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CriticalCareNurseF E B R U A R Y 2 0 1 5 • V O L U M E 3 5 N U M B E R 1
T h e j o u r n a l f o r h i g h a c u i t y , p r o g r e s s i v e , a n d c r i t i c a l c a r e n u r s i n g
Stroke VolumeOptimization
Therapeutic Hypothermia
Delirium
Exertional Heat Stroke
ECMO for Pediatric
Cardiac Arrest
CNE
CNE
CNE
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CriticalCareNurseT h e j o u r n a l f o r h i g h a c u i t y , p r o g r e s s i v e , a n d c r i t i c a l c a r e n u r s i n g
President TERI LYNN KISS, RN, MS, MSSW, CNML, CMSRN
President-elect KAREN MCQUILLAN, RN, MS, CNS-BC, CCRN, CNRN, FAAN
Secretary LISA RIGGS, RN, MSN, ACNS-BC, CCRN
Treasurer CHRISTINE S. SCHULMAN, RN, MS, CNS, CCRN
Directors LINDA M. BAY, RN, MSN, ACNS-BC, CCRN, PCCN
MEGAN BRUNSON, RN, MSN, CNL, CCRN-CSC
NANCY FREELAND, RN, MSN, CCRN
KAREN L. JOHNSON, RN, PhD
DEBORAH KLEIN, RN, MSN, ACNS-BC, CCRN, CHFN, FAHA
PAULA S. MCCAULEY, DNP, APRN, ACNP-BC, CNE
RIZA V. MAURICIO, RN, PhD, CCRN, CPNP-PC/AC
KATHLEEN K. PEAVY, RN, MS, CCRN, CNS-BC
MARY ZELLINGER, RN, MN, ANP, CCRN-CSC, CCNS
Chief Executive Officer DANA WOODS
Editorial OfficeAmerican Association of Critical-Care Nurses101 Columbia, Aliso Viejo, CA 92656 (800) 899-1712, (949) 362-2000Website: www.ccnonline.org e-mail: [email protected]
Publishing Manager MICHAEL MUSCATManaging Editor REBECKA WULFArt and Production Director LeROY HINTONCopy Editors BARBARA HALLIBURTON, PhD
KATIE SPILLER, MS
Book Review Editor MARY PAT AUST, RN, MS
Graphic Artist MATTHEW EDENSSenior Publishing Associate SAM MARSELLAPeer-Review Coordinator DENISE GOTTWALD
Advertising Sales OfficeSLACK Incorporated6900 Grove Road, Thorofare, NJ 08086(800) 257-8290, (856) 848-1000
National Account Manager KATHY HUNTLEYRecruitment Manager MONIQUE McLAUGHLIN Administrator ASHLEY SEIGFRIED
Editor JoAnn Grif Alspach, RN, MSN, EdD
THOMAS AHRENS, RN, PhD, CCRN, CS
Clinical Specialist/Research Scientist, Nursing DepartmentBarnes-Jewish Hospital, St Louis, Missouri
SUSAN D. BELL, RN, MS, CNRN, CNP
Nurse Practitioner, NeurosurgeryOhio State University Medical Center, Columbus, Ohio
SUZETTE CARDIN, RN, DNSc, CNAA
Adjunct Assistant Professor, Graduate Nursing Administration Program UCLA School of Nursing, Los Angeles, California
BONNIE M. JENNINGS, RN, PhD, FAAN
Professor, Nell Hodgson Woodruff School of NursingEmory University, Atlanta, Georgia
SUSAN G. TREVITHICK, RN, MS, CNA
Clinical Support Manager, Specialty Care CenterSalt Lake City Veterans Administration Medical Center, Utah
GLENNA TRAIGER, RN, MSN, CCRN
Clinical Nurse Specialist, Pulmonary Arterial Hypertension Program Greater LA VA Medical Center, Los Angeles, California
Editorial Board
Contributing EditorsAdvanced PracticeANDREA M. KLINE-TILFORD, CPNP-AC/PC, CCRN, FCCM
Bariatric CareBRENDA K. HIXON VERMILLION, RN, DNP, ACNS-BC,
ANP-BC, CCRN
Basic and Advanced Life SupportPRISCILLA K. GAZARIAN, RN, PhD
Cardiovascular SurgeryKRISTINE CHAISSON, RN, BSN, MS, CCRN
Certification Test PrepCAROL RAUEN
Cochrane Review SummaryDAPHNE STANNARD, RN, PhD, CCRN, CCNS
Complementary TherapiesDEBRA KRAMLICH, RN, MSN, CCRN
Critical Care AppsCLAIRE CURRAN, RN, MSN, CCRN
Cultural DiversityMAJELLA S. VENTURANZA, RN, MA, CCRN
ECGs and PacemakersJANE N. MILLER, RN, DNP, CCRN, CCNS
Emergency DepartmentDOROTHY DUNCAN, RN, DNP, ACNP-BC, CCRN, CEN
End-of-Life CareKATHLEEN OUIMET PERRIN, RN, PhD, CCRN
Evidence-Based PracticeMARCIA BELCHER, RN, MSN, BBA, CCRN-CSC, CCNS
Family-Centered CarePATRICIA BROWN, DNP, APN, CNS, CCRN
Gastrointestinal DisordersROSEMARY K. LEE, DNP, ARNP, ACNP-BC, CCNS, CCRN
Geriatric CareSONYA R. HARDIN, RN, PhD, CCRN, ACNS-BC, NP-C
Healthy Work EnvironmentsVIRGINIA C. HALL, BSN, CCRN
Heart FailureKAREN L. COOPER, RN, MSN, CCRN, CNS
Management/AdministrationMARIA CHRISTABELLE CASTRO, RN, MSHA, CCRN, NE-BC
Military Critical Care Nursing: Air ForceBENJAMIN SCHULTZE, RN, ACNP-BC, MEd, MSN
Military Critical Care Nursing: ArmyLINDA A. VALDIRI, COL, ANC, USA, RN, MS, CCNS
Military Critical Care Nursing: NavyCARL GOFORTH, RN, MSN, CCRN
Neonatal CareRACHEL A. JOSEPH, PhD, CCRN
Neurology/NeurosurgeryGLENN CARLSON, MSN, ACNP-BC, CCRN
NutritionCOLLEEN O’LEARY-KELLEY, RN, PhD, CNE
Pain ManagementDIANE GLOWACKI, RN, MSN, CNS, CNRN-CMC
Patient Education and Discharge PlanningFLORENCE M. SIMMONS, RN, MSN, CCRN
Patient SafetyELIZABETH MATTOX, RN, MSN, ARNP
Patient TransportMELISSA RACH, RN, BSN, CCRN, CMC
Pediatric CareJODI E. MULLEN, RN-BC, MS, CCRN, CCNS
PharmacologyKELLY THOMPSON-BRAZILL, RN, MSN, ACNP, CCRN-CSC, FCCM
Postanesthesia RecoveryTITO D. TUBOG, RN-BC, CRNA, APRN, CCRN-CSC-CMC, CEN
PreceptingLIZ ROGAN, RN, EdD-c, CNE
Progressive CareMARGARET M. ECKLUND, RN, MS, CCRN, ACNP-BC
Pulmonary CareDEBRA SIELA, RN, PhD, ACNS-BC, CCNS, CCRN, CNE, RRT
Quality Improvement ReportsJULIE M. STAUSMIRE, RN, MSN, ACNS-BC
Rural SettingsCHARLENE A. WINTERS, PhD, APRN, ACNS-BC
SimulationKATE MOORE, RN, DNP, CCRN, CEN, AGACNP-BC, AGPCNP-BC
Staff DevelopmentLESLIE SWADENER-CULPEPPER, APRN-CNS, MSN,
CCRN, CCNS
Tele-ICUPAT JUAREZ, APN, CCRN, CCNS
ToxicologyDANA BARTLETT, RN, MSN, MA, CSPI
TraumaMICHAEL W. DAY, RN, MSN, CCRN
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 1
CriticalCareNurseT h e j o u r n a l f o r h i g h a c u i t y , p r o g r e s s i v e , a n d c r i t i c a l c a r e n u r s i n g
F E B R U A R Y 2 0 1 5 • V O L U M E 3 5 N U M B E R 1
Stroke Volume Optimization:
The New Hemodynamic Algorithm
CNE
Alexander Johnson and Thomas Ahrens
Page 11
CRITICAL CARE NURSE (ISSN 0279-5442, eISSN 1940-8250) is published bimonthly (February, April, June, August, October, December) by theAmerican Association of Critical-Care Nurses (AACN), 101 Columbia, Aliso Viejo, CA 92656. Telephone: (949) 362-2000. Fax: (949) 362-2049.E-mail: [email protected]. Copyright 2015 by AACN. All rights reserved. CRITICAL CARE NURSE is an official publication of AACN. No part of thispublication may be reproduced or transmitted in any form or by any means, electronic or mechanical, in cluding photocopying, recording orby any information storage retrieval system without permission of AACN. For all permission requests, please contact the Copyright ClearanceCenter, Customer Service, 222 Rosewood Drive, Danvers, MA 01923. (978) 750-8400. The statements and opinions contained herein aresolely those of individual contributors and not of the editor or AACN. The editor and AACN assume that articles emanating from a particularinstitution are submitted with the approval of the requisite authority, including all matters pertaining to human studies and patient privacyrequirements. Advertisements in this journal are not a warranty, endorsement, or approval of the products by the editor or AACN, who dis-claim all responsibility for any injury to persons or property resulting from any ideas or products referred to in articles or advertisements.Individual subscriptions (print and online): US, $39; outside of US, US$60. Student rates: US, $25; outside of US, $38. Institutional rates (printand online): US, $412; outside of US, US$504. Institutional rates (print only): US, $294; outside of US, US$387. Institutional rates (online only):US, $276; outside of US, US$276. Single copies and back issues: US, $40; outside of US, US$50. Fax requests to CCN Back Issues at (949) 362-2049 or write to CCN, 101 Columbia, Aliso Viejo, CA 92656, or phone (800) 899-1712; (949) 362-2050, ext 532. Prices on single copies orbulk reprints of articles are available on request from AACN at (949) 362-2050, ext 532.
Printed in the USA. Periodicals postage paid at Laguna Beach, Calif, and additional mailing offices. Postmaster: Send address changes to CRITICAL CARENURSE, 101 Columbia, Aliso Viejo, CA 92656. Allow 4 to 6 weeks for change to take effect. For subscription questions please call toll-free: AACN mem-bers, (800) 899-2226 or (949) 362-2000; nonmembers, (800) 336-6348 or (818) 487-2075.
The name and title CRITICAL CARE NURSE are protected through a trademark registration in the US Patent Office. CRITICAL CARE NURSE is indexed in Cumu-lative Index to Nursing & Allied Health Literature (CINAHL), Medline, and RNdex Top 100 and is a participant in the UMI Article Clearinghouse andNurseSearch, as well as Nursing Abstracts.
2 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
CCN FAST FACTSUse of a Nursing Checklist to Facilitate
Implementation of TherapeuticHypothermia After Cardiac Arrest
Page 38
Nonpharmacological Interventions toPrevent Delirium: An Evidence-Based
Systematic ReviewPage 50
Cover illustration by Kimberly Martens
OnlineNOWAbstracts of articles available exclusively
online at www.ccnonline.org
Page 10
Methods Used by Critical CareNurses to Verify Feeding TubePlacement in Clinical Practice
Annette M. Bourgault, Janie Heath, Vallire Hooper, Mary Lou Sole, and Elizabeth G. NeSmith
Page e1
FEATURESUse of a Nursing Checklist to
Facilitate Implementation of Therapeutic Hypothermia After
Cardiac ArrestKathleen Ryan Avery, Molly O’Brien, Carol Daddio Pierce,
and Priscilla K. Gazarian
Page 29
Nonpharmacological Interventionsto Prevent Delirium: An Evidence-
Based Systematic ReviewRyan M. Rivosecchi, Pamela L. Smithburger, Susan Svec,
Shauna Campbell, and Sandra L. Kane-Gill
Page 39
MILITARY CRITICAL CARE NURSING: NAVY
Exertional Heat Stroke in Navy andMarine Personnel: A Hot Topic
Carl W. Goforth and Josh B. Kazman
Page 52
PEDIATRIC CAREExtracorporeal Membrane Oxygenation
for Pediatric Cardiac ArrestJennie Ryan
Page 60
EDITORIALImproving Cardiac Arrest ResuscitationOutcomes: A Valentine Worth Sending
JoAnn Grif Alspach, Editor
Page 6
CERTIFICATION TEST PREPCelebrate and Be Proud!
Carol Rauen, Kirtley Ceballos, and Steve Risch
Page 71
ASK THE EXPERTSComparing Blood Pressure Measures:
Does One Measurement Equal Another?Barbara McLean
Page 75
IN OUR UNITImplementation of Early Exercise and
Progressive Mobility: Steps to SuccessMelody R. Campbell, Julie Fisher,
Lyndsey Anderson, and Erin Kreppel
Page 82
COLUMNS
DEPARTMENTS
ALSO IN THIS ISSUE
CNE
CNE
4 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
ContributorsPage 5
CorrectionsPage 9
Book ReviewsPage 89
Education DirectoryPage 91
I Am a Critical Care NursePage 92
Venous cannula
Rightatrium
Leftatrium
Rightventricle
Leftventricle
Aortic cannula
Aorta
Superior venacava
Page 60
Normalsystole
Normaldiastole
Constantmean
Overestimatedsystole
UnderestimateddiastoleComparing normal
with underdamped
Page 75 Page 89
pharmacy and therapeutics at the University of
Pittsburgh School of Pharmacy.
Coauthor of Exertional Heat Stroke in Navy
and Marine Personnel, Josh Kazman is a
research associate with the Consortium for
Health and Military Performance at Uniformed
Services University of the Health Sciences.
Elizabeth G. NeSmith, coauthor of Methods
Used to Verify Feeding Tube Placement, is an
associate professor and chair of the Depart-
ment of Physiological and Technological
Nursing at Georgia Regents University, College
of Nursing, in Augusta.
Molly O’Brien, coauthor of Implementation
of Therapeutic Hypothermia After Cardiac
Arrest, is the research coordinator in the car-
diac ICU at Shapiro Cardiovascular Center at
Brigham and Women’s Hospital.
Coauthor of Use of a Nursing Checklist to
Facilitate Implementation of Therapeutic
Hypothermia After Cardiac Arrest, Carol
Daddio Pierce is the clinical educator in the
medical ICU at Brigham and Women’s Hospital.
Ryan M. Rivosecchi, coauthor of Nonphar-
macological Interventions to Prevent Delirium,
is a pharmacy resident in critical care at the
University of Pittsburgh Medical Center, Pres-
byterian Hospital.
Author of Extracorporeal Membrane Oxygena-
tion for Pediatric Cardiac Arrest, Jennie Ryan
in a nurse practitioner in the ICU at Nemours
Cardiac Center, Wilmington, Delaware.
Coauthor of Nonpharmacological Inter-
ventions to Prevent Delirium, Pamela L.
Smithburger is an assistant professor of
pharmacy and therapeutics, University of
Pittsburgh School of Pharmacy.
Mary Lou Sole, coauthor of Methods Used to
Verify Feeding Tube Placement, is the Orlando
Health Distinguished Professor at University of
Central Florida, College of Nursing.
Coauthor of Nonpharmacological Interventions to
Prevent Delirium, Susan Svec is the clinical director of
the medical ICU, University of Pittsburgh Medical Cen-
ter, Presbyterian Hospital.CCN
Coauthor of Stroke Volume
Optimization, Thomas Ahrens
is a research scientist, Barnes-
Jewish Hospital, St Louis, Missouri.
Kathleen Ryan Avery, coauthor of
Implementation of Therapeutic
Hypothermia After Cardiac Arrest, is
the clinical educator for the cardiac ICU
at Brigham and Women’s Hospital,
Boston, Massachusetts.
Coauthor of Methods Used to Verify
Feeding Tube Placement, Annette M.
Bourgault is an assistant professor at
Georgia Regents University, College of
Nursing, in Augusta.
Shauna Campbell, coauthor of Non-
pharmacological Interventions to Prevent
Delirium, is the nursing director of the
medical ICU at the University of Pittsburgh
Medical Center, Presbyterian Hospital.
Priscilla K. Gazarian, coauthor of
Implementation of Therapeutic Hypother-
mia After Cardiac Arrest, is the nursing
program director for resuscitative clinical
practice at Brigham and Women’s Hospital.
Coauthor of Exertional Heat Stroke in
Navy and Marine Personnel, Carl Goforth
is the clinical subject matter expert for the
Marine Corps Combat Development
Command located in Quantico, Virginia.
Janie Heath, coauthor of Methods to
Verify Feeding Tube Placement, is dean of
the College of Nursing at University of
Kentucky in Lexington.
Coauthor of Methods Used to Verify
Feeding Tube Placement, Vallire Hooper
is the manager of nursing research at Mis-
sion Hospital in Asheville, North Carolina.
Coauthor of Stroke Volume Optimiza-
tion, Alexander Johnson is a clinical nurse
specialist, Central DuPage Hospital–North-
western Medicine, Winfield, Illinois.
Sandra L. Kane-Gill, coauthor of Non-
pharmacological Interventions to Prevent
Delirium, is an associate professor of
Contributors
KANE-GILL
AHRENS KAZMAN
AVERY
BOURGAULT
GAZARIAN
GOFORTH
HEATH
HOOPER
JOHNSON SVEC
SOLE
SMITHBURGER
RIVOSECCHI
PIERCE
NeSMITH
RYAN
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 5
Improving Cardiac Arrest ResuscitationOutcomes: A Valentine Worth Sending
Survival Rates Remain DishearteningEach year nearly 568 500 sudden cardiac
arrests occur in the United States. Of these,
approximately 359400 (63%) are out-of-hospital
cardiac arrests (OHCAs) and 209 000 (37%)
are in-hospital cardiac arrests.1 Of the nearly
360 000 cardiac arrests that happen outside
hospitals, 88% occur in the home.3 If effective
cardiopulmonary resuscitation (CPR) can be
delivered immediately after cardiac arrest, the
victim’s probability of survival is doubled or
tripled.3 However, despite decades of research,
the instruction of millions of laypersons and
professional heath care providers, countless
public service announcements, and national
programs provided by organizations such as the
AHA and American Red Cross, only 32%3 to 40%
of OHCAs are responded to with bystander CPR.1
Among all OHCA victims, only 8%3 to 9.5%
survive to hospital discharge.4
A few distinctions between out-of-hospital
and in-hospital patient populations are worth
noting. An OHCA can be defined as “cessation
of cardiac mechanical activity that occurs out-
side of the hospital setting and is confirmed by
the absence of signs of circulation.”5 Although
it may develop from a variety of noncardiac
etiologies such as trauma or drug overdose, a
substantial majority of OHCAs is attributable
to cardiac causes.5
An in-hospital cardiac arrest occurs in a
hospital and typically includes resuscitation
efforts such as defibrillation, chest compressions,
or both.6 As admission to a hospital becomes
Editorial
In the United States, February 14 is Valentine’s
Day, when expressions of love are sent to
those we care about most. The American
Heart Association’s (AHA’s) designation of
February as American Heart Month reminds
us that we could extend those sentiments
beyond a single day by demonstrating how to
protect our loved ones from cardiac disease,
still ranked as the nation’s number 1 cause of
death.1 In recognition of the burden that heart
disease represents in our patient populations,
this issue of Critical Care Nurse is devoted to
the topic of cardiac arrest, a challenging condi-
tion that teeters its victims between life and
death. One of the particularly vexing and long-
standing attributes of this disorder is our lim-
ited success in prevailing against its potentially
ominous outcomes.
Definition of Cardiac Arrest Cardiac arrest is defined as the abrupt loss
of cardiac function in someone who may or
may not have a diagnosis of heart disease. It
arises instantaneously, often without preceding
symptoms,2 making it virtually impossible to
anticipate and challenging to correctly recog-
nize, manage, and reverse before irreversible
and fatal consequences ensue. Although it
may arise from a number of distinct etiologies,
most cases of cardiac arrest are associated with
development of a cardiac arrhythmia, typically
ventricular fibrillation.1
JoAnn Grif Alspach
©2015 American Association of Critical-Care Nursesdoi: http://dx.doi.org/10.4037/ccn2015167
6 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
more selective based on need for services, in-hospital
patients who experience cardiac arrest are likely to be
sicker and have more clinically significant comorbidities
compared to their neighbors living at home. As a result,
despite the greater availability of health care profession-
als to provide CPR, in-patient cardiac arrest victims may
have more clinically advanced systemic disorders that
could limit their ability to benefit from CPR.
During the 1990s, reports of survival to discharge
rates following in-hospital cardiac arrest and CPR ranged
from 7% to 26%.7,8 In the United States, the most recent
in-hospital cardiac arrest statistics from the Resuscitation
Outcomes Consortium Cardiac Epistry and Get With The
Guidelines-Resuscitation data show an overall survival rate
to hospital discharge for adult victims of cardiac arrest of
23.9%.4 For patients in the United Kingdom, the
National Cardiac Arrest Audit found an overall survival
to hospital discharge rate of 18.4%.9 As in the United
States, higher rates of survival to hospital discharge are
found in patients with shockable rhythms (ventricular
fibrillation or pulseless ventricular tachycardia) compared
to those with nonshockable rhythms (asystole or pulse-
less electrical activity).9
For patients over 70 years, the chance of survival to
hospital discharge following in-hospital CPR ranges at a
lower plateau between 11.6% and 18.7%, with declining
survival associated with increasing age.10 Although some
improvements in cardiac arrest survival can be noted,
the body of research in this area suggests that significant
improvements have not yet been realized. Until those
advances can be identified to influence clinical practice,
critical care nurses might consider making their contribu-
tions by pursuing alternative efforts that represent poten-
tial inroads toward improving cardiac arrest outcomes.
Critical Care Nurses Can Contribute toImproved Outcomes
Recent research suggests that 2 of the inroads that
may lead to better cardiac arrest resuscitation outcomes
include doing more and doing less than we are currently
doing in managing this condition.
Doing MoreThe Doing More strategy recognizes that 92% of the
360 000 Americans who suffer an OHCA each year will
die, that a majority of those deaths might have been
avoided if timely and effective interventions known
to improve survival from cardiac arrest had been
provided, and that one of those timely and effective
interventions is provision of bystander CPR. As a recent
AHA Science Advisory explained,11 OHCA survival
rates have increased in communities where bystander
CPR participation was expanded. These are especially
important initiatives in poor, non–English-speaking,
Black, and Latino neighborhoods, where few know
how to provide bystander CPR. Instructional and
recruitment programs to inform, involve, and teach
CPR to residents of these neighborhoods could launch
lifesaving efforts with immediate impact.
Doing LessAs in many aspects of life, doing less at times yields
more. Two approaches to doing less with resuscitation
for cardiac arrest suggested by recent literature include
focusing on immediate and effective provision of Basic
Life Support (BLS) rather than delaying or interrupt-
ing that to provide Advanced Life Support (ALS) and
teaching laypersons to perform chest compressions-only
CPR rather than standard CPR that includes intermit-
tent breaths.
An intriguing study reported by Sanghavi and
colleagues12 at Harvard University used a nationally
representative sample of Medicare beneficiaries from
nonrural areas of the United States that included 1643
patients managed with BLS and 31 292 managed with
ALS. The researchers concluded that OHCA patients
had higher survival at discharge (BLS 13.1% vs ALS
9.2%, 95% CI, 2.3-5.7), higher survival at 90 days (BLS
8.0% vs 5.4% for ALS; 95% CI, 1.2-4.0), and lower rates
of poor neurological functioning (BLS 21.8% vs ALS
44.8%; 95% CI, 18.6-27.4) when they received only BLS
rather than ALS from emergency medical services.
These results need to be interpreted with caution (the
ALS was provided by emergency medical services staff
rather than hospital physicians or nurses, the timing
of initiation of either form of resuscitation is not
included in data, data rely on billing record rather than
clinical documentation of measures provided, and ALS
is usually preceded by BLS, so it is not clear how those
influences were distinguished to capture measurement
of ALS alone, some patients require the medications,
equipment, and therapies reserved for ALS) to ensure
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 7
that the methodology and analysis are sufficiently vetted
and not found wanting. Despite that customary admo-
nition, the results are thought-provoking and worthy
of further consideration and repeat testing.
A second avenue of Doing Less involves the use of
compression-only CPR in place of traditional CPR
procedures that include intermittent use of mouth-to-
mouth breaths. Since the AHA updated its CPR guide-
lines in 2005 to recommend use of chest-compression
CPR by untrained rescuers as well as in dispatcher-
assisted CPR in an effort to expand the quality and
provision of bystander CPR, a number of reports13,14
have heralded support for compression-only CPR
(hands-only) as an effective form of CPR with survival
outcomes comparable to those of conventional CPR.
Additional studies15 have noted better neurological
outcomes at 1 month with hands-only CPR compared
to conventional CPR when hands-only CPR is com-
bined with public-access automated external defib-
rillators. More recently, a meta-analysis of studies
including more than 92 000 adult patients with OHCAs
further supported the efficacy of hands-only CPR in
producing survival rates comparable to those achieved
with conventional CPR for patients whose arrest was
of cardiac etiology.16
Because nearly 90% of cardiac arrests occur within
the home, most of us will encounter victims who are
family members, close friends, or neighbors, as stated
by the AHA mantra: “The life you save with CPR is
mostly likely to be someone you love.”3 For those of us
already thoroughly trained and certified to provide
lifesaving resuscitation, our ability to respond to that
emergency is automatic, immediate, and competent.
In addition, critical care nurses could join with colleagues
in home health, school and community health, and
numerous other surrounding organizations to instruct
and empower residents in our neighborhoods, schools,
communities, places of worship or recreation, towns
or cities to serve their own loved ones as bystander-CPR
providers. Sending them a text, e-mail, tweet, card, or
brochure that reads “If you love someone, learn how
to save their life” and invites them to see the brief video
of how easily and quickly they can learn hands-only
CPR17 can represent the best valentine’s gift they ever
received. Critical care nurses can do that. We know
you can.
Join the ConversationIf you can suggest other strategies for improving
patient outcomes following cardiac arrest, please send
them to us at [email protected] so Critical Care Nurse can
share these with our readers. CCN
JoAnn Grif Alspach, RN, MSN, EdD
Editor, Critical Care Nurse
References1. Go AS, Mozaffarian D, Roger VL, et al; for the American Heart Associa-
tion Statistics Committee and Stroke Statistics Subcommittee. Executivesummary: heart disease and stroke statistics—2014 update: a reportfrom the American Heart Association. Circulation. 2014;129:399-410.
2. American Heart Association. Cardiac Arrest. http://www.heart.org/HEARTORG/Conditions/More/CardiacArrest/About-Cardiac-Arrest_UCM_307905_Article.jsp. Accessed December 2, 2014.
3. American Heart Association. CPR Statistics. Last updated September 3,2014. http://www.heart.org/HEARTORG/CPRAndECC/WhatisCPR/CPRFactsandStats/CPR-Statistics_UCM_307542_Article.jsp. AccessedDecember 2, 2014.
4. American Heart Association. Cardiac Arrest Statistics. Last updated Sep-tember 11, 2014. http://www.heart.org/HEARTORG/General/Cardiac-Arrest-Statistics_UCM_448311_Article.jsp. Accessed December 2, 2014.
5. McNally B, Robb R, Mehta M, et al; Centers for Disease Control andPrevention. Out-of-hospital cardiac arrest surveillance—Cardiac ArrestRegistry to Enhance Survival (CARES), United States, October 1, 2005-December 31, 2010. MMWR Surveill Summ. 2011;60(8):1-19.
6. Morrison LJ, Neumar RW, Zimmerman JL, et al; for the American HeartAssociation Emergency Cardiovascular Care Committee, Council onCardiopulmonary, Critical Care, Perioperative and Resuscitation,Council on Cardiovascular Nursing, Council on Clinical Cardiology,and Council on Peripheral Vascular Disease. Strategies for improvingsurvival after in-hospital cardiac arrest in the United States: 2013 con-sensus recommendations: a consensus statement from the AmericanHeart Association. Circulation. 2013;127:1538-1563.
7. Ebell MH, Becker LA, Barry HC, et al. Survival after in-hospital cardiopul-monary resuscitation: a meta-analysis. J Gen Intern Med. 1998;13:805-816.
8. Tresch D, Heudebert G, Kutty K, et al. Cardiopulmonary resuscitationin elderly patients hospitalized in the 1990s: a favorable outcome. J AmGeriatr Soc. 1994;42:137-141.
9. Nolan JP, Soar J, Smith GB, et al. National Cardiac Arrest Audit. Incidenceand outcome of in-hospital cardiac arrest in the United Kingdom NationalCardiac Arrest Audit. Resuscitation. 2014;85(8):987-992.
10. van Gijn MS, Frijns D, van de Glind EM, C van Munster B, HamakerME. The chance of survival and the functional outcome after in-hospitalcardiopulmonary resuscitation in older people: a systematic review. AgeAgeing. 2014;43(4):456-463.
11. Sasson C, Meischke H, Abella BS, et al; for the American Heart Associa-tion Council on Quality of Care and Outcomes Research, EmergencyCardiovascular Care Committee, Council on Cardiopulmonary, CriticalCare, Perioperative and Resuscitation, Council on Clinical Cardiology,and Council on Cardiovascular Surgery and Anesthesia. Increasing car-diopulmonary resuscitation provision in communities with lowbystander cardiopulmonary resuscitation rates: a science advisory fromthe American Heart Association for healthcare providers, policymakers,public health departments, and community leaders. Circulation.2013;127:1342-1350.
12. Sanghavi P, Jena AB, Newhouse JP, Zaslavsky AM. Outcomes after out-of-hospital cardiac arrest treated by basic vs advanced life support. JAMAIntern Med. In press. http://archinte.jamanetwork.com /journal.aspx.Accessed December 2, 2014.
13. Bohm K, Rosenqvist M, Herlitz J, Hollenberg J, Svensson L. Survivalis similar after standard treatment and chest compression only inout-of-hospital bystander cardiopulmonary resuscitation. Circulation.2007;116(25):2908-2912.
8 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
14. Iwami T, Kawamura T, Hiraide A, et al. Effectiveness of bystander-initi-ated cardiac-only resuscitation for patients with out-of-hospital cardiacarrest. Circulation. 2007;116(25):2900-2907.
15. Iwami T, Kitamura T, Kawamura T, et al. Chest-compression-only car-diopulmonary resuscitation for out-of-hospital cardiac arrest withpublic-access defibrillation. Circulation 2012;126:2844-2851. http://circ.ahajournals.org/content/126/24/2844.full?sid=f1d8c729-f6cc-4041-8d91-817fde1c97a0. Accessed December 2, 2014.
16. Yao L, Wang P, Zhou L, et al. Compression-only cardiopulmonary resus-citation vs standard cardiopulmonary resuscitation: an updated meta-analysis of observational studies. Am J Emerg Med. 2014;32(6):517-523.
17. American Heart Association. Two Steps to Staying Alive With Hands-Only CPR. http://www.heart.org/HEARTORG/CPRAndECC/HandsOnlyCPR/Hands-Only-CPR_UCM_440559_SubHomePage.jsp.Accessed December 2, 2014.
Corrections
In the December article by Chaisson et al, “Improving Patients’ Readiness forCoronary Artery Bypass Graft Surgery”(Crit Care Nurse. 2014;34[6]:29-38),the e-mail address listed for the cor-responding author (Kristine Chaisson)was invalid. The correct e-mail [email protected].
©2015 American Association of Critical-Care Nurses doi:http://dx.doi.org/10.4037/ccn2015359
TemporalScanner™
The Exergen TemporalScanner Temporal Artery Thermometer
More than 50 published studies - supporting accuracy from preemies to geriatrics in all areas of care.
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10 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
OnlineNOW
Methods Used by Critical Care Nurese to Verify FeedingTube Placement in Clinical Practice
ANNETTE M. BOURGAULT, RN, PhD, CNL
JANIE HEATH, PhD, APRN-BC
VALLIRE HOOPER, RN, PhD, CPAN
MARY LOU SOLE, RN, PhD, CCNS
ELIZABETH G. NeSMITH, PhD, APRN-BC
BACKGROUND The American Association of Critical-Care Nurses practice alert on verification of feeding tube placement makes
evidence-based practice recommendations to guide nursing management of adult patients with blindly inserted feeding tubes.
Many bedside verification methods do not allow detection of improper positioning of a feeding tube within the gastrointestinal
tract, thereby increasing aspiration risk.
OBJECTIVES To determine how the expected practices from the American Association of Critical-Care Nurses practice alert were
implemented by critical care nurses.
METHODS This study was part of a larger national, online survey that was completed by 370 critical care nurses. Descriptive
statistics were used to analyze the data.
RESULTS Seventy-eight percent of nurses used a variety of methods to verify initial placement of feeding tubes, although 14% were
unaware that tube position should be confirmed every 4 hours. Despite the inaccuracy of auscultation methods, only 12% of
nurses avoided this practice all of the time.
CONCLUSIONS Implementation of expected clinical practices from this guideline varied. Nurses are encouraged to implement
expected practices from this evidence-based, peer reviewed practice alert to minimize risk for patient harm. (Critical Care Nurse.
2015;35[1]:e1-e7)
©2015 American Association of Critical-Care Nurses http://dx.doi.org/10.4037/ccn2015984
Critical Care Nurse offers an online publication process that provides current, relevant and useful information about the bedsidecare of critically and acutely ill patients in the most timely and efficient manner possible. The abstracts below represent full-textarticles available exclusively on the Critical Care Nurse website, www.ccnonline.org. These OnlineNOW articles are fully peerreviewed, edited, formatted, and citable. Reprints of the full-text articles are available by calling (800) 899-1712 or (949) 362-2050(ext 532) or by e-mailing [email protected].
Do you have a QR scanner app on youriPhone or Android? Scan this QR code withyour phone to access this article instantly.
Nurses commonly experience scenarios where hemodynamic monitoring is focused
on hypovolemia (see case study) in clinical practice. In this article, we provide
an overview of the use of stroke volume (the amount of blood ejected from the left
ventricle with each beat) for hemodynamic management of critically ill patients.
We also discuss the limitations of conventional assessment parameters, methods
of measuring stroke volume, hemodynamic variables that influence stroke volume, the stroke volume
optimization (SVO) replacement algorithm, supporting literature, and nursing considerations.
Much of the supporting literature (mostly studies in perioperative patients) on stroke volume as a
primary hemodynamic monitoring parameter focuses on the treatment of hypovolemia, as in the case
Stroke Volume Optimization: The NewHemodynamic AlgorithmALEXANDER JOHNSON, RN, MSN, ACNP-BC, CCNS, CCRN
THOMAS AHRENS, RN, PhD
This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article,which tests your knowledge of the following objectives:
1. Discuss the use of stroke volume optimization in a hypovolemic patient2. Define corrected flow time, peak velocity, stroke distance, and stroke index3. State various methods used to obtain blood flow measurement
©2015 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2015427
CNE Continuing Nursing Education
Cover
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 11
Critical care practices have evolved to rely more on physical assessments for monitoring cardiac output
and evaluating fluid volume status because these assessments are less invasive and more convenient to
use than is a pulmonary artery catheter. Despite this trend, level of consciousness, central venous pressure,
urine output, heart rate, and blood pressure remain assessments that are slow to be changed, potentially
misleading, and often manifested as late indications of decreased cardiac output. The hemodynamic
optimization strategy called stroke volume optimization might provide a proactive guide for clinicians to
optimize a patient’s status before late indications of a worsening condition occur. The evidence supporting
use of the stroke volume optimization algorithm to treat hypovolemia is increasing. Many of the cardiac
output monitor technologies today measure stroke volume, as well as the parameters that comprise stroke
volume: preload, afterload, and contractility. (Critical Care Nurse. 2015;35[1]:11-28)
study. In the following section, we review the clinical
importance of hypovolemia that may go undetected
(occult hypovolemia) when conventional assessment
techniques are used.
Importance of Occult HypovolemiaTo illustrate the nature of subclinical or occult
hypovolemia and to test the sensitivity of gastrointestinal
tonometry for detecting such hypovolemia, Hamilton-
Davies et al1 conducted a study on 6 healthy volunteers
in the critical care unit at University College of London
Hospitals, London, England. Each of the volunteers had
a mean of 25% (21%-31%) of their overall blood volume
removed during a 1-hour period, and the volunteers’
response was measured. Variables such as heart rate,
blood pressure, serum levels of lactate, and stroke volume
were measured every 30 minutes throughout the study.
After 90 minutes, decreases in gut intramucosal pH were
observed, as well as marked decreases in stroke volume,
by a mean of 16.5 mL (P < .01). Despite this compromised
flow, no clinically significant or consistent postinterven-
tional changes were noted in serum levels of lactate,
arterial blood pressure, heart rate, or arterial blood gases
according to serial measurements obtained throughout
the study period. Retransfusion was started after 90 min-
utes. The results of this study1 may provide insight into
the reliability of routinely used measurements such as
heart rate and systolic blood pressure as volume deple-
tion progressed in these volunteers.
Hypovolemia (defined as inadequate left ventricular
filling volumes)2 affects the cardiovascular system in a
characteristic sequence of events as the hypovolemia
worsens3-6 (Table 1). First, stroke volume decreases
Alexander Johnson is a clinical nurse specialist, Central DuPage Hospital, Cadence Health System–Northwestern Medicine, Winfield, Illinois.
Thomas Ahrens is a research scientist, Barnes-Jewish Hospital, St Louis, Missouri.
Corresponding author: Alexander Johnson, 4007 Schillinger Dr, Naperville, IL 60564 (e-mail: [email protected]).
To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].
Authors
12 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Acritical care nurse cares for a patient who had
a 3-vessel coronary artery bypass graft approx-
imately 30 minutes earlier. No indications of
bleeding are present, and both cardiac output and urine
output are within the reference limits. However, the
patient’s systolic arterial blood pressure has decreased
to 77 mm Hg 3 times in the past 20 minutes. Because
the decrease seems to respond to fluid administration,
the nurse begins administering a fourth bottle of 5%
albumin via the rapid infuser in accordance with the sur-
geon’s standing orders. Even though the patient’s central
venous pressure has remained at 3-4 mm Hg since the
patient arrived from surgery, the nurse notes that the
stroke volume has remained between 75 and 80 mL
since the second bottle of albumin. On the basis of the
patient’s hemodynamic profile and this recent
sequence of events, the nurse calls the surgeon to inquire
about an order to administer a vasoactive agent. In
this case, decreased stroke volume response to fluid
suggests adequate volume expansion even though low
central venous pressure values suggest hypovolemia.
CASE STUDY
Blood loss, %
Heart rate, beats per minute
Blood pressure, mm Hg
Pulse pressure
Respiratory rate, breaths per minute
Mental status
Class 4
> 40%
> 140
Decreased
Decreased
> 35
Confused, lethargic
Class 3
30%-40%
> 120
Decreased
Decreased
30-40
Anxious, confused
Class 2
15%-30%
> 100
Normal
Decreased
20-30
Mildly anxious
Class 1
< 15%
< 100
Normal
Normal or increased
14-20
Slightly anxious
Table 1 Classes of shock by Advanced Trauma Life Support (ATLS) designationa
a Reprinted from American College of Surgeons,5 with permission.
because of decreased overall circulating volume (class 1).
Next, heart rate increases and vasoconstriction occurs to
maintain blood pressure and cardiac output (the volume
of blood pumped by the heart per minute)7 (class 2). A
surge of endogenous catecholamines helps shunt blood
from the periphery and splanchnic circulation to the brain
and great vessels to preserve vital organs. Once compen-
satory mechanisms are exhausted, cellular respiration
begins to change from aerobic metabolism to anaerobic
metabolism, and tissue oxygenation is threatened. Oxy-
gen extraction rates increase, and mixed venous oxygen
saturation (Sv̄O2) and central venous oxygen saturation
(ScvO2) decrease because of decreased cardiac output,
compromised blood flow, and decreased oxygen deliv-
ery to tissues (class 3).2,7 Finally, urine output, level of
consciousness, and blood pressure decrease (class 4).3-5
Each event may take minutes to hours. Despite this known
sequence, aggressive intervention often is not implemented
until hypotension occurs.8,9 Traditionally, clinicians are
trained to monitor for early indications of decompensa-
tion, and the first hemodynamic monitoring parameter
to decrease in hypovolemia is stroke volume.1-5
Hypovolemia frequently occurs in patients during
surgery and in the critical care unit because of bleeding,
hypoalbuminemia, capillary leak and interstitial edema,
diarrhea, vomiting, and insensible water loss. If the hypo-
volemia is left untreated (or undertreated), circulatory
hypoxia may develop because of the decreased blood flow
and hypoperfusion. Compensatory diversion of blood
flow centrally, away from the peripheral and splanchnic
circulation, often masks hypoperfusion.2
If not recognized and treated promptly, decreased
circulating volume (particularly at the microvascular level)
leads to diminished oxygen delivery, depletion of intra-
cellular energy reserves, acidosis, anaerobic glycolysis,
and lactate accumulation. Hypovolemia can also lead to
ischemic gastrointestinal complications, including nau-
sea, vomiting, and intolerance of oral intake. Therefore,
diligent monitoring, via accurate assessment of cardiac
output and stroke volume, for hypovolemia is important
for monitoring blood flow.
Limitations of Conventional AssessmentsCurrent conventional assessments such as heart rate,
blood pressure, urine output, central venous pressure
(CVP), and level of consciousness often lack precision as
indicators of changes in a patient’s status. Although the
values obtained in these assessments somewhat correlate
with hemodynamic variables, the values are slow to
change and the changes are often late indications of a
patient’s worsening condition.3-5 Several studies10-17 suggest
that using physical assessment to evaluate cardiac output
may yield inaccurate findings. More recent data18-20 sug-
gest that the predictive power of blood lactate levels for
mortality and morbidity are independent of blood pres-
sure and common physiological triage variables (eg,
heart rate, blood pressure, mental status, capillary refill).
Despite these limitations, assessments such as blood
pressure are still considered a standard of care, and cur-
rent practice mandates use of the assessments. However,
blood pressure itself is a composite of so many factors2-5
(Figure 1) that it is of limited value as an early sign of
hemodynamic derangements such as hypovolemia.
Compensatory mechanisms such as vasoconstriction
and tachycardia influence the cardiovascular system to
keep blood pressure normal,2 making the correlation
between blood pressure and blood flow slow to change
as circulating volume decreases.1-5 The terms compensated
shock and cryptic shock are now being used to define
patient scenarios that meet clinical criteria for shock in
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 13
Figure 1 A, Complexity of blood pressure (BP): interrela-tionship of variables comprising BP. BP is the cardiacoutput (CO) multiplied by systemic vascular resistance(SVR). CO is the product of heart rate (HR) and strokevolume (SV). SV is influenced by preload, afterload, contractility, and rhythm. SVR is calculated by dividingthe difference between mean arterial pressure (MAP) and central venous pressure (CVP) by the CO and thenmultiplying by 80. (Derivation of content as described inAlspach.2) B, CO and SVR coexist in a balanced “seesaw”-type relationship. In general, when one decreases, the otherincreases (and vice versa) to maintain normal blood pressure.
BP = CO x SVR
A
B
HR x SV
MAP – CVP x 80
• Preload• Afterload• Contractility• Rhythm
CO
CO SVR
the presence of normal blood pressures.18 Blood pressure
measurements are more useful for conditions that involve
treatment of hypertension rather than treatment of
hypovolemia or shock.21,22 International guidelines such
as the Seventh Report of the Joint National Committee on
Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure22 help guide care providers in the man-
agement of hypertension according to a systematic and
stepwise approach. However, currently no such guidelines
exist for the management of hypotension.
Reconsidering Fluid Replacement End Points
In an article published in 1996, Connors et al23 sug-
gested that use of a pulmonary artery catheter (PAC) was
associated with an increased likelihood of patient death.
Since then, use of PACs has generally decreased. Although
values obtained via a PAC were once considered the gold
standard for bedside hemodynamic monitoring,24,25 the
precision of a PAC for assessing preload status via filling
pressures is limited. As early as 1971, Forrester et al26
pointed out the inaccuracies of CVP monitoring. In a more
recent systematic review of CVP as a predictor of cardiac
output and fluid responsiveness, Marik et al27 concluded
that CVP should
not be used as a
basis for clinical
decisions on fluid
management. In
fact, Marik et al27
noted that the
only published study28 suggesting CVP could be an accurate
indication of preload was done in horses. Even though
guidelines such as those of the Surviving Sepsis Campaign29
recommend using CVP to monitor preload, no study of
CVP or pulmonary artery occlusive pressure (PAOP) has
shown that these pressures consistently correlate with
blood flow or volume status.30 Early and aggressive use
of fluid replacement to preestablished end points such
as ScvO2 is more likely than the measurement of CVP
itself to provide patients benefit.31,32 The limitations of
CVP are further pointed out in the landmark study on
septic shock by Rivers et al33 published in 2001. These
investigators randomized 263 patients with septic shock
to receive either treatment according to a protocol on
fluid replacement known as early goal-directed therapy
or conventional care (control group). The patients treated
according to the protocol had a 17% reduction in mortality,
even though CVP was used as part of the basis for treat-
ment in both the interventional and the control group.33
PAOP is also an inaccurate predictor of fluid respon-
siveness in critically ill patients, further indicating that
blood pressures do not correlate with blood flow param-
eters such as cardiac output and stroke volume.34,35 This
lack of correlation occurs because many factors can
alter the pressure-volume relationship within the heart.
For example, conditions that increase PAOP but not
preload include, but are not limited to, positive-pressure
mechanical ventilation, positive end-expiratory pressure,
and decreased ventricular compliance. Conditions that
alter cardiac compliance include aging, obesity, diabetes,
myocardial ischemia, and sepsis.36 The challenge encoun-
tered with interpreting PAOP is further illustrated in
Figure 2; the 3 hearts in the drawing have different cardio -
myopathies and various left ventricular end-diastolic vol-
umes (LVEDVs), but each heart has the same PAOP. As a
result, the baseline Frank-Starling pressure-volume
curves for the 3 hearts differ vastly (Figure 3). When
LVEDV increases in normal hearts, pressure increases in
a characteristic curvilinear relationship. However, in con-
ditions such as left ventricular hypertrophy, decreased
wall compliance increases intracardiac pressure without
a concomitant increase in volume. Measurements based
on blood flow, such as stroke volume, help clinicians
avoid incorrect assumptions based on pressure-volume
curves.36 Ultimately, blood flow is more reliable and pre-
cise than are blood pressures, and blood flow can decrease
before blood pressures decrease.1,3,5,18
CVP and PAOP were never intended to be used alone;
both are filling pressures meant to guide the optimiza-
tion of stroke volume.27,32 The fundamental reason to
administer a fluid bolus to a patient is to increase stroke
volume.27,35,37 Although stroke volume monitoring is not
considered a standard of care, as is conventional moni-
toring of vital signs, plotting or documenting stroke
volume in response to a fluid challenge may be the clos-
est clinicians can come to using the Frank-Starling curve
in routine bedside practice. Stroke volume is more likely
to indicate hypovolemia before other monitoring param-
eters do because the former is not influenced by most
compensatory mechanisms.1-5 Treatments that include
giving fluids and medications such as drugs that improve
contractility (inotropes) are often administered with the
goal of improving stroke volume. Specifically targeting
14 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Ultimately, blood flow is more reliableand precise than blood pressures, andblood flow can decrease before bloodpressures decrease.
stroke volume for hemodynamic management is termed
SVO. Indications for use of SVO include age, heart failure,
low urine output, bleeding, monitoring of fluid boluses
and vasoactive infusions, cardiac conditions, and risk for
hypoperfusion or organ dysfunction. Awareness of con-
traindications is just as important: for example, esophageal
Doppler monitoring is contraindicated in patients with
esophageal strictures or varices.
Stroke Volume As the Newest CardiacVital SignAssessing for Adequate Perfusion
Using mean arterial pressure to evaluate a patient for
adequate perfusion to the vital organs is a controversial
but important idea for bedside clinicians to consider.38,39
As oxygen supply decreases or oxygen demand increases,
tissue hypoxia can develop. However, exactly when the
hypoxia occurs in an individual patient is unclear. ScvO2
can be a helpful global indicator; however, monitoring
microcirculatory perfusion at the end-organ level is not
readily available yet.40 When compromised perfusion
progresses to the point of eventual acidosis, organ dam-
age most likely is occurring, even when blood pressures
are normal.1
The complexity of these changes defies overreliance
on parameters such as blood pressure. Ongoing fluid
replacement decisions should be based on stroke volume,
variations in pulse pressure, cardiac output derived by
using a minimally invasive method, and passive leg-raising
maneuvers supported by integrated assessment to more
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 15
Figure 2 Challenges associated with interpreting pulmonary artery occlusion pressure (PAOP). Left ventricular end-diastolicvolume (LVEDV) can be independent of PAOP. A, PAOP is 22 mm Hg. Normal left ventricle has very high LVEDV. B, PAOP is22 mm Hg. Dilated right ventricle creates increased juxtacardiac pressure; LVEDV is normal. C, PAOP is 22 mm Hg. Left ventric-ular hypertrophy with noncompliant myocardium creates decreased space within the left ventricle; LVEDV is low. Use of PAOPalone to reflect LVEDV may not be accurate.Based on data from Marik et al27 and Turner.36
Illustration courtesy of Lisa Merry, RN, Merry Studio, Bloomington, Illinois.
B CA
Figure 3 Fluid replacement to optimize stroke volume(SV) vs cardiac filling pressures as primary end point.Information in blue is displayed when filling pressuresform the basis for routine bedside preload monitoring.Patient-specific differences in myocardial compliance and filling capacity markedly limit ability to estimate end-diastolic volume and thus, SV, on the basis of cardiac fill-ing pressures. Note also the widening of the Doppleraortic pulse waveform (systolic flow time, or FTc) as pre-load increases. SV measurements (in red) are the primarytarget for fluid in SV optimization. Blood-flow-based tech-nology allows clinicians to estimate SV more directlyalong this pressure-volume curve. This approach helpseliminate “guesstimation” of blood flow based on cardiacfilling pressures.
Stro
ke v
olum
e, m
L
25
Fluid bolus administered
Pulmonary arteryocclusive pressure
50
SV 100 mL
SV 75 mL
SV 40 mL
500 mL 1000 mL 1500 mL4 mm Hg➔➔
12 mm Hg 18 mm Hg
75
100
120
precisely determine the response to the replacement
efforts.32,35,41,42 Methods of actually measuring blood flow
by more direct methods are becoming increasingly
available. These methods can provide true blood-flow
measurements, such as stroke volume, stroke distance,
variation in stroke volume, and systolic flow time.
Methods of Measuring Stroke VolumeTraditionally, echocardiography has been the most
commonly used method to measure stroke volume at the
bedside. However, this method is expensive and technically
difficult and continuous or serial measurements are often
not practical in critical care. Several new technologies
enable ongoing measurement of stroke volume at the
bedside, including noninvasive Doppler imaging
(USCOM), esophageal Doppler imaging (Deltex Medical;
Figure 4), bioimpedance (SonoSite), endotracheally applied
bioimpedance (ConMed Corporation), bioreactance
(Cheetah Medical), pulse contour methods (Edwards
Lifesciences, LidCo Ltd, Pulsion Medical Systems), an
exhaled carbon dioxide method (Philips, Respironics),
and the PAC. All use various methods to calculate stroke
volume, and the results have various degrees of accuracy.
Some devices measure stroke volume directly (eg,
esophageal Doppler imaging) and may be considered
the preferred method because of the high degree of
accuracy of the results.43 Other technologies simply
divide the cardiac output by the heart rate to obtain
stroke volume (eg, PAC). Table 2 provides a more
detailed comparison.44-59
Clinical application of technology is based on
knowledge and experience in obtaining and applying
the information received. If a care provider targets the
wrong hemodynamic end points or interprets a poor
waveform as an
accurate tracing,
benefits may be
limited. These
concerns were
cited in the tech-
nology assessment report published by the Agency for
Healthcare Research and Quality60 in 2008 as some of the
most likely reasons studies have collectively suggested
no benefit for monitoring with PACs.
Disagreement may exist about which technology is best
for monitoring stroke volume because none of the tech-
nologies is appropriate for all patients in all situations.
Each technology has a unique profile of advantages and
limitations, and a patient’s situation may dictate which
technology is best at a given time. Regardless of the
technology used, the device will provide measurements
of preload, afterload, and contractility for optimizing
stroke volume.
Hemodynamic Variables That InfluenceStroke Volume
Three variables affect stroke volume: preload,
contractility, and afterload.
Measurement of Preload: Corrected Flow TimeCorrected flow time (FTc) is a measure obtained in
esophageal and noninvasive Doppler imaging via ultra-
sound technology. The FTc is an estimate of circulating
blood volume based on the amount of red blood cells
16 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Each technology has a unique profileof advantages and limitations, and apatient’s situation may dictate whichtechnology is best at a give time.
Figure 4 Examples of minimally invasive hemodynamicmonitoring. A, Esophageal Doppler monitor: displayallows real-time measurement of preload (flow time, cor-rected, FTc), contractility (peak velocity, PV), stroke vol-ume (SV), and stroke distance (SD). B, Sagittal view ofesophageal Doppler probe in place to monitor cardiac out-put variables. Ultrasound transducer measures blood flowin the descending thoracic aorta.Images courtesy of Deltex Medical, Inc, West Sussex, England.
A
B
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 17
Description
Stroke volume estimate obtained viaultrasound probe placed at the sternalnotch or parasternally; ultrasound beamdirected at the aortic or pulmonic valve
Stroke volume estimate directly obtainedvia Doppler signal of descending aorta;typically, patient must be sedated;inserted similarly to a nasogastric tube
Bioimpedance technology via endotra-cheal tube; stroke volume obtainedfrom impedance signal from ascendingaorta; patient must be intubated
Transcutaneous electrodes placed onneck and chest; electrical impedancebetween electrodes during cardiaccycle entered into nomogram to com-pute stroke volume; for best readings,patient must have normal anatomy
Stroke volume estimated from arterialpressure waveform via methods suchas lithium infusion, pulse pressurevariation, or thermodilution; continu-ous cardiac output and beat-to-beatvariability proportional to stroke volume; changes in systemic vascularresistance and arterial pressure neces-sitate recalibration; dampening, dys-rhythmias, and ventilator triggeringalso limit accuracy
Exhaled carbon dioxide method, withFick equation; needs controlledmechanical ventilation to work; addi-tional personnel, such as respiratorytherapist, may be required; patientmust be intubated
Measures cardiac output via thermodi-lution, temperature sensed by thecatheter thermistor; stroke volumecalculated by dividing cardiac outputby heart rate; central venous accessrequired via catheterization of rightside of heart
Like bioimpedance, uses transcutaneouselectrodes; however, signal acquisitioneliminates impedance errors presentwith the first-generation technology
Randomized controlled trials regarding patient outcome
None
9 trials44-52 (2 trials hadconflicts of interest todisclose) showing reducedlength of stay, complica-tions, use of vasopres-sors, renal insufficiency, and mortality and lowerlactate levels
None
None
3 trials (each with conflictsof interest to disclose)suggesting decreasedcomplications and length of stay (LidCO),53
(FloTrac),54 and (PiCCO)55
3 trials suggesting unclearbenefit (PiCCO)56 (conflictof interest disclosed) orno benefit (FloTrac)57
and (PiCCO)58
None
Several trials,59,60 with both pro and con findings
None
Where used
Anywhere
Operating room,intensive careunit, emergencydepartment
Operating room,intensive care unit
Anywhere
Operating room,intensive care unit
Operating room,intensive care unit
Operating room,intensive care unit
Operating room,intensive care unit
Manufacturer
USCOM, Sydney, Australia
Deltex Medical, WestSussex, England
ConMed Corporation,Utica, New York
SonoSite, Bothell,Washington
FloTrac, Edwards Lifesciences, IrvineCalifornia
LidCo Ltd, Cambridge,United Kingdom
PiCCO, Pulsion Medical Systems,Munich, Germany
Philips Respironics,Andover, Massachusetts
Cheetah Medical, Portland, Oregon
Technology
External Dopplerimaging
Esophageal Doppler imaging
Endotrachealbioimpedance
Transcutaneousbioimpedance
Pulse contour
Exhaled carbondioxide method
Pulmonary arterycatheter
Bioreactance
Table 2 Technology for measuring stroke volume
that cross the ultrasound transducer beam through the
aorta during the systolic phase (Figures 4A and 4B). FTc
corresponds to the width of the pulse waveform base
and can be used to estimate preload. For example, a longer
FTc suggests that the left ventricle is pumping forward
an increased amount of blood (ie, increased preload).
The width of the pulse wave is measured in milliseconds
and represents the amount of time spent in systole com-
pared with total cardiac cycle time, and FTc is also cor-
rected for heart rate.61 The correction is based on a heart
rate of 60/min,
although the
current heart
rate is taken into
account. If a
patient’s heart
rate is 60/min, then each cardiac cycle will last 1 second,
or 1000 ms. Normal FTc is 330 to 360 ms.61,62 In other
words, for a cardiac cycle lasting 1 second, the systolic flow
period should last approximately 330 to 360 ms, provided
that adequate preload exists. An easy way to remember
the reference range is to remember that the heart is in
diastole two-thirds of the time and that normal FTc
multiplied by 3 equals 1 second, or 1000 ms62 (Figure 5).
But normal reference ranges are really just reference points,
not necessarily static physiological targets to be used for
all patients. The most important value of FTc is the degree
to which it changes in response to intravenous adminis-
tration of fluids.62 Increases in FTc in response to volume
challenge help confirm hypovolemia, which is manifested
as a narrow waveform base and a low FTc (Figure 3).
The accuracy of FTc has been questioned.63-65 However,
a complete understanding of the variable is critical before
FTc and be used effectively in clinical practice.66-68 Simply
put, FTc is suggestive of the amount of circulating volume
that passes the tip of the ultrasound probe during systole.36
Therefore, conditions such as bleeding (hypovolemia),
heart failure (low contractility), and high afterload (eg,
vasoconstriction) may contribute to low blood-flow
states and thus low FTc. These influences must be con-
sidered before FTc is accepted as a surrogate for preload
in individual patients. Several investigators66,69-72 have
suggested that FTc is as good as or better than PAOP for
indicating changes in preload. Most important, however,
improvement in stroke volume after fluid administration
is what was intended to form the basis on which preload
18 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
The most important value of correctedflow time is the degree to which itchanges in response to intraveousadministration of fluids.
Figure 5 Waveform components for stroke volume optimization (SVO): aortic pulse waveform from an esophageal Dopplerexamination. Corrected flow time (ie, the time spent in systole) corresponds to the width of the pulse waveform and is an indexof preload. Peak velocity corresponds to the height of the wave and is a measure of contractility. Stroke distance represents thearea under the curve and is used to compute stroke volume.
Peak velocity (cm/s)
Velo
city
, cm
/s
Flow time, ms
Stroke distance (cm)= area under curve
1/3 Systole 2/3 Diastole
1 Cardiac cycle
responsiveness is ultimately determined (in each of the
outcome trials studying SVO).44-52,73,74 In other words,
FTc (as well as CVP and PAOP) is best used as a decision-
making aid for optimizing stroke volume.
Measurement of Contractility: Peak VelocityPeak velocity, a measure of contractility, is indicated
by the amplitude of a Doppler waveform (Figure 5). It
indicates the acceleration of blood flow in the systolic
phase, or the speed at which a pressure wave goes from
baseline to the peak height of contraction. An overall
reference range is 50 to 120 cm/s. Peak velocity can be
age dependent; the expected range for a 20- to 30-year-
old is 90 to 120 cm/s, with gradually decreasing expected
peak velocity as a person ages. Patients more than 65
years old are expected to have a peak velocity greater
than 50 cm/s. Values less than 50 cm/s are suggestive
of poor left ventricular contractility, as in heart failure.
However, peak velocity should be evaluated with respect
to a patient’s baseline values and how those values
respond to treatments. For example, an increase in peak
velocity is expected with administration of an inotrope.
A low stroke volume can occur for 1 of 2 main rea-
sons: hypovolemia or decreased ventricular contractility.
The immediate measured availability of peak velocity
with Doppler techniques provides better information
than do the derived contractility parameters of the PAC
regarding why stroke volume may be low. For example,
if stroke volume is low but peak velocity is normal, the
problem most likely is hypovolemia.21 However, if both
stroke volume and peak velocity are low, the problem
most likely is left ventricular dysfunction.62 A patient’s
response to medications such as preload reducers, after-
load reducers, or inotropes can help differentiate the
cause of the left ventricular dysfunction (eg, fluid over-
load, high afterload, or low contractility, respectively).
Peak velocity may also help detect acute decompen-
sating systolic heart failure earlier than do other tech-
niques for monitoring cardiac output. In critical illness,
poor left ventricular contractility (low ejection fraction)
may initially lead to a compensatory increase in end-
diastolic volume, a change that implies a normal stroke
volume. The ability to monitor peak velocity allows cli-
nicians to recognize this decrease in contractility in real
time and intervene before a decrease in stroke volume
occurs. Further research is needed to better establish
SVO treatment guidelines for patients with heart failure.
Measurement of Afterload: Systemic Vascular Resistance
Systemic vascular resistance (SVR) is the resistance
that must be overcome by the ventricles to develop force
and contract, propelling blood into the arterial circulation.2
Most of the newer hemodynamic monitoring technolo-
gies (eg, esophageal Doppler imaging, bioimpedance,
pulse contour methods) have the capability to calculate
SVR. However, SVR was not a major parameter in the
algorithms used in any of the SVO trials that showed
improved outcomes in surgical patients.44-52,73,74
Evidence of lack of inclusion suggests that SVR is a
more of a secondary monitoring parameter. Elevated SVR
usually occurs in response to systemic hypertension or
as a compensatory mechanism due to decreased cardiac
output, as in shock states (Figures 1A and 1B). Therefore,
nurses must know why the SVR is elevated. If the value is
elevated in response to low cardiac output, once cardiac
output is improved with treatment (eg, fluid, inotropes),
SVR should decrease because of a decreased need for
compensatory vasoconstriction. If SVR is elevated
because of systemic hypertension, treatment may include
administration of an afterload reducer.2
When SVR decreases, the left ventricular ejection of
blood encounters lower resistance. Low afterload states
may be less problematic when blood pressure and car-
diac output are normal (Figure 1A). However, attempts
to increase low SVR generally include administration of
vasopressors.2 ScvO2 and stroke volume should also be
followed as end points to ensure that blood flow and tis-
sue oxygenation improve in response to the vasopressor21
(Figure 6). Titrating the dose of a vasopressor used to
alter ScvO2 and stroke volume allows clinicians to focus
on optimizing blood flow to both the microcirculation
and the macrocirculation. Several studies of fluid replace-
ment protocols that include use of vasopressors suggest
that optimizing ScvO231,33,75 and stroke volume47,76 improve
patients’ outcomes. However, further research is needed
to better establish how vasopressors and ScvO2 are best
used in SVO protocols.
Stroke Volume, Stroke Index, and Stroke Distance
Stroke volume is one of the primary end points for
detecting fluid responsiveness and guiding goal-directed
therapy.27,32,62 Stroke index is a standardized parameter in
which a patient’s body surface area is taken into account.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 19
However, monitoring both stroke volume and stroke index
is generally not necessary, because they use different units
of measure to quantify the same value. Table 3 gives ref-
erence ranges for these parameters.21,77-79 However, the
ideal stroke volume value is the one that contributes to
adequate blood flow for tissue oxygenation without
increasing heart rate.
Despite the unique advantages of measuring stroke
volume, available technologies to measure this parameter
at the bedside have some limitations. Even esophageal
Doppler imaging, which provides a highly flow-directed
estimation of stroke volume, uses a calculated estimation
of aortic diameter based on the patient’s height and
weight.80 Stroke distance may be a more accurate reflec-
tion of the Doppler estimation of stroke volume. Stroke
distance is the distance a column of blood moves through
the descending thoracic aorta during each systolic phase.61
Because stroke distance is used to calculate stroke vol-
ume, the recommendation is that stroke distance be
evaluated to determine if the measurement of stroke
volume is accurate.
The SVO Algorithm: Putting It All Together
The Frank-Starling principle states that the strength
of cardiac contraction is directly related to the length of
muscle fibers at end diastole, or preload.81 Administration
of fluid on the basis of stroke volume allows clinicians to
directly apply this principle. Figure 7 displays a standard
example of an SVO fluid replacement algorithm, cited by
Schober et al,62 that is based on a synthesis of experimen-
tal SVO protocols and literature.44-52,73,74 In this type of
algorithm, determination of fluid responsiveness is used:
fluid boluses are administered as long as stroke volume
continues to improve by 10% or more. When administra-
tion of fluid boluses ceases to improve stroke volume by
20 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Figure 6 Response of stroke volume to norepinephrine. Increasing vasopressor doses to previously established, prescribedthresholds for mean arterial pressure (MAP) and systemic vascular resistance may in turn decrease stroke volume and overallblood flow. The case example graph suggests that stroke volume is optimized at 8 μg/min of norepinephrine, even though aMAP of only 55 mm Hg is achieved at that dose. Note: patients’ responses to norepinephrine dosing may vary.
Stro
ke v
olum
e, m
L
MAP response to increasing doses of norepinephrine, mm Hg
Increasing norepinephrine dose, μg/min 2 5
75
50
25
10 15 20
65605550
Parameter
Cardiac output, L/min
Stroke volume, mL
Stroke indexb
Flow time corrected, ms
Peak velocity, cm/s
Stroke distance, cm
Cardiac indexc
Systemic vascular resistance, dyne sec cm-5
Saturation of central venous oxyhemoglobin, %
Central venous pressure, mm Hg
Stroke volume variation, %
Referencerange
4-8
50-100
25-45
330-360
30-120
10-20
2.8-4.2
900-1600
65-80
2-8
< 10-15
Table 3 Reference ranges for hemodynamic parametersa
a Based on data from Ahrens,21 Lynn-McHale Wiegand,77 Lynn-McHale Wiegand and Carlson,78 and Edwards Lifesciences.79
b Calculated as stroke volume in milliliters per heartbeat divided by bodysurface area in square meters.
c Calculated as cardiac output in liters per minute divided by body surfacearea in square meters.
10% or more, no more fluid is needed. Using this method
of fluid administration can mitigate the risk of pulmonary
edema, and bedside clinicians can be better assured that
the patient is receiving enough fluid to optimize the
macrocirculation but not more fluid than is needed.
SVR and blood pressure are usually not included in
SVO algorithms and are considered secondary monitor-
ing parameters in SVO.44-52 According to the SVO algo-
rithm, SVR and blood pressure are evaluated only after
peak velocity (contractility) and stroke volume are opti-
mized, because SVR and blood pressure are more indi-
rect reflections of cardiac output and are influenced by
other factors (see Figures 1A and 1B). Furthermore,
when blood flow and tissue oxygenation are measured
rather than assumed, doses of vasopressors can be adjusted
to optimize the end points of stroke volume (macrocir-
culation) and ScvO2 (microcirculation) rather than SVR
and blood pressure (Figure 6). Stroke volume may improve
initially with initiation and escalating doses of vasopres-
sors, but changes in afterload due to further increases in
the medication may impede stroke volume and cardiac
output.82 Surveillance of ongoing stroke volume and
cardiac output may help clinicians avoid this decrease
in stroke volume and cardiac output.
Challenges to SVO implementation may include incor-
porating new hemodynamic monitoring technology into
daily practice (eg, esophageal Doppler imaging, pulse
contour method), education of staff members, support
from physicians and leaders, and the paucity of literature
to support use in nonsurgical patients. However, potential
benefits include use of minimally invasive techniques,
allowing earlier detection of unstable hemodynamic status,
and reductions in morbidity, mortality, and length of stay.
More research is needed to determine how values
such as peak velocity and ScvO2 can be incorporated into
the SVO algorithm. The following case studies illustrate
these points and indicate how SVO can be applied in cases
involving alterations in preload, afterload, and contractility.
Case Study 1: Decreased PreloadA 59-year-old man was admitted to the surgical
intensive care unit after having a partial liver lobectomy
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 21
Figure 7 Example of an algorithm for stroke volume optimization.
Other therapies as appropriate, for example:
• High afterload state: dilators (± more fluid) if low correctedflow time, low peak velocity, and blood pressure acceptable
• Low contractility state: inotropic agents if low peak velocityand blood pressure
• Low afterload state: vasopressors if high corrected flowtime, high stroke volume, and low blood pressure
If stroke volume or correctedflow time is low
Give 200 mL of colloid or500 mL of crystalloid
Stop giving fluids;monitor stroke
volume as indicated
If stroke volume decreased > 10%
Yes (stroke volumeincreased < 10%)
No (stroke volumeincreased > 10%)
Is the heart pumping
enough blood?
after a motor vehicle accident (Table 4). On postopera-
tive day 5, he was evaluated for discharge to a general
care unit. His urine output had decreased during the
preceding 12 hours, suggestive of hypovolemia. The
hypovolemia was evidenced by low stroke volume, low
FTc, and low ScvO2 in the presence of a normal peak
velocity. After injection of a 1000-mL bolus of physiolog-
ical saline, stroke volume improved from 34 mL to 48
mL, more than a 10% (3.4 mL) improvement. So,
another bolus was given. Satisfactory response to the
bolus was manifested by normal FTc and ScvO2. Stroke
volume improved to 49 mL only with the second bolus
(<10% improvement), indicating the beginning of the
plateau along the Frank-Starling curve where increased
stretching of the ventricular myocytes does not improve
stroke volume. Thus, no further administration of fluid
was indicated.
Case Study 2: Decreased Preload Leads toDecreased Afterload
A 55-year-old woman was admitted because of sepsis
(Table 5). The patient had a dangerously reduced stroke
volume, decreased FTc, decreased ScvO2, and a normal
peak velocity, indicating hypovolemia. She was deemed
fluid responsive as indicated by an improvement in
stroke volume from 26 mL to 50 mL, a greater than 10%
(2.6 mL) improvement, after administration of a bolus of
1000 mL of physiological saline. So, another saline bolus
was indicated. However, the patient did not respond to
the second bolus, as evidenced by an improvement in
stroke volume from 50 mL to only 51 mL (<10%), suggest-
ing that the macrocirculation had been optimized. Nor-
epinephrine was started because of the reduced ScvO2
and persistent hypotension despite volume correction.
The patient responded appropriately as evidenced by the
22 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Heart rate, beats
per minute
102
100
99
Central venousoxygen
saturation, %
49
69
70
Central venouspressure,mm Hg
3
5
6
Blood pres-sure, mean
(SD), mm Hg
100/48 (64)
94/55 (68)
100/60 (73)
Peak velocity,
cm/s
96
95
95
Flow time, corrected, ms
300
335
337
Stroke volume,
mL
34
48
49
Intervention
Administer 1000-mLbolus of physio-logical saline
Administer 1000-mLbolus of physio-logical saline
Response
Table 4 Interventions used and response of 59-year-old man admitted after a motor vehicle accident
Heart rate, beats
per minute
107
105
105
106
Central venousoxygen
saturation, %
26
48
50
68
Central venouspressure,mm Hg
4
9
9
8
Blood pres-sure, mean
(SD), mm Hg
68/36 (47)
76/42 (53)
80/44 (59)
92/62 (72)
Peak velocity,
cm/s
78
76
76
72
Flow time, corrected, ms
254
341
341
344
Stroke volume,
mL
26
50
51
55
Intervention
Administer 1000-mLbolus of 0.9% normal saline
Administer 1000-mLbolus of physio-logical saline
Administer norepinephrine 10 μg/min
Response
Table 5 Interventions used and response of 55-year-old woman admitted for sepsis
increase in ScvO2 to 68%, suggesting normalization of
the microcirculation.
Literature Supporting Clinical Usefulness of SVO
Before they adopt a new practice, astute clinicians
want to know that the practice is strongly supported in
the literature. Randomized controlled trials are the
highest-level research design, and the number of well-
designed randomized controlled trials is directly correlated
with the level of evidence assigned to a given practice.83-85
The findings of 11 randomized controlled trials,44-52,73,74
including 9 prospective trials,44-52 suggest that SVO results
in improved patient outcomes. Despite a thorough liter-
ature review, we were unable to find a fluid replacement
strategy supported by more research. The results of the
9 prospective trials,44-52 which included a total of about
1000 patients, consistently suggested that compared with
conventional fluid replacement, SVO fluid replacement
protocols contribute to decreases in overall hospital length
of stay (by 2 days or more), complication rates, renal
insufficiency, infection, use of vasopressors, blood lactate
levels, and time-to-tolerance of oral intake. Appropriately
implemented SVO programs that replicate these outcomes
may also be associated with decreased costs.86
Notably, the sample in all 11 trials44-52,73,74 included
perioperative patients. Although 2 of these trials44,47 also
focused on postoperative care in the critical care unit,
more research is needed to indicate the efficacy of SVO
in nonsurgical patients. However, in perioperative
patients, the strength of the supporting evidence in
favor of SVO has been substantiated by large-scale sys-
tematic literature reviews conducted by the Agency for
Healthcare Research and Quality,87 the National Health
Service,86 and third-party payers such as the Centers for
Medicare and Medicaid Services88 and Aetna.89
In 3 of these studies,86-88 the agencies recommended
SVO protocols be used for monitoring cardiac output of
patients receiving mechanical ventilation in the critical
care unit and for surgical patients who require intra -
operative fluid optimization. Esophageal Doppler imag-
ing,88 bioimpedance,90 and PACs91 are all reimbursed by
the Centers for Medicare and Medicaid Services88 on the
basis of systematic literature reviews. However,
esophageal Doppler imaging is the only technology also
supported by the Agency for Healthcare Research and
Quality.87
Similarly, the Cochrane Collaborative59 and the
Agency for Healthcare Research and Quality60 have pub-
lished technology assessments based on meta-analyses
of outcomes related to use of PACs. The analyses indi-
cated that the patients studied showed no evidence of
benefit or harm from PACs. Among the reasons cited
for the perceived lack of benefit was clinician-to-clinician
variability in management of hemodynamic data obtained
via PACs. In addition, the authors59,60 questioned the
accuracy of the interpretation of the hemodynamic
information in the studies analyzed and whether or not
patient management strategies based on hemodynamic
data were appropriate. Furthermore, none of the studies
included use of a specific protocol for PAC use. This lack
of a protocol is a key difference between PAC studies and
SVO studies. Each of the 9 randomized control trials44-52
on SVO
included a
protocol for
use of SVO.
Use of a pro-
tocol is con-
sistent with
other studies of replacement protocols that include
fluid therapy, which can be lifesaving when initiated
early in the course of treatment. Findings from a meta-
analysis of hemodynamic optimization by Poeze et al92
also suggest that replacement strategies such as SVO
improve outcomes, including patient mortality, in
high-risk surgical patients.
Nursing ConsiderationsNursing considerations associated with incorporat-
ing SVO into bedside practice include acquiring and
evaluating hemodynamic data, maintenance of skin
integrity, sedation and analgesia, and nursing research.
Acquisition and Evaluation of Hemodynamic Information
Clinical proficiency with applying or inserting the
hemodynamic monitoring device and adequate signal
acquisition are key.93 Each device has its own unique signal
acquisition technique and competency requirements.
Inappropriate application of the device may produce inac-
curate hemodynamic readings, leading to improper treat-
ment decisions.77,78 Once accurate readings are obtained,
understanding the appropriate application of “normal”
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 23
Stroke volume may improve initially with initiation and escalating doses ofvasopressors, but changes in afterloaddue to further pressor dose increases mayimpede stroke volume and cardiac output.
hemodynamic reference ranges to all patients is crucial.
Tracking trends in hemodynamic values over time is
generally more useful than is monitoring and treating
on the basis of single data points, because transient
changes in values may not be clinically importantly.
When readings are considered accurate and hypo -
volemia is identified, rapid infusion of a fluid bolus may
optimize a patient’s response. Fluid infused via a pres-
sure bag often produces a more dramatic increase in
stroke volume than does fluid administered via an intra-
venous infusion pump. A maximum rate of commonly
used intravenous pumps is 999 mL/h. Because hypo -
volemia and hypoperfusion are time-sensitive conditions,
the provider’s judgment and the patient’s condition may
determine that a more rapid infusion rate is needed.
The latest revision of the Surviving Sepsis Campaign
guidelines also suggests an increased emphasis on earlier
and more aggressive fluid replacement. For example, the
2008 guidelines94 recommended a 20 mL/kg crystalloid
fluid challenge in a 6-hour replacement bundle. In the
2012 revised guideline,29 the recommended amount of
fluid was increased (to 30 mL/kg) in a shorter time (3-hour
bundle). Clinicians must strongly consider strategies to
infuse such a volume rapidly enough, in accordance with
institutional policy as appropriate.
Maintenance of Skin IntegrityCare must be taken to avoid skin breakdown under
and around skin electrodes. With bioimpedance and
bioreactance, signals are acquired transcutaneously, and
skin care should be in accordance with the manufacturer’s
recommendations and institutional policy. Mouth ulcer-
ations are also possible with monitoring devices such as
those used for esophageal Doppler imaging93 and endo-
tracheally applied bioimpedance. Diligent oral care should
be performed as
needed while
those devices are
in place. Site care
is also important
when caring for
patients moni-
tored with intravenous pulse contour devices or PACs.
Catheter infections can be minimized by using sterile
conditions during insertion and aseptic technique during
dressing changes.77,78
Sedation and AnalgesiaSedation is sometimes required with techniques such
as the exhaled carbon dioxide method, which requires
controlled mechanical ventilation, and esophageal Doppler
imaging. These techniques may have limited accuracy
when increased respiratory rates or restlessness, respec-
tively, occur. Therefore, sedative agents or analgesics
may be administered as needed.77,78 Although not a major
focus with respect to SVO, pain cannot be overlooked;
it is not only an overall priority but can also influence
hemodynamic readings.
Nurse ResearchThe implications of patient advocacy extend beyond
routine patient care and include nurses’ participation in
designing and implementing future research on the clini-
cal usefulness of SVO in critical care. Critical care nurses
monitor and treat hypovolemia daily and have a unique
opportunity to contribute to the existing scientific body
of knowledge through participation in SVO studies in
medical critical care patients.
SummaryThe growing body of evidence supporting SVO
suggests that implementation of SVO into daily practice
should be considered.61,62,88 A new era is emerging in
which blood-flow monitoring is taking precedence over
the monitoring of blood pressures. Cardiac pressures
help provide estimates of blood volume; however, normal
cardiac pressures can be observed in a patient in shock
and provide little information about blood flow.30,95-97
Interpretation and treatment of blood pressures incor-
porate assumptions, whereas stroke volume may be
considered a more precise measure of fluid responsive-
ness and an earlier warning sign of volume depletion
than are urine output, altered mental status, CVP, heart
rate, and blood pressure.1-5 Earlier signals allow clini-
cians to anticipate rather than react to changes, improv-
ing the likelihood for maintaining a stable metabolic
state at the organ and cellular level. In addition to the
evidence supporting SVO, minimally invasive applica-
tions and improvements in accuracy also add to safety
advantages when inherent limitations of the various
methods are considered.
For years, strategies for use of SVO were not feasible
because no practical measurement method for SVO
24 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Earlier signals such as stroke volumeallow clinicians to anticipate rather thanreact to changes, improving the likeli-hood of maintaining a stable metabolicstate at the organ and cellular level.
existed for bedside clinicians. Fortunately, technology
has improved the hemodynamic monitoring landscape.
Compared with old devices, newer technology is less inva-
sive, safe, evidence based, flow directed, cost-effective,
easier to use, and accurate. Although further research
on SVO and dynamic indices are needed to establish the
clinical efficacy of SVO in critical care units, the current
body of literature indicates that SVO is associated with
fewer complications and reduced hospital lengths of stay,
particularly in patients receiving mechanical ventilation
and in surgical patients. Until more randomized trials
on the impact of SVO protocols on the outcomes of
critical care patients are published, SVO is supported
by more evidence than is use of filling pressures for fluid
replacement in critical care units.27,32,44-52,73,74,86-88 On the
basis of our review of the current available literature, we
suggest that the SVO algorithm for fluid replacement be
considered in place of use of cardiac filling pressures for
patients in critical care, as appropriate, with attention to
outcomes. In the meantime, more research is needed to
evaluate the impact of SVO on patients other than peri-
operative patients and on nonintubated patients. CCN
AcknowledgmentsThe authors thank Terry Sears and Julie Stielstra for their contributions. Wealso thank the critical care staff, physicians, and leaders at Central DuPageHospital–Northwestern Medicine. Without their help and support, this man-uscript would have been much more difficult to complete.
Financial DisclosuresTom Ahrens has lectured for hemodynamic monitoring companies (includingDeltex Medical Inc) and is a hemodynamic monitoring consultant.
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14 Iregui MG, Prentice D, Sherman G, Schallom L, Sona C, Kollef MH.Physicians’ estimates of cardiac index and intravascular volume basedon clinical assessment versus transesophageal Doppler measurementsobtained by critical care nurses. Am J Crit Care. 2003;12(4):336-342.
15. Neath SX, Lazio L, Guss DA. Utility of impedance cardiography toimprove physician estimation of hemodynamic parameters in the emer-gency department. Congest Heart Fail. 2005;11(1):17-20.
16. Staudinger T, Locker GJ, Laczika K, et al. Diagnostic validity of pulmonaryartery catheterization for residents at an intensive care unit. J Trauma.1998;44(5):902-906.
17. Celoria G, Steingrub J, Vickers-Lahti M, et al. Clinical assessment ofhemodynamic values in two surgical intensive care units: effects of ther-apy. Arch Surg. 1990;125(8):1036-1039.
18. Bakker J, Jansen T. Don’t take vitals, take a lactate. Intensive Care Med.2007;33:1863-1865.
19. Howell MD, Donnino M, Clardy P, Talmor D, Shapiro NI. Occult hypop-erfusion and mortality in patients with suspected infection. Intensive CareMed. 2007;33(11):1892-1899.
20. Mikkelsen M, Miltiades A, Gaieski D, et al. Serum lactate is associatedwith mortality in severe sepsis independent of organ failure and shock.Crit Care Med. 2009;37(5):1670-1677.
21. Ahrens T. Hemodynamics in sepsis. AACN Adv Crit Care. 2006;17(4):435-445.
22. Department of Health and Human Services, National Institutes ofHealth, National Heart, Lung, and Blood Institute. The Seventh Report ofthe Joint National Committee on Prevention, Detection, Evaluation, andTreatment of High Blood Pressure. Bethesda MD: National Heart, Lung,and Blood Institute; August 2004. NIH Publication No. 04-5230.
23. Connors A, Speroff T, Dawson N, et al. The effectiveness of right heartcatheterization in the initial care of critically ill patients. SUPPORTInvestigators. JAMA. 1996;276(11):889-897.
24. Smartt S. The pulmonary artery catheter: gold standard or redundantrelic. J Perianesth Nurs. 2005;20(6):373-379.
25. Pugsley J, Lerner A. Cardiac output monitoring: is there a gold standardand how do the newer technologies compare? Semin Cardiothorac VascAnesth. 2010;14(4):274-282.
26. Forrester JS, Diamond G, McHugh TJ, Swan HJ. Filling pressures in theright and left sides of the heart in acute myocardial infarction: a reappraisalof central-venous-pressure monitoring. N Engl J Med. 1971;285(4):190-193.
27. Marik P, Baram M, Vahid B. Does central venous pressure predict fluidresponsiveness? A systematic review of the literature and the tale ofseven mares. Chest. 2008;134(1):172-178.
28. Magdesian KG, Fielding CL, Rhodes DM, Ruby RE. Changes in centralvenous pressure and blood lactate concentration in response to acuteblood loss in horses. J Am Vet Med Assoc. 2006;229(9):1458-1462.
29. Dellinger RP, Levy MM, Rhodes A, et al; Surviving Sepsis CampaignGuidelines Committee including the Pediatric Subgroup. SurvivingSepsis Campaign: International guidelines for management of severesepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580-637.
30. Ahrens T. Stroke volume optimization vs central venous pressure influid management. Crit Care Nurse. 2010;30(2):71-73.
31. Pope JV, Jones AE, Gaieski DF, Arnold RC, Trzeciak S, Shapiro NI; Emer-gency Medicine Shock Research Network (EMShockNet) Investigators.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 25
Now that you’ve read the article, create or contribute to an online discussionabout this topic using eLetters. Just visit www.ccnonline.org and select the articleyou want to comment on. In the full-text or PDF view of the article, click“Responses” in the middle column and then “Submit a response.”
To learn more about stroke volume optimization, read “StrokeVolume Optimization Versus Central Venous Pressure in FluidManagement” by Ahrens in Critical Care Nurse, April 2010;30:71-72. Available at www.ccnonline.org.
Multicenter study of central venous oxygen saturation (ScvO2) as a pre-dictor of mortality in patients with sepsis. Ann Emerg Med. 2010;55(1):40-46.e1.
32. Marik P. Surviving sepsis: going beyond the guidelines. Ann IntensiveCare. 2011;1(17):1-6.
33. Rivers E, Nguyen B, Havstad S, et al; Early Goal-Directed Therapy Col-laborative Group. Early goal-directed therapy in the treatment of severesepsis and septic shock. N Engl J Med. 2001;345(19):1368-1377.
34. Benington S, Ferris P, Nirmalan M. Emerging trends in minimally inva-sive haemodynamic monitoring and optimization of fluid therapy. Eur JAnaesthesiol. 2009;26(11):893-905.
35. Marik P, Monnet X, Teboul JL. Hemodynamic parameters to guide fluidtherapy. Ann Intensive Care. 2011;1(1):1-9.
36. Turner MA. Doppler-based hemodynamic monitoring: a minimallyinvasive alternative. AACN Clin Issues. 2003;14(2):220-231.
37. Michard F, Teboul J. Predicting fluid responsiveness in ICU patients: acritical analysis of the evidence. Chest. 2002;121:2000-2008.
38. Dünser M, Takala J, Brunauer A, Bakker J. Re-thinking resuscitation:leaving blood pressure cosmetics behind and moving forward to permis-sive hypotension and a tissue perfusion-based approach. Crit Care. 2013;17:326. doi:10.1186/cc12727.
39. Marik P, Bellomo R. Re-thinking resuscitation goals: an alternativepoint of view! Crit Care. 2013;17:458. doi:10.1186/cc12775.
40. Knotzer H, Hasibeder W. Microcirculation function monitoring at thebedside—a view from the intensive care. Physiol Meas. 2007;28(9):R65-R86.
41. Marik P, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterialwaveform derived variables and fluid responsiveness in mechanicallyventilated patients: a systematic review of the literature. Crit Care Med.2009;37(9):2642-2647.
42. Marik P. Techniques for assessment of intravascular volume in criticallyill patients. Intensive Care Med. 2009;24(5):329-337.
43. Dark P, Singer M. The validity of trans-esophageal Doppler ultrasonog-raphy as a measure of cardiac output in critically ill adults. Intensive CareMed. 2004;30:2060-2066.
44. Chytra I, Pradl R, Bosman R, Pelnar P, Kasal E, Zidkova A. EsophagealDoppler-guided fluid management decreases blood lactate levels inmultiple-trauma patients: a randomized controlled trial. Crit Care.2007;11(1):R24.
45. Conway DH, Mayall R, Abdul-Latif MS, Gilligan S, Tackaberry C. Ran-domized controlled trial investigating the influence of intravenous fluidtitration using esophageal Doppler monitoring during bowel surgery.Anaesthesia. 2002;57(9):845-849.
46. Gan TJ, Soppitt A, Maroof M, et al. Goal-directed intraoperative fluidadministration reduces length of hospital stay after major surgery. Anes-thesiology. 2002;97(4):820-826.
47. McKendry M, McGloin H, Saberi D, Caudwell L, Brady AR, Singer M.Randomised controlled trial assessing the impact of a nurse delivered,flow monitored protocol for optimisation of circulatory status after car-diac surgery. BMJ. 2004;329(7460):258-261.
48. Mythen MG, Webb AR. Perioperative plasma volume expansionreduces the incidence of gut mucosal hypoperfusion during cardiac sur-gery. Arch Surg. 1995;130(4):423-429.
49. Sinclair S, James S, Singer M. Intraoperative intravascular volume opti-misation and length of hospital stay after repair of proximal femoralfracture: randomised controlled trial. BMJ. 1997;315(7113):909-912.
50. Venn R, Steele A, Richardson P, Poloniecki J, Grounds M, Newman P.Randomized controlled trial to investigate influence of the fluid chal-lenge on duration of hospital stay and perioperative morbidity inpatients with hip fractures. Br J Anaesth. 2002;88(1):65-71.
51. Wakeling HG, McFall MR, Jenkins CS, et al. Intraoperative oesophagealDoppler guided fluid management shortens postoperative hospital stayafter major bowel surgery. Br J Anaesth. 2005;95(5):634-642.
52. Noblett S, Snowden C, Shenton B, Horgan A. Randomized clinical trialassessing the effect of Doppler-optimized fluid management on out-come after elective colorectal resection. Br J Surg. 2006;93(9):1069-1076.
53. Pearse R, Dawson D, Fawcett J, Rhodes A, Grounds RM, Bennett ED.Early goal-directed therapy after major surgery reduces complicationsand duration of hospital stay: a randomized, controlled trial[ISRCTN38797445]. Crit Care. 2005;9(6):R687-R693.
54. Mayer J, Boldt J, Mengistu AM, Röhm KD, Suttner S. Goal-directedintraoperative therapy based on autocalibrated arterial pressure wave-form analysis reduces hospital stay in high-risk surgical patients: a ran-domized, controlled trial. Crit Care. 2010;14(1):R18. doi:10.1186/cc8875.
55. Goepfert M, Richter H, Eulenburg C, et al. Individually optimizedhemodynamic therapy reduces complications and length of stay in theintensive care unit: a prospective, randomized controlled trial. Anesthe-siology. 2013;119(4):824-836.
56. Salzwedel C, Puig J, Carstens A, et al. Perioperative goal-directed hemo-dynamic therapy based on radial arterial pulse pressure variation andcontinuous cardiac index trending reduces postoperative complicationsafter major abdominal surgery: a multi-center, prospective, randomizedstudy. Crit Care. 2013;17(5):R191. doi:10.1186/cc12885.
57. Van der Linden PJ, Dierick A, Wilmin S, Bellens B, De Hert SG. A ran-domized controlled trial comparing an intraoperative goal-directedstrategy with routine clinical practice in patients undergoing peripheralarterial surgery. Eur J Anaesthesiol. 2010;27(9):788-793.
58. Szakmany T, Toth I, Kovacs Z, et al. Effects of volumetric vs pressure-guided fluid therapy on postoperative inflammatory response: a prospec-tive, randomized clinical trial. Intensive Care Med. 2005;31(5):656-663.
59. Rajaram SS, Desai NK, Kalra A, et al. Pulmonary artery catheters foradult patients in intensive care. Cochrane Database Syst Rev. 2013;2:CD003408. doi:10.1002/14651858.CD003408.pub3.
60. Balk E, Raman G, Chung M, et al. Evaluation of the Evidence on Benefitsand Harms of Pulmonary Artery Catheter Use in Critical Care Settings.Rockville, MD: Agency for Healthcare Research and Quality; March 28,2008. http://www.cms.gov/determinationprocess/downloads/id55TA.pdf. Accessed October 29, 2014.
61. Roche A, Miller T, Gan T. Goal-directed fluid management with trans-oesophageal Doppler. Best Pract Res Clin Anaesthesiol. 2009;23(3):327-334.
62. Schober P, Loer S, Schwarte L. Perioperative hemodynamic monitoringwith transesophageal Doppler technology. Anesth Analg. 2009;109:340-353.
63. Chew HC, Devanand A, Phua GC, Loo CM. Oesophageal Doppler ultra-sound in the assessment of haemodynamic status of patients admittedto the medical intensive care unit with septic shock. Ann Acad Med Sin-gapore. 2009;38(8):699-703.
64. Bendjelid K. Assessing fluid responsiveness with esophageal Dopplerdynamic indices: concepts and methods [comment]. Intensive Care Med.2006;32(7):1088.
65. Monnet X, Pinsky M, Teboul J. FTc is not an accurate predictor of fluidresponsiveness. Intensive Care Med. 2006;32:1090-1091.
66. Johnson A, Schweitzer D. Putting the wedge under pressure [comment].Ann Acad Med Singapore. 2010;39(10):815.
67. Singer M. The FTc is not an accurate marker of left ventricular preload:reply to the comment by Chemla and Nitenberg. Intensive Care Med.2006;32(9):1456-1457.
68. Singer M. The FTc is not an accurate marker of left ventricular preload.Intensive Care Med. 2006;32(7):1089.
69. Madan AK, UyBarreta VV, Aliabadi-Wahle S, et al. Esophageal Dopplerultrasound monitor versus pulmonary artery catheter in the hemody-namic management of critically ill surgical patients. J Trauma. 1999;46(4):607-611.
70. Seoudi H, Perkal M, Hanrahan A, Angood P. The esophageal Dopplermonitor in mechanically ventilated surgical patients: does it work[abstract]? J Trauma. 1999;47(6):1171.
71. DiCorte CJ, Latham P, Greilich PE, Cooley MV, Grayburn PA, Jessen ME.Esophageal Doppler monitor determinations of cardiac output and pre-load during cardiac operations. Ann Thoracic Surg. 2000;69(6):1782-1786.
72. Kincaid H, Fly M, Chang M. Noninvasive measurements of preloadusing esophageal Doppler are superior to pressure-based estimates incritically injured patients [abstract]. Crit Care Med. 1999;27(1):A111.
73. Mark JB, Steinbrook RA, Gugino LD, et al. Continuous noninvasivemonitoring of cardiac output with esophageal Doppler ultrasound dur-ing cardiac surgery. Anesth Analg. 1986;65(10):1013-1020.
74. Valtier B, Cholley BP, Belot JP, Coussay JE, Mateo J, Payen DM. Nonin-vasive monitoring of cardiac output in critically ill patients using trans-esophageal Doppler. Am J Respir Crit Care Med. 1998;158:77-83.
75. Micek ST, Roubinian N, Heuring T, et al. Before-after study of a stan-dardized hospital order set for the management of septic shock. CritCare Med. 2006;34(11):2707-2713.
76. Saberi D, Caudwell L, McGloin H, Singer M. Proactive circulatory man-agement in the first 4 hours postcardiac surgery: interim analysis of anurse-led, oesophageal Doppler-guided protocol [abstract]. IntensiveCare Med. 2000;26(3 suppl):S220.
77. Lynn-McHale Wiegand D, ed. AACN Procedure Manual for Critical Care.6th ed. St Louis, MO: Elsevier Saunders: 2011.
78. Lynn-McHale Wiegand D, Carlson K, eds. AACN Procedure Manual forCritical Care. 5th ed. St Louis, MO: Elsevier; 2005.
79. Edwards Lifesciences. Advanced hemodynamic monitoring. The FloTracsensor: stroke volume variation. http://www.edwards.com/products/mininvasive/Pages/strokevolumevariationwp.aspx. Accessed October30, 2014.
80. Singer M. Continuous Haemodynamic Monitoring by Oesophageal Doppler[doctoral dissertation]. London, England: University of London; April 1989.
81. Starling EH. The Linacre Lecture on the Law of the Heart. London, England:Longmans, Green & Co; 1918.
26 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
82. Ahrens T, Taylor L. Hemodynamic Waveform Analysis. St Louis, MO: WBSaunders; 1992:432, 444-447.
83. Atkins D, Best D, Briss PA, et al; GRADE Working Group. Grading quality ofevidence and strength of recommendations. BMJ. 2004;328(7454):1490-1498.
84. Guyatt G, Gutterman D, Baumann MH, et al. Grading strength of recom-mendations and quality of evidence in clinical guidelines: report from anAmerican College of Chest Physicians task force. Chest. 2006;129(1):174-181.
85. Schünemann HJ, Jaeschke R, Cook DJ, et al; ATS Documents Developmentand Implementation Committee. An official ATS statement: grading thequality of evidence and strength of recommendations in ATS guidelinesand recommendations. Am J Respir Crit Care Med. 2006;174(5):605-614.
86. Mowatt G, Houston G, Hernández R, et al. Systematic review of the clini-cal effectiveness and cost-effectiveness of oesophageal Doppler monitor-ing in critically ill and high-risk surgical patients. Health Technol Assess.2009;13(7):iii-iv, ix-xii, 1-95. doi:10.3310/hta13070.
87. Agency for Healthcare Research and Quality. Esophageal Doppler ultra-sound-based cardiac output monitoring for real-time therapeutic manage-ment of hospitalized patients: a review. http://www.cms.hhs.gov/determinationprocess/downloads/id45TA.pdf. Published January 16,2007. Accessed October 30, 2014.
88. Centers for Medicare and Medicaid Services. CMS manual system: pub100-03 Medicare national coverage determinations. http://www.cms.hhs.gov/Transmittals/Downloads/R72NCD.pdf. Published August 28,2007. Accessed October 31, 2014.
89. Aetna Health Insurance. Clinical policy bulletin: esophageal Dopplermonitoring. Publication No. 0793. http://www.aetna.com/cpb/medical/data/700_799/0793.html. Accessed October 31, 2014.
90. Centers for Medicare and Medicaid Services. CMS manual system: pub100-03 Medicare national coverage determinations. https://www.cms.gov/transmittals/downloads/R63NCD.pdf. Published December 15, 2006.Accessed October 31, 2014.
91. CMS.gov. Billing and coding guidelines. Cardiac catheterization andcoronary angiography. http://downloads.cms.gov/medicare-coverage-database/lcd_attachments/30719_6/L30719_CV006_CBG_010111.pdf. Accessed November 24, 2014.
92. Poeze M, Greve J, Ramsay G. Meta-analysis of hemodynamic optimization:relationship to methodological quality. Critical Care. 2005;9(6):R771-R779.
93. Prentice D, Sona C. Esophageal Doppler monitoring for hemodynamicassessment. Crit Care Nurs Clin North Am. 2006;18:189-193.
94. Dellinger P, Levy M, Carlet J, et al; International Surviving Sepsis Cam-paign Guidelines Committee; American Association of Critical-CareNurses; American College of Chest Physicians; American College ofEmergency Physicians; Canadian Critical Care Society; European Societyof Clinical Microbiology and Infectious Diseases; European Society ofIntensive Care Medicine; European Respiratory Society; InternationalSepsis Forum; Japanese Association for Acute Medicine; Japanese Soci-ety of Intensive Care Medicine; Society of Critical Care Medicine; Societyof Hospital Medicine; Surgical Infection Society; World Federation ofSocieties of Intensive and Critical Care Medicine. Surviving Sepsis Cam-paign: international guidelines for management of severe sepsis and sep-tic shock: 2008 [published correction appears in Crit Care Med.2008;36(4):1394-1396]. Crit Care Med. 2008;36(1):296-327.
95. Wo CC, Shoemaker WC, Appel PL, Bishop MH, Kram HB, Hardin E.Unreliability of blood pressure and heart rate to evaluate cardiac outputin emergency resuscitation and critical illness. Crit Care Med. 1993;21(2):218-223.
96. Shippy C, Appel P, Shoemaker W. Reliability of clinical monitoring to assessblood volume in critically ill patients. Crit Care Med. 1984;12:107-112.
97. Ferrer R, Artigas A, Suarez D, et al; Edusepsis Study Group. Effectivenessof treatments for severe sepsis: a prospective, multicenter, observationalstudy. Am J Respir Crit Care Med. 2009;180(9):861-866.
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CNE Test Test ID C1513: Stroke Volume Optimization: The New Hemodynamic AlgorithmLearning objectives: 1. Discuss the use of stroke volume optimization in a hypovolemic patient 2. Define corrected flow time, peak velocity, stroke distance,and stroke index 3. State various methods used to obtain blood flow measurement
Program evaluation Yes No
Objective 1 was met � �Objective 2 was met � �Objective 3 was met � �Content was relevant to my
nursing practice � �My expectations were met � �This method of CNE is effective
for this content � �The level of difficulty of this test was:
� easy � medium � difficultTo complete this program,
it took me hours/minutes.
5. Which of the following explains why clinicians prefer blood flow
monitoring versus blood pressure monitoring?
a. Compensatory mechanisms mask hypoperfusion
b. Afterload, preload, and contractility are influenced by medications
c. Blood pressure, MAP, and heart rate are late indicators of hypoperfusion
d. All of the above
6. Which of the following changes is expected in a patient who
received a 1000-mL fluid challenge that confirms hypovolemia?
a. Increase in PAOP
b. Increase in urine output
c. Increase in stroke volume, corrected flow time, and cardiac output
d. Increase in CVP and MAP
7. Volume and vasopressors are often the treatment of choice in a
patient with shock. Which of the following parameters are best used
as end points to guide therapy?
a. Stroke volume, peak velocity, and corrected flow time
b. Stroke volume, systemic vascular resistance, and central venous
oxygen saturation (ScvO2)
c. ScvO2, corrected flow time, and peak velocity
d. ScvO2 and stroke volume
8. Nursing implications in obtaining hemodynamic data include
which of the following?
a. Proficiency in application of monitoring device
b. Application of data obtained to patient population
c. Achieving optimal signal acquisition
d. All of the above
9. Mechanical ventilation with positive end-expiratory pressure can
impede blood flow and increase PAOP. How can clinicians deter-
mine proper interventions for this patient population?
a. Trend and optimize stroke volume
b. Trend cardiac filling pressures
c. Closely follow pulmonary vascularity on the chest radiograph
d. Trend blood pressure
For faster processing, takethis CNE test online at
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AACN, 101 Columbia Aliso Viejo, CA 92656.
Test ID: C1513 Form expires: February 1, 2018 Contact hours: 1.0 Pharma hours: 0.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 7 correct (78%) Synergy CERP Category A Test writer: Carol Ann Brooks, BSN, RN, CCRN-K, CSC
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1. �a �b �c �d
9. �a �b �c �d
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6. �a �b �c �d
5. �a �b �c �d
4. �a �b �c �d
3. �a �b �c �d
2. �a �b �c �d
1. Which of the following hemodynamic values help determine
responsiveness to fluid replacement?
a. Stroke volume within normal values
b. Normal stroke volume with normal filling pressures
c. Adequate blood flow for tissue oxygenation without increasing
heart rate
d. Afterload and preload stabilized
2. Which of the following is the first hemodynamic parameter to
decrease in hypovolemia?
a. Pulmonary artery occlusive pressure (PAOP)
b. Central venous pressure (CVP)
c. Cardiac output
d. Stroke volume
3. After mitral valve replacement, your patient’s urine output
decreases over 3 hours. The monitor displays sinus tachycardia
with heart rate 108 beats/min, CVP 8 mm Hg, cardiac output 4
L/min, and mean arterial pressure (MAP) 80 mm Hg. The MAP
remains within normal range because of which of the following?
a. Normal cardiac output
b. No change in circulating volume
c. Compensatory mechanisms
d. MAP is an independent parameter
4. Monitoring stroke volume gives the clinician insight into which
of the following?
a. Blood flow and circulating volume
b. Cardiac filling pressures
c. Oxygenation
d. Contractility
In the United States, 359 400 people experience an out-of-hospital cardiac arrest each year, andless than 9.5% of those people survive.1 Out-of-hospital cardiac arrest continues to be associated
with high mortality, and among those patients who do survive the initial cardiac arrest, two-thirds die
as a result of neurological injury.2 Postresuscitation care is increasingly recognized as an integral component
in improving the quality of survival and neurological outcomes. Although advances have been made in
initial resuscitative efforts; anoxic neurological injury remains a major concern after return of spontaneous
circulation (ROSC).2,3 Therapeutic hypothermia improves neurological outcomes after ROSC.3
Use of a Nursing Checklist toFacilitate Implementation ofTherapeutic HypothermiaAfter Cardiac ArrestKATHLEEN RYAN AVERY, RN, MSN, CCRN
MOLLY O’BRIEN, MPH
CAROL DADDIO PIERCE, RN, MSN, CCRN
PRISCILLA K. GAZARIAN, RN, PhD
©2015 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2015937
Feature
Therapeutic hypothermia has become a widely accepted intervention that is improving neurological outcomes
following return of spontaneous circulation after cardiac arrest. This intervention is highly complex but infre-
quently used, and prompt implementation of the many steps involved, especially achieving the target body
temperature, can be difficult. A checklist was introduced to guide nurses in implementing the therapeutic
hypothermia protocol during the different phases of the intervention (initiation, maintenance, rewarming, and
normothermia) in an intensive care unit. An interprofessional committee began by developing the protocol, a
template for an order set, and a shivering algorithm. At first, implementation of the protocol was inconsistent,
and a lack of clarity and urgency in managing patients during the different phases of the protocol was apparent.
The nursing checklist has provided all of the intensive care nurses with an easy-to-follow reference to facilitate
compliance with the required steps in the protocol for therapeutic hypothermia. Observations of practice and
feedback from nursing staff in all units confirm the utility of the checklist. Use of the checklist has helped reduce
the time from admission to the unit to reaching the target temperature and the time from admission to continuous
electroencephalographic monitoring in the cardiac intensive care unit. Evaluation of patients’ outcomes as related
to compliance with the protocol interventions is ongoing. (Critical Care Nurse. 2015;35[1]:29-38)
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 29
Despite recommendations from the American Heart
Association,3 the European Resuscitation Council and
the International Liaison Committee on Resuscitation4
that therapeutic hypothermia be used in comatose sur-
vivors following ROSC, challenges to implementation of
therapeutic hypothermia in clinical practice remain.
Therapeutic hypothermia is a complex but uncommon
intervention, and because of this, prompt implementation
of the many steps involved and quickly achieving the
desired temperature goal can be difficult.
BackgroundIn 2002, researchers in 2 studies5,6 reported improved
neurological outcomes and a decrease in mortality with
the use of therapeutic hypothermia after out-of-hospital
cardiac arrest. Recently published guidelines from both
the American Heart Association and the International
Liaison Committee on Resuscitation incorporated evi-
dence from research
and recommended
that clinicians imple-
ment therapeutic
hypothermia to increase the likelihood of improved
neurological outcome.3,7 Brain cells die because of several
biochemical processes resulting from cardiac arrest and
the inflammatory process following that injury. Therapeu-
tic hypothermia is believed to be effective because it reduces
cerebral metabolism, decreases cerebral blood flow, and
decreases intracranial pressure.8-10 The neuroprotective
mechanisms of therapeutic hypothermia are now widely
recognized and implemented as a standard of care.3
The American Heart Association recommended that
comatose adult patients with ROSC following out-of-
hospital cardiac arrest be cooled to 32ºC to 34ºC (90ºF-
93ºF) for 12 to 24 hours, with the strongest evidence of
survival for those patients who had pulseless ventricular
tachycardia or ventricular fibrillation rhythms.3 Less
well understood is how the timing of these therapeutic
hypothermia interventions affects patients’ outcomes. In
the 2002 studies published by Bernard et al5 and the
Hypothermia After Cardiac Arrest Study Group,6 target
temperature was reached within 8 hours after ROSC.
Although a prospective observational study11 of 986
patients did not reveal an association between the timing
of therapeutic hypothermia and neurological outcomes,
observational evidence demonstrates a 20% increase in
risk of death for every hour delay in initiating therapeu-
tic hypothermia.12 The evidence is not conclusive; how-
ever, the American Heart Association’s 2010 guidelines
recommended initiating therapeutic hypothermia as
soon as possible after ROSC.3 Our institution’s policy
states that therapeutic hypothermia should be initiated
within 6 hours of ROSC with a goal of achieving target
temperature within 4 hours of initiation of therapeutic
hypothermia. Therapeutic hypothermia has few absolute
contraindications. The ultimate decision to initiate ther-
apeutic hypothermia should be based on an assessment
of the potential risks and benefits of hypothermia in
each individual patient while considering the complete
clinical situation and comorbid conditions.9,13
Recommendations for the Use of Checklists
The implementation of institution-specific standard-
ized protocols, order sets, and a bundled care approach
have proven a successful method in combating the bar-
riers to implementation of therapeutic hypothermia14-20
and were associated with an increased efficiency in
achieving target temperature.21,22
The effectiveness of a surgical safety checklist on rates
of postoperative death and complications was documented
by Haynes et al,23 who reported a decrease in death rate
and complication rate after implementation of a check-
list. In addition to decreasing mortality and complica-
tion rates, surgical checklists have improved compliance
with safety measures, teamwork, and communication.24
Kathleen Ryan Avery is the clinical educator for the cardiac intensivecare unit and co-chair of the Therapeutic Hypothermia Committeeat Brigham and Women’s Hospital, Boston, Massachusetts.
Molly O’Brien is the research coordinator in the cardiac intensivecare unit at Shapiro Cardiovascular Center at Brigham andWomen’s Hospital.
Carol Daddio Pierce is the clinical educator in the medical intensivecare unit at Brigham and Women’s Hospital.
Priscilla K. Gazarian is the nursing program director for resuscita-tive clinical practice at Brigham and Women’s Hospital and anassociate professor of nursing at Simmons College, Boston, Massachusetts.
Corresponding author: Priscilla K. Gazarian, RN, PhD, The Center for Nursing Excel-lence, Brigham and Women’s Hospital, 1 Brigham Circle, 4th Floor, Suite 6, BostonMA 02120 (e-mail: [email protected]).
To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949)362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].
Authors
The effectiveness of a surgical safetychecklist has been documented.
30 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Beginning in 2009, checklists have been adapted and
used to improve patients’ outcomes in other practice
situations such as in interdisciplinary rounds and
meetings, during shift handoff, and at discharge.25-29
Researchers have documented that tools such as check-
lists can increase adherence to evidence-based practice
guidelines,30 so we considered adding a checklist to our
therapeutic hypothermia bundle to support the safe,
effective, and efficient implementation of the therapeutic
hypothermia protocol.
Local ProblemAt our hospital, we have implemented therapeutic
hypothermia in 182 patients in the past 5 years. Until
2009, therapeutic hypothermia was exclusively imple-
mented in the coronary care unit (CCU). Although most
patients who are treated with therapeutic hypothermia
continue to be admitted to the CCU (73%) or the medical
intensive care unit (18%), therapeutic hypothermia is
sometimes provided in the other intensive care units
(ICUs). The number of patients receiving therapeutic
hypothermia has increased steadily each year to a total
of 59 patients in 2013 (Figure 1). Because of the low fre-
quency of therapeutic hypothermia cases and the large
number of nursing staff across different ICUs, months
can pass between case exposures, and each exposure
could be at a different phase of the protocol.
In a review of cases of therapeutic hypothermia at
our institution, we found inconsistencies in the implemen-
tation of the protocol and a lack of clarity and urgency in
managing the patients during the different phases of
the protocol (initiation, maintenance, rewarming, and
normothermia). Despite our having a standardized order
template and nursing policy for therapeutic hypothermia,
our data indicated a need for improvement in our imple-
mentation of the therapeutic hypothermia protocol.
Intended ImprovementCaring for patients after cardiac arrest in a critical
care unit is a complex, tense, and time-sensitive under-
taking. Applying an infrequently used but multifaceted
procedure such as therapeutic hypothermia under these
conditions is challenging and may diminish reliable and
consistent implementation of the intervention. Barriers
to timely implementation exist, including a delayed
decision to implement therapeutic hypothermia, lack of
protocols to guide implementation, the volume of cardiac
arrest patients treated, training, and experience of staff.31
Providing therapeutic hypothermia requires an interdis-
ciplinary collaborative approach initiated in the field by
emergency medicine services (EMS) and continued by
the emergency department, catheterization laboratory,
and the ICUs. The different phases of therapeutic
hypothermia cause physiological changes that require
intense assessment, monitoring, and intervention to
manage shifts in hemodynamics (bradycardia, hypoten-
sion, hypovolemia), electrolytes (hyper- and hypo-
glycemia, hypo- and hyperkalemia), achieving desired
temperature,
managing infec-
tion, and assessing
for evidence of
myoclonus and
seizure activity.8,9,32 Successful implementation of the
therapeutic hypothermia protocol requires collaboration
among many disciplines and is a labor-intensive task
that requires continuous monitoring, assessment, and
multitasking by the bedside nurse to rapidly initiate the
many required protocol interventions during the 4 dif-
ferent phases of therapeutic hypothermia in a 3- to 5-day
period.31-33 In addition, nurses are responsible for pro-
moting patients’ comfort and providing support to
patients’ families during the tenuous period after car-
diac arrest.33-35
Although we were decreasing the time it took to achieve
target temperature, we were not reliably achieving our
Figure 1 Number of patients who had therapeutic hypothermiaby type of intensive care unit.
Abbreviations: CCU, coronary care unit; MICU, medical intensive care unit;SICU, surgical intensive care unit. Other includes neurological, cardiac surgery,and thoracic intensive care units.
40353025201510502009 2010
CCU MICU SICU Other
2011 2012 2013
No. o
f pat
ient
s
Year
Caring for patients after cardiac arrestin a critical care unit is a complex,tense, and time-sensitive undertaking.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 31
target temperature in fewer than 4 hours after the initia-
tion of therapeutic hypothermia (see Table). We proposed
a checklist as an intervention to improve achieving the
desired temperature goal within the recommended 4
hours and to manage the various protocol interventions
and minimize complications.
Since the release of the World Health Organization’s
surgical safety checklist study,23 checklists have gained
prominence in clinical care as visual tools for stan-
dardizing communi-
cation, especially
during high-risk
processes.24 Because
checklists have been
documented as effective tools to improve teamwork
and communication,24 we theorized that a checklist
could improve performance in reaching target tempera-
ture during therapeutic hypothermia.
Study PurposeThe purpose of our checklist was to guide ICU nurses
and the health care team in safely, effectively, and effi-
ciently implementing the therapeutic hypothermia
protocol during the different phases of the intervention
in the ICU to decrease the time required to achieve the
target temperature.
MethodsEthics
Our cardiac arrest registry was reviewed by the
Human Research Committee and was approved as
research limited to health medical records. Data from
the cardiac arrest registry were collected and managed
by using REDCap electronic data capture tools hosted
at Brigham and Women’s Hospital. REDCap (Research
Electronic Data Capture) is a secure, web-based appli-
cation designed to support data capture for research
studies.36 All patient identifiers (date of birth, medical
record number) are restricted from data reporting
within REDCap to protect the confidentiality of the data.
SettingBrigham and Women’s Hospital is a 793-bed academic
medical center with 100 adult ICU beds in 6 units and a
total of 436 critical care staff nurses.
Planning the Intervention: Improving Therapeutic Hypothermia ImplementationWith a Checklist
To achieve optimal, consistent standardized care
for patients receiving therapeutic hypothermia in our
hospital, an interprofessional committee on therapeutic
hypothermia was established in 2008 with representa-
tion from nursing, pharmacy, cardiology, neurology,
pulmonary critical care, emergency medicine, and
interventional cardiology.37 Our committee began by
developing a protocol in 2009, an order template in
2010, and a shivering algorithm in 2011. These resources
had been developed as we gained experience with the
implementation of therapeutic hypothermia and were
based on current evidence. Nurses received ongoing
education on the therapeutic hypothermia protocol via
in-service training sessions and annual competency ses-
sions. As we gained experience in caring for patients
receiving therapeutic hypothermia and as new data
were published, our hospital’s protocol for therapeutic
hypothermia underwent annual revisions.
Based on the positive feedback from the ICU nursing
staff on the 1-page shivering algorithm and building on
the success of the World Health Organization’s surgical
Time measured
Start of therapeutic hypothermia to target temperature
Admission to unit to target temperature
Admission to unit to placement of Arctic Sun
Admission to unit to continuous electroencephalographicmonitoring
After checklist (n = 61)
6:30 (4:32-9:57)
4:00 (2:00-6:56)
0:30 (0:30-1:00)
14:17 (9:15-22:42)
Goal time
< 4:00
< 3:00
—
< 18:00
Before checklist (n = 60)
7:00 (5:30-8:11)
5:47 (4:22-8:03)
1:05 (0:30-2:29)
37:27 (15:00-55:27)
Time, hours:minutes, median (interquartile range)
Table Times needed to complete therapeutic hypothermia interventions after admission to coronary care unit
Checklists have been documented aseffective tools to improve teamworkand communication.
32 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
safety checklist,23 the nursing representatives on the
Therapeutic Hypothermia Committee proposed devel-
oping a checklist on therapeutic hypothermia for inten-
sive care nurses. The goal of this checklist was to improve
the timeliness of achieving the target temperature within
the recommended 4 hours and to manage the various
interventions at all phases of the therapeutic hypother-
mia protocol while minimizing complications and main-
taining safe and high-quality patient care. Relying on a
standardized protocol improves the quality and outcomes
of an intervention such as therapeutic hypothermia.9,16-
18,20,22 Checklists have also been used as tools to increase
the quality and safety in many industries and have gained
popularity in health care. Checklists standardize the
tasks that must be completed and provide a transparent
framework to ensure protocol adherence, all while
establishing a process to share information and support
among caregivers.38
Checklist DevelopmentThe design of our checklist was motivated by our
desire to shorten the time required to reach the target
temperature and provide direction to managing the many
treatment interventions at each stage of the therapeutic
hypothermia protocol. Our existing guideline and order
template became the key interventions captured on the
checklist. Based on the American Heart Association’s
guidelines for postresuscitation care and our guidelines
of care for use of therapeutic hypothermia after cardiac
arrest, we divided interventions into the 4 stages of the
therapeutic hypothermia protocol. The first phase is the
“initiation of cooling” from 0 to 4 hours. The goal is that
the patient will reach the target temperature of 33°C
(91.4°F) within 4 hours of initiation of therapeutic
hypothermia. The next phase is “maintenance of cool-
ing” from 4 to 24 hours. Cooling is maintained for 24
hours from the initiation of therapeutic hypothermia.
Twenty-four hours after the initiation of therapeutic
hypothermia, the “rewarming” phase begins. Rewarming
is done very slowly at a rate of 0.25°C (0.5°F) per hour
and takes 12 to 16 hours. Once the patient reaches 37°C
(98.6°F), the last phase, “normothermia,” is maintained
for 48 hours. We were now able to identify all of the
interventions that needed to be completed to achieve
our first goal of target temperature within 4 hours.
The checklist is designed as 1 page to be kept at the
bedside. It is a quick, easy, just-in-time resource for
nurses, includes a box to be checked when each item is
completed, and is used during handoff communication.
The checklist was first pilot tested in the CCU and was
revised on the basis of staff feedback. We incorporated
the checklist into the hospital policy available online,
and we placed hard copies in a reference book on the unit
for nurses to integrate into patient care. This therapeutic
hypothermia checklist (Figure 2) for intensive care nurses
has been in use since September 2012.
Evaluation and AnalysisData are collected in real time by our research coor-
dinator. An initiation of therapeutic hypothermia report
is generated each time orders for therapeutic hypothermia
are implemented and is sent to all members of the thera-
peutic hypothermia committee for review. This report
includes patients’ demographics (eg, age), initial rhythm,
downtime, times from ROSC to arrival in the emergency
department, from emergency department to ICU admis-
sion, from ROSC to target temperature, from ICU
admission to target temperature, from ICU admission
to placement of Arctic Sun surface cooling device, and
from ICU admission to electroencephalography. The
reports allow us to accurately track the use of therapeu-
tic hypothermia throughout the hospital and to review
cases both as they occur and over time.
The development and implementation of the thera-
peutic hypothermia checklist have provided the nurs-
ing staff in all ICUs with an easy-to-follow reference to
facilitate compliance with the required interventions in
the therapeutic hypothermia protocol. Since 2009, we
have cared for 183 patients receiving therapeutic hypother-
mia at our institution. Despite the various systems in
place, the median time
to target temperature
from ROSC was 8 hours,
double our desired goal
of 4 hours. Since we
began using the checklist, we have reduced our time
from CCU admission to target temperature from a
median time of 5 hours 47 minutes (2009-2011) to 4
hours (2012-2013) in the CCU, where the checklist was
first pilot tested and used consistently. The time from
CCU admission to placement of the Arctic Sun cooling
device has decreased from 1 hour before use of the
checklist to 30 minutes since implementation of the
checklist (see Table).
Nurses report that the checklisthelps them prepare, prioritize,and organize their interventions.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 33
Figure 2 Therapeutic hypothermia (TH) after cardiac arrest: ICU nursing checklist.
Abbreviations: ABG, arterial blood gas analysis; BBG, bedside blood glucose; BHIP, Brigham and Women’s Hospital intravenous insulin protocol; BICS OE, Brigham Inte-grated Computing System order entry; BIS, bispectral index monitoring; BSAS, Bedside Shivering Assessment Scale; Ca, calcium; CBC, complete blood cell count;CK, creatine kinase; CK-MB, creatine kinase–MB fraction; cTnt, cardiac troponin T; CVP, central venous pressure; D/C, discontinue; EEG, continuous electroen-cephalographic monitoring; Glu, glucose; ICU, intensive care unit; IVB, intravenous bolus; K, potassium; labs, samples for laboratory tests; MAP, mean arterial pres-sure; Mg, magnesium; NMBA, neuromuscular blocking agent; q, every; temp, temperature; TOF, train of four.
Courtesy Brigham and Women’s Hospital, Boston, Massachusetts.
This is intended to be a quick reference only—Refer to the ADM 1.4.18 and Nursing NCPM ICU-44 policies for detailson patient management of therapeutic hypothermia. This document is not part of the medical record.
Patient ID stamp Date/Time TH initiated:________
Initiation of cooling 0-4 hours(goal: target temp within 4 hours)
❒ BICS OE template completed by house staff♢ EEG ordered in Precipio
❒ Establish 2 sources of temperature Monitoring to Arctic Sun —preferred order is Foley, esophageal, rectal
❒ Place Arctic Sun pads onadmission to ICU
❒ Sedation infusion (propofol ormidazolam)
❒ Analgesia infusion (fentanyl or hydromorphone)
❒ BIS monitoring❒ Baseline TOF❒ Magnesium 4 g IVB over 4
hours❒ Cover head, hands, feet with
towels/blankets❒ BSAS every hour
♢ If BSAS ≥ 1, follow shiver-ing algorithm
❒ BBG q 1 hour♢ If Glu > 200, start modified
BHIP♢ Turn insulin OFF if
Glu < 200❒ Draw baseline admission labs:
Chem 20, CBC, CK, CK-MB, cTnt, lactic acid, ABG
____ ♢ 4 hours after initiation: serum GLU, K
❒ Target temp (91.4°F) achieved within 4 hours of initiating THIF NOT—refer to shivering algorithm and Arctic Sun troubleshooting chart/guidelines
❒ Document hourly: Patient temperature, Arctic Sun flow, water temperature
❒ Determine time to begin rewarming
Maintenance of cooling4-24 hours
❒ BIS monitoring❒ Continue sedation/analgesia
infusions❒ BSAS q 1 hour
♢ If BSAS ≥ 1, follow shivering algorithm
❒ BBG q 1 hour♢ If Glu > 200, start modified
BHIP♢ Turn insulin OFF if Glu < 200
❒ MAP goal > 75 mm Hg❒ CVP goal > 12 mm Hg❒ Document hourly: Patient temp,
Arctic Sun flow, water temp❒ EEG performed❒ Draw labs q 4 hours after TH
initiation at:____ ♢ 8 hours: Chem 7,
CBC, CK, CK-MB, cTnt, lactic acid, ABG
____ ♢ 12 hours: Glu, K, cultures: blood, sputum,urine
____ ♢ 16 hours: Chem 7, CBC, CK, CK-MB, cTnt, lactic acid, ABG
____ ♢ 20 hours: Glu, K____ ♢ 24 hours: Chem7,
CBC, CK, CK-MB, cTnt,lactic acid, ABG
❒ Hold K+ replacement 4 hours prior to rewarming (unless K < 3.5)
Normothermia x 48 hours AFTER target temp 98.6ºF
❒ Keep Arctic Sun pads on andtarget temp set at 98.6°F/37°C for 48 hours
❒ Wean/discontinue sedation/ analgesia infusions
❒ If NMBA infusion ♢ D/C NMBA infusion♢ Assess TOF every hour♢ When TOF 4/4, wean/
discontinue sedation/ analgesia
❒ Observe for temp spikes andrigors♢ Refer to normothermia
section of shivering algorithm
❒ Document hourly: patient temp, Arctic Sun flow, water temp
❒ Draw labs every 8 hours x 2:♢ Glu, K, Mg, Ca
_______ _______
Rewarming 24-38 hours Date/time:______
❒ Rewarming begins 24 hoursafter initiation of TH
❒ Set Arctic Sun to:♢ target temp of
98.6°F/37°C ♢ rewarm at rate of 0.5°F
(0.25°C) per hour (it will take 12-16 hours to rewarm)
♢ Refer to directions on Arctic Sun and in nursing policy
❒ Continue sedation/analgesia infusions
❒ Draw labs q 4 hours after TH initiation at:____ ♢ 28 hours: Glu, K____ ♢ 32 hours: Glu, K____ ♢ 36 hours: Glu, K❒ BIS monitoring❒ BSAS q 1 hour
♢ If BSAS ≥ 1, follow shivering algorithm during rewarming
❒ BBG q 1 hour♢ If insulin infusion, check
BBG every 30 minutes♢ Turn insulin OFF if
Glu < 200❒ Document hourly: Patient
temp, Arctic Sun flow, water temp
❒ Once target temp of 98.6°F/37°C achieved: Normothermia phase♢ Wean off of sedation
34 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
the management of shivering. The checklist has provided
an opportunity for case discussions with the clinical nurse
educator and has led to an increased understanding of
the rationale for the different therapeutic hypothermia
interventions, including the early use of electroencephalo-
graphic monitoring. We have noted a decrease in time
from CCU admission to initiation of continuous electroen-
cephalographic monitoring from 37.5 hours to 14.25
hours (see Table). The nurses have stated that the thera-
peutic hypothermia checklist aids in clinical decision
making by providing prompts to assist with maintaining
hemodynamic stability and preventing complications
from therapeutic hypothermia.
DiscussionThe use of the therapeutic hypothermia checklist helps
maintain consistent care of patients in the dynamic ICU
Observations of practice and feedback from the
nursing staff in all the ICUs all support the utility of the
therapeutic hypothermia checklist for intensive care
nurses. The checklist has been implemented in units
other than the CCU where therapeutic hypothermia is
used less often. Nurses have reported that using the
therapeutic hypothermia checklist helps them prepare,
prioritize, and organize their interventions when admit-
ting a critically ill patient. Nurses have reported that the
checklist guides nursing documentation and ensures
that future interventions remain on schedule, while also
supporting teamwork and communication. The check-
list helps the nurses to focus on the immediate tasks
and simultaneously view the entire process from begin-
ning to end so that they can anticipate changes as the
patient progresses. We have observed increased use of
the shivering algorithm and nursing documentation of
Mr C, a 55-year-old man, was out jogging one
evening when he experienced a witnessed ven-
tricular fibrillation cardiac arrest. Bystander
cardiopulmonary resuscitation was initiated, and EMS-
activated prompt defibrillation and ROSC were achieved
within 10 minutes. EMS initiated therapeutic hypothermia
with an infusion of iced normal saline (4°C) and ice packs
applied to the neck, axillae, and groin. Mr C arrived in the
emergency department at 9:05 PM with a body temperature
of 36.5°C (97.8°F). Despite Mr C’s history of hypertension
and coronary artery disease (drug-eluting stent to circumflex
artery 5 years earlier), the 12-lead electrocardiogram did
not show evidence of myocardial ischemia or infarction.
An assessment by the emergency department’s team and a
neurology consultant confirmed that Mr C met the criteria
for therapeutic hypothermia: he had experienced a ventric-
ular fibrillation cardiac arrest with ROSC after 10 minutes,
he was comatose (no meaningful response to verbal stimuli),
and there were no contraindications for therapeutic hypother-
mia. The emergency department continued cooling with
ice packs and initiated continuous infusions of propofol
and fentanyl.
Mr C was admitted to the CCU at 12:30 AM with a body
temperature of 35°C (95.2°F). The CCU nursing staff had
prepared for his arrival and anticipated Mr C’s care needs
by using the therapeutic hypothermia checklist. The physi-
cians had entered the therapeutic hypothermia order set and
the necessary equipment including the Arctic Sun surface
cooling device was ready for placement upon Mr C’s arrival
and was started at 12:40 AM. Interventions to prevent shiver-
ing and maintain comfort were initiated. Bispectral monitor-
ing was initiated, and a baseline train of 4 was obtained. Blood
samples for laboratory tests were collected per the therapeutic
hypothermia protocol. Mr C did experience some shivering
that was promptly treated by referring to the shivering algo-
rithm from the therapeutic hypothermia checklist and a target
temperature of 32.7°C (90.9°F) was achieved at 2 AM. Electroen-
cephalographic monitoring was initiated at 9 AM. Cooling
was maintained for 24 hours from the start of therapeutic
hypothermia. The nurse coming on for the next shift was
alerted that Mr C would be due to be rewarmed in 2 hours.
Using the checklist, the nurses reviewed the completed inter-
ventions during the maintenance phase. A potassium level of
3.2 mEq/L had been repleted per protocol 2 hours previously.
The glucose levels had remained less than 200 mg/dL, so
insulin had not been initiated during the cooling phase. Mr C
rewarmed at a rate of 0.25°C (0.5°F) per hour without signif-
icant hypotension, hypoglycemia, or hyperkalemia. Nor-
mothermia (37°C, 98.6°F) was achieved in 14 hours and
maintained per protocol for 48 hours. Mr C’s neurological
and cardiac status improved during his 5-day stay in the CCU,
and he was discharged home on day 10 after receiving an
implantable cardioverter defibrillator. He had good neurolog-
ical recovery as evidenced by a Cerebral Performance Category
score of 1. Mr C returned to work 2 weeks after discharge
from the hospital and resumed his exercise regimen.
CASE STUDY
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 35
environment, where many team members need to col-
laborate with one another. Further, it supports nursing
practice by decreasing the uncertainty for nurses less
familiar with implementing the protocol in this complex
time-pressured situation.
We have introduced a novel checklist for the imple-
mentation of therapeutic hypothermia and demonstrated
further support for the growing body of evidence indi-
cating that checklists and other types of cognitive aids
are effective in improving various complex processes.30
Using a checklist for therapeutic hypothermia has many
implications in addition to the potential to improve
patients’ outcomes. Given that checklists have been
documented as improving teamwork and communica-
tion, their use in therapeutic hypothermia could lead to
improved interdisciplinary collaboration. Further, this
type of support for nursing work increases nurses’
autonomy and allows them more time to focus on pro-
viding holistic care to patients and patients’ families.
LimitationsThis report of the implementation of an ICU nursing
checklist for therapeutic hypothermia to integrate the
evidence for therapeutic hypothermia into practice is
limited by the lack of control over possible confounding
variables that may have affected the time to achieve the
temperature target. Although our practice has improved,
we cannot conclude that this is solely a result of using
the checklist. Nonetheless, we easily integrated the
checklist into practice, and it can be adapted for use in
other institutions.
SummaryThus far, the therapeutic hypothermia checklist for
intensive care nurses has helped the CCU improve 2
metrics related to the implementation of evidence-based
practice of therapeutic hypothermia: the time from CCU
admission to achieving the target temperature and the
time from CCU admission to continuous electroen-
cephalographic monitoring.
Our next challenge will be to focus on the processes
within our system to continue the cooling initiated by
EMS and decrease the time from ROSC to ICU admis-
sion. Further evaluation of compliance with the thera-
peutic hypothermia checklist and the effects on
patients’ outcomes is needed for continuous quality
improvement. CCN
AcknowledgmentsThe authors thank Annmarie Chase, RN, MSN, CEN ED, clinical flow manager, Benjamin M. Scirica, MD, MPH (co-chair), and all members of the TherapeuticHypothermia Committee at Brigham and Women’s Hospital for their guidanceand support in the development of the therapeutic hypothermia checklist forintensive care nurses and the nursing staff of the CCU and medical ICU for theirfeedback on the implementation of the checklist.
Financial DisclosuresNone reported.
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20. Walters EL, Morawski K, Dorotta I, et al. Implementation of a post-car-diac arrest bundle including therapeutic hypothermia and hemodynamicoptimization in comatose patients with return of spontaneous circulationafter out-of-hospital cardiac arrest: a feasibility study. Shock. 2011;35(4):360-366.
21. Kilgannon JH, Roberts BW, Stauss M, et al. Use of a standardized orderset for achieving target temperature in the implementation of therapeutichypothermia after cardiac arrest: a feasibility study. Acad Emerg Med.2008;15(6):499-505.
22. Gessner P, Dugan G, Janusek L. Target temperature with 3 hours: com-munity hospital’s experience with therapeutic hypothermia. AACN AdvCrit Care. 2012;23(3):246-257.
23. Haynes AB, Weiser TG, Berry WR, et al. A surgical safety checklist toreduce morbidity and mortality in a global population. N Engl J Med.2009;360(5):491-499.
24. Lyons VE, Popejoy LL. Meta-analysis of surgical safety checklist effects onteamwork, communication, morbidity, mortality, and safety. Western JNurs Res. 2014;36(2):245-261.
25. Alvarado K, Lee R, Christoffersen E, et al. Transfer of accountability:transforming shift handover to enhance patient safety. Healthcare Quar-terly (Toronto, Ont). 2006;9 Spec No:75-79.
26. Amin Y, Grewcock D, Andrews S, Halligan A. Why patients need leaders:introducing a ward safety checklist. J R Soc Med. 2012;105(9):377-383.
27. Halasyamani L, Kripalani S, Coleman E, et al. Transition of care for hos-pitalized elderly patients—development of a discharge checklist for hos-pitalists. J Hosp Med. 2006;1(6):354-360.
28 Lamb BW, Sevdalis N, Vincent C, Green JSA. Development and evalua-tion of a checklist to support decision making in cancer multidisciplinaryteam meetings: MDT-QuIC. Ann Surg Oncol. 2012;19(6):1759-1765.
29. Piotrowski MM, Hinshaw DB. The safety checklist program: creating aculture of safety in intensive care units. Jt Comm J Quality Improve. 2002;28(6):306-315.
30. Halm MA. Daily goals worksheets and other checklists: are our criticalcare units safer? Am J Crit Care. 2008;17(6):577-580.
31. Foedisch MJ, Viehoefer A. Standard operating procedures: therapeutichypothermia in CPR and post-resuscitation care. Crit Care Med. 2012;12(suppl 2):A4.
32. Olson D, Grissom J, Dombrowski K. The evidence base for nursing careand monitoring of patients during therapeutic temperature management.Ther Hypothermia Temp Manag. 2011;1(4):209-217.
33. Olson DM, Kelly AP, Washam NC, Thoyre SM. Critical care nurses’workload estimates for managing patients during induced hypothermia.Nurs Crit Care. 2008;13(6):305-309.
34. Cushman L, Warren ML, Livesay S. Bringing research to the bedside: therole of induced hypothermia in cardiac arrest. Crit Care Nurs Q.2007;30(2):143-153.
35. McKean S. Induced moderate hypothermia after cardiac arrest. AACNAdv Crit Care. 2009;20(4):342-353.
36. Harris PA, Taylor R, Thielke R, Payne J, Gonzalez N, Conde JG. Researchelectronic data capture (REDCap)—a metadata-driven methodology andworkflow process for providing translational research informatics sup-port. J Biomed Inform. 2009;42(2):377-381.
37. Szumita PM, Baroletti S, Avery KR, et al. Implementation of a hospital-wideprotocol for induced hypothermia following successfully resuscitatedcardiac arrest. Crit Pathw Cardiol. 2010;9(4):216-220.
38. Winters BD, Gurses AP, Lehmann H, Sexton JB, Rampersad CJ, PronovostPJ. Clinical review: checklists—translating evidence into practice. Crit Care.2009;13(6):210.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 37
CCN Fast Facts
Use of a Nursing Checklist to FacilitateImplementation of Therapeutic HypothermiaAfter Cardiac Arrest
CriticalCareNurseThe journal for high acuity, progressive, and critical care nursing
begins. Rewarming is done very slowly at a rate of
0.25°C (0.5°F) per hour and takes 12 to 16 hours.
• Once the patient reaches 37°C (98.6°F), the last
phase, “normothermia,” is maintained for 48 hours.
• The checklist is a quick, easy resource for nurses,
and is used during handoff communication. The
nursing checklist has provided all of the intensive
care nurses with an easy-to-follow reference to
facilitate compliance with the required steps in
the protocol for therapeutic hypothermia.
• Using a checklist for therapeutic hypothermia has
many implications in addition to the potential to
improve patients’ outcomes. Given that checklists
have been documented as improving teamwork
and communication, their use in therapeutic
hypothermia could lead to improved interdiscipli-
nary collaboration. Further, this type of support
for nursing work increases nurses’ autonomy and
allows them more time to focus on providing
holistic care to patients and patients’ families.
• Use of the checklist has helped reduce the time from
admission to the unit to reaching the target tem-
perature and the time from admission to continu-
ous electroencephalographic monitoring in the
cardiac intensive care unit. Evaluation of patients’
outcomes as related to compliance with the proto-
col interventions is ongoing. CCN
FactsTherapeutic hypothermia has become a widely
accepted intervention that is improving neurological
outcomes following return of spontaneous circulation
(ROSC) after cardiac arrest. This intervention is highly
complex but infrequently used, and prompt implemen-
tation of the many steps involved, especially achieving
the target body temperature, can be difficult.
• A checklist was introduced to guide nurses in
implementing the therapeutic hypothermia
protocol during the different phases of the inter-
vention (initiation, maintenance, rewarming,
and normothermia) in an intensive care unit.
• We divided interventions into the 4 stages of
the therapeutic hypothermia protocol so that we
were able to identify all of the interventions that
needed to be completed to achieve our first goal
of target temperature within 4 hours.
• The first phase is the “initiation of cooling” from
0 to 4 hours. The goal is that the patient will reach
the target temperature of 33°C (91.4°F) within 4
hours of initiation of therapeutic hypothermia.
• The next phase is “maintenance of cooling” from
4 to 24 hours. Cooling is maintained for 24 hours
from the initiation of therapeutic hypothermia.
• Twenty-four hours after the initiation of thera-
peutic hypothermia, the “rewarming” phase
Avery KR, O’Brien M, Pierce CD, Gazarian PK. Use of a Nursing Checklist to Facilitate Implementation of Therapeutic Hypothermia After Cardiac Arrest. Critical CareNurse. 2015;35(1):29-38.
38 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Delirium has a substantial impact on health care. This complication is associated with a
15-day increase in hospital length of stay (LOS),1 a financial impact of $4 billion to $16 billion
annually,2 and a 19% increase in 6-month mortality.3 Delirium is common across all patient
settings; the prevalence, however, varies according to acuity of illness. Delirium develops in general
medicine patients at rates ranging from 11% to 42%.4 The highest prevalence of delirium, as high as 87%,
occurs in critically ill patients.5 Understanding the impact of delirium on hospitalized patients makes
prevention and optimal treatment of this complication a priority. Two approaches are used to manage
delirium: use of pharmacological agents and application of nonpharmacological therapies.
NonpharmacologicalInterventions to PreventDelirium: An Evidence-Based Systematic ReviewRYAN M. RIVOSECCHI, PharmD
PAMELA L. SMITHBURGER, PharmD, MS, BCPS
SUSAN SVEC, RN, BSN, CCRN
SHAUNA CAMPBELL, RN, BSN
SANDRA L. KANE-GILL, PharmD, MS
©2015 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2015423
Feature
Development of delirium in critical care patients is associated with increased length of stay, hospital costs, and
mortality. Delirium occurs across all inpatient settings, although critically ill patients who require mechanical
ventilation are at the highest risk. Overall, evidence to support the use of antipsychotics to either prevent or
treat delirium is lacking, and these medications can have adverse effects. The pain, agitation, and delirium
guidelines of the American College of Critical Care Medicine provide the strongest level of recommendation
for the use of nonpharmacological approaches to prevent delirium, but questions remain about which non-
pharmacological interventions are beneficial. (Critical Care Nurse. 2015;35[1]:39-51)
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 39
This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article,which tests your knowledge of the following objectives:
1. Describe the nursing literature on nonpharmacological interventions to prevent delirium2. Discuss nonpharmacological interventions that have been shown to be effective in preventing delirium3. Explain the tools developed for the measurement of delirium in intensive care unit patients
CNE Continuing Nursing Education
The 2013 pain, agitation, and delirium guidelines6 of
the American College of Critical Care Medicine provide
recommendations for the use of pharmacological agents
in the prevention and treatment of delirium. Because of
a lack of compelling data, the guidelines do not provide
a recommendation for a pharmacological protocol or for
a combined nonpharmacological and pharmacological
protocol for prevention of delirium. Furthermore, the
guidelines give a -2C recommendation for pharmacologi-
cal prevention with either haloperidol or atypical
antipsychotics. The lack of evidence supporting the use
of pharmacological agents creates a void in the effective
management of delirium.
The guidelines6 give the highest grade within the
delirium section (1B) to a nonpharmacological preven-
tion strategy, meaning the recommendation is a strong
one backed by a moderate level of evidence. Unfortu-
nately, most of the literature is on nonpharmacological
interventions used in either general medicine, geriatric,
or perioperative patients.7-16 Although critically ill
patients certainly differ from most of the populations of
patients studied, one can reasonably assume that critically
ill patients, who are at the highest risk for delirium, would
also benefit from nonpharmacological interventions. Large
randomized controlled trials with a multi-interventional
approach that includes pharmacological and nonphar-
macological approaches to prevent delirium are needed.17
Any appropriate attempt at such a study requires a strong
understanding of nonpharmacological approaches. The
purpose of this systematic review is to summarize the
available literature on nonpharmacological management
of delirium among all populations of patients. The ulti-
mate goal is to identify which strategies are beneficial to
facilitate the development of a nonpharmacological pro-
tocol that could be implemented for critically ill patients.
MethodsA literature search was completed by using MEDLINE
and EMBASE. With PubMed, the following terms were
used to search MEDLINE for material from 1946 to
October 15, 2013: delirium AND (critically ill, intensive
care, ICU, intensive care unit, OR critical illness), AND
(treatment, prevention, prophylaxis, adjunctive therapy,
OR adjunct therapy). Additional searches in MEDLINE
were then performed with the terms (mobility, animation,
exercise, rehabilitation, physical therapy, OR bicycle),
(light, window, curtains, shades, OR blinds), (earplugs,
ear, noise, OR hearing aid), (sleep, sleep hygiene, OR
sleep deprivation), (eyeglasses, glasses, OR magnifying
lens), orientation, and hydration, each combined with
AND delirium, AND (critically ill, intensive care, ICU,
intensive care unit, OR critical illness). EMBASE was
searched by using the same strategy. The search was
restricted to studies conducted in humans and reported
in English. A second reviewer independently performed
the same search for validation. The titles of all citations
retrieved from the search were reviewed for relevance.
On the basis of the relevance of the title, articles were
selected to be reviewed at the abstract level. Abstracts were
considered for full-text review if delirium was measured
as an outcome (incidence or severity), and the screening
for delirium was completed by using a standardized screen-
ing tool. No further review of an abstract was done if the
study covered was not original research, addressed exclu-
sively pharmacological approaches, or used a combination
of pharmacological and nonpharmacological approaches.
If, after review, the abstract was still deemed applicable,
a full-text review was done in which the same inclusion
40 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Ryan M. Rivosecchi is a second-year pharmacy resident in criticalcare at the University of Pittsburgh Medical Center, PresbyterianHospital, Pittsburgh, Pennsylvania.
Pamela L. Smithburger is an assistant professor of pharmacy andtherapeutics, University of Pittsburgh School of Pharmacy, Pittsburgh,Pennsylvania, and a clinical specialist in the medical intensive careunit at the University of Pittsburgh Medical Center, PresbyterianHospital.
Susan Svec is the clinical director of the medical intensive care unit,University of Pittsburgh Medical Center, Presbyterian Hospital. Sherecently graduated from the master’s of leadership and administrationprogram at California University of Pennsylvania, California,Pennsylvania.
Shauna Campbell is the nursing director of the medical intensive careunit at the University of Pittsburgh Medical Center, PresbyterianHospital.
Sandra L. Kane-Gill is an associate professor of pharmacy andtherapeutics at the University of Pittsburgh School of Pharmacy.She has secondary appointments in the School of Medicine in theClinical Translational Science Institute, Department of CriticalCare Medicine, and the Department of Biomedical Informatics.She is also the critical care medication safety pharmacist at the Uni-versity of Pittsburgh Medical Center in the Department of Pharmacy.
Corresponding author: Sandra Kane-Gill, 918 Salk Hall, 3501 Terrace St, Pittsburgh,PA 15261 (e-mail: [email protected]).
To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949)362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].
Authors
and exclusion criteria were applied
to the text of the article. No inclusion
restrictions were placed on the study
setting or population of patients
(critically ill or not critically ill).
Studies with mixed nonpharmaco-
logical interventions, including non-
pharmacological protocols with
many interventions, were included.
The exclusion of any involvement of
pharmaceuticals was necessary to
evaluate the true benefit of a non-
pharmacological protocol and mini-
mize confounding variables. The
references of the included articles
were reviewed to ensure a compre-
hensive assessment.
ResultsAll Studies
A total of 17 articles7-24 met the
inclusion criteria and were selected
for review (see Figure and Tables 1
and 2). Seven studies18-24 were done
in critically ill patients, 5 in geriatric
general medicine patients,9-13 3 in postoperative patients,14-16
and 2 in patients who had a hip fracture.7,8 A total of 13
of the studies were prospective investigations,7-11,13,15,16,18,21-24
and 4 were randomized control trials.14-16,24 The Confusion
Assessment Method or the Confusion Assessment Method
for the Intensive Care Unit (CAM-ICU) was the most fre-
quently used tool and was used in 10 studies.7-10,13,19-23 The
Neelon and Champagne Confusion Scale was used in 4
evaluations,14-16,24 and the Intensive Care Delirium Screen-
ing Checklist,18 the Diagnostic and Statistical Manual of
Mental Disorders (Fourth Edition; DSM-IV),12 and the
Delirium Screening Scale12 were each used once. The
frequency of delirium screening ranged from less than
daily to 3 times per day.
The incidence of delirium was determined in 12
studies.7-15,18-21 Among these, 9 revealed a benefit of the
nonpharmacological intervention.8-10,12-15,20,21 Table 3 gives
the interventions used in the individual studies. Among
the interventions that were beneficial, the mean reduc-
tion in the incidence of delirium was 24.7%, with a
range of 9.7% to 31.8%. In 6 studies,7,8,10,11,22,23 the dura-
tion of delirium decreased after the addition of the
nonpharmacological intervention. Additionally, among
the 6 evaluations7-10,13,18 of the severity of delirium, all but
1 study9 indicated a reduction in severity. Patients’ LOS
was examined in 6 studies.7,8,11,18-20 Of the 6 studies, the
results of 2 revealed a decrease in LOS.11,19 Among the 3
studies18-20
done in the
ICU, only 1
indicated a
reduction in
LOS.19 When
any outcome related to delirium (incidence, duration,
severity) was examined, only 2 studies11,19 did not show
any benefit from the addition of a nonpharmacological
intervention.
A total of 28 unique nonpharmacological interven-
tions were used in the clinical studies. The most com-
mon interventions associated with any clinical benefit
were mobilization,8,10,20-23 reorientation,9,10,13,18,21 education
of nurses,7,10,12,18,23 and music therapy.9,16,18,20,21 A single
nonpharmacological intervention was examined in 5
studies,12,14-16,24 and multiple nonpharmacological inter-
ventions were examined in 12 investigations.7-10,11,13,18-23
Delirium is associated with multiple negativeconsequences, including increased lengthof stay, higher health care costs, and evenincreased mortality.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 41
Figure Breakdown of articles selected in literature search.
44 Excluded▪ 24 were not original research▪ 6 did not measure delirium or did not
use standard delirium measurement▪ 5 contained pharmacological intervention▪ 5 were not full-text articles▪ 4 did not involve an intervention
Abstracts screened outcomes, delirium screening, and pharmacologicalinterventions
Limit to English and humans 821
54 Selected for full-textreview
17 Included in review
10 Included
References reviewed for inclusion
7 Included
89 Selected for further review of abstract
EMBASE1540 citations
MEDLINE1104 citations
Titles screened for relevance
42 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Reference,year
Milisen et al,7
2001
Marcantonio et al,8 2001
Inouye et al,9
1999
Vidán et al,10
2009
Lundström et al,11 2005
Tabet et al,12
2005
Caplan andHarper,13 2007
Ono et al,14
2011
Taguchi et al,15
2007
McCaffrey,16
2009
Design
Prospective
Prospective,randomized,double-blind
Prospective,individualmatching
Prospective,controlled
Prospective
Case-control,single-blind
Prospective
Randomized,randomizedcontrolled trial
Prospective,randomizedcontrolled trial
Prospective,randomizedcontrolled trial
Screening tool used (frequency)
CAM, modified CAM
CAM (daily)
CAM (daily)
CAM (daily)
DSM-IV criteria(days 1, 3, and 7)
Delirium Rating Scale
CAM (every other day)
MDAS for severity ifCAM positive
NEECHAM (no com-ment on how often)
NEECHAM (twice a day)
NEECHAM (daily for 3 days)
Population (N)
Hip fracture, emergencydepartment/trauma, (26)
Hip fracture, ≥ 65 years old(126)
General medicine,> 70 years old(852)
Geriatric unit, age> 70 years (542)
Age > 70 years,geriatric unit (400)
Age > 70 years,geriatric unit (250)
Age > 70 years,geriatric unit (37)
Esophagectomy(22)
Esophagectomy(11)
Hip or knee surgery, > 75years old (22)
Notable exclusions
Metastatic cancer,life expectancy < 6 months
Inability to completeinterview, low riskfor delirium
Expected hospitalstay <48 hours
None
Patient not presenton unit duringassessment
Severe dementiaDischarged within 48
hours
Nonpharmacological interventions
Nursing educationPoster in units
Module: dehydration, dentures, nutrition supplements, mobilization (physical/occu-pational therapy), glasses, hearing aids,clock, calendar, family presence
Protocol: orientation with care-team namesand day’s schedule, cognitive stimulationactivities, sleep protocol (warm drink,relaxing music, back massage, noise reduction, medication reschedule), mobilization, visual aids, adaptive equipment,hearing aids, hydration
Staff educationPoster in unitsOrientation: clock, calendar, reason for
admission, date, place, family letterGlasses, hearing aidsSleep: warm drink, reschedule medications
and proceduresMobilization: out of bed, catheter removal,
change positions, avoid restraintsHydration: schedule water if ratio of blood urea
nitrogen to serum level of creatinine > 40Nutrition
Medical team educationReorganization of nursing staff
Medical team education
ReorientationCognitive stimulation activitiesFeeding assistanceHydrationVision protocolHearing protocol
Bright light therapy
Bright light therapy
Music therapy
Table 1 Studies included that involved patients who were not critically ill
Abbreviations: CAM, Confusion Assessment Method; DSM-IV, Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition); LOS, length of stay;MDAS, Memorial Delirium Assessment Scale; NEECHAM, Neelon and Champagne Confusion Scale.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 43
Outcomes
No difference in incidence3-day reduction in duration Reduction in the severity (2.94 points)No difference in LOS
18% reduction in incidence17% reduction in severity1.2-day reduction in durationNo difference in LOS
5.1% reduction in incidence56 fewer days delirious28 fewer episodes No difference in severity No difference in recurrence
6.8% reduction in incidence0.4 decrease in severity2.5-hour reduction in durationNo difference in recurrenceNo difference in functional declineNo difference in death
No difference in prevalence at 24 and 72 hours4-day reduction in LOS
9.7% reduction in point prevalence of delirium
31.8% reduction in incidence3.9-point reduction in MDAS score
31.7% reduction in prevalence
34% reduction in incidence at day 3
Decrease in delirium each of the 3 days
Comments
Used resource study nursesScreened only patients with CAM if NEECHAM identified them as
high riskScreened only on days 1, 3, 5, and 8
Recommendations by geriatric consultant based on moduleRecommendations not made if team was already doing them
Less than 50% screened met inclusion criteriaUsed research nursesGeared intervention against risk factorsSame medical team provided care to both groups
Must have risk factor for inclusion Disposition to either geriatric or general medicine decided by
emergency department physicianBaseline characteristics not very similarNote intervention more helpful in intermediate risk
Extensive nursing training for the intervention
Investigators had no role in day-to-day managementUse of daytime assessment and point prevalence could be
underestimated
Patient must have 1 risk factor for enrollmentMean intervention time 14-19 h/wkVery small sample sizeCost analysis
Mean LOS 24.8 daysTwo dropped out because light was too brightAll male populationScreening stopped on postoperative day 5
All male population
All patients received standard pain, mobilization protocolMusic set to play 4 times a day for 1 hour; patients could do
more if they wished to
Antipsychotic use
Not reported
Yes
Not reported
Not reported
Not reported
Not reported
Not reported
Not reported
Not reported
Not reported
In 6 of those studies,8-10,13,20,21 the interventions were
incorporated into a protocol. The mean number of
interventions used per study was 4.1.
ICU StudiesOf the 7 studies18-24 (Table 2) conducted in ICU patients,
6 investigations18,20-24 indicated a benefit in at least 1
delirium-related outcome, including incidence, duration,
or severity. In the remaining study,19 a 0.6-day reduction
in ICU LOS occurred. Only 1 study18 indicated a reduction
in subsyndromal delirium. In all but 1 study,24 more than
1 nonpharmacological intervention was used; mobiliza-
tion, a noise-reduction protocol, and a sleep protocol
were used most often. All studies20-24 that included either
mobilization or noise-reduction or sleep protocols indi-
cated a statistically significant benefit in at least 1 delirium-
related outcome.
DiscussionICU delirium is associated with numerous adverse
consequences, ranging from increased cost to mortality.3,5
As in a multitude of other ailments, prevention is the opti-
mal strategy, especially when effective treatment options
are unavailable. Haloperidol has been studied for preven-
tion and treatment of ICU delirium, but the results have
been inconclusive.25,26 Because of the unconvincing evidence
44 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Reference,year
Skrobik et al,18
2010
Arenson et al,19
2013
Kamdar et al,20
2013
Colombo et al,21 2012
Schweickert et al,22 2009
Needham et al,23 2010
Van Rompaeyet al,24 2012
Design
Prospective
Randomized,cohort
Observational,pre-postdesign
Prospective,observational,2 stage
Prospective,randomized
Prospective
Prospective,randomizedcontrolled trial
Screening tool used (frequency)
ICDSC (3 times a day)
CAM, CAM-ICU (3 times a day)
CAM-ICU (2 times a day)
CAM-ICU (2 times a day)
CAM-ICU (daily)
CAM-ICU (daily)
NEECHAM (daily)
Population (N)
Medical-surgicalICU (1133)
Cardiac surgery(ICU/medicine)(1010)
Medical ICU (300)
Medical-surgicalICU (314)
Medical ICU (104)
Medical ICU (57)
ICU (136)
Notable exclusions
Inpatient death, preexisting structuralbrain disease
Visual or hearingimpairment
Absent limbs, 6-month mortality<50%, cardiac arrest
No exclusions
Minimum score of 10 on GlasgowComa Scale
Hearing impairmentSedation
Nonpharmacological interventions
Nursing educationRadio or compact disc player, reorientation
Private room, no barriersWindows
Sleep: minimize overhead page, turn off television, dim hallway, group care activities
Open blindsPrevent nappingMobilizationMinimize caffeine before bed Sleep: earplugs, eye mask, music
Reorientation: follow mnemonic—use firstname, give information about location, LOS,and illness
ClockRead paper or book, music, radioReduction of night noise
Mobilization, physical/occupational therapyPassive range-of-motion exercises
Mobilization, physical/occupational therapyNursing education
Ear plugs
Table 2 Studies included that involved patients who were critically ill
Abbreviations: CABG, coronary artery bypass graft; CAM, Confusion Assessment Method; ICDSC, Intensive Care Delirium Screening Checklist; ICU, intensive care unit;LOS, length of stay; NEECHAM, Neelon and Champagne Confusion Scale; RASS, Richmond Agitation-Sedation Scale.
for pharmacological management of delirium, nonphar-
macological strategies need to be further evaluated.
The nonpharmacological intervention specifically
discussed in the pain, agitation, and delirium guidelines6
of the American College of Critical Care Medicine is
early mobilization. Our review fully supports this recom-
mendation, and we think early mobilization should be
included, when feasible, in any nonpharmacological
prevention protocols implemented across all practice
settings. Some type of mobilization was used in 6 stud-
ies,8,10,20-23 and 4 of the types8,10,20,21 were included in proto-
cols with many interventions. The 2 studies22,23 in which
mobilization was not part of a protocol were conducted
in medical ICU patients receiving mechanical ventilation,
and the results showed benefits for all outcomes evaluated.
The onus then switches to the development of a
nonpharmacological protocol to prevent delirium, but
the ideal protocol has not yet been developed. One start-
ing point would be to use the known risk factors for
delirium and target interventions to patients who have
these risk factors. This strategy was used by Inouye et al,9
who created a standardized protocol to combat 6 risk
factors: cognitive impairment, sleep deprivation, immo-
bility, visual impairment, auditory impairment, and
dehydration. The observational PRE-DELIRIC (PREdic-
tion of DELIRium in ICu patients) study27 was done in
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 45
Outcomes
No difference in rate of delirium8.7% reduction in ICDSC score = 08.4% reduction in subsyndromal deliriumNo difference in LOS (patients with delirium)
No difference between environmentsDay 3 median day of onset0.6-day reduction in ICU LOS
5% increase in delirium-free or coma-free days20% reduction in incidence of delirium or comaNo difference in ICU mortalityNo difference in ICU LOS
13.5% reduction in incidenceMean onset on day 2Delirium increased ICU LOS by 2 days
2-day reduction in ICU delirium days24% decrease in ICU time with delirium13% decrease in hospital days with delirium
8% reduction in days delirious32% increase in days not delirious24% decrease in days unable to assess
2-point reduction on NEECHAM score25% reduction when delirium and mild confusion
grouped together
Comments
Hospital does not provide cardiac surgery or trauma careNurses could give haldoperidol if ICDSC score > 3No difference in antipsychotic administered
Same anesthetic used63.9% underwent CABG, 71.7% men6.2% delirium in < 65-year-olds vs 21.4% in > 65-year-oldsBaseline characteristics very different
Primary outcome delirium-coma combination according toCAM/RASS
Delirium secondary outcomeCompared ICU with post-ICUPrimarily respiratory failure patientsPrimary outcome of sleep quality: no difference
Used research nursesStandardized sedation protocolAll treatment haloperidol or olanzapineMedical ICU significantly higher rates of deliriumMidazolam use hazard ratio of 2.145
All patients received mechanical ventilationLess than 10% of patients in medical ICU includedDelirium a secondary outcome
Inclusion was mechanical ventilation ≥ 4 daysRoutine delirium screening not part of standard care before
project startedNo delirium assessments on 15 (pre) and 28 (post) patient days
NEECHAM scorer blinded to use of ear plugsLowest NEECHAM score used for calculation of incidence
Antipsychotic use
Yes
Not reported
Yes
Yes
Yes
Not reported
Not reported
an ICU, and multivariate logistic regression analysis
indicated that 10 of the 25 risk factors evaluated were
predictive of delirium. Unfortunately, the majority of
the predictors, such as age and scores on the Acute
Physiology and Chronic Health Evaluation II, were
characteristics
that could not
be altered by
use of a
nonpharmaco-
logical inter-
vention. Although creation of a protocol based on risk
factors is an excellent starting point, efforts must be
directed toward modifiable health care–associated
exposures and not nonmodifiable susceptibilities.
Protocols with many interventions would be needed
in order to include the many risk factors for delirium
identified through the literature and to combat each fac-
tor appropriately. Marcantonio et al8 attempted to devise
such a protocol. They developed a geriatric consultation
that encompassed 10 modules with at least 2 recommen-
dations to be made for each module. Collectively, 31
recommendations potentially could have been used.
Implementation of the appropriate recommendations
for each patient resulted in one of the largest reductions
in both incidence and severity of delirium. Vidán et al10
also used a multicomponent intervention and had results
similar to those of Marcantonio et al.8 The inevitable
follow-up question becomes, Is a certain aspect of these
multicomponent interventions leading to the positive
results, and, if so, what aspect?
The importance of a protocol that includes multiple
interventions is evident when the outcomes of studies with
2 or fewer interventions7,11,12,14-16,18,19,22-24 are compared with
the outcomes of studies with many interventions.8-10,13,20,21
For incidence of delirium, the multi-interventional pro-
tocols resulted in a 15.9% mean reduction, whereas those
with 2 or fewer interventions showed an 11% reduction.
The 11% reduction is slightly misleading because 4 of the
11 studies7,11,18,19 with 2 or fewer interventions did not
46 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Implementation of the appropriate recommendations for each patientresulted in one of the largest reductionsin both incidence and severity of delirium.
Table 3 Interventions showing benefita
a Key: X, trial in patients who were not critically ill; #, trial in critically ill patients.
Refe
renc
e
Nurs
ing
educ
atio
n
Visu
al d
ispl
ays
Hydr
atio
n
Dent
ures
Nutri
tion
Mob
ility
Eye
prot
ocol
Hear
ing
prot
ocol
Cloc
k
Cale
ndar
Fam
ily
Reor
ient
atio
n
Mus
ic
Daily
sch
edul
e
Cogn
itive
stim
ulat
ion
War
m d
rink
Back
mas
sage
Ligh
t the
rapy
Nois
e re
duct
ion
Med
icat
ion/
proc
edur
e re
sche
dule
Adap
tive
equi
pmen
t
Cath
eter
rem
oval
Avoi
danc
e of
rest
rain
ts
Open
blin
ds
Min
imiza
tion
of c
affe
ine
befo
re b
ed
Eye
mas
k
Dim
hal
lway
s at
nig
ht
7 X X8 X X X X X X X X X18 # # #9 X X X X X X X X X X X X X10 X X X X X X X X X X X X X20 # # # # # # #21 # # # # # #22 #23 # #12 X13 X X X X X X14 X15 X24 #16 X
indicate any difference in the incidence of delirium,
whereas all 6 of the multi-interventional studies8-10,13,20,21
indicated a reduction in incidence of at least 5.1%.
Another strategy, included in 6 studies,7,10-12,18,23 was
extensive education of nurses. The specifics of the educa-
tion were typically not reported, but the material tended
to focus on the effects of delirium, screening for delirium,
and, at times, implementation of the investigators’ pro-
tocol. This strategy was used as the sole intervention in
2 studies.11,12 Milisen et al7 used education of nurses and
prominent display of educational material, both of which
resulted in no difference in the incidence of delirium or
the LOS, but a positive reduction in both the duration
and the severity of delirium. Tabet et al12 concentrated
on an education-only strategy for both nurses and
physicians and reported a 9.7% reduction in the point-
prevalence of delirium. However, the investigators used
the Delirium Rating Scale, a screening tool that is not
recommended in the guidelines6 of the American College
of Critical Care Medicine. Whether or not the results
would be the same if either the Intensive Care Delirium
Screening Checklist or the CAM-ICU were used is not
clear. Last, Lundström et al11 used a similar strategy but
also included a reorganization of the nursing staff. These
investigators noted no difference in the prevalence of
delirium at 24 or 72 hours. Patients in the study were
tested for delirium by using the DSM-IV on hospital days
1, 3, and 7. Because the DSM-IV is a set of diagnostic
criteria and not a delirium screening tool, whether or
not these results can reliably be compared with the
results of other studies in which screening for delirium
was used is unclear.12
We would be remiss if we did not address the notion
that perhaps the best protocol simply involves high-level
nursing care. Most of the unique interventions used in
the studies reviewed could be easily incorporated into
everyday nursing for every patient regardless of the
patient’s risk factors for delirium. Notable exceptions
would be early mobility, nutrition, and catheter removal.
An inability to determine if certain aspects of a newly
implemented protocol were already routine nursing
practice before the protocols were implemented is a lim-
itation of most published studies of nonpharmacological
interventions. Unfortunately, a study that could indicate
a true level of the benefit of each intervention would not
be feasible, because such a study would require nurses
to stop providing standard care. Additionally, any future
studies must include use of a standardized screening
tool, preferably either the CAM-ICU or the Intensive
Care Delirium Screening Checklist, to allow accurate
interpretation of the impact of any future interventions
or protocol.
Implications for Critical Care NursesAlthough we reviewed of studies of both critically ill
and non–critically ill patients, we think that a variety of
interventions that benefit patients who are not critically
ill would still be useful in an ICU. The evidence shows
that targeting interventions to prevent or treat known
risk factors for delirium have the greatest benefit (eg,
cognitive stimulation, reorientation), and a great deal
of overlap exists between risk factors for both critically
and non–critically ill patients. A wide variety of patients
are treated in ICUs, and the variety of specialized ICUs
can be as unique as the patients treated within the units.
For these reasons, strong consideration should be given
to having ICUs implement nonpharmacological inter-
ventions that have been beneficial for patients who were
not critically ill.
Multicomponent intervention protocols to combat
delirium have proved beneficial. On the basis of guideline
recommendations and the strength of literature, these
protocols should include early mobilization, education
of nurses, and cognitive stimulation with reorientation.
Depending on the severity of a patient’s illness, a variety
of ways can
be used to
accomplish
early mobi-
lization.
Mobilization can be as complete as full physical or occu-
pational therapy treatments or merely passive range-of-
motion exercises. Bedside nurses and other members of
the medical team work together to decide the level of
mobilization a patient can complete. Additionally, nurses
can advocate for removal of tubes, catheters, or restraints
that may prevent early mobilization.
Second, education of nurses is an essential component
of the success of any new intervention or initiative. The
literature describes a variety of strategies for educating
nurses, including didactic lectures, visual displays, and
one-on-one sessions. In order to include the potentially
large number of nurses who need to be educated, educa-
tion should be directed at all types of learners.28,29 Last,
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 47
All studies that included mobilization, noise-reduction, or sleep protocols displayeda benefit in the reduction of delirium.
cognitive stimulation and reorientation is a rather broad
term that allows each nurse to develop a strategy that
works for him or her. Still, each nurse’s intervention
should incorporate a few key components, such as
determining how the patient would like to be addressed,
frequent reorientation to date and time, providing updates
on the patient’s schedule and clinical status, and convers-
ing with the patient in a manner that requires memory
recall by the patient.
The implementation of a new intervention or initiative
is often met with resistance to change. In order to mini-
mize this resistance, obtaining nurses’ acceptance of and
willingness to support the change becomes imperative.
One strategy to eliminate high levels of resistance is to
educate nurses about the dangers and implications of
the development of delirium while stressing that patients
become increasingly difficult to care for once delirium
occurs. Another frequent reason for resistance is an
overall lack
of time during
the nursing
shift to add
additional
tasks to be completed; however, most interventions we
have mentioned in this review could be worked into a
nurse-implemented protocol that would require no more
than 5 to 10 minutes per nursing shift to accomplish.
Assembling a multidisciplinary team (physician, nurse,
pharmacist, and respiratory therapist) to determine
which nonpharmacological interventions are feasible
within each specific unit is important. Ultimately the
success of a nonpharmacological protocol to prevent
delirium lies with the bedside nurses, who have the
most frequent contact with patients.
ConclusionUse of nonpharmacological interventions is essential
for the prevention of delirium. These interventions can
be a low-risk, low-cost strategy that has shown a benefit
in most studies. Nonpharmacological therapy also has
the potential to decrease the off-label use of antipsychotics
for the treatment of delirium. The largest challenge in
developing a nonpharmacological protocol is determin-
ing what interventions to include. Although a “one-size-
fits-all” protocol may not be available, a strong body of
evidence supports the inclusion of education of the med-
ical team, reorientation with cognitive stimulation, and
early mobility in any protocol created. ICU staff should
assemble a multidisciplinary team to review interven-
tions of known benefit to determine which ones can be
implemented within the staff ’s specific unit. CCN
Financial DisclosuresNone reported.
References1. Salluh JI, Soares M, Teles JM, et al; Delirium Epidemiology in Critical
Care Study Group. Delirium epidemiology in critical care (DECCA): an international study. Crit Care. 2010;14(6):R210. doi:10.1186/cc9333.
2. Pun BT, Ely EW. The importance of diagnosing and managing ICUdelirium. Chest. 2007;132(2):624-636.
3. Ely EW, Shintani A, Truman B, et al. Delirium as a predictor of mortal-ity in mechanically ventilated patients in the intensive care unit. JAMA.2004;291(14):1753-1762.
4. Siddiqi N, House AO, Holmes JD. Occurrence and outcome of deliriumin medical in-patients: a systematic literature review. Age Ageing. 2006;35(4):350-364.
5. Balas MC, Rice M, Chaperon C, Smith H, Disbot M, Fuchs B. Managementof delirium in critically ill older adults. Crit Care Nurse. 2012;32(4):15-26.
6. Barr J, Fraser GL, Puntillo K, et al; American College of Critical Care Med-icine. Clinical practice guidelines for the management of pain, agitation,and delirium in adult patients in the intensive care unit. Crit Care Med.2013;41(1):263-306.
7. Milisen K, Foreman MD, Abraham IL, et al. A nurse-led interdisciplinaryintervention program for delirium in elderly hip-fracture patients. J AmGeriatr Soc. 2001;49(5):523-532.
8. Marcantonio ER, Flacker JM, Wright RJ, Resnick NM. Reducing deliriumafter hip fracture: a randomized trial. J Am Geriatr Soc. 2001;49(5):516-522.
9. Inouye SK, Bogardus ST Jr, Charpentier PA, et al. A multicomponentintervention to prevent delirium in hospitalized older adults. N Engl JMed. 1999;340(9):669-676.
10. Vidán MT, Sánchez E, Alonso M, Montero B, Ortiz J, Serra JA. An inter-vention integrated into daily clinical practice reduces the incidence ofdelirium during hospitalization in elderly patients. J Am Geriatr Soc.2009;57(11):2029-2036.
11. Lundström M, Edlund A, Karlsson S, Brännström B, Bucht G,Gustafson Y. A multifactorial intervention program reduces the dura-tion of delirium, length of hospitalization, and mortality in deliriouspatients. J Am Geriatr Soc. 2005;53(4):622-628.
12. Tabet N, Hudson S, Sweeney V, et al. An educational intervention canprevent delirium on acute medical wards. Age Ageing. 2005;34(2):152-156.
13. Caplan GA, Harper EL. Recruitment of volunteers to improve vitality inthe elderly: the REVIVE study. Intern Med J. 2007;37(2):95-100.
14. Ono H, Taguchi T, Kido Y, Fujino Y, Doki Y. The usefulness of brightlight therapy for patients after oesophagectomy. Intensive Crit Care Nurs.2011;27(3):158-166.
15. Taguchi T, Yano M, Kido Y. Influence of bright light therapy on postop-erative patients: a pilot study. Intensive Crit Care Nurs. 2007;23(5):289-297.
16. McCaffrey R. The effect of music on acute confusion in older adultsafter hip or knee surgery. Appl Nurs Res. 2009;22:107-112.
17. Khan BA, Zawahiri M, Campbell NL, et al. Delirium in hospitalizedpatients: implications of current evidence on clinical practice and futureavenues for research—a systematic evidence review. J Hosp Med. 2012;7(7):580-589.
48 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Multicomponent protocols targetingknown risk factors for delirium appear tohave benefits over single interventions.
Now that you’ve read the article, create or contribute to an online discussionabout this topic using eLetters. Just visit www.ccnonline.org and select the articleyou want to comment on. In the full-text or PDF view of the article, click“Responses” in the middle column and then “Submit a response.”
To learn more about caring for patients with delirium, read“Impact of a Delirium Screening Tool and Multifaceted Educationon Nurses’ Knowledge of Delirium and Ability to Evaluate It Correctly” by Gesin et al in the American Journal of Critical Care,January 2012;21:e1-e11. Available at www.ajcconline.org.
18. Skrobik Y, Ahern S, Leblanc M, Marquis F, Awissi DK, Kavanagh BP.Protocolized intensive care unit management of analgesia, sedation,and delirium improves analgesia and subsyndromal delirium rates[published correction appears in Anesth Analg. 2012;115(1):169]. AnesthAnalg. 2010;111(2):451-463.
19. Arenson BG, MacDonald LA, Grocott HP, Heibert BM, Arora RC. Effectof intensive care unit environment on in-hospital delirium after cardiacsurgery. J Thorac Cardiovasc Surg. 2013;146(1):172-178.
20. Kamdar BB, Yang J, King LM, et al. Developing, implementing, andevaluating a multifaceted quality improvement intervention to promotesleep in an ICU. Am J Med Qual. 2014;29(6):546-554.
21. Colombo R, Corona A, Praga F, et al. A reorientation strategy for reducingdelirium in the critically ill: results of an interventional study. MinervaAnestesiol. 2012;78(9):1026-1033.
22. Schweickert WD, Pohlman MC, Pohlman AS, et al. Early physical andoccupational therapy in mechanically ventilated, critically ill patients: arandomised controlled trial. Lancet. 2009;373(9678):1874-1882.
23. Needham DM, Korupolu R, Zanni JM, et al. Early physical medicineand rehabilitation for patients with acute respiratory failure: a qualityimprovement project. Arch Phys Med Rehabil. 2010;91(4):536-542.
24. Van Rompaey B, Elseviers MM, Van Drom W, Fromont V, Jorens PG.
The effect of earplugs during the night on the onset of delirium andsleep perception: a randomized controlled trial in intensive care patients.Crit Care. 2012;16(3):R73.
25. Wang W, Li HL, Wang DX, et al. Haloperidol prophylaxis decreasesdelirium incidence in elderly patients after noncardiac surgery: a ran-domized controlled trial. Crit Care Med. 2012;40(3):731-739.
26. Page VJ, Ely EW, Gates S, et al. Effect of intravenous haloperidol on theduration of delirium and coma in critically ill patients (Hope-ICU): arandomised, double-blind, placebo-controlled trial. Lancet Respir Med.2013;1(7):515-523.
27. van den Boogaard M, Pickkers P, Slooter AJ, et al. Development and val-idation of PRE-DELIRIC (PREdiction of DELIRium in ICu patients)delirium prediction model for intensive care patients: observationalmulticentre study. BMJ. 2012;344:e420.
28. Devlin JW, Marquis F, Riker RR, et al. Combined didactic and scenario-based education improves the ability of intensive care unit staff to recog-nize delirium at the bedside. Crit Care. 2008;12(1):R19.
29. Gesin G, Russell BB, Lin AP, Norton HJ, Evans SL, Devlin JW. Impact ofa delirium screening tool and multifaceted education on nurses’ knowl-edge of delirium and ability to evaluate it correctly. Am J Crit Care. 2012;21(1):e1-e11.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 49
CCN Fast Facts
Nonpharmacological Interventions to Prevent Delirium: An Evidence-Based Systematic Review
CriticalCareNurseThe journal for high acuity, progressive, and critical care nursing
patient can complete. Additionally, nurses can advo-
cate for removal of tubes, catheters, or restraints that
may prevent early mobilization.
• Education of nurses is an essential component of the
success of any new intervention. In order to include
the potentially large number of nurses who need to
be educated, education should be directed at all
types of learners.
• Cognitive stimulation and reorientation is a broad
term that allows each nurse to develop an individual
strategy. Still, each nurse’s intervention should
incorporate a few key components, such as deter-
mining how the patient would like to be addressed,
frequent reorientation to date and time, providing
updates on the patient’s schedule and clinical status,
and conversing with the patient in a manner that
requires memory recall by the patient.
• Obtaining nurses’ acceptance of and willingness to
support the new intervention is imperative.
• One reason for resistance is a lack of time during the
nursing shift to add additional tasks. Assembling a
multidisciplinary team (physician, nurse, pharma-
cist, respiratory therapist) to determine which non-
pharmacological interventions are feasible within
each specific unit is important.
• Ultimately the success of a nonpharmacological protocol
to prevent delirium lies with the bedside nurses, who
have the most frequent contact with patients. CCN
FactsDevelopment of delirium in critical care patients is
associated with increased length of stay, hospital costs,
and mortality. The pain, agitation, and delirium guide-
lines of the American College of Critical Care Medicine
provide the strongest level of recommendation for the
use of nonpharmacological approaches to prevent
delirium, but questions remain about which nonphar-
macological interventions are beneficial.
• Prevention is the optimal strategy, especially
when effective treatment options are unavailable.
Haloperidol has been studied for prevention and
treatment of intensive care unit (ICU) delirium,
but the results have been inconclusive.
• A variety of interventions that benefit patients
who are not critically ill would still be useful in
an ICU. The evidence shows that targeting inter-
ventions to prevent or treat known risk factors
for delirium have the greatest benefit (eg, cogni-
tive stimulation, reorientation), and a great deal
of overlap exists between risk factors for both
critically and non–critically ill patients.
• Multicomponent intervention protocols to
combat delirium have proved beneficial. These
protocols should include early mobilization,
education of nurses, and cognitive stimulation
with reorientation.
• Mobilization can be as complete as full physical
or occupational therapy treatments or merely
passive range-of-motion exercises. Bedside nurses
and other members of the medical team work
together to decide the level of mobilization a
Rivosecchi RM, Smithburger PL, Svec S, Campbell S, Kane-Gill SL. Nonpharmacological Interventions to Prevent Delirium: An Evidence-Based Systematic Review.Critical Care Nurse. 2015;35(1):39-51.
50 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
CNE Test Test ID C1512: Nonpharmacological Interventions to Prevent Delirium: An Evidence-Based Systematic ReviewLearning objectives: 1. Describe the nursing literature on nonpharmacological interventions to prevent delirium 2. Discuss nonpharmacological interven-tions that have been shown to be effective in preventing delirium 3. Explain the tools developed for the measurement of delirium in intensive care unit patients
Program evaluation Yes No
Objective 1 was met � �Objective 2 was met � �Objective 3 was met � �Content was relevant to my
nursing practice � �My expectations were met � �This method of CNE is effective
for this content � �The level of difficulty of this test was:
� easy � medium � difficultTo complete this program,
it took me hours/minutes.
7. Which of the following is the nonpharmacological intervention specificallydiscussed in the pain, agitation, and delirium guidelines of the AmericanCollege of Critical Care Medicine?a. Music therapyb. Reorientationc. Nursing educationd. Early mobilization
8. Which of the following is used to allow accurate interpretation of theimpact of future interventions to reduce delirium?a. Biostatisticsb. Multiple regression analysisc. Bonferroni multiple comparison testd. Standardized screening tool
9. The evidence-based literature supports which of the following nonphar-macological interventions to combat delirium?a. Nursing education, mobility, and cognitive stimulation with reorientationb. Nursing education, mobility, and art therapyc. Mobility, cognitive stimulation with reorientation, and art therapyd. Mobility, exercise therapy, and cognitive stimulation with reorientation
10. Which of the following nonpharmacological interventions allows eachnurse to develop a strategy that works for him or her?a. Mobilizationb. Nursing educationc. Cognitive stimulation and reorientationd. Music therapy
11. Which of the following is a strategy for educating nurses about non-pharmacological interventions that help reduce delirium?a. Visual displaysb. Case study analysisc. Excel spread sheetd. PowerPoint self-learning modules
12. Which of the following is essential for the prevention of delirium?a. Pharmacological therapyb. Nonpharmacological interventionsc. Occupational therapyd. Speech therapy
For faster processing, takethis CNE test online at
www.ccnonline.org or mail this entire page to:
AACN, 101 Columbia Aliso Viejo, CA 92656.
Test ID: C1512 Form expires: February 1, 2018 Contact hours: 1.0 Pharma hours: 0.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%) Synergy CERP Category A Test writer: Lynn C. Simko, PhD, RN, CCRN
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Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1. �a �b �c �d
12. �a �b �c �d
11. �a �b �c �d
10. �a �b �c �d
9. �a �b �c �d
8. �a �b �c �d
7. �a �b �c �d
6. �a �b �c �d
5. �a �b �c �d
4. �a �b �c �d
3. �a �b �c �d
2. �a �b �c �d
1. The highest prevalence of delirium occurs in which of the followingpatient populations?a. Nursing home patientsb. Critically ill patientsc. General medicine patientsd. Perioperative patients
2. Exclusion criteria of the research described in this manuscript includewhich of the following?a. Not original researchb. Delirium measured as an outcomec. Screening for delirium using a standardized screening toold. Incidence or severity of delirium was an outcome measure
3. Excluding any manuscripts involved with pharmaceuticals was necessaryto evaluate the true benefit of a nonpharmacological protocol and to minimizewhich of the following?a. Validity and reliability issuesb. Hierarchies of evidencec. Confounding variablesd. Cleaning and coding data
4. Which of the following tools was used most frequently in the deliriumresearch?a. Delirium Screening Scaleb. Neelon and Champagne Confusion Scalec. Intensive Care Delirium Screening Checklistd. Confusion Assessment Method for the Intensive Care Unit
5. In several studies, the duration of delirium decreased after the additionof which of the following?a. Nonpharmacological interventionsb. Pharamacological interventionsc. Haloperidold. Lorazepam
6. Which of the following factors were examined in outcomes related todelirium?a. Incidence, duration, and severityb. Decreasing length of stayc. Mobilityd. Reorientation
Heat stroke is a persistent problem among firefighters,1 athletes,2 and militarypersonnel,3 all of whom have occupations that require physical exertion inhumid or hot environments. Military occupations in particular involve physically
demanding tasks, such as carrying heavy loads for extended periods, often with
unpredictable rest periods.4 When protective equipment such as body armor is
worn, heat dissipation is further blocked.5 These extreme conditions place US military personnel
and the military nurses who care for them at risk for heat injuries.6
Heat stress is determined by environmental (ie, radiant and ambient temperature, air movement,
and humidity) and behavioral (eg, ergogenic agents, work intensity, and protective clothing) factors.7,8
Just a few of these risk factors combined can quickly lead to an exertional heat injury. The less severe
conditions can be treated on site with the person resuming normal activities the same day. Conversely,
exertional heat stroke (EHS) is a life-threatening emergency, and rapid cooling must be administered
immediately to ensure survival.9 The high incidence of heat illnesses3 in the US military might indicate
that rapid recognition of heat injury and use of sound clinical nursing practices are not being applied
consistently from ship to ship or unit to unit. Because EHS morbidity and mortality are preventable,
it is important that critical care nurses in the Navy and other branches of the military rapidly recognize
Exertional Heat Stroke inNavy and Marine Personnel:A Hot TopicCARL W. GOFORTH, RN, PhD, CCRN
JOSH B. KAZMAN, MS
©2015 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2015257
Military Critical Care Nursing: Navy
Although exertional heat stroke is considered a preventable condition, this life-threatening emergency affects
hundreds of military personnel annually. Because heat stroke is preventable, it is important that Navy critical
care nurses rapidly recognize and treat heat stroke casualties. Combined intrinsic and extrinsic risk factors
can quickly lead to heat stroke if not recognized by deployed critical care nurses and other first responders.
In addition to initial critical care nursing interventions, such as establishing intravenous access, determining
body core temperature, and assessing hemodynamic status, aggressive cooling measures should be initiated
immediately. The most important determinant in heat stroke outcome is the amount of time that patients
sustain hyperthermia. Heat stroke survival approaches 100% when evidence-based cooling guidelines are fol-
lowed, but mortality from heat stroke is a significant risk when care is delayed. Navy critical care and other
military nurses should be aware of targeted assessments and cooling interventions when heat stroke is sus-
pected during military operations. (Critical Care Nurse. 2015;35[1]:52-59)
52 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
and treat patients with potential EHS during military
operations. Previous military reviews have focused on
organizational practices and the onus of responsibility
for EHS up the chain of command.10 For critical care mil-
itary nurses, however, it is crucial to rapidly recognize
and treat heat stroke in the field. Therefore, the aim of
this column is to discuss the definition, risk factors,
treatment, and nursing implications of EHS.
Definition of Heat StrokeHeat stroke is a life-threatening emergency charac-
terized by a rapid increase in the body’s core temperature
(Tcore) to greater than 40°C (104°F), multiple organ dys-
function,9 and central nervous system abnormalities (eg,
delirium, confusion, agitation),11 with a mortality rate as
high as 18% in military populations.12 Exertional heat
stroke, especially when combined with strenuous activity,
can occur during exposure to hot or mild climates. Con-
versely, classic heat stroke occurs only in hot climates.
The heat injury spectrum is listed in Table 1.
Incidence of Exertional Heat StrokeEHS mortality is significant in athletes and certain
occupations, such as agricultural workers.14 Among
athletes, EHS is the third leading cause of mortality.15
Moreover, among athletes and military personnel, the
frequency of EHS continues to increase despite safety
measures.12,15-18 Despite knowledge of EHS risk factors,
the incidence of heat stroke or heat exhaustion in the
US military has not decreased in the past 5 years, esti-
mated in 2013 at 0.25 and 1.57 per 1000 person years,
respectively.3 Highly motivated individuals might be
tempted to ignore heat safety rules, especially during
Authors
Carl Goforth is the clinical subject matter expert for the Marine CorpsCombat Development Command located in Quantico, Virginia.He has more than 20 years of combined Navy and Marine serviceand has deployed as a critical care and flight nurse attached to USMarine units overseas.
Josh Kazman is a research associate with the Consortium for Healthand Military Performance at Uniformed Services University of theHealth Sciences. He has worked on a variety of projects and publi-cations related to health disparities, heat tolerance, cardiovasculardisease, and injury prevention.
Corresponding author: CDR Carl Goforth, Combat Development & Integration,HQMC, 3300 Russell Road, Quantico, VA 22134-5001 (e-mail: [email protected]).
To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or(949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].
Clinical condition
Heat syncope
Heat cramps
Heat exhaustion
Classic heat stroke
Exertional heat stroke
Core temperature
Normal
Normal or elevatedbut < 40°C (104°F)
37°C-40°C (98.6°F-104°F)
> 40°C (104°F)
> 40°C (104°F)
Related symptoms
Generalized weakness,syncope
Painful muscle contrac-tions (commonly in calf,quadriceps, or abdominalmuscles)
Fatigue, nausea, vomiting,headache
Heat exhaustion symptomspresent before mentalstatus changes
Heat exhaustion symptomspresent before mentalstatus changes
Related signs
Postural syncope with rapidrecovery once supine
Affected muscles are stiffand tender to palpation
Flushed, profuse sweatingwith or without clammyskin, normal mental status
Hot skin with or withoutsweating, mental statuschanges (disorientation,ataxia, loss of conscious-ness); can develop slowlyover several days
Hot skin with or withoutsweating, mental statuschanges (disorientation,ataxia, loss of conscious-ness); rapid onset
Definitiona
Dizziness or fainting in a hotenvironment due to pos-tural blood pooling in lowerextremities
Painful muscle spasms during exercise in the heat
Diminished physical activityin the heat due to cardio-vascular compromise
Severe hyperthermia primarilydue to heat exposure
Severe hyperthermia primarilydue to strenuous exercise
Table 1 Heat-related illness criteria
a Definitions from Pryor et al9 and Epstein and Roberts.13
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 53
dangerous operations, placing them at even greater risk
of EHS.10 Military units’ awareness of heat injury is also
important. One military unit or ship might place greater
emphasis on work/rest cycles, environmental monitor-
ing, and so on than another unit.
Risk FactorsRecognizing inherent risk factors can help Navy criti-
cal care nurses make informed clinical decisions during
training and deployments. Additionally, US Navy medical
missions, such as
disaster response,
usually include the
care of diverse, vul-
nerable popula-
tions, such as the young and the elderly.19 EHS risk factors
(Table 2) are commonly classified into 1 of 2 areas:
intrinsic (related to the individual) and extrinsic (envi-
ronmental, task-related, or contextual).
Intrinsic Risk FactorsIn addition to a history of heat illness, intrinsic risk
factors can range from sickle cell trait to high motiva-
tion.6,16,22,23 Military training includes the indoctrination
of military culture, such as “mission first,” which can
lead motivated persons to ignore important physiologi-
cal warning signs. Other data from the US military show
that overweight military personnel have a higher risk
for sustaining heat injuries.22 Low aerobic fitness has
been cited as a predisposing factor for EHS.24 Poorly
conditioned athletes must work harder to keep up with
fit teammates and thus may ignore warning signs such
as dehydration, tachycardia, or sweating cessation.
Numerous classes of medications have also been impli-
cated in heat stroke (Table 3).
The mechanism by which common medications
contribute to heat stroke depends on the class of drug.
Anticholinergics (antihistamines, antidepressants, or
antipsychotics) decrease production of sweat.11 Cardio-
vascular agents, such as antihypertensives or diuretics,
decrease the natural physiological responses to dehy-
dration and hyperthermia.25 Of special concern to
young, healthy populations is the recent increase in
use of dietary supplements.
Recent publications indicate that US Marines are
among the highest military users of dietary supplements.26
Ergogenic stimulants, such as amphetamines or ephedra,
increase heat production. Ephedra, from the Chinese plant
ma-huang,27 along with 1,3-dimethylamyamine (DMAA),
is associated with serious heat injury in athletes28,29 and
with EHS30 and death31 in the military. Although the exact
mechanism underlying heat injury in many ergogenic
aids is not fully characterized, published reports clearly
Table 2 Risk factors for heat illnessa
Intrinsic (internal) factors
History of heat-related event
Age (< 15 or > 65 years)
Alcohol consumption
Existing medical conditions (ie, respiratory, hematologic,or cardiovascular)
Dehydration
Sleep deprivation
Medications or supplements
Obesity
Overmotivation
Inadequate acclimatization, pooraerobic conditioning, or both
Recent illness
Sickle cell trait
Extrinsic (environmental) factors
Level of exertion
Excess clothing or protectiveequipment
Lack of water
Temperature (ambient)
Humidity
Wet bulb globe temperature
a Based on information from Armstrong et al,2 Epstein et al,10 Casa et al,17
Glahn et al,20 and Wallace et al.21
Table 3 Medications implicated in exertional heat illnessa
Effect
Reduces rate of sweating
Alters skin blood flow
Lowers cardiac contractility
Increases heat production(ergogenic), hypothalamic setpoint, or both
Type of medication
AntihistaminesAnticholinergics
Calcium channel blockersFemale reproductive hormonesCapsaicin
β-Blocking medicationsCalcium channel blockers
SympathomimeticsAmphetaminesEphedra1,3-dimethylamyamine(sympathomimetic properties)
Salicylates (supratherapeuticdoses)
a Based on information from Howe and Boden,11 Seto et al,25 Kao et al,26 Lee,27
Lopez and Casa,28 Fink et al,29 Oh et al,30 and Eliason et al.31
54 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Exertional heat stroke develops as aresult of many complex factors andcan vary from person to person.
indicate that US Navy and other critical care nurses should
screen EHS patients for recently used medications or
ingestion of dietary supplement.
Extrinsic Risk FactorsProfessions in the US Armed Forces are particularly
hazardous, with constant exposure to strenuous physical
exertion and climate extremes. For instance, summer
temperatures in Afghanistan routinely reach 51°C (124°F).32
During military operations, personnel perform tasks while
wearing body armor, which weighs a mean of 12.3 kg
(27 lbs),33 often without sufficient rest. Because of the
nature of military operations, these factors are difficult to
modify and might place military personnel in scenarios
that exceed their physical capacity. Therefore, these indi-
viduals are at increased risk when subjected to individual
and environmental factors that predispose them to EHS.
It is clear from the evidence that EHS develops as a
result of many complex factors and can vary from per-
son to person. However, hyperthermia is always the
common denominator underlying any risk factor.6
HyperthermiaHyperthermia is an increase in Tcore above the body’s
natural set point.6 Human homeostasis requires a narrow
operating temperature around 37°C.34 To accomplish this,
a thermoregulatory system composed of compensatory
and noncompensatory systems communicate together for
thermoregulation when Tcore fluctuates.35 During strenu-
ous physical activity, body temperature increases in
healthy persons, but as metabolic processes and/or envi-
ronmental conditions exceed cardiovascular and central
nervous system compensation, hyperthermia (Tcore >
40°C) ensues13 and the risk of EHS increases.10
Temperatures as high as 46.5°C (116°F) have been
reported in patients who have recovered from heat stroke,36
but survival at such an extreme Tcore is rare. The severity
of tissue injury due to hyperthermia depends on the crit-
ical thermal maximum,37 defined as the maximum inten-
sity and duration of tissue heating before cellular death
occurs.38 At extreme core temperatures, thermoregulatory
mechanisms are overwhelmed, cellular proteins begin
denaturing, and apoptosis (programmed cellular death)
can occur within 5 minutes.39,40 Failure to promptly rec-
ognize and treat hyperthermia can lead to EHS within
minutes, a life-threatening medical emergency. The inte-
grated effects of hyperthermia leading to derangement
of the central nervous system and multiorgan dysfunc-
tion are typical of EHS (Figure 1). More extensive reviews
are available.13
Clinical ManagementThe extent and severity of EHS might not be read-
ily apparent in the chaos of military operations.
Because mild forms of heat illness, if not recognized,
might rapidly progress to EHS, immediate evaluation
is necessary to assess the severity of symptoms and, if
needed, to initiate cooling rapidly. When cooling is
provided immediately, survival is near 100%.18 Reduc-
ing Tcore to less than 40.5°C in less than 30 minutes is
the current recommendation.9
Supportive InterventionsThe initial priorities most relevant to EHS are
hemodynamic status, Tcore, and mental status. Upon
presentation of EHS, critical care nursing staff must
assess and stabilize vital signs, correctly recognize
signs and symptoms of EHS, and begin cooling. The
hallmark of EHS is altered function of the central
nervous system, such as confusion and combativeness.
Nursing management for EHS starts with assessing air-
way, breathing,
and circulation
(ABCs). Baseline
consciousness
should also be
immediately established, along with an initial score on
the Glasgow Coma Scale. Additional assessments
include, when possible, medical history, medications,
and/or dietary supplements used, body temperature at
admission and maximum known temperature, clinical
features apparent at admission, and vital signs. Critical
care nursing interventions also include advanced
hemodynamic monitoring and initiating fluid resuscita-
tion with crystalloid intravenous solutions per the insti-
tution’s protocol, preferably chilled (4°C) 0.9% sodium
chloride solution.41 Lactated Ringer solution is not
used, because liver function can be suppressed by over-
heated tissues, leading to unmetabolized lactate and
worsening lactic acidosis.20 Numerous studies42-44 have
demonstrated that axillary, aural (tympanic), oral, and
skin temperatures often indicate a falsely low Tcore,
especially after intense exercise in the heat. Rectal tem-
perature remains the reference standard for assessment
Central nervous system abnormalitiessuch as confusion and agitation oftenare the first signs of heat stroke.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 55
of Tcore in a potential EHS patient and the end point is
a Tcore less than 39°C (102°F).
CoolingOnce hyperthermia is confirmed by rectal temperature,
or if a high suspicion of hyperthermia exists while one is
waiting for positive confirmation, cooling measures should
begin without delay. Effective heat dissipation relies on
the rapid transfer of heat from the body’s core to the skin
and from the skin to the environment.9
The most important determinant in an EHS out-
come is the amount of time that patients’ core body
temperature is above the threshold (38.6°C) for cellular
damage.45 Reducing the Tcore to less than 40°C within
30 minutes or less is critical.6 When in doubt, the maxim
“cool first, transport second” should be employed to ensure
rapid treatment.
The fastest way to decrease Tcore is to remove restrictive
clothing and equipment and immerse the body (trunk
and extremities) in a pool or tub of cold water (approxi-
mately 1°C-14°C, or 35°F-57.2°F).46 Once the patient is
immersed in cold water, aggressive stirring or continu-
ous water motion will replace warmed water at the skin
with cold water. Additionally, wrapping a cold, wet towel
Figure 1 The event sequence leading to heat stroke and death from the compensatory to the uncompensable phase. Physicalactivity, especially during hot conditions, initiates a “compensable” thermoregulatory response (above the dashed horizontal line).When individual ability to compensate is surpassed, central venous pressure decreases, core temperature increases leading tothermoregulatory failure if prompt treatment is not initiated. This thermoregulatory failure triggers cellular death, intracellularimbalance (energy depletion), and circulatory failure. The multiple body system failures, if not immediately treated, lead to death.
Abbreviations: ATP, adenosine triphosphate; CNS, central nervous system; DIC, dissemiated intravascular coagulation.
Adapted with permission from Epstein and Roberts,13 ©2011, John Wiley and Sons A/S.
Com
pens
ator
yNo
ncom
pens
ator
yIntrinsic factors
Sweat
Hypovolemia Central venous pressure decreases
Core temperature increase
Systemic inflammation
Blood brain barrier breakdown
CNS derangement
ATP depletion
Cellular anoxia
*Liver dysfunction*Renal failure*Coagulopathy (DIC)*Cardiac dysrythmia*Myoglobin release*Intestinal permeability
Circulatory collapse
Increased metabolic rate
Core temperature increase
Cardiac output increase
Extrinsic factors
Heat stroke
Death
Heat stress
Core temperature increase
56 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
around the top of the head will enhance rapid cooling
further.45 It is recognized that cold water is not always
available in remote areas. One alternative, when resources
are limited, is to douse the victim with immediately
available water. This method can reach a cooling rate of
0.1°C to 0.2°C per minute.47 Cooling rates for the most
common cooling methods are presented in Figure 2.9
Civilian Nursing ImplicationsHeat exposure is one of the most deadly natural
hazards in the United States. The Centers for Disease
Control and Prevention48 estimates that between 1992
and 2006, heat stroke claimed the lives of 423 Americans,
more than hurricanes, lightning, floods, tornados, and
earthquakes combined. These injuries require aggressive
clinical treatments consisting of rapid cooling and sup-
portive nursing care, such as fluid resuscitation to preserve
organ function. Therefore, although this article is focused
on Navy critical care nursing, the concepts of rapid recog-
nition and cooling are universal and apply to any critical
care nurse caring for a heat stroke victim.
ConclusionEHS requiring critical care nursing intervention rep-
resents a substantial risk of morbidity and mortality to
Navy and Marine Corps personnel. With military EHS
rates at high levels despite scientific advances, never
before has it been so clinically important to recognize
and rapidly treat potential EHS casualties. EHS rates in
the Marine Corps, for instance, were more than 5 times
higher than the rates in other military branches in
2011.49 Data also suggest that military heat stroke sur-
vivors have twice the mortality risk from cardiovascular,
kidney, and liver failure within 30 years of initial hospi-
talization compared with military survivors of nonheat
injuries.21 According to the best evidence available, ice-
water or cold-water immersion is the most effective cool-
ing treatment and is recommended as the definitive
treatment.46 If this method is unavailable, case reports
demonstrate that continual water dousing combined
with fanning is a practical alternative until advanced treat-
ment is available. Practical resources for the implemen-
tation of EHS prevention and emergency procedures can
Figure 2 Relative cooling rates by heat stroke nursing intervention. Optimal cooling rates (> 0.155°C/min), acceptable coolingrate (> 0.079°C/min and < 0.154°C/min), or unacceptable cooling rates (< 0.078°C/min).
Abbreviation: IVF, intravenous fluids.Adapted with permission from Pryor et al,9 ©2013 with permission from Elsevier.
Mea
n co
olin
g ra
te, º
C/m
in
2ºC cold-water immersion
0.00
0.05
0.10
0.15
0.20
0.25
Unac
cept
able
Acce
ptab
leOp
timal
0.30
0.35
0.40
4ºC cooling blanket
8ºC cold-water immersion
20ºC cold-water immersion
Chilled IVF and water-room temperature immersion
Ice packs at major arteries
Gastric lavage
Ice-water immersion
IVF-room temperature, ice packs at major arteries
IVF-room temperature only
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 57
be found in multiple locations (Table 4). The evidence
underscores the need for prompt identification of poten-
tial EHS victims and aggressive cooling measures in the
field as key critical care nursing actions. CCN
AcknowledgmentsThe views expressed are those of the authors and do not reflect the officialpolicy or position of the US Marine Corps, the Uniformed Services Universityof the Health Sciences, the Department of Defense, or the US government.
Financial DisclosuresWork on this manuscript was funded by the Office of Naval Research, grantno. N0001411MP20023.
References1. Murakoshi M, Sekine M. Measures by local government—actions to
take in dealing with heat stroke for firefighters. Nihon Rinsho. 2012;70(6):1052-1056.
2. Armstrong LE, Johnson EC, Casa DJ, et al. The American football uniform:uncompensable heat stress and hyperthermic exhaustion. J Athl Train.2010;45(2):117-127.
3. Update: Heat Injuries, Active Component, US Armed Forces, 2012. MSMR.2013;20(3):17-20.
4. Simpson R, Gray S, Florida-James G. Physiological variables and perform-ance markers of serving soldiers from two “elite” units of the BritishArmy. J Sports Sci. 2006;24(6):597-604.
5. Chinevere T, Cadarette B, Goodman D, Ely B, Cheuvront S, Sawka M.Efficacy of body ventilation system for reducing strain in warm and hotclimates. Eur J Appl Physiol. 2008;103(3):307-314.
6. Casa D, Armstrong L, Kenny G, O’Connor F, Huggins R. exertional heatstroke: new concepts regarding cause and care. Curr Sports Med Rep.2012;11(3):115-123.
7. Epstein Y, Moran D. Thermal comfort and the heat stress indices. IndHealth. 2006;44(3):388-398.
8. Haller C, Benowitz N. Adverse cardiovascular and central nervous systemevents associated with dietary supplements containing ephedra alkaloids.N Engl J Med. 2000;343(25):1833-1838.
9. Pryor RR, Casa DJ, Holschen JC, O’Connor FG, Vandermark LW. Exertionalheat stroke: strategies for prevention and treatment from the sports fieldto the emergency department. Clin Pediatr Emerg Med. 2013;14(4):267-278.
10. Epstein Y, Druyan A, Heled Y. Heat injury prevention—a military per-spective. J Strength Cond Res. 2012;26:S82-S86.
11. Howe AS, Boden BP. Heat-related illness in athletes. Am J Sports Med.2007;35(8):1384-1395.
12. Carter R III, Cheuvront S, Williams J, et al. Epidemiology of hospitaliza-tions and deaths from heat illness in soldiers. Med Sci Sports Exerc. 2005;37(8):1338-1344.
13. Epstein Y, Roberts W. The pathopysiology of heat stroke: an integrative viewof the final common pathway. Scand J Med Sci Sports. 2011;21(6):742-748.
14. Centers for Disease Control. Heat-related deaths among crop workers—United States, 1992-2006. MMWR. 2008;57:649-653.
15. Stearns R, O’Connor F, Casa D, Kenny G. Exertional Heat Stroke. Sudbury,MA: Jones and Bartlett Learning, LLC; 2011.
16. Armstrong L, Casa D, Millard-Stafford M, Moran D, Pyne S, RobertsWO. American College of Sports Medicine position stand: exertionalheat illness during training and competition. Med Sci Sports Exerc. 2007;39(3):556-572.
17. Casa D, Almquist J, Anderson S. Inter-association task force on exertionalheat illnesses consensus statement. NATA News. 2003;6:24-29.
18. Casa D, Guskiewicz K, Anderson S, et al. National Athletic Trainers’Association position statement: preventing sudden death in sports. J Athl Train. 2012;47(1):96-118.
19. Faulk J, Hanly M. Tales From the Sea: Critical Care Nurses Serving Aboardthe USNS Comfort and USNS Mercy. Crit Care Nurse. 2013;33(4):61-67.
20. Glahn K, Ellis F, Halsall P, et al. Recognizing and managing a malignanthyperthermia crisis: guidelines from the European Malignant Hyperther-mia Group. Br J Anaesth. 2010;105(4):417-420.
21. Wallace RF, Kriebel D, Punnett L, Wegman DH, Amoroso PJ. Prior heatillness hospitalization and risk of early death. Environ Res. 2007;104(2):290-295.
22. Bedno S, Li Y, Han W, et al. Exertional heat illness among overweightUS Army recruits in basic training. Aviat Space Environ Med. 2010;81(2):107-111.
23. Carter R, Cheuvront S, Sawka M. Heat related illnesses. Sports Sci Exchange.2006;19(3):1-6.
24. Gardner JW, Kark JA, Karnei K, et al. Risk factors predicting exertionalheat illness in male Marine Corps recruits. Med Sci Sports Exerc. 1996;28(8):939-944.
Now that you’ve read the article, create or contribute to an online discussion aboutthis topic using eLetters. Just visit www.ccnonline.org and select the article youwant to comment on. In the full-text or PDF view of the article, click “Responses”in the middle column and then “Submit a response.”
To learn more about military critical care nursing, read “Tales Fromthe Sea: Critical Care Nurses Serving Aboard the USNS Comfortand USNS Mercy” by Faulk and Hanly in Critical Care Nurse,August 2013;33:61-67. Available at www.ccnonline.org.
Resource
Uniformed Services University, Consortiumfor Health and Military Performance
US Army Research Institute of Environmental Medicine
US Army Medical Department
American College of Sports Medicine
US Marine Corps Heat Injury PreventionProgram
Description
Clinical consultation for exertional heat illnessand related conditions such as exertional rhabdomyolysis
Army clinical and educational resources regardingheat physiology, acclimation, and related operational issues
Provides a link to Medical Aspects of Harsh Environments, Volume 1
Civilian guidelines and consensus regarding exertional heat illness
Marine Corps resource for the prevention of heatinjury guidance per MCO 6200.1E, includingacclimatization and work-rest cycles
Website
http://champ.usuhs.mil
http://www.usariem.army.mil
http://www.cs.amedd.army.mil
www.acsm.org
http://www.imef.marines.mil/portals/68/Docs/IMEF/Surgeon/MCO_6200.1E_W_CH_1_Heat_Injury_Prevention.pdf
Table 4 Military and civilian resources for exertional heat illness guidelines
58 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
25. Seto C, Way D, O’Connor N. Environmental illness in athletes. Clin SportsMed. 2005;24(3):695-718.
26. Kao T-C, Deuster PA, Burnett D, Stephens M. Health behaviors associatedwith use of body building, weight loss, and performance enhancingsupplements. Ann Epidemiol. 2012;22(5):331-339.
27. Lee M. The history of Ephedra (ma-huang). J R Coll Physicians Edinb.2011;41(1):78-84.
28. Lopez R, Casa D. The influence of nutritional ergogenic aids on exercise heattolerance and hydration status. Curr Sports Med Rep. 2009;8(4):192-199.
29. Fink E, Brandom BW, Torp KD. Heatstroke in the super-sized athlete.Pediatr Emerg Care. 2006;22(7):510-513.
30. Oh R, Henning J. Exertional heatstroke in an infantry soldier takingephedra-containing dietary supplements. Mil Med. 2003;168(6):429-430.
31. Eliason M, Eichner A, Cancio A, Bestervelt L, Adams B, Deuster P. Casereports: death of active duty soldiers following ingestion of dietary sup-plements containing 1, 3-dimethylamylamine (DMAA). Mil Med. 2012;177(12):1455-1459.
32. NOAA. Climate of Afghanistan. http://www.ncdc.noaa.gov/oa/climate/afghan/afghan-narrative.html. Accessed November 11, 2014.
33. Konitzer L, Fargo M, Brininger T, Lim Reed M. Association betweenback, neck, and upper extremity musculoskeletal pain and the individualbody armor. J Hand Ther. 2008;21(2):143-148.
34. Hall J. Guyton and Hall Textbook of Medical Physiology. 12th ed. Philadelphia,PA: Saunders: Elsevier; 2011.
35. Ha S, Talbott E, Kan H, Prins CA, Xu X. The effects of heat stress and itseffect modifiers on stroke hospitalizations in Allegheny County, Pennsyl-vania. Int Arch Occup Environ Health. 2014;87(5):557-565.
36. Ghaznawi H, Ibrahim M. Heat stroke and heat exhaustion in pilgrimsperforming the Haj (annual pilgrimage) in Saudi Arabia. Ann Saudi Med.1987;7(3):323-326.
37. Sherwood SC, Huber M. An adaptability limit to climate change due to
heat stress. Proc Natl Acad Sci U S A. 2010;107(21):9552-9555.38. Lutterschmidt WI, Hutchison VH. The critical thermal maximum: history
and critique. Can J Zool. 1997;75(10):1561-1574.39. Bouchama A, Knochel J. Heat stroke. N Engl J Med. 2002;346(25):1978-1988.40. Leon L, Helwig B. Heat stroke: role of the systemic inflammatory response.
J Appl Physiol. 2010;109(6):1980-1988.41. Badjatia N. Hyperthermia and fever control in brain injury. Crit Care Med.
2009;37(7):S250-S257.42. Casa DJ, Becker SM, Ganio MS, et al. Validity of devices that assess body
temperature during outdoor exercise in the heat. J Athl Train. 2007;42(3):333-342.
43. Ganio MS, Brown CM, Casa DJ, et al. Validity and reliability of devicesthat assess body temperature during indoor exercise in the heat. J AthlTrain. 2009;44(2):124-135.
44. Ronneberg K, Roberts W, McBean A, Center B. Temporal artery temper-ature measurements do not detect hyperthermic marathon runners.Med Sci Sports Exerc. 2008;40(8):1373-1375.
45. Gagnon D, Lemire BB, Casa DJ, Kenny GP. Cold-water immersion andthe treatment of hyperthermia: using 38.6ºC as a safe rectal temperaturecooling limit. J Athl Train. 2010;45(5):439-444.
46. McDermott BP, Casa DJ, Ganio MS, et al. Acute whole-body cooling forexercise-induced hyperthermia: a systematic review. J Athl Train. 2009;44(1):84-93.
47. Rav-Acha M, Hadad E, Epstein Y, Heled Y, Moran D. Fatal exertionalheat stroke: a case series. Am J Med Sci. 2004;328(2):84-87.
48. Centers for Disease Control and Prevention. Preventing heat-relatedillness or death of outdoor workers. Workplace Solutions. 2013. http://www.cdc.gov/niosh/docs/wp-solutions/2013-143/. Accessed November11, 2014.
49. Update: Heat injuries, active component, U.S. Armed Forces, 2011.MSMR. 2012;19(3):14-16.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 59
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It is only fitting that the first neonate to be supported by extracorporeal membraneoxygenation (ECMO) was named Esperanza, which when translated from Spanishmeans hope.1 Indeed, to the more than 50 000 patients who have survived because of ECMO,
this revolutionary treatment has provided hope where there was none before.2 In the past 5
decades, the use of artificial oxygenation and perfusion has revolutionized the care of critically
ill patients, both in the operating room and in the intensive care unit. Use of artificial oxygenation and
perfusion has evolved from bypass during cardiac surgery to advanced life support, to complex extracorpo-
real cardiopulmonary resuscitation (ECPR). Within the past 20 years, ECPR has been initiated when
traditional resuscitation methods have failed and has proven its effectiveness with a survival to discharge
rate of approximately 40%.3-13 However, the appropriate use of this therapy and delineated criteria for
initiating and withdrawing this therapy have yet to be defined. Furthermore, implementation of this
Extracorporeal Membrane Oxygenationfor Pediatric Cardiac ArrestJENNIE RYAN, MS, CPNP-AC
©2015 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2015655
Pediatric Care
Extracorporeal cardiopulmonary resuscitation (ECPR) remains a promising treatment for pediatric patients
in cardiac arrest unresponsive to traditional cardiopulmonary resuscitation. With veno-arterial extracorporeal
support, blood is drained from the right atrium, oxygenated through the extracorporeal circuit, and transfused
back to the body, bypassing the heart and lungs. The use of artificial oxygenation and perfusion thus provides
the body a period of hemodynamic stability, while allowing resolution of underlying disease processes. Survival
rates for ECPR patients are higher than those for traditional cardiopulmonary resuscitation (CPR), although
neurological outcomes require further investigation. The impact of duration of CPR and length of treatment
with extracorporeal membrane oxygenation vary in published reports. Furthermore, current guidelines for
the initiation and use of ECPR are limited and may lead to confusion about appropriate use of this support.
Many ethical concerns arise with this advanced form of life support. More often than not, the dilemma is not
whether to withhold ECPR, but rather when to withdraw it. Although clinicians must decide if ECPR is
appropriate and when further intervention is futile, the ultimate burden of choice is left to the patient’s care-
givers. Offering support and guidance to the patient’s family as well as the patient is essential. (Critical Care
Nurse. 2015;35[1]:60-70)
This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article,which tests your knowledge of the following objectives:
1. Determine the difference between venovenous and venoarterial extracorporeal membrane oxygenation (ECMO)2. Describe the benefits of extracorporeal cardiopulmonary resuscitation3. Discuss the ethical considerations related to management of patients undergoing ECMO
CNE Continuing Nursing Education
60 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
extraordinary therapy introduces
many ethical dilemmas concerning
advanced life support. This article
addresses the use of ECMO during
CPR, as well as the ethical problems
we face with the continued advance-
ment of end-of-life care.
Extracorporeal Cardiopulmonary Resuscitation
ECPR is considered the initiation
of ECMO, following refractory cardiac
arrest unresponsive to conventional
cardiopulmonary resuscitation (CPR).
During the initiation of ECPR, tradi-
tional resuscitation measures are con-
tinued, including chest compressions
and emergency administration of
medication. Practitioners initiating
this treatment should aim to maxi-
mize cardiac output and flow to opti-
mize outcomes. While traditional
resuscitation continues, surgeons place the ECMO cannu-
las in large arterial and venous vessels. Location of can-
nula placement is based on the type of ECMO that the
patient will receive. There are 2 forms of ECMO, venove-
nous and venoarterial. During venovenous ECMO, blood
is drained from the right atrium, oxygenated through the
circuit, then perfused back into the right atrium where the
heart pumps it to the rest of the body, bypassing only the
lungs. However, this form of ECMO requires adequate
cardiac function, which is always severely impaired or
absent in ECPR patients.14 Therefore, venoarterial extra-
corporeal support is initiated for ECPR patients. In this
technique, 1 cannula is placed for venous drainage,
similar to venovenous ECMO, but the oxygenated blood
is returned to the aorta, bypassing both the lungs and
heart (see Figure). Placement of the cannulas is depend-
ent on the ease of access and the size of the patient.14 If
access to intracardiac placement is available, such as
with postoperative cardiac patients, this method is usu-
ally preferable, with direct cannulation of the right atrium
and aorta. Other methods include the cannulation of the
femoral artery and vein. However, this use is restricted
to adolescents and adults because the size of their vessels
is large enough to support adequate drainage and reinfu-
sion.14 Still, the most common method of cannulation is
venous access through the internal jugular vein directly
into the right atrium and arterial access through the
right carotid artery into the aorta.3
Once a patient is successfully cannulated, the patient
is immediately connected to the ECMO circuit. For this
reason, most centers have developed a “rapid deployment
system,” in which a circuit is preprimed with a crystalloid
solution or is able to be primed with blood products within
a very short period, usually 10 to 20 minutes.15 Although
a large immediate infusion of crystalloid solution can be
tolerated by older children and adolescents, some centers
are reluctant to administer such an infusion to a neonate
because of the significant hemodilution.15 However, the
Author
Jennie Ryan in a nurse practitioner in the intensive care unit atNemours Cardiac Center. She is also a per diem faculty member inthe Helene Fuld Pavillion Simulation Lab at the University ofPennsylvania, School of Nursing, in Philadelphia.
Corresponding author: Jennie Ryan, MS, CPNP-AC, Nemours Cardiac Center, A. I. duPont Hospital for Children, 1600 Rockland Road, Wilmington, DE 19803 (e-mail: [email protected]).
To purchase electronic or print reprints, contact the American Association of Criti-cal-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or(949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].
Figure Venoarterial extracorporeal support for extracorporeal cardiopulmonaryresuscitation.
Venous cannula
Rightatrium
Leftatrium
Rightventricle
Leftventricle
Aortic cannula
Aorta
Superior venacava
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 61
benefits of immediate end-organ perfusion often outweigh
the risks of low hematocrit, which can be resolved with
blood transfusions once the circuit has been established.15
The Benefits of ECPRThe postresuscitation phase in pediatric patients
remains a high-risk period, complicated by significant
myocardial dysfunction, hyperthermia, hyperglycemia,
impaired autoregulation of blood pressure, and ischemia/
reperfusion response.14-16 Upon return of spontaneous
circulation and reperfusion, a decrease in contractility
of the heart, known as myocardial stunning, often occurs.
Decreased function of the heart can lead to hypotensive
shock, with further damage arising from increased pro-
duction of inflammatory mediators and nitric oxide.16
Treatment of hypotension and myocardial dysfunction
often requires aggressive hemodynamic support with
fluid resuscitation and vasoactive agents including epi-
nephrine, dobutamine, and dopamine.16
In contrast, mechanical circulation via ECMO
allows the body a period of hemodynamic stability
and the possibility of resolution of underlying disease
processes.15,16
Perfusion of
organs with
fully oxygenated
blood via the
ECMO circuit
allows decreased myocardial oxygen demand, gener-
ally without the use of high-dose vasoconstrictors and
inotropic agents.15 This stability in the postresuscita-
tion period may further improve survival rates.17
Large, multi-institutional studies16-18 show that overall
survival to discharge rates in pediatric patients resusci-
tated with conventional CPR remains at approximately
25% to 27%. However, survival statistics for ECPR are
more encouraging, with a general rate of success of near
40% to 60%.2-5,7-13,19-26 Multi-institutional data obtained in
2012 from the Extracorporeal Life Support Organization
(ELSO), an international registry and database of ECMO
treatment, demonstrated that ECPR was successful for
934 out of 2236 neonatal and pediatric patients, with
survival to discharge of 39% for neonates and 40% for
children. Other retrospective, single-institution studies
have shown survival rates as high as 72% to 80%.25,27-29
The Table provides more detailed information from the
current studies of ECPR in pediatric patients. Critical
analysis of this information is imperative when deter-
mining the utility of ECPR.
Most studies rate ECPR’s success solely on survival to
discharge statistics; only a few studies address neurologi-
cal outcome. A void remains in the literature as far as
addressing quality of life after ECPR. Furthermore, “good
neurological outcome” is often a subjective measure,
with terminology varying among researchers. Some
studies have shown that ECPR patients have an increased
likelihood of central nervous system complications
developing compared with patients treated with ECMO
without CPR.4 Other studies examining ECPR patients
have shown favorable neurological outcomes, as meas-
ured by the Pediatric Cerebral Performance Category
Scale, with a score of 2 or less in most patients.8,9,19,20,32
Further investigation into long-term neurological seque-
lae is needed and should be included in future studies.
When to Initiate Therapy?In 2005, the American Heart Association recom-
mended the use of ECPR for in-hospital patients in car-
diac arrest when the duration of no-flow arrest is brief
and the condition leading to the cardiac arrest is
reversible.35 This broad recommendation does not offer a
definition of “brief,” nor does it differentiate between
time of no-flow arrest and duration of traditional CPR.
More recent recommendations from the 2010 Interna-
tional Consensus on Cardiopulmonary Resuscitation36
specifies that ECPR is appropriate for patients with heart
disease that is “amenable to treatment or heart trans-
plantation,” where the cardiac arrest occurs in the inten-
sive care unit in a facility with the personnel, equipment,
and training to provide ECPR. Use of ECPR is indicated
in only 1 situation after out-of-hospital cardiac arrest,
which is in cases of environmentally induced severe
hypothermia (< 30°C), again, only if the appropriate
equipment and expertise are available.36 Medical institu-
tions providing ECPR should have established protocols
for its implementation and use. Often centers lacking
these resources are unable to offer ECPR at all.
The advantages of ECPR after prolonged conven-
tional resuscitation remain a source of controversy.
Despite the large number of studies performed regarding
ECPR use, no criteria or guidelines for timing of initia-
tion of this therapy have been clearly established. The
International Consensus on Cardiopulmonary Resuscita-
tion recognizes that evidence is insufficient for establishing
62 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Mechanical circulation via extracorporealmembrane oxygenation allows the bodya period of hemodynamic stability andthe possibility of resolution of underlyingdisease processes.
Reference
Aharon et al28
Alsoufi et al21
Alsoufi et al30
Cengiz et al4
Chan et al5
Chrysostomous et al29
Conrad et al3
de Mos et al10
Del Nido23
Delmo Walter et al11
Duncan et al22
Huang et al13
Huang et al9
Joffe et al19
Kane et al20
Kelly and Harrison31
Kumar et al12
Population ofpatients
Postoperative, cardiac
Postoperative, cardiac
ICU and cardiac
ELSO registry
ELSO registry ofcardiac patients
Cardiac
ELSO registry
ICU
Cardiac
ICU
Cardiac
Pediatric
Pediatric
Meta-analysis
Cardiac
Pediatric and cardiac
Postoperative, cardiac
No. ofpatients
10
48
80
161
492
40
151 Neonatal
282 Pediatric
5
11
42
11
54
27
762
172
31
29
No. (%) ofsurvivors todischarge
8 (80)
23 (46)
27 (34)
64 (40)
208 (42)
30 (75)
Neonatal: 65 (43)
Pediatric: 111 (39)
2 (40)
6 (55)
17 (40.4)
6 (55)
25 (46)
11 (41)
361 (49)
88 (51)
7 (23)
12 (41)
Duration of cardiopulmonaryresuscitation, min
Mean (range), 42 (5-110)
> 30 min associated with poor survival
Not reported
Median (range)Survivors: 46 (14-95) Nonsurvivors: 41 (19-110)
Not reported
Not reported
Median (IQR)Survivors: 40 (25-50)Nonsurvivors: 37 (35-50)
Not reported
RangeAll: 31-77Survivors: 35-48
Mean (SD): 65 (9)
Mean (SD)Survivors: 35 (1.3)Nonsurvivors: 46 (4.2)
Median (range)55 (20-103)
Mean (SD)Survivors: 39 (17)Nonsurvivors: 52 (45)
Median (IQR)Survivors: 45 (25-50)Nonsurvivors: 60 (37-81)
Not reported
Median (interquartile range)Survivors: 32 (25-41)Nonsurvivors: 36 (21-45)
MedianSurvivors: 40Nonsurvivors: 47
Mean (SD)Survivors: 42 (8)Nonsurvivors: 51 (10)
Duration of ECMO therapy
Not reported
Not reported
4 days for both survivors andnonsurvivors
Mean (SD)Survivors: 4.7 (3.5) daysNonsurvivors: 4.4 (6.4) days
Median (IQR) Survivors: 87 (51-137) hours Nonsurvivors: 87 (37-171) hours
Median (IQR)Survivors: 53 (29-98) hoursNonsurvivors: 48 (28-102) hours
Not reported
Not reported
Mean (SD): 112 (18) hours
Mean (SD)Survivors: 4.0 (2.2) days Nonsurvivors: 6.0 (0.9) days
Not reported
Not reported
Median (IQR), rangeSurvivors: 102 (68-135), 43-
419 hoursNonsurvivors: 89.2 (26.9-221),
6-637 hours
Not reported
Median (interquartile range)Survivors: 84 (52-118) hoursNonsurvivors: 119 (57-183)
hours
MeanSurvivors: 4 daysNonsurvivors: 6 days
Not reported
Continued
Table Retrospective pediatric studies of extracorporeal membrane oxygenation (ECMO) in cardiopulmonary resuscitation
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 63
any specific threshold for CPR duration beyond which
survival is unlikely.36
A substantial amount of debate can be found in pub-
lished reports about when ECPR should be initiated and
when further intervention would be futile. Several pedi-
atric studies have shown increased mortality rates for
patients cannulated after 30 minutes of conventional
CPR.7,11,28,34 However, other retrospective studies8-10,12,20,26,27,29,31,32
of pediatric patients have shown positive outcomes with
median CPR duration of 30 to 50 minutes. Even more
interesting are the multiple case reports24,27,30,32,37 of suc-
cessful cannulation and survival to discharge in patients
receiving CPR of up to 90 to 220 minutes.
Other research has focused on parameters that may
act as predictors for positive outcome. ECPR patients
with a preexisting diagnosis of cardiac illness have
shown improved survival outcomes, when compared
with patients with noncardiac illnesses.5,6,8,30,32 Perhaps
patients with cardiac illness have less multiorgan dysfunc-
tion before cardiac arrest and therefore are more likely to
Reference
Morris et al32
Paden et al2
Polimenakos et al26
Prodhan et al27
Raymond et al8
Shah et al33
Sivarajan et al34
Thiagarajan et al6
Tajik and Cardarelli7
Wolf et al24
Thourani et al25
Population ofpatients
ICU
ELSO registry
Cardiac single ventricle,neonates
ICU, cardiac
AHA/NRCPR
Cardiac
Cardiac
ELSO registry
Meta-analysis
Cardiac
Cardiac
No. ofpatients
64
Neonatal: 784
Pediatric: 1562
14
32
199
27
37
682
288
90
15
No. (%) ofsurvivors todischarge
21 (33)
Neonatal: 304 (39)
Pediatric: 630 (40)
8 (57)
24 (72)
87 (44)
9 (33)
14 (38)
261 (38)
114 (39.6)
50 (55.5)
11 (73.3)
Duration of cardiopulmonaryresuscitation, min
Median (range)Survivors: 50 (5-105)Nonsurvivors: 46 (15-90)
Not reported
Mean (SD)Survivors: 38.6 (6.3)Nonsurvivors: 42.1 (7.7)
Median (range)Survivors: 43 (15-142)Nonsurvivors: 60 (20-76)
Median (range)Survivors: 46 (26-68)Nonsurvivors: 57 (38-71)
Not reported
MedianSurvivors: 15 Nonsurvivors: 40
Not reported
Not reported
Survivors: 42 (16-98)Nonsurvivors: 43 (20-75)
Not reported
Duration of ECMO therapy
Median (range)Survivors: 55 (2-359) hoursNonsurvivors: 64 (1-506) hours
Not reported in ECPR group
Median (IQR)Survivors: 4 (3-6.5) daysNonsurvivors: 8 (5-11.5) days
Median (range)Survivors: 122 (41-816) hoursNonsurvivors: 59 (7-905)
hours
Not reported
Mean (SD)Survivors: 79.3 (40.7) hoursNonsurvivors: 128.6 (193.3)
hours
Not reported
Median (interquartile range)Survivors: 88 (51-140) hoursNonsurvivors: 66 (26-157)
hours
Median (range)4.3 (0.03-90) days
Median (range)Survivors: 3 (1-20) daysNonsurvivors: 5 (1-21) days
Median (range)66 (18-179)
Table Continued
Abbreviations: AHA/NRCPR, American Heart Association/National Registry of Cardiopulmonary Resuscitation; ELSO, Extracorporeal Life Support Organization; ICU,intensive care unit; IQR, interquartile range.
64 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
survive after treatment with ECPR.8 Few published data
support preexisting measurements as indicators for sur-
vival. Arterial blood gas values have been postulated to
be predictive variables in several studies, with pH less
than 7.2 associated with higher mortality.4,19,20,34 However,
Thiagarajan et al6 noted that although pre-ECMO arterial
pH less than 6.9 was strongly associated with negative
outcome, 12% of children who survived after ECPR use
had a pre-ECMO pH less than 6.9.6 Multiple studies5,6,8,9,19,20
have shown that preexisting renal insufficiency and
metabolic electrolyte abnormalities are associated with
worse survival to discharge.
This discordance in published results is of extreme
importance to practitioners initiating ECPR in pediatric
patients. The absence of clearly defined parameters and
inconsistencies in published reports may lead some cli-
nicians to initiate ECPR when attempts may be futile,
but also may inhibit its use when there is the possibility
of success.
When to Withdraw ECMO?Transition from ECPR to standard ECMO care occurs
once the child is cannulated and placed on the ECMO
circuit. Further management of the patient focuses on
treatment of underlying disease processes. The use of
artificial oxygenation and perfusion in this time allows
the child a period of hemodynamic stability and decreased
myocardial oxygen demand, during which vital organ
function may return. However, the precise amount of
time it takes the organs to regain adequate function to
support the body remains unknown. Several studies4,5,30
of duration of ECMO after CPR show similar amounts of
time on the circuit for both survivors and nonsurvivors.
Historically, data in pediatric patients indicate that
ECMO for cardiac failure after cardiothoracic surgery
continued beyond 3 to 6 days results in poor outcomes,
and ECMO beyond 2 weeks may not improve respiratory
failure.33 However, a recent review38 of ELSO data in car-
diac ECMO patients shows no significant difference in
survival to discharge between patients who receive
ECMO for 14 to 20.9 days (25% survival) and patients
who received ECMO for 21 to 27.9 days (23% survival);
but, survival decreased significantly after 28 days to
13%.38 In pediatric patients receiving ECMO for acute
respiratory failure, review of ELSO data showed survival
rates were inversely related to duration of ECMO.
Patients receiving ECMO support for 3 weeks or longer
had a survival to discharge rate of 38%, significantly
decreased from the rate of survival of patients who
received ECMO support for 2 weeks or less (61%).39
If separation from the ECMO circuit is not possible
because of ongoing cardiac or pulmonary failure, then
transition to other modes of mechanical support may be
an option. Patients with prolonged pulmonary failure
but recovery of cardiac function may be transitioned to
venovenous extracorporeal support, potentially decreas-
ing the risk of oxygenator-associated thrombi. Patients
with continued cardiac dysfunction may be converted to
a ventricular assist device to act as a bridge for transplant.
To date, only 2 ventricular assist devices are approved
for pediatric use, the Berlin Heart and HeartWare. How-
ever, no current research supports the use of a ventricu-
lar assist device in children after cardiac arrest.
The only clear indicator for withdrawal of ECMO
support is neurological devastation evidenced by brain
death, in which termination of all life support is war-
ranted. Other clear criteria for withdraw of ECMO
include hemorrhagic stroke or intraventricular hemor-
rhage in which anticoagulation must be discontinued to
prevent wors-
ening intracra-
nial bleeding.
Other indica-
tors for termi-
nation of
ECMO
include wors-
ening end-organ dysfunction. Renal insufficiency follow-
ing ECPR is a poor prognostic factor.5,6,8,9,19 Acute renal
injury can occur during cardiac arrest and resuscitation
as a result of hypoperfusion of the kidneys. Again, the
question of how long it will take for these organs to recover,
or if recovery is possible at all, has yet to be answered.
Ethical ConsiderationsThe judicious use of ECPR in pediatric critical care is
complicated by a vast number of factors, including the
high cost of care, questionable effectiveness, and intensi-
fied emotions of families and providers caring for a criti-
cally ill child. ECPR is an advanced form of life support,
so its use in patient care must be in accordance with the
principles of medical ethics. The first principle is benefi-
cence, which requires that practitioners offer care that
is beneficial to their patients.40 Unnecessary surgical
The use of artificial oxygenation and perfusion allows a period of hemodynamicstability, during which vital organ functionmay return. However, the amount of timeit takes the organs to regain adequatefunction remains unknown.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 65
procedures and unauthorized research are common
problems that arise when addressing beneficence.41 The
second principle is nonmaleficence, meaning do no
harm. This principle requires that the benefits of a treat-
ment must outweigh the potential negative aspects such
as overburdensome pain and unavoidable suffering.40
When discussing the continued use of ECMO, practi-
tioners must decide if prolonged therapy to enhance the
possibility of survival prevails over the risk of unneces-
sary discomfort and extended suffering of the child. The
third ethical principle is autonomy, which refers to the
patient’s right to decide what is appropriate in their
care. In critically ill pediatric patients, a dependent
child’s autonomy is delegated to the surrogate decision
maker, most often the parents.40 Their values and judg-
ments must be respected by practitioners and incorpo-
rated into decision making at every level.
The fourth principle is justice, which is often a source
of controversy in modern medicine.40 This principle
demands that therapies be provided equally to all
patients despite differences in socioeconomic status,
race, gender, and
so on. However,
medical resources
are not limitless,
and societies must
strive to ensure appropriate distribution of health care.40
Median hospital charges of ECPR patients has been
quoted at $310824, which is significantly greater than
charges for propensity-matched conventional CPR
patients, which are $147817.42 Financial burdens of
ECMO support may far exceed reimbursement from
insurance companies and may place the hospital at
financial risk.40,43 Offering excess treatment in one
patient may conceivably lead to a decrease in resources
for another patient.43
Taking into account the ethical principles of medicine,
practitioners in the intensive care unit must be acutely
aware of the potential for benefit and the medically
futility of the therapies they provide. Most often, such
awareness means that advanced life support is initiated
and removed appropriately depending on the patient’s
chance of survival and the desires of the patient’s family.
These concepts are more commonly known as initiating,
withholding, and withdrawing treatment.
Ethical guidelines have determined that, withholding
and withdrawing life support are no different.44,45 However,
many professionals recognize that a psychological differ-
ence clearly exists.44 Based on this assumption, the Presi-
dent’s Commission on Ethical Problems in Medicine
concluded that, contrary to widespread feelings on the
matter, withdrawing treatment was preferable to with-
holding treatment for 2 reasons.45,46 Primarily, withdraw-
ing allows a time-limited trial of therapy in which the
patient’s status can be reassessed and prognosis deter-
mined.45,46 Second, a traditional reluctance to withdraw
treatment had led many practitioners to forgo lifesaving
therapies altogether for fear of eventual “failure.”44 For
this reason, most intensivists now offer advanced life
support to their patients with the hope that therapies
will be successful, or at the very least “buy some time.”44
Withholding ECPR is often a debate between physi-
cians involved in the patient’s care. Most families are not
aware of ECPR and would not know to request that their
child be treated with ECPR. Often ECPR is recommended
by a physician, and therefore withholding ECPR may
come to mean simply not offering it. Withholding ECPR
often becomes an intraprofessional dilemma, where the
effectiveness of treatment is controversial. As discussed
previously, the lack of parameters to guide physicians is
detrimental to evidence-based practice, and decisions in
this scenario are often based on personal reasoning,
experience, and values. In these difficult situations, prac-
titioners most often decide to treat, possibly against their
better judgment.44 Solomon et al44 examined perceptions
of physicians and nurses caring for critically ill children
and reported that 80% of critical care attending physicians
agreed that “sometimes I feel we are saving children who
should not be saved,” whereas only 8% agreed that
“sometimes I feel we give up on children too soon.”
The ethical dilemma of ECPR is therefore most often
not whether to withhold it, but when to withdraw it.
Again, the literature does not support a definitive
timetable for withdrawal of ECMO. Obviously, neurolog-
ical devastation as evidenced by brain death is a defini-
tive indicator for withdrawal of treatment. But no other
parameters exist, and the decision to withdraw is often
at the recommendation of the provider.40,47 Maintaining
ethical principles at this time is essential for practitioners
as they address the medical futility of further treatment.40
There must be a level of assurance that prolonged time
on ECMO will enhance patients’ outcomes and that this
possibility outweighs the risks of further suffering and
discomfort for the child.47
66 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
The ethical dilemma of ECPR is mostoften not whether to withhold support,but when to withdraw it.
The Final DecisionAlthough clinicians must decide if ECMO is appro-
priate and when further intervention is futile, the ultimate
burden of choice is left to the patient’s parents. As prac-
titioners, we must be aware of, and respect, the tremendous
responsibility of this decision. ECPR is initiated as the
most advanced form of life support available to patients,
when death without ECMO is most certainly imminent.
Furthermore, many patients remain alive purely through
the use of ECMO and cannot be supported with traditional
medicine. Removal of the pump often equates to death.
In 2003, Curley and Meyer48 examined parental
experiences with ECMO and reported that 61% of par-
ents felt that they had no other choice but to consent to
treatment, since death was the only other option. In the
study, most parents understood that ECMO was an
extraordinary intervention, even in the technologically
dominant intensive care unit environment.
As practitioners, we must be aware of our communi-
cation with parents in this very difficult and anxious time.
Honesty concerning the many complications and uncer-
tainties of ECMO is paramount to effective discussions.48
Furthermore, when a decision is made to treat a child
with ECMO, parents must be cautioned that its use
involves a time-limited trial.48 Reasonable expectations of
length of duration and outcome must be clear to par-
ents.47 Finally, all members of the team must be prepared
to answer questions and provide support throughout the
use of ECMO.47 The importance of offering support and
guidance can never be underestimated in this setting,
where parents are very aware that every moment with
their child may be their last.
Nursing ImplicationsThe use of ECMO during CPR is a technologically
advanced and complex treatment that requires extensive
knowledge from every member of the health care team.
Bedside nurses should be well educated on the physiol-
ogy of the patient, as well as the mechanical aspects of
the ECMO pump. Centers providing this treatment must
offer educational programs to train nurses in rapid
deployment of the ECMO circuit. Familiarity with the
circuit and experience with the cannulation procedure
will ensure a smooth transition from cardiopulmonary
resuscitation to artificial circulation.
Once the patient is cannulated, highly skilled nurses
are needed to manage daily treatment. Nursing care of
ECMO patients is both physically and mentally demand-
ing. These patients require frequent laboratory and
physical assessments, as well as frequent neurological
checks. Neurological injury is common in ECMO patients
owing to the acuity of their illness and the risk of cerebral
vascular injury from stroke or hemorrhage. Daily ultra-
sound imaging of the head are routine in most centers,
and continuous electroencephalographic monitoring is
also implemented with concerns for subclinical seizure
activity. Because
of the immense
workload associ-
ated with ECMO
patients, 2
nurses are gener-
ally needed to
care for these acutely ill children. One nurse is tasked
with the care of the patient, while the other nurse tends
to the needs of the ECMO pump. Most centers have
implemented the use of perfusionists and specially
trained respiratory therapists to manage the ECMO cir-
cuit in an effort to reduce the strain on nursing staffing.
Furthermore, the bedside nurse is often depended on
to provide support to patients’ families. This responsibil-
ity is difficult and challenging, and it requires a large
amount of dedication. Most intensive care nurses are well
versed in end-of-life care and must continue to use this
skill during ECMO trials. Although the physical care of
these patients can be burdensome, bedside nurses must
strive to ensure that time is allocated for family support.
When needed, nurses should be aware of the resources
available for patients’ families, including palliative care
teams, social workers, and chaplain services. These serv-
ices can help by offering assistance to family members
during periods of critical illness and end of life.
The Future of ECPRUse of ECMO as a final therapy during CPR in the
care of critically ill patients remains promising. As
providers continue to broaden the boundaries of use of
ECMO, it is imperative that judicious decision making
be maintained in the clinical setting. Further data and
research are needed to create guidelines and parameters
for withholding and withdrawing ECMO. It is essential
that clinicians providing this treatment be thoroughly
educated and knowledgeable about the literature, so that
decisions are based on evidence.
The importance of offering support andguidance can never be underestimatedin this setting, where parents are veryaware that every moment with theirchild may be their last.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 67
Finally, as with all end-of-life care, it is essential that
all members of the health care team be aware of parental
presence and concern. Support must be provided to
patients’ families on a constant basis to ensure that their
needs are met. It is very easy for physicians and nurses
to become overwhelmed by the technical aspects of
caring for these critically ill patients and focus solely on
maintaining life. However, a holistic approach to care
should remain a focus, with appropriate support of the
patient as well as the patient’s family. CCN
Financial DisclosuresNone reported.
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8. Raymond TT, Cunnyngham CB, Thompson MT, et al. Outcomes amongneonates, infants, and children after extracorporeal cardiopulmonaryresuscitation for refractory inhospital pediatric cardiac arrest: a reportfrom the National Registry of Cardiopulmonary Resuscitation. PediatrCrit Care Med. 2010;11(3):362-371.
9. Huang SC, Wu ET, Chen YS, et al. Extracorporeal membrane oxygena-tion rescue for cardiopulmonary resuscitation in pediatric patients. CritCare Med. 2008;36(5):1607-1613.
10. de Mos N, Van Litsenburg RR, McCrindle B, Bohn DJ, Parshuram CS.Pediatric in intensive care unit cardiac arrest: incidence, survival, andpredictive factors. Crit Care Med. 2006;34(4):1209-1215.
11. Delmo Walter EM, Alexi-Meskishvili V, Huebler M, et al. Rescue extra-corporeal membrane oxygenation in children with refractory cardiacarrest. Interact Cardiovasc Thorac Surg. 2011;12(6):929-934.
12. Kumar TKS, Zurakowski D, Dalton H, et al. Extracorporeal membraneoxygenation in postcardiotomy patients: factors influencing outcome.J Thorac Cardiovasc Surg. 2010;140(2):330-336.
13. Huang SC, Wu ET, Wang CC, et al. Eleven years of experience withextracorporeal cardiopulmonary resuscitation for pediatric patientswith in-hospital cardiac arrest. Resuscitation. 2012;83(6):710-714.
14. Fuhrman BP, Zimmerman J. Pediatric Critical Care. 3rd ed. Philadelphia,PA: Mosby; 2006.
15. Fiser RT, Morris MC. Extracorporeal cardiopulmonary resusciation inrefractory pediatric cardiac arrest. Pediatr Clin North Am. 2008;55(4):929-941.
16. Young KD, Seidel JS. Pediatric cardiopulmonary resuscitation: a collectivereview. Ann Emerg Med. 1999;33(2):195-205.
17. Nadkarni VM, Larkin GL, Peberdy MA, et al. First documented rhythmand clinical outcome from inhospital cardiac arrest among children andadults. JAMA. 2006;295(1):50-57.
18. Topijan AA, Nadkarni VM, Berg RA. Cardiopulmonary resuscitation inchildren. Curr Opin Crit Care. 2009;15(3):203-208.
19. Joffe AR, Lequier L, Robertson CMT. Pediatric outcomes after extracor-poreal membrane oxygenation for cardiac disease and for cardiac arrest:a review. ASAIO J. 2012;58(4):297-310.
20. Kane DA, Thiagarajan RR, Qypij D et al. Rapid response extracorporealmembrane oxygenation to support cardiopulmonary resuscitation inchildren with cardiac disease. Circulation. 2010;122(11 suppl):S241-S248.
21. Alsoufi B, Al-Radi O, Gruenwald C, et al. Extracorporeal life supportfollowing cardiac surgery in children: analysis of risk factors and sur-vival in a single institution. Eur J Cardiothorac Surg. 2009;35(6):1004-1011.
22. Duncan B, Ibrahim A, Hraska V, et al. Use of rapid-deployment extra-corporeal oxygenation for the resuscitation of pediatric patients withheart disease after cardiac arrest. J Thorac Cardiovasc Surg. 1998;116(2):305-311.
23. Del Nido P. Extracorporeal membrane oxygenation for cardiac supportin children. Ann Thorac Surg. 1996;61(1):336-339.
24. Wolf MJ, Kanter KR, Kirshbom PM, Kogon BE, Wagoner SF. Extracor-poreal cardiopulmonary resuscitation for pediatric cardiac patients. AnnThorac Surg. 2012;94(3):874-880.
25. Thourani VH, Kirshbom PM, Kanter KR, et al. Venoarterial extracorpo-real membrane oxygenation (VA-ECMO) in pediatric cardiac support.Ann Thorac Surg. 2006;82(1):138-144.
26. Polimenakos AC, Wojtyla P, Smith PJ, et al. Post-cardiotomy extracorpo-real resuscitation in neonates with complex single ventricle: analysis ofoutcomes. Eur J Cardiothorac Surg. 2011;40(6):1395-1404.
27. Prodhan P, Fiser RT, Dyamenahalli U, et al. Outcomes after extracor-poreal cardiopulmonary resuscitation (ECPR) following refractorypediatric cardiac arrest in the intensive care unit. Resuscitation. 2009;80(10):1124-1129.
28. Aharon AS, Drinkwater DC, Churchwell KB, et al. Extracorporeal mem-brane oxygenation in children after repair of congenital cardiac lesions.Ann Thorac Surg. 2001;72(6):2095-2101.
29. Chrysostomou C, Morell VO, Kuch BA, O’Malley E, Munoz R, WeardenPD. Short- and intermediate-term survival after extracorporeal membraneoxygenation in children with cardiac disease. J Thorac Cardiovasc Surg.2013;146(2):317-325.
30. Alsoufi B, Al-Radi O, Nazer R, et al. Survival outcomes after rescueextracorporeal resuscitation in pediatric patients with refractory cardiacarrest. J Cardiovasc Surg. 2007;134(4):952-959.
31. Kelly RB, Harrison RE. Outcome predictors of pediatric extracorporealcardiopulmonary resuscitation. Pediatr Cardiol. 2010;31(5):626-633.
32. Morris MC, Wernovsky G, Nadkarni VM. Survival outcomes followingextracorporeal cardiopulmonary resuscitation from inhospital pediatriccardiac arrest. Pediatr Crit Care Med. 2004;5(5):440-446.
33. Shah SA, Shankar V, Churchwell KB, et al. Clinical outcomes of 84 chil-dren with congenital heart disease managed with extracorporeal mem-brane oxygenation after cardiac surgery. ASAIO J. 2005;51(5):504-507.
34. Sivarajan VB, Best D, Brizard CP, et al. Duration of resuscitation priorto rescue extracorporeal membrane oxygenation impacts outcome inchildren with heart disease. Intensive Care Med. 2011;37(5):853-860.
35. American Heart Association. 2005 American Heart Association guidelinefor cardiopulmonary resuscitation and emergency cardiovascular care.Circulation. 2005;112(24):47-50.
36. de Caen AR, Kleinman ME, Chameides L, et al. Part 10: Pediatric basicand advanced life support: 2010 International Consensus on Cardiopul-monary Resuscitation and Emergency Cardiovascular Care Science withtreatment recommendations. Resuscitation. 2010;81(suppl 1):e213-e259.
37. Kelly RB, Porter PA, Meier AH, Myers JL, Thomas NJ. Duration of car-diopulmonary resuscitation before extracorporeal rescue: how long isnot long enough? ASAIO J. 2005;51(5):665-667.
38. Merril ED, Schoeneberg L, Sandesara P, et al. Outcomes after prolongedextracorporeal membrane oxygenation support in children with cardiacdisease: Extracorporeal Life Support Organization registry study. J Thorac
Now that you’ve read the article, create or contribute to an online discussionabout this topic using eLetters. Just visit www.ccnonline.org and select the articleyou want to comment on. In the full-text or PDF view of the article, click“Responses” in the middle column and then “Submit a response.”
To learn more about extracorporeal membrane oxygenation, read“Discharge Outcome in Adults Treated With ExtracorporealMembrane Oxygenation” by Guttendorf et al in the AmericanJournal of Critical Care, September 2014;23:365-377. Available atwww.ajcconline.org.
68 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Cardiovasc Surg. 2014;148(2):582-588.39. Brogan TV, Zabrocki L, Thiagarajan RR, Rycus PT, Bratton SL. Prolonged
extracorporeal membrane oxygenation for children with respiratoryfailure. Pediatr Crit Care Med. 2012;13(4):e294-e254.
40. Steinhorn DM. Termination of extracorporeal membrane oxygenationfor cardiac support. Artif Organs. 1999;23(11):1026-1030.
41. Lantos JD, Frader J. Extracorporeal membrane oxygenation and the ethicsof clinical research in pediatrics. N Engl J Med. 1990;326(6):409-413.
42. Lowry AW, Morales DL, Graves DE, et al. Characterization of extracor-poreal membrane oxygenation for pediatric cardiac arrest in the UnitedStates: analysis of the kids’ inpatient database. Pediatr Cardiol.2013;34(6):1422-1430.
43. Truog RD, Brett AS, Frader J. The problem with futility. N Engl J Med.1992;326(23):1560-1564.
44. Solomon MZ, Sellers DE, Heller KS, et al. New and lingering controver-sies in pediatric end-of-life care. Pediatrics. 2005;116(4):872-883.
45. President’s Commission for the Study of Ethical Problems in Medicineand Biomedical and Behavioral Research. Deciding to Forgo Life-Sustain-ing Treatment: A Report on the Ethical, Medical, and Legal Issues in Treat-ment Decisions. Washington, DC: US Government Printing Office; 1983.
46. American Academy of Pediatrics, Committee on Bioethics. Guidelineson forgoing life-sustaining medical treatment. Pediatrics. 1994;93(3):532-536.
47. Gamulka BD. Ethical uncertainty: an approach to decisions involving extra-corporeal membrane oxygenation. Can Med Assoc J. 1994;150:565-568.
48. Curley MA, Meyer EC. Parental experience of highly technical therapy:Survivors and nonsurvivors of extracorporeal membrane oxygenationsupport. Pediatr Crit Care Med. 2003;4(2):214-219.
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 69
CNE Test Test ID C151: Extracorporeal Membrane Oxygenation for Pediatric Cardiac ArrestLearning objectives: 1. Determine the difference between venovenous and venoarterial extracorporeal membrane oxygenation (ECMO) 2. Describe thebenefits of extracorporeal cardiopulmonary resuscitation 3. Discuss the ethical considerations related to management of patients undergoing ECMO
Program evaluation Yes No
Objective 1 was met � �Objective 2 was met � �Objective 3 was met � �Content was relevant to my
nursing practice � �My expectations were met � �This method of CNE is effective
for this content � �The level of difficulty of this test was:
� easy � medium � difficultTo complete this program,
it took me hours/minutes.
7. The use of ECPR in pediatric critical care is complicated by all except which of
the following?
a. High cost of care
b. Questionable effectiveness
c. Intensified emotions of families and providers
d. Absence of standardized clinical guidelines for withdrawal
8. Which of the following is the term for the concept of initiating and removing
advanced life support?
a. Initiating
b. Withholding
c. Withdrawing
d. All of the above
9. Nursing care of patients receiving ECMO include which of the following?
a. Neurologic assessment
b. Highly skilled nursing care
c. Early mobility
d. A and B
10. Which of the following can help nurses assist families with emotional
support during hospitalization?
a. Child life specialists
b. Palliative care, social workers, and chaplain services
c. Physician support
d. Leadership support
11. Studies examining parents’ experiences with ECMO report which of the
following?
a. Parents felt they had no other choice as death was the only other option.
b. ECMO is one of several treatments available to improve their child’s condition.
c. Parents preferred optimistic reports on their child’s condition over reasonable prognosis.
d. Parents relied heavily on the physicians to guide them through the daily stressors
of having a child undergoing supportive measures.
12. Which of the following statements is true regarding treatment of neonates
with ECMO?
a. Large immediate infusion of crystalloids is a standard of care for neonates.
b. Immediate infusion with crystalloids is well tolerated by neonates.
c. Benefits of immediate end-organ perfusion often outweigh the risks of low hematocrit.
d. Hemodilution is not a significant risk with neonates.
For faster processing, takethis CNE test online at
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AACN, 101 Columbia Aliso Viejo, CA 92656.
Test ID: C151 Form expires: February 1, 2018 Contact hours: 1.0 Pharma hours: 0.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%) Synergy CERP Category A Test writer: Tina Cronin
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Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1. �a �b �c �d
12. �a �b �c �d
11. �a �b �c �d
10. �a �b �c �d
9. �a �b �c �d
8. �a �b �c �d
7. �a �b �c �d
6. �a �b �c �d
5. �a �b �c �d
4. �a �b �c �d
3. �a �b �c �d
2. �a �b �c �d
1. Venoarterial extracorporeal membrane oxygenation (ECMO) is the preferred
extracorporeal support for extracorporeal cardiopulmonary resuscitation
(ECPR) patients over venovenous ECMO because of which of the following?
a. Risk of hemodilution in neonates
b. Absence of adequate cardiac function
c. Impaired renal function
d. None of the above
2. Complications in the postresuscitation phase in pediatric patients include all
except which of the following?
a. Impaired autoregulation of blood pressure
b. Myocardial dysfunction
c. Increased contractility of the heart
d. Hyperglycemia
3. Benefits of mechanical circulation via ECMO include which of the following?
a. Decreased risk of hypotensive shock
b. Decreased risk of aggressive vasoactive resuscitation
c. Promotion of autoregulation of blood pressure in the initial resuscitation period
d. Promotion of hemodynamic stability
4. ECPR is recommended for use in which of the following types of patient settings?
a. Heart transplant surgery
b. Brief no-flow cardiac arrest in the hospital setting
c. Severe hyperthermia
d. Prolonged cardiopulmonary resuscitation with spontaneous return of circulation
5. Which of the following preexisting measurements can help determine survival
potential?
a. Preexisting diagnosis of cardiac illness has shown to improve survival outcomes
b. A pre-ECMO pH of less than 7.2 is associated with higher mortality
c. A pre-ECMO pH of less than 6.9% is associated with negative outcomes
d. All of the above
6. Which of the following is the only clear indicator for withdrawal of ECMO
support?
a. Neurological deterioration
b. Ongoing cardiac dysfunction
c. Ongoing pulmonary failure
d. Oxygenator-associated thrombi
Carol Rauen, RN, MS, CCNS, CCRN, PCCN, CEN, RN-BC, the department editor,
is an independent clinical nurse specialist in The Outer Banks of North Carolina.
Carol welcomes feedback from readers and practice questions from potential
contributors at [email protected].
Kirtley Ceballos, MSN, RNC-NIC, PCNS-BC, clinical nurse specialist in the
neonatal intensive care unit at University of Colorado Hospital, University of
Colorado Health, Colorado Institute for Maternal Fetal Health, Aurora, Colorado,
contributed the pediatric CCRN questions.
Steve Risch, RN, MSN, CCRN, CCNS, a critical care clinical nurse specialist at
Holy Cross Hospital, Silver Spring, Maryland, contributed the adult CCRN
questions.
Adult CCRN Practice Questions1. Following a craniotomy, a
patient has a decreased serum
sodium level. Which other labo-
ratory findings would lead the
nurse to suspect syndrome of
inappropriate antidiuretic hor-
mone (SIADH)?
A. High serum osmolality and low
urine sodium
B. Low serum osmolality and high
urine sodium
C. High urine specific gravity and
high urinary output
D. Low urine specific gravity and
low urinary output
Test plan topic: Endocrine, 6% of the
CCRN questions
2. A multiple trauma patient has
received 4 L of normal saline and
2 units of packed red blood cells
but continues to be hypotensive.
Which recent assessment finding
of this patient would best reflect
improving tissue perfusion?
A. Increasing creatinine level
B. Increasing hematocrit
C. Decreasing heart rate
D. Decreasing lactic acid levels
Test plan topic: Multisystem, 8% of
the CCRN questions
3. A patient who continues to
experience full-body tonic-clonic
Contributors
Celebrate and Be Proud!
©2015 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2015495
Certification Test Prep
RAUEN
Thirty years ago this month (February 1985) I took the CCRN
exam. Achieving and maintaining my critical care certification
is one of the accomplishments, in my 34 years as a critical care
nurse, of which I am most proud. Many of the nurses who are read-
ing this column were not yet born when I became certified. My
efforts to help others prepare for and achieve this coveted certifica-
tion is exciting and humbling. The recent changes that have
occurred in the eligibility criteria have allowed more nurses to
obtain and maintain their CCRN certification. Now all nurses who
affect the care of critically ill patients and their families, whether
electronically (CCRN-e), in the classroom, at the bedside, or from an
administrative office (CCRN-K), can proudly wear the CCRN creden-
tial. I feel honored to be a member of this group. Please join me in
celebrating my anniversary and remember to celebrate your own!
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 71
CEBALLOS RISCH
Test plan topic: Cardiovascular, 20% of the CCRN questions
Correct Answers and Rationales for Adult CCRN Practice Questions1. Correct Answer: B
RationaleSIADH or diabetes insipidus (DI) can develop after
craniotomy. The posterior lobe of the pituitary gland,
which is regulated by the hypothalamus, releases antidi-
uretic hormone (ADH). In SIADH, increased release of
ADH causes fluid retention. The fluid retention causes
the patient to have a low urinary output, low serum
osmolality, low serum level of sodium, high specific
gravity of urine, and high sodium level in the urine.
SourceMorton P, Fontaine D. Critical Care Nursing: A Holistic Approach. 10th ed.
Philadelphia, PA: Lippincott, Williams & Wilkins; 2013:391.
2. Correct Answer: D
RationaleThe best indicator of improved oxygen delivery to
the cells during resuscitation is a decreasing level of lactic
acid, which is a byproduct of anaerobic metabolism.
Creatinine and hematocrit are not good indicators of oxy-
genation at the cellular level, and a decrease in heart rate
can reflect adequate resuscitation, but is not as specific
an indicator of tissue perfusion as are lactic acid levels.
SourceMorton P, Fontaine D. Critical Care Nursing: A Holistic Approach. 10th ed.
Philadelphia, PA: Lippincott, Williams & Wilkins; 2013:1408-1418.
3. Correct Answer: C
RationaleStatus epilepticus is a seizure that is continuous for a
prolonged period of time and typically does not respond
to single/initial administration of antiepileptic medica-
tion and benzodiazepine. Simple and partial complex
seizures last only 5 to 7 minutes. Myoclonic seizures are
associated with hypoxic brain injury and have a single
jerklike presentation, not full-body involvement.
SourcesBardwaj A, Mireski M. Handbook of Neurocritical Care. 2nd ed. New York, NY:
Springer; 2012:499.Morton P, Fontaine D. Critical Care Nursing: A Holistic Approach. 10th ed.
Philadelphia PA: Lippincott, Williams & Wilkins; 2013:902.
movements with no apparent response despite
administration of lorazepam (Ativan) and pheny-
toin (Dilantin) is most likely experiencing which
type of seizure?
A. Partial complex
B. Simple complex
C. Status epilepticus
D. Myoclonic seizure
Test plan topic: Neurological, 12% of the CCRN questions.
4. A patient who sustained a cervical (C5) spinal
cord injury 8 weeks ago and is quadriplegic has
sudden development of hypertension, blurred
vision, flushing, and diaphoresis of the face and
neck. The nurse should immediately:
A. Lower the head of the bed to flat position
B. Coach the patient to breathe deeply and cough
effectively
C. Check the patient’s temperature and administer an
antipyretic as needed
D. Irrigate the patient’s urinary catheter
Test plan topic: Neurological, 12% of the CCRN questions.
5. A patient has these hemodynamic findings after
mitral valve replacement:
Heart rate (HR), 65/min
Systolic blood pressure (SBP), 70 mm Hg
Mean arterial pressure (MAP), 55 mm Hg
Cardiac output (CO), 3.8 L/min
Cardiac index (CI, calculated as CO in liters per
minute divided by body surface area in square
meters), 1.8
Central venous pressure (CVP), 12 mm Hg
Pulmonary artery occlusion pressure (PAOP),
15 mm Hg
Which of the following interventions should the
nurse perform?
A. Increase epinephrine infusion from 4 μg/min to
6 μg/min.
B. Decrease the norepinephrine infusion from 8 μg/min
to 4 μg/min
C. Prepare to administer a 1-L bolus of normal saline
D. Attach the epicardial pacing wires to a pacemaker
and begin ventricular (VVI) pacing
72 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
4. Correct Answer: D
RationaleThe most common cause of autonomic dysreflexia is
obstruction of the urinary catheter, so irrigation might
correct the problem. The head of the bed (A) should be
elevated, not lowered. Although C5-level quadriplegics
must be monitored carefully for airway and pulmonary
issues, assisting the patient with effectively coughing (B)
will not help to treat the current problem. Fever (C) is
not a symptom of autonomic dysreflexia.
SourcesBardwaj A, Mireski M. Handbook of Neurocritical Care. 2nd ed. New York, NY:
Springer; 2012:499. Morton P, Fontaine D. Critical Care Nursing: A Holistic Approach. 10th ed.
Philadelphia, PA: Lippincott, Williams & Wilkins; 2013:391.
5. Correct Answer: A
RationaleIncreasing the epinephrine infusion would further
increase - and -receptor stimulation to increase heart
rate, contractility, and blood pressure. Decreasing the
norepinephrine (B) could further decrease the blood
pressure. The CVP and the PAOP are both high, indicat-
ing that more volume (C) is not needed at this time. No
need to pace for a heart rate of 65/min.
SourceMorton P, Fontaine D. Critical Care Nursing: A Holistic Approach. 10th ed.
Philadelphia, PA: Lippincott, Williams & Wilkins; 2013:392.
Pediatric CCRN Practice Questions1. A 13-year-old is now permanently disabled after a
motor vehicle collision (MVC) in which the
mother was driving. What is an effective way for
the nurse to promote coping for this patient and
family?
A. Instruct the parents to recognize how different the
child will be from their peers.
B. Discourage expression of feelings of anger by the
patient toward the mother.
C. Provide information about other children in similar
situations who are doing well.
D. Do not include the child in discussions or decisions
about care.
Test plan topic: Professional Caring and Ethical Practices,
20% of the pediatric CCRN questions
2. A 3-week-old infant is newly admitted to the
pediatric intensive care unit (PICU) with a heart
rate of 246/min. The parents report the baby has
refused feeding for 8 hours and is difficult to
console. The infant is pale and sweating. What
intervention will be tried first?A. Digoxin
B. Applying ice to the face
C. Synchronized cardioversion
D. Intravenous (IV) adenosine
Test plan topic: Cardiac, 14% of the pediatric CCRN
questions
3. An 11-year-old admitted for bacterial meningitis
has complained of headache and abdominal pain
for the past 4 hours and is now febrile, tachy-
cardic, and vomiting. The nurse contacts the
physician immediately because the nurse suspects:
A. Acute adrenocortical insufficiency
B. Appendicitis
C. Hyponatremia
D. Cushing syndrome
Test plan topic: Neurological, 14% of the pediatric CCRN
questions
4. A 6-kg infant is in the PICU after 6 days of having
bloody diarrhea, vomiting, and fever at home.
Urine output in the past 12 hours is 10 mL and is
amber in color. Blood pressure is 110/85 mm Hg.
What diagnostic test do you expect to evaluate
these new symptoms?
A. Liver function tests
B. Magnetic resonance imaging
C. Renal scan
D. Echocardiogram
Test plan topic: Renal, 6% of the pediatric CCRN questions
5. An 8-year-old recovering from an open femoral
fracture is moved from the medical-surgical unit
to the PICU because of signs of infection. What
symptom of osteomyelitis may be masked by
treatment of the primary injury?
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 73
A. Local signs infection
B. Fever
C. Dehydration
D. Pain
Test plan topic: Multisystem, 11% of the pediatric CCRN
questions
Correct Answers and Rationales for Pediatric CCRN Practice Questions1. Correct Answer: C
RationaleFostering hopefulness (C) may help improve the
patient’s sense of well-being. It is important to promote
normalization by emphasizing abilities, rather than
focusing on differences (A). If the child is not allowed to
express anger (B), this family will not be able to develop
a nurturing environment. Allowing the patient to partic-
ipate in decisions (D) will encourage a positive self-image.
SourceHockenberry MJ, Wilson D. Wong's Nursing Care of Infants and Children. St
Louis, MO: Elsevier Health Sciences; 2013:857-858.
2. Correct Answer: B
RationaleThis patient has clinical signs of supraventricular
tachycardia (SVT). A vagal maneuver, like applying ice
to the face, can immediately reverse SVT. IV adenosine
(D) may be used in the emergency setting when vagal
maneuvers fail. Digoxin (A) is first-line medical man-
agement for chronic SVT. Synchronized cardioversion
(C) can be used to treat SVT in the ICU setting if cardiac
output is compromised.
SourceHockenberry MJ, Wilson D. Wong's Nursing Care of Infants and Children. St Louis,
MO: Elsevier Health Sciences; 2013:1400.
3. Correct Answer: A
RationaleAlthough rare, acute adrenocortical insufficiency
can be caused by damage of the adrenal gland from
meningococcemia. Early symptoms include headache,
diffuse abdominal pain, nausea, and vomiting. Although
abdominal pain and vomiting can be symptoms of
appendicitis (B), classic signs include anorexia and peri-
umbilical pain followed by nausea and pain in the right
lower quadrant. Hyponatremia (C) should always be con-
sidered in patients with central nervous system infection
and can be a result of adrenal insufficiency. Cushing syn-
drome (D) is rare in children and most often caused by
steroid therapy.
SourceHockenberry MJ, Wilson D. Wong's Nursing Care of Infants and Children. St
Louis, MO: Elsevier Health Sciences; 2013:1586.
4. Correct Answer: C
RationaleOliguria, amber urine, and hypertension are clinical
manifestations of hemolytic-uremic syndrome (HUS),
the leading cause of acute renal failure in infants and young
children. HUS generally follows an episode of gastroenteritis.
A renal scan to assess renal perfusion is an expected diag-
nostic procedure.
SourcePotts NL, Mandleco BL. Pediatric Nursing: Caring for Children and Their Families.
Independence, KY: Cengage Learning; 2011:723.
5. Correct Answer: D
RationaleBecause the patient is most likely receiving pain med-
ication for the fracture, increased pain and tenderness may
not be perceived. The nurse should monitor for signs of
acute infection and alterations in thermoregulation while
continuing to provide pain-relief measures.
SourcePotts NL, Mandleco BL. Pediatric Nursing: Caring for Children and Their Families.
Independence, KY: Cengage Learning; 2011:1312.
AACN Certcorp publishes a study bibliography that
identifies the sources from which items are validated. The
document may be found in the AACN Certification exam
handbook. The contributor of each question written for
this column has listed the source used in developing each
item. CCN
74 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Barbara McLean is a critical care clinicalnurse specialist at Grady Health Systemsin Atlanta, Georgia.
complexity of variables requires a
physiological appreciation of a
constellation of signs and symp-
toms, not just the blood pressures
or the mean pressure.1
In 1896, the mercury sphyg-
momanometer was designed and
then adopted and disseminated in
part by Harvey Cushing. In 1905,
Korotkoff developed methods for
auscultating Korotkoff sounds,
which were related primarily to
diastolic pressures. The clinical
techniques of direct measurement
of blood pressure by intra-arterial
cannula were initially developed
in the 1930s but were not used
effectively until the 1950s. These
measurements were soon accepted
as representing true systolic and
diastolic pressures.2 Since that time,
a significant amount of research
and engineering has produced a
variety of invasive and alternative
indirect methods of measuring
blood pressure. Following a brief
summary of the current methods
of evaluating blood pressure, a
simple overview of validation of
invasive arterial blood pressure
will simplify the comparisons.
Providers can indirectly moni-
tor blood pressure by using a num-
ber of techniques, most of which
describe the external pressure
of correlating with the NIBPvalues so often, it makes mewonder if I have misunder-stood my previous trainingon arterial catheters.
A Barbara McLean, RN, MN,
CCNS-BC, NP-BC, CCRN,
replies:
Many critically ill patients are
monitored with continuous blood
pressure measurements, which
provide clinicians with the impor-
tant measures of systolic blood
pressure (reflecting the change of
pressure in the artery related to
ventricular stroke volume) and
diastolic blood pressure (related
to vascular tone), as well as the
calculated mean arterial pressure
and pulse pressure. The physiology
of blood pressure monitoring is
quite complex, and the meanings
of the different values are often
misunderstood. Although most
providers use target end points for
pressure monitoring and interven-
tion, little evidence supports the
use of a single blood pressure tar-
get. When measuring noninvasively,
the points of measure are static,
versus the invasive measures, which
are dynamic (beat to beat). The
Author
Corresponding author: Barbara McLean, RN, MN,
CCNS-BC, NP-BC, CCRN, Grady Health Systems, 80 JesseHill Jr. Drive SE, Atlanta, GA 30303 (e-mail:[email protected]).
To purchase electronic and print reprints, contact theAmerican Association of Critical-Care Nurses, 101Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].
Comparing Blood Pressure Measures: Does One Measurement Equal Another?
Is it prudent to corre-late noninvasive bloodpressure (NIBP) meas-urements with arterialblood pressure meas-urements? My under-standing is that theaccuracy of arterialblood pressure meas-urements is assessedby doing the square-wave test and level-ing, not by correlatingthe arterial measure-ments with the NIBPvalues. However, Iobserve the practice
©2015 American Association of Critical-Care Nursesdoi: http://dx.doi.org/10.4037/ccn2015557
Ask the Experts
Q
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 75
applied to block flow to an artery
distal to the occlusion. These
methods actually detect the effects
of blood flow, not intra-arterial
pressure. These differences in what
is actually measured are the major
points of discrepancy between
direct and indirect measurements.
Five methods are currently used
for noninvasive monitoring of blood
pressure: Doppler flow, infrasound,
oscillometry, the volume clamp
technique, and arterial tonometry.
Doppler FlowSystems that operate on the
Doppler principle take advantage
of the change in frequency of an
echo signal when there is move-
ment between 2 objects. Doppler
devices emit brief pulses of sound
at a high frequency that are reflected
back to the transducer. In an uncom-
pressed artery, the small amount
of motion of the artery wall does
not cause a change in frequency of
the reflected signal. The compressed
artery exhibits a large amount of
wall motion when flow first appears
in the vessel distal to the inflated
cuff, which changes the frequency
of the signal, causing what is known
as a Doppler shift. The first appear-
ance of flow in the distal part of the
artery represents systolic pressure.
When the Doppler shift in the echo
signal disappears, that represents
diastolic pressure.
InfrasoundInfrasound devices use a
microphone to detect low-frequency
(20-30 Hz) sound waves associated
with the oscillation of the arterial
wall. These sounds are processed by
a minicomputer, and the processed
signals are usually displayed in
digital form.
OscillometryMost automated NIBP devices
are based on oscillometry. Oscillo-
metric devices operate on the same
principle as manual oscillometric
measurements. The cuff senses
pressure fluctuations caused by
vessel wall oscillations in the pres-
ence of pulsatile blood flow. Maxi-
mum oscillation is seen at mean
pressure, whereas wall movement
greatly decreases below diastolic
pressure. As with the other auto-
mated methods described, the
signals produced by the system
are processed electronically and
displayed in numeric form.3 In
oscillometry, variations in cuff
pressure resulting from arterial
pulsations during cuff deflation
are sensed by the monitor and
used to determine arterial blood
pressure values. The pressure at
which the peak amplitude of arte-
rial pulsations occurs corresponds
closely to directly measured mean
arterial pressure, and values of
systolic and diastolic pressure are
derived from proprietary formulas
that examine the rate of change of
the pressure pulsations. Conse-
quently, systolic and diastolic val-
ues obtained with this technique
are less reliable than mean arterial
pressure values.
Indirectly measured pressures
vary depending on the size of the
cuff used. Cuffs of inadequate width
and length can provide falsely ele-
vated measurements. Bladder width
should equal 40% and bladder
length at least 60% of the circum-
ference of the extremity measured.
When a cuff is slowly deflated and
blood first begins to flow through
the occluded artery, the artery’s
walls begin to vibrate. This vibra-
tion can be detected as an oscilla-
tion in pressure and has served as
the basis for the development of
several automated devices for mon-
itoring blood pressure. The disad-
vantages include the inability to
measure diastolic pressure, poor
correlation with directly measured
pressures, and lack of utility in
situations in which Riva-Rocci
(auscultation) measurements are
also unobtainable.4
Volume Clamp TechniqueThe volume clamp method
avoids the use of an arm cuff. A
finger cuff is applied to the proxi-
mal or middle phalanx to keep
the artery at a constant size. The
pressure in the cuff is changed as
necessary by a servocontrol unit
strapped to the wrist. The feed-
back in this system is provided by
a photoplethysmograph that esti-
mates arterial size. The pressure
needed to keep the artery at its
unloaded volume can be used to
estimate the intra-arterial pressure.5
Arterial TonometryArterial tonometry provides
continuous noninvasive measure-
ment of arterial pressure, includ-
ing pressure waveforms. It slightly
compresses the superficial wall of
an artery (usually the radial artery).
Pressure tracings obtained in this
manner are similar to intra-arterial
tracings. A generalized transfer
76 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
function can convert these tracings
to an estimate of aortic pressure.
This method has not yet achieved
widespread clinical use.
In summary, automated non-
invasive measurement of blood
pressure is a major component of
modern critical care monitoring.
Oscillometric and Doppler-based
devices are adequate for frequent
blood pressure checks in patients
without hemodynamic instability,
in patient transport situations
where arterial catheters cannot be
easily used, and in patients with
severe burns, in whom direct arte-
rial pressure measurement would
be associated with an unacceptably
high risk of infection. Automated
NIBP monitors have a role in fol-
lowing trends of pressure change;
however, the averaging over time is
the value-laden data, not the single
measure, or its comparison to
invasive arterial pressure. In gen-
eral, such automated devices have
significant limitations in patients
with rapidly fluctuating blood
pressures, and blood pressure val-
ues obtained with such devices
may differ substantially from
directly measured intra-arterial
pressures.
Given these limitations, critical
care practitioners should be wary
of relying solely on NIBP measure-
ments in patients with rapidly
changing hemodynamics or in
whom very exact measurements
of blood pressure are important.6
It is vital to remember that regard-
less of the method by which blood
pressure is measured, it is a poor
surrogate for the true value of con-
cern, that is, the stroke volume
that forces itself (via cardiac ejec-
tion) into the resistant arteries. For
most trials conducted in humans
or animals, blood pressure meas-
ures obtained by using a wide vari-
ety of methods correlate poorly with
invasive arterial pressure measure-
ments, particularly in patients
with edema, who are receiving
vasoactive medications, or who
have significant hypoperfusion.7-9
In the clinical environment,
monitoring of direct arterial
pressure uses an underdamped
catheter-transducer system. The
arterial response to ventricular
ejection is a frequency response,
that is, the stroke volume bolus of
blood goes into the artery, gener-
ating a vibration column that emits
many responses (arterial wall
oscillations) that are averaged into
the systolic pressure. These frequen-
cies transmit into the system,
which transmits the frequencies
through the fluid-filled tubing and
transducer.10 Nowadays, monitors
offer internal calibration, filtering
of artifacts, and printouts of the
display. The digital display shows
an average of values over time and
thus does not show beat-to-beat
variability accurately. Beat-to-beat
differences in amplitude can be
measured precisely by freezing the
monitor display with on-screen
calibration, allowing assessment
of the effect of ectopic beats on
blood pressure, variations in pulse
pressure or systolic pressure, and
the severity of pulsus paradoxus.
Direct measurement of arterial
blood pressure requires that the
pressure waveform from the can-
nulated artery be reproduced
accurately on the bedside monitor.
The displayed pressure signal is
markedly influenced by the meas-
uring system, including the arterial
catheter, extension tubing, stop-
cocks, flush devices, transducer,
amplifier, and recorder.
Zeroing and leveling are com-
mon procedures for most providers,
but the importance of the dynamic
response to fluid flush is not gen-
erally well understood or used to
test the accuracy of the system.
The length, width, and compliance
of the tubing all affect the system’s
response to change. Small-bore
catheters are preferable because
they minimize the mass of fluid
that can oscillate and amplify the
pressure. The compliance of the
system (the change in volume of
the tubing and the transducer for
a given change in pressure) should
be low. In addition, bubbles in the
tubing can affect measurements
in 2 ways. Large amounts of air in
the measurement system damp
the system response and cause
the system to underestimate the
pressure. Large amounts of air
are usually easily detectable.
Small air bubbles cause an increase
in the compliance of the system
and can markedly amplify the
reported pressure.
Testing the Accuracy ofthe Monitoring SystemZero Reference
When pressure measurements
seem inaccurate or differ markedly
from indirect measurements, the
system’s accuracy can be checked
quickly. The most likely source of
error is improper zeroing of the
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 77
system, which can be caused either
by a change in the patient’s position
or by zero drift. Opening the trans-
ducer stopcock to air and aligning
the transducer with the midaxillary
line should confirm that the moni-
tor displays zero (a transducer that
is below the zero reference line will
result in falsely high measurements
and vice versa). The monitor should
be zeroed whenever the patient’s
position changes, when blood pres-
sure changes significantly, and rou-
tinely every 6 to 8 hours because
of zero drift. Disposable pressure
transducers are standardized and
do not require calibration. If zero
referencing is correct, a fast-flush
test can be done to assess the sys-
tem’s dynamic response.10,11
Square-Wave TestTwo major factors affect the
validity of pressures measured:
resonant frequency response, the
vibration of the fluid column in
response to a change in the system
(eg, flush), and the damping coef-
ficient, evaluating the end of the
vibrations.
Overdamped tracings are usu-
ally caused by problems that are
correctable, such as air bubbles,
kinks in tubing, clots, overly
compliant tubing, loose connec-
tions, a deflated pressure bag, or
anatomical factors that affect the
catheter. An underdamped trac-
ing results in systolic overshoot
and can be due to excessive tub-
ing length or patient-related fac-
tors such as increased inotropic
or chronotropic state, as the vessel
wall is more rigid and oscillates
at a higher level. Many monitors
can be adjusted to filter out fre-
quencies above a certain limit,
which can eliminate frequencies
in the input signal that are caus-
ing ringing, although elimination
of important frequencies will result
in inaccurate measurements.10
Although other techniques can
be used, the easiest way to test the
damping coefficient and resonant
frequency of a monitoring system
is by doing a fast-flush test (also
known as a square-wave test). This
test is performed at the bedside
by briefly opening and closing the
continuous flush device, producing
a square-wave displacement on
the monitor followed by a return
to baseline, usually after a few
smaller oscillations. Visual inspec-
tion is usually sufficient to ensure
a proper frequency response. An
optimal fast-flush test causes an
undershoot followed by a small
overshoot, then settles back into
the patient’s waveform (Figure 1).
When air is present in the tubing,
a clot is on the tip of the catheter,
or the catheter is not properly
positioned, the waveform will
Figure 1 Crisp systole, dicrotic notch, and diastole. When flush test is applied, 2 oscillations follow before return to baseline.
300 mm Hg
DicroticnotchSystole
Diastole
Systolic
MeanDiastolic
Time →
Pres
sure→
“Square wave” or flush test,natural resolution to normal oscillation,only 2 oscillations before return to baseline
78 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
appear more rounded and less
defined. When the square-wave
flush is applied, no resonance is
seen (Figure 2). Finally, when the
system is underdamped, the tub-
ing is too long, or the catheter is
the wrong size, multiple oscilla-
tions are apparent after the square-
wave test is applied (Figure 3).
Dynamic response validation by
fast-flush test should be performed
frequently: at least every 8 hours,
with every significant change in
the patient’s hemodynamic status,
after each opening of the system
(zeroing, blood sampling, tubing
change), and whenever the wave-
form appears damped.
Components of the monitoring
system are designed to optimize
the frequency response of the entire
system. The 18- and 20-gauge
catheters used to gain vascular
access are not a major source of
distortion but can become kinked
or occluded by thrombus, resulting
in overdamping of the system.
Standard, noncompliant tubing
is provided with most disposable
transducer kits and should be as
short as possible to minimize sig-
nal amplification (overdamping).
Air bubbles in the tubing and con-
necting stopcocks are a notorious
source of overdamping of the trac-
ing and can be cleared by flushing
through a stopcock.
Despite technical problems,
direct arterial pressure measure-
ment offers several advantages.
Arterial catheters actually measure
the end-on pressure propagated by
the arterial pulse. In contrast, indi-
rect methods report the external
pressure necessary either to obstruct
flow or to maintain a constant
transmural vessel pressure. Arterial
catheters can also detect pressures
at which Korotkoff sounds are
either absent or inaccurate. Arte-
rial catheters provide a continuous
measurement, with heartbeat-to-
heartbeat blood pressures.
Problems With ComparingNoninvasive and InvasivePressure Monitoring
Indirect methods of measur-
ing blood pressure estimate the
arterial pressure by reporting
the external pressure necessary to
either obstruct flow or maintain a
constant transmural vessel size. A
recently published meta-analysis12
of 28 studies involving 919
patients concluded that
inaccuracy and imprecision
of continuous noninvasive
arterial pressure monitoring
devices are larger than what
was defined as acceptable.
This may have implications
Figure 2 When the arterial pressure loses its sharp visualization or the digital measure is lower than oscillated or anticipated,check the patient first. Then check all connections on the monitoring system, starting at the patient all the way to the transducerand then the pressure bag. An overdamped picture can occur when connections are loose, the pressure bag is inflated at lessthan 300 mm Hg, there is air in the tubing, or a clot forms on the tip. Validate the mean pressure of both the arterial catheterand the oscillated pressure.
300 mm Hg
Normalsystole
Normal diastole
Constantmean
Underestimatedsystole
Overestimateddiastole
Comparing normalwith overdamped
Systolic
Oscillations absent,indicates overdamping
Mean
Diastolic
Time →
Pres
sure→
“Square wave” or flush test
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 79
for clinical situations where
continuous noninvasive arte-
rial pressure is being used for
patient care decisions.
Direct arterial catheters measure
the end-on pressure propagated by
the arterial pulse with every beat.
They are not measuring the same
end points as indirect methods
measure. Rigorous validation of
the accuracy of the monitoring
system can be done with the square-
wave flush test, but that does not
ensure the value of the blood
pressure measurements, just the
accuracy of the system.11
Direct arterial pressure meas-
urement offers several advan-
tages in many but not all patients.
Although an invasive catheter is
required, the reported risk of com-
plications is low. Arterial catheters
provide a heartbeat-to-heartbeat
measurement, can detect pressures
at which Korotkoff sounds are
either absent or inaccurate, and
do not require repeated inflation
and deflation of a cuff. Regardless
of the method used, the mean
arterial pressure should generally
be the value used for decision
making in most critically ill
patients, because it is the most sta-
ble (least affected) measurement
(calculation) across all methods of
blood pressure monitoring.
So to answer the first question,
“Is it prudent to correlate NIBP
measurements with arterial blood
pressure measurements?” No.
Most noninvasive methods provide
an average calculation for systolic
and diastolic blood pressures,
based on a measured mean pres-
sure. Compare the mean pressures
and consider the tested and zeroed
invasive arterial pressure to be the
true measure whether you like the
numbers or not. These 2 types of
measurements evaluate something
quite different: direct pressure
monitors beat-to-beat pressure
pulse, whereas the commonly used
noninvasive methods measure
peak oscillations related to blood
flow. Especially in patients treated
with vasopressors, inotropic agents,
and vasodilators, these measure-
ments may differ significantly.
The second question was, “My
understanding is that the accuracy
of arterial blood pressure meas-
urements is assessed by doing the
square-wave test and leveling, not
by correlating the arterial meas-
urements with the NIBP values.
However, I observe the practice of
correlating with the NIBP values
so often, it makes me wonder if I
have misunderstood my previous
training on arterial catheters.”
Leveling and square-wave test-
ing provide an evaluation of the
system and validation of system
acceptability. Neither test validates
the patient’s arterial pressure, but
the tests validate the integrity of
Figure 3 Spiked systole with a lower diastole should alert the provider to a possible underdamping issue. Underdamping usuallyoccurs when the tubing is too long or the catheter is the wrong size. The problem is usually not physiologic. Reduce the tubinglength and stabilize or replace the catheter. Observe that the mean pressure remains constant between oscillated and invasive.
300 mm Hg
Normalsystole
Normaldiastole
Constantmean
Overestimatedsystole
UnderestimateddiastoleComparing normal
with underdamped
Systolic
“Ringing oscillations”indicate underdamping
Mean
Diastolic
Time →
Pres
sure→
“Square wave” or flush test
80 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
the monitoring system that meas-
ures the pressure. If zeroing is
performed and the square-wave
test is passed, you can rest assured
that the direct pressure is being
monitored correctly. When inva-
sive arterial pressure monitor is
zero referenced, leveled, and passes
the frequency response test, then
the invasive pressure is what should
be monitored. At the very best,
correlation can be made between
noninvasive and invasive meas-
urements at the mean pressure
measure only.
Remember that the primary
role of the circulation is to provide
tissues with dissolved and bound
oxygen as well as other energy
substrates, so it is always best to
correlate pressure readings with
indicators of tissue perfusion, no
matter what method(s) you choose
for monitoring. Recommendations
for pressure targets must take into
consideration the site and method
of measurement as well as the true
value of blood pressure versus
oxygen adequacy. Trends in blood
pressure and the relationship to
metabolic measures are the most
important measures in today’s
critical care environment. CCN
Financial DisclosuresNone reported.
References1. Magder SA. The highs and lows of blood
pressure: toward meaningful clinical targetsin patients with shock. Crit Care Med. 2014;42(5):1241-1251.
2. Pierce EC. Percutaneous arterial catheteriza-tion in man with special reference to aortog-raphy. Surg Gynecol Obstet. 1951;93:56.
3. Borow KM, Newberger JW. Non-invasiveestimation of central aortic pressure usingthe oscillometric method for analyzingsystemic artery pulsatile blood flow: com-parative study of indirect systolic, dias-tolic, and mean brachial artery pressurewith simultaneous direct ascending aorticpressure measurements. Am Heart J.1982;103:879.
4. Bruner JM, Krenis LJ, Kunsman JM, Sher-man AP. Comparison of direct and indirectmethods of measuring arterial blood pres-sure: Pt III. Med Instrum. 1981;15(3):182-188.
5. Bogert LW, van Lieshout JJ. Non-invasivepulsatile arterial pressure and stroke volumechanges from the human finger. Exp Physiol.2005;90:437-446.
6. Van Egmond J, Hasenbros M, Crul JF. Inva-sive v. non-invasive measurement of arterialpressure. Br J Anaesth. 1985;57(4):434-444.
7. Aarnes TK, Hubbell JAE, Lerche P, Bed-narski RM. Comparison of invasive andoscillometric blood pressure measurementtechniques in anesthetized sheep, goats, andcattle. Vet Anaesth Analg. 2014;41:174-185.
8. Hohn A, Defosse JM, Becker S, et al. Non-invasive continuous arterial pressure moni-toring with Nexfin does not sufficientlyreplace invasive measurements in criticallyill patients. Br J Anaesth. 2013;111(2):178-184.
9. Stover JF, Stocker R, Lenherr R, et al. Non-invasive cardiac output and blood pressuremonitoring cannot replace an invasivemonitoring system in critically ill patients.BMC Anesthesiol. 2009;9:6.
10. Troy P, Smyrnios NA, Howell MD. Routinemonitoring of critically ill patients. In:Irwin RS, Rippe JM, eds. Irwin and Rippe’sIntensive Care Medicine. Philadelphia, PA:Lippincott Williams & Wilkins; 2011:258-276.
11. McGhee BH, Bridges EJ. Monitoring arte-rial blood pressure: what you may notknow. Crit Care Nurse. 2002;22(2):60-79.
12. Kim SH, Lilot M, Sidhu KS, Rinehart J, YuZ, Canales C, Cannesson M. Accuracy andprecision of continuous noninvasive arterialpressure monitoring compared with invasivearterial pressure: a systematic review andmeta-analysis. Anesthesiology. 2014;120(5):1080-1097.
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Ask the ExpertsDo you have a clinical, practical,or legal question you’d like to haveanswered? Send it to us and we’llpass it on to our Ask the Expertspanel. Questions may be mailed toAsk the Experts, Critical Care Nurse,101 Columbia, Aliso Viejo, CA 92656;or sent by e-mail to [email protected] of the greatest generalinterest will be answered in thisdepartment each and every issue.
www.ccnonline.org
Melody R. Campbell is a critical care clinical nurse specialist and trauma programmanager at Kettering Medical Center, Kettering, Ohio.
Julie Fisher is a physical therapist and the lead therapist in the physical medicineand rehabilitation department at Good Samaritan Hospital, Dayton, Ohio.
Lyndsey Anderson is an occupational therapist in the physical medicine and rehabilitation department at Good Samaritan Hospital, Dayton, Ohio.
Erin Kreppel is a physical therapist in the physical medicine and rehabilitationdepartment at Little Company of Mary Hospital, Evergreen Park, Illinois.
Corresponding author: Melody R. Campbell, RN, DNP, CEN, CCRN, CCNS, Trauma Program, Kettering MedicalCenter, 3535 Southern Blvd, Kettering, Ohio 45429 (e-mail: [email protected]).
To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].
Literature Review,Appraisal, and Synthesis
Electronic databases searched for
evidence included Cochrane, PubMed,
and CINAHL. Key words included
mechanical ventilation, critically ill,
critical illness, early mobilization proto-
col, delirium, intensive care unit, early
mobility, sedation, physical rehabilita-
tion, and physical therapy. In CINAHL,
limits included research, English,
human, and all adults. Related cita-
tions were reviewed in PubMed with
limitations of clinical trials, human,
English, and publication between 2007
and 2012. References from key articles
were reviewed to search for additional
evidence. Articles were included in
the appraisal if content focused on
early mobility in critically ill patients
receiving mechanical ventilation.
Articles were rated by strength of
evidence.4 Level 1 evidence, that estab-
lished by meta-analysis or systemic
review (and also the highest level of
evidence) was not found. No Cochrane
reviews or national practice guidelines
that were related to the subject had
been published between 2007 and
2012. Since that time, a clinical practice
guideline2 related to pain, agitation,
and delirium in the critically ill has
Anew bundle of interventions to improve the care of critically ill
patients receiving mechanical ventilation has been identified.1,2
This bundle incorporates performance and coordination of
spontaneous awakening trials and spontaneous breathing trials; careful
selection of sedatives; assessment, prevention, and management of delir-
ium; and early exercise with progressive mobility.1,2 In collaboration with
the Institute for Healthcare Improvement, and as a part of a critical care
collaborative, our hospital had implemented many parts of the bundle,
but early exercise and progressive mobility had not yet been incorpo-
rated into care. In this article, we share our process for literature review,
appraisal, and synthesis along with protocol development. An evidence-
based performance improvement (EBPI) model was used to plan, imple-
ment, and disseminate the change.3 High-fidelity human simulation
boosted confidence and teamwork and also underscored important
safety aspects before implementation. Unit champions and daily multi-
disciplinary rounding assisted with culture change.
Authors
Implementation of Early Exercise and Progressive Mobility: Steps to Success
©2015 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2015701
In Our Unit
Melody R. Campbell, RN, DNP, CEN, CCRN, CCNSJulie Fisher, PT, MPTLyndsey Anderson, MOT, OTR/LErin Kreppel, PT, MPT
82 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
been published. Seven keeper articles
were identified.5-11
The articles were shared and
discussed with our multidiscipli-
nary team. From these articles, the
team determined that early activity
had been demonstrated to be safe
and feasible7,8 and that early mobil-
ity was associated with an increase
in both delirium-free days and
ventilator-free days.5,6,10 Some stud-
ies noted that the implementation
of early mobility contributed to
decreases in length of stay in both
intensive care units (ICUs) and
hospitals.9,10 An additional article11
discussed barriers and facilitators
to implementation of early mobility.
Barriers included sedation, decreased
level of consciousness, and agitation.
Factors that facilitated change were
the presence of a protocol and the
presence of unit champions.11 The
multidisciplinary team decided that
the evidence was sufficient for us to
implement the practice of early
mobility for our patients.
Planning for ChangeWhile our team was planning
implementation of early mobility,
we elected to be a part of an expedi-
tion on early mobility sponsored by
the Institute for Healthcare Improve-
ment. The expedition was a series of
webinars that included presenta-
tions of the science surrounding early
mobility and assisted with protocol
development and implementation
planning. We invited various depart-
ments (respiratory therapy, physical
and occupational therapy, pharmacy)
and our medical director to attend
the webinars. We ensured that ICU
nursing staff, who would act as unit
champions, could attend. The webi-
nar communicated the importance
of early mobility and the evidence
supporting the change.
Our early mobility protocol
(Figure 1) was developed after careful
reading of 2 key articles: a random-
ized controlled trial and a descriptive
study that detailed the intervention
arm of that same trial.5,6 The protocol
was reviewed by the multidisciplinary
team and by several critical care
intensivists. The protocol included
contraindications to initiating early
mobility designated by a yellow text
box indicating caution. Once the
patient had no contraindications,
preparation of early mobility would
begin, designated by a green text box
indicating that the patient was ready
to go. Preparing for early mobility
would include assessing and securing
all devices, stopping tube feeding, and
moving all catheters, intravenous
pumps, and the urinary catheter
drainage bag to the side of the bed
with the ventilator. Activity would
progress from active range-of-motion
exercises to bed mobility exercises
(lateral rolling, move from semire-
cumbent to upright), sitting on the
edge of the bed, sitting to/from stand-
ing and bed to/from chair transfers,
and finally ambulation. An addi-
tional red box was included in the
protocol that delineated contraindi-
cations to continuing early mobility.
If the patient experienced physiolog-
ical changes such as hemodynamic
instability, or oxygen desaturation,
activity would be stopped.
An additional flowchart (Figure
2) was created to visualize and teach
others how early mobility would fit
into our process of coordination of
spontaneous awakening trials and
spontaneous breathing trials.
Our plan for implementation was
written and reviewed by our hospital’s
Human Institutional Review Com-
mittee and the university’s institu-
tional review board. We wanted to
collect patient data during the imple-
mentation of our project to monitor
process and outcomes and wanted
to ensure the safety of that data col-
lection and dissemination of results.
The final aspects of planning for
practice change included creating
an aim statement. Using our EBPI
model, an aim statement would
help us to know whether we had
reached a short-term goal in our
implementation. Working with our
medical director, we determined
that our aim statement would be:
By month 3 of the project, early
mobility would be incorporated
into the care of 25% of patients
receiving mechanical ventilation
(as appropriate). The implementa-
tion steps in accordance with our
EBPI model are listed in Table 1.
Practicing With High-Fidelity Human Simulation
One of our physical therapists
had read an article about the use of
high-fidelity human simulation to
teach physical therapy students.
Training with simulation helped
improve the students’ confidence
before they started getting clinical
experience in an actual ICU.13 The
physical therapist expressed a
desire to try our protocol by using
simulation first so that the team
could practice together to ensure
that the protocol was easy to under-
stand and that safety concerns were
addressed. Her main concern was
related to accidental extubation of
a patient, and she wanted us to plan
the steps of how we would care for
a patient who experienced that seri-
ous adverse event. We developed 3
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 83
simulation scenarios (see Table 2 for
examples):
• Assessment of the patient to
determine whether any contraindi-
cations for beginning early mobility
were present.
• Preparation of the patient and
beginning activity with recognition
of changes in condition that would
require stopping activity.
• Inadvertent extubation during
activity.
The project leader/clinical nurse
specialist worked with the personnel
in the simulation laboratory to pre-
pare for practice. Intravenous pumps,
a tube feeding pump, a sequential
compression device, a ventilator, a
manual resuscitation bag, a cardiac
monitor, a walker, and a transport
ventilator were transported to the
laboratory. The simulation labora-
tory was set up with the appropriate
equipment to look like one of our
ICU rooms. Nursing unit champions,
physical therapists, occupational
therapists, and respiratory thera-
pists participated. The clinical
nurse specialist reviewed the draft
protocol, including the sections on
contraindications for early mobil-
ity, preparation of the patient,
progression of activity, and when
to stop activity if the patient’s
condition changed. Additionally,
the flowchart of how early mobility
Figure 1 Early mobility protocol.
Contraindications to initiating early mobility5,6
1. Mean arterial pressure, < 65 mm Hg2. Heart rate, < 60/min or > 120/min3. Respiratory rate, < 10/min or > 32/min4. Oxygen saturation (pulse oximetry), < 90%5. Actively undergoing a procedure6. Patient’s agitation requiring increased sedation in past 30 minutes7. Insecure airway device or difficult airway
Contraindications to continuing earlymobility5,6
1. Mean arterial pressure, < 65 mm Hg2. Heart rate, < 60/min or > 120/min3. Respiratory rate, < 10/min or > 32/min4. Oxygen saturation (pulse oximetry),
< 90%5. Marked patient-ventilator dyssynchrony6. Patient distress
a. Evidenced by nonverbal cues and gestures
b. Physically combative7. New arrhythmia8. Concern for myocardial ischemia9. Concern for airway integrity
10. Fall to knees11. Inadvertent removal of endotracheal
tube12. Judgment of nurse, physical thera-
pist, or occupational therapist
Prepare for early mobility5,6
1. Assess all devices before beginning2. Secure all devices3. Stop tube feeding4. Remove or detach unnecessary
devices (eg, sequential compres-sion systems)
5. Move urinary catheter drainagebag, intravenous poles, and fecal collection bag to side of bed next toventilator
6. Always mobilize to side of bed nextto ventilator
7. For ambulation, use transport venti-lator. Always have wheelchairbehind patient to use in event ofweakness, intolerance of activity.
Prepare for early mobility
Active or active assisted range-of-motion exercises
Bed mobility exercises: lateral rolling, move semirecumbent to upright
Sitting balance activities, apply gaitbelt, assist to sit at side of bed,
incorporate activities of daily living
Improve standing balance and tolerance: reach, march in place, weight shift
Ambulation with assistance
Work on transfers: sit to stand, bed to chair, bed to commode, repetition
84 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
would be incorporated into our
current process was reviewed and
discussed.
The simulation began and the
group focused on how to begin to
move the patient. Discussion was
intense, with brainstorming about
the roles and responsibilities of
each of the team members. When
the patient needed to move from
sitting at the edge of the bed to
standing or transfering to a chair, a
team member was substituted for
the patient simulator so that the
team could practice standing the
patient at the bedside and ambula-
tion in the hallway. Proper body
mechanics and safe handling of
patient were emphasized. The group
thoroughly enjoyed the simulation
and found that the “hands-on”
approach boosted confidence. Four
priorities were identified for imple-
mentation of the protocol with a
“real” patient:
• The nurse caring for the patient
could begin to prepare all tubes
and catheters anticipating the
other team members’ arrival.
Doing so decreased the prepa-
ration time for the other disci-
plines, thereby increasing the
number of other patients that
they were able to see in their
work day.
• One person should be desig-
nated to communicate with
the patient and provide direc-
tion to the team during early
mobility. The physical thera-
pist or occupational therapist
was positioned immediately
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 85
Figure 2 Incorporation of early mobility into our current process.
Considerations for spontaneous breathing trial6,12:
(1) spontaneous breathing trial should be done daily when indicated, (2) coordinate tim-ing of early mobility with spontaneous breathing trial: (a) perform spontaneous breath-ing trial earlier in day, (b) perform early mobility session later in day after spontaneousbreathing trial if trial is unsuccessful, (c) patient to be extubated? Extubate, and dophysical/occupational therapy later in day
Proceed with early mobility withphysical/occupational therapist6
Patient meets criteria for spontaneous awakening trial12
Assess wakefulness
Patient is awake and calm: (1) opens eyes to voice,
(2) squeezes hand of nurse, (3) sticks out tongue6
Patient with decreased responsiveness5:(1) perform passive range-of-motionexercises, (2) continue sedation vaca-tion, (3) continue to monitor and assess
Agitation: restart sedation at half dose6,12
Perform spontaneous awakening trial
in front of the patient while
the patient was moving and
the group determined that
this team member would
direct the patient and lead
communications for the team.
The goal was to help the
patient understand what to
do next and to decrease con-
fusion for team members.
• Additional roles were delineated.
The respiratory therapist would
be responsible at all times for
monitoring endotracheal tube
security and oxygenation status.
The nurse would monitor other
tubes and catheters as well as
vital signs. The physical and
occupational therapists would
assess and monitor motor
strength, balance, and toler-
ance of activity. The decision
to stop the intervention and
return the patient to a supine
position would be a team
decision led by the nurse. The
patient also could stop the
activity.
• Specific equipment would
be helpful for mobilization.
A reclining-back manual
wheelchair would be posi-
tioned behind the patient
when walking in the hall in the
event of change of condition.
This specific type of wheel-
chair would allow supine posi-
tioning for ease in transferring
the patient back into the bed.
The transport ventilator would
be used when the patient was
ambulating in the hall.
ImplementationSmall tests of change were used
to begin the implementation. After
each test, the multidisciplinary
team reviewed how things went.
The protocol flowed well and was
easily understood. The team, having
gained confidence through the use
of simulation, worked well together
and the patients were safe. Next steps
involved teaching others about early
mobility and disseminating the
practice. The physical medicine and
rehabilitation department conducted
several in-service training sessions
with their staff and added written
and oral competencies to ensure staff
knowledge and patient safety. Nurses
and respiratory therapists conducted
training during staff meetings as
well as special educational confer-
ences focused on the bundle. We
used a slogan of “Mobility Is Medi-
cine” and provided slogan buttons
to those staff members who had
cared for a patient during early
mobility. We also purchased cook-
ies shaped like feet and emphasized
“Feet to the Floor.” This added fun
and helped create some excitement
regarding the change. Daily multi-
disciplinary rounding helped to
determine which patients were ready
for early mobility and supported
staff during implementation. The
team met every 2 weeks in conjunc-
tion with the medical director. Prob-
lems encountered with the practice
change were discussed and methods
to improve implementation were
developed. Constant communica-
tion with all the specialties involved
was done through staff meetings,
electronic mail, bulletin boards,
and departmental publications.
The patient’s experience was
also explored. One patient whom
we interviewed after he had been
extubated indicated that he enjoyed
being up while connected to the
ventilator. He had severe chronic
obstructive disease and had received
mechanical ventilation before. He
felt that he was ready to move
before the team was ready, and
when he began to ambulate out of
his room, he felt that he could
have walked much further but the
team was “nervous.” He walked
the next day around the whole
perimeter of the ICU. He stated
that “it felt good to get out and walk
because there is nothing else to do
in the ICU” and “it made it more
interesting.” The exercise made
him feel like he was improving.
Table 1 Plan for implementing the evidence-based performance improvement modela
1. Describe the problem: Need for implementation of early mobility into practice.
2. Formulate focused clinical question: What is the effect of an early mobility protocolon delirium and length of stay in the intensive care unit over the course of 3 months?
3. Search for evidence.
4. Appraise and synthesize evidence.
5. Develop aim statement: By month 3 of project, early mobility will be incorporatedinto care of 25% of patients receiving mechanical ventilation (as appropriate).
6. Engage in small tests of change.• Ensure safety: high-fidelity human simulation• Ensure safety and reproducibility: protocol refinement
7. Disseminate practice to all staff and patients.
8. Utilize plan-do-study-act process to monitor/evaluate implementation of new practice.a Based on information from Levin et al.3
86 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
Sustaining PracticeCreating organizational memory
and knowledge reservoirs were
important mechanisms in our
hospital to help with sustaining
practice.14 In our electronic medical
record, we were able to create files
to hold resource documents. Our
early mobility protocol was placed
Cardiac monitor
Normal sinusrhythm
Heart rate = 80/minNoninvasive blood
pressure = 130/80mm Hg
Oxygen saturation(pulse oximetry) =98%
Respiratory rate =16/min
Change in conditionSinus tachycardiaHeart rate=116/minNoninvasive blood
pressure =150/84 mm Hg
Oxygen saturation(pulse oximetry) =90%
Respiratory rate =30/min
Instructor content
Patient is improv-ing. Yesterdaypatient was ableto sit and danglelegs at bedside,sit to stand with2-person assist.Gait was steady.Plan for today isto march in place,weight shift, and determine if patient canambulate in room.
Patient’s conditionhas changed.Please work as a team to remedythe situation.
Expectations of student group
Verbalize the contraindi-cations to initiating early mobility. Examinepatient and infusions.Review ventilator settingsand vital signs.
Verbalize preparing patientfor early mobility.
Prepare patient for sit tostand, march in place,weight shift, possibleambulation in room.Verbalize:• Secure all devices• Turn off tube feeding• Move urinary catheter,
and intravenous poles to side of bed next to ventilator.
• Remove unnecessary devices (eg, sequentialcompression system)
• Obtain portable ventilator• Walker with support
for portable cardiac monitor
• Recumbent wheelchair
Nurse: talks to patient andassures them of theirsafety, tells them whatwill happen.
Team assists patient backto bed.
Respiratory therapistapplies face mask 100%oxygen. Team assessespatient’s tolerance ofextubation. Nurse notifiesphysician/provider ofextubation.
Important learning considerations
Have chart of contraindica-tions for early mobilityavailable for team toreview.
Note that patient has nocontraindications.
Have chart of items forconsideration for plan-ning for early mobility.
Discuss roles and responsibilities of different personnel.
Respiratory therapist:responsible for endotra-cheal tube and tubing toventilator. Setup ofportable ventilator.
Nurse: responsible forintravenous poles andintravenous catheters.Cardiac monitor ontowalker.
Patient care technician:remove sequential com-pression device, andmove urinary drainagebag to side of bed byventilator. Attach towalker. Emphasize main-taining drainage bagbelow level of bladder.
Physical/occupationaltherapist: apply gait belt,instruct patient. Assesstrunk stability, balance.Assist to sit at side ofbed. Determine whethermay sit to stand, marchin place, begin ambula-tion in room.
Calm approach to patientvery important.
Indications that patientmay need reintubation:
Tachypnea, decreasedoxygen saturation, circumoral cyanosis,tachycardia, hypotension.
Resources for reintubation:nurse practitioner, physi-cian, or anesthesiologist.
Ventilator
Assist controlFraction of
inspired oxygen=40%
Positive end-expiratorypressure =5 cm H2O
Low pressurealarm fromventilator
Simulation
Oral endotrachealtube to subglotticsuction
Sequential com-pression device(both legs)
Nasogastric tube–tube feeding/pump
Urinary catheter
Peripherallyinserted centralcatheter
Infusions:Dexmedetomidine
(Precedex)0.7 μg/kg per hour
Inadvertent endotrachealtube removal,patient is anxious, tachypneic.
Table 2 Simulation scenario 3 for early mobility: inadvertent removal of endotracheal tube
www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 87
in these files for ease of reference at
each computer terminal. We revised
our mechanical ventilator order set
(computer physician order entry) to
include prechecked orders for early
mobility as well as consultation with
physical and/or occupational thera-
pists for evaluation and treatment.
Then when the patient met criteria
for initiation of early mobility, the
appropriate orders were there. We
also used documents called standards
of nursing practice. These docu-
ments were a blend of nursing art
and science that helped to delineate
the important aspects of nursing
care for a specific type of patient.
They were used to help with orien-
tation of new staff. Our standard of
nursing practice for patients receiv-
ing mechanical ventilation was
updated to include concepts related
to early mobility. Lectures for criti-
cal care class also were updated to
include early mobility.
Lessons LearnedAfter 3 months, we were excited
that we had met our aim. More
than 25% of critically ill patients
receiving mechanical ventilation in
that third month had received early
mobility. No serious adverse events
had occurred. Staff were not only
readily identifying patients who were
appropriate for early mobility but
also were obtaining orders for
physical and occupational therapy
for patients who were not receiving
mechanical ventilation. A physical
therapist and an occupational ther-
apist were assigned to the ICU daily.
We had collected data related to
incidence and duration of delirium
and found a problem with the flow-
sheet design in our electronic medical
record. Additional changes were
the intensive care unit. Crit Care Med. 2013;32(4):15-26.
3. Levin RF, Keefer JM, Marren J, et al. Evidence-based practice improvement: merging 2paradigms. J Nurs Qual. 2010;25(2):117-126.
4. Melynk BM, Fineout-Overholt E. Evidence-BasedPractice in Nursing and Healthcare: A Guide toBest Practice. 2nd ed. Philadelphia, PA: Wolters/Kluwer/Lippincott Williams & Wilkins.
5. Schweikert WD, Pohlman MC, Pohlman AS,et al. Early physical and occupational therapyin mechanically ventilated, critically ill patients:a randomized controlled trial. Lancet. 2009;373(9678):1874-1882.
6. Pohlman MC, Schweickert WD, PohlmanAS, et al. Feasibility of physical and occupa-tional therapy beginning from initiation ofmechanical ventilation. Crit Care Med. 2010;38(11):2089-2094.
7. Bailey P, Thomsen GE, Spuhler V, et al. Earlyactivity is feasible and safe in respiratorytherapy. Crit Care Med. 2007;35(1):139-145.
8. Thomsen GE, Snow GL, Rodriguez L, et al.Patients with respiratory failure increase ambu-lation after transfer to an intensive care unitwhere early activity is a priority. Crit Care Med.2008;138(5):1224-1233.
9. Morris PE, Goad A, Thompson C, et al. Earlyintensive care unit mobility therapy in thetreatment of acute respiratory failure. CritCare Med. 2008;36(8):2238-2243.
10. Needham DM, Korupolu R, Zanni JM, et al.Early physical medicine and rehabilitationfor patients with acute respiratory failure: aquality improvement project. Arch Phys MedRehabil. 2010;91(4):536-542.
11. Winkelman C, Peereboom K. Staff-perceivedbarriers and facilitators. Crit Care Nurse. 2010;30(2):S13-S16.
12. Girard TD, Kress JP, Fuchs BD, et al. Efficacyand safety of a paired sedation and ventilatorweaning protocol for mechanically ventilatedpatients in intensive care units (awakeningand breathing trial): a randomized controlledtrial. Lancet. 2008;371(9607):126-134.
13. Shoemaker MJ, Riermersma L, Perkins R.Use of high fidelity simulation to teach physi-cal therapist decision-making skills for theintensive care setting. Cardiopulm Phys Ther J.2009;20(1):13-18.
14. Virani T, Lemieux-Charles L, Davis DA, et al.Sustaining change: once evidence-based prac-tices are transferred, what then? Healthcare Q.2009;12(1):89-96.
made to add detail to the 4 features of
the Confusion Assessment Method-
ICU (CAM-ICU) to support critical
thinking and accuracy of documen-
tation. We also noted problems with
sedation and analgesia practices and
are in the process of implementing a
nonverbal pain assessment tool and
an analgesia-first approach. As always,
change continues.
SummaryOur purposeful approach to the
implementation of early mobility by
using an EBPI model resulted in sus-
tainment of the practice a year later.
Critical appraisal and synthesis of
the literature resulted in a good pro-
tocol for early mobility. High-fidelity
human simulation built confidence
with working together, and this
translated to experiences with early
mobility in actual patients. Lessons
learned from others related to the
use of unit champions and multidis-
ciplinary rounding to help support
the practice change. We continue to
find opportunities to improve our
practice related to the care of patients
receiving mechanical ventilation. CCN
AcknowledgmentsThe authors acknowledge the leadership and sup-port of Mary Jo Trout, PharmD, RPh, BCPS, Robyn R.Razor, RN, MSN, and Thomas M. Yunger, Jr, MD,
FCCP, DABSM.
Financial DisclosuresNone reported.
References1. Vasilevskis EE, Ely EW, Speroff T, et al.
Reducing iatrogenic risks: ICU-acquireddelirium and weakness—crossing the qual-ity chasm. Chest. 2012;138(5):1224-1233.
2. Barr J, Fraser GL, Puntillo K, et al. Clinicalpractice guidelines for management of pain,agitation and delirium in adult patients in
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In Our UnitIn Our Unit highlights uniquepractices, innovations, research, orresourceful solutions to commonlyencountered problems in criticalcare areas and settings where criti-cally ill patients are cared for. Ifyou have an idea for an In OurUnit article, send it to Critical CareNurse, 101 Columbia, Aliso Viejo,CA 92656; e-mail, [email protected].
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www.ccnonline.org CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 89
Book Reviews
I had this book all those years agowhen I was becoming nursey so Iwould not have been so surprised byhow different working as a nurse,responsible and accountable for thecare of really sick patients, was fromwhat I learned in school. Second, Ihave had some great preceptorsthrough the years and I wish Kati Kleber had been one of them. Third, Iwish this book was available to give toall new nurses who crossed my path.It will make them feel as though theyare not alone, prepare them for whatis to come, and allow them to makeinformed choices as they move fromschool to becoming nursey.
Mary Pat Aust is a clinical practicespecialist at the American Associationof Critical-Care Nurses in Aliso Viejo,California.
©2015 American Association of Critical-CareNurses doi: http://dx.doi.org/10.4037/ccn2015997
Anatomy ofResearch forNursesHedges C, Williams B.
Indianapolis, IN: Sigma
Theta Tau International;
2014. Paperback; 352
pages. ISBN-13: 978-1938835117
This book is part of the Anatomyseries, published by Sigma Theta TauInternational, that uses the concept ofanatomical structure and function todevelop the content. The foundationof the book rests on distinguishingresearch from quality improvement andevidence-based practice, with additionaldiscussion about where these 3 com-ponents intersect.
through school, transi-tioning to working as anurse in a hospital,and transitioning fromthe acute care medical-surgical unit to aneuro/trauma intensivecare unit.
Kleber’s confident,compassionate, andwitty demeanor isevident throughoutthe book, as she dis-cusses combining thetechnical and emo-tional work of nursingand how to find yourplace along the con-tinuum. She offers tipsfor conquering study-ing for the NCLEXexam and strategiesfor landing a job. She
calls out some of the most fright-ening things about being a newnurse (eg, calling physicians,rounding with physicians, givingand receiving report from col-leagues, and assessing patients)and provides very practical, action-able tips.
Kleber offers advice on somecommon areas where new nursesstumble, such as time management,shift work, and, the ultimate in stress,the code blue. With wit and wisdom,she shares stories from her ownexperiences. She also shares herperspective on the work-life bal-ance, which is essential to becom-ing a resilient nurse.
As a nurse with more than 30years of experience, I had 3 wishesafter reading this book. First, I wish
Becoming NurseyKleber K. Portland, OR: Book Baby
Publishing; 2014. Paperback; 186 pages;
$12.99 (print), $7.99 (eBook). ISBN-13:
978-1483542460
Reviewed by Mary Pat Aust, RN, MS
The decision to become a nurseis a long-term commitmentthat sends nursing students on
a potentially confusing and frighten-ing journey. The transition betweenthe safety and structure of nursingschool and becoming a licensedhealth care provider in a hospitalnever seems long or structuredenough to avoid the inevitable fearand anxiety associated with it. Inher book, Becoming Nursey, Klebercovers topics such as getting
Many well-known names in theworld of nursing research haveauthored chapters in this book.Their contributions are significantlysupported by the inclusion of amedical librarian who coauthoredthe chapter on conducting the litera-ture search and review. In addition tothe process of conducting research,the book includes legal and ethicalaspects, research involving specialand vulnerable populations, where tofind funding, and the impact of theInternet and social media on theconduct of research.
Foundations ofClinical NurseSpecialist Practice2nd editionFulton JS, Lyon BL,
Goudreau KA, eds.
New York, NY: Springer Publishing; 2014.
Paperback; 512 pages. ISBN-13: 978-
0826129666
This book is both a text for edu-cating new clinical nurse specialists(CNSs) and for the benefit of CNSsin practice to continue their profes-sional development journey. Whilegiving the history and context of therole, this edition reaches into thepresent and future opportunitieswithin the health care system for theunique contributions of the CNS. Ashealth care continues to change, sodo the ways in which a CNS affectspatients and families, nurses, andsystems in the 3 spheres of influence.
The authors also discuss entre-preneurship, billing and reimburse-ment, and regulation of practice.Finally, short exemplar chaptersdemonstrate how the CNS role canbe implemented to achieve positiveoutcomes in multiple settings.
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Palliative CareNursing: QualityCare to the End of Life4th editionMatzo M, Sherman DW,
eds. New York, NY:
Springer Publishing; 2015. Hardcover;
704 pages. ISBN-13: 978-9826196354
This statement in the preface ofthe 4th edition truly describes therole and function of palliative care:
Unlike hospice care, pallia-tive care is not dependenton prognosis and can beprovided in the context ofcurative treatments, curingwhat can be cured, but withthe concurrent attempt ofalleviating symptomscaused by disease or itstreatment.
Palliative Care Nursingdescribes the ethical and legalaspects of palliative and end-of-lifecare, and presents the process ofproviding that care within the frame-work of the whole person (includingfamily and caregivers). Provision ofnursing care is divided into 2 sec-tions: (1) addressing the physicalaspects of dying for particular diag-noses and (2) addressing symptommanagement for all patients. Pallia-tive care nursing is a crucial aspectof providing care across patients’life span, whether faced with con-genital issues, chronic disease, oraging. CCN
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make a positive difference in the life of someone who issuffering is truly a blessing.
What are the challenges you encounter andhow do you overcome them?
Fear of failing to do my very best as a nurse is thegreatest challenge I face every day. I turn to God forstrength and I pray diligently that He continues to useme to help improve patients’ lives.
What has your journey as a nurse been like?My journey as a nurse has been a beautiful educa-
tional experience and a true blessing. There have been(and will continue to be) challenging days when I havedone all I can do and nothing helps, but knowing I didmy best gives me some satisfaction.
At the end of a busy day, how do you find balance in your life?
I find balance in my faith and belief in God. I tryto live my life and treat others as I want to be treated.
What would we be surprised to know about you?
I am a vegetarian!
How has AACN played a role in your career?AACN has played a major role in my career. I look to
AACN for standards and resources, and I use the con-tinuing nursing education to evolve and learn as a nurse.AACN mandates excellence and I accept the challengeto uphold, meet, and exceed this mandate. CCN
I Am a Critical Care Nurse
Why did you become a nurse?I was made to be a nurse. It is in my nature to
care for, assess, troubleshoot, reassure, and encour-age patients. Being a nurse is all I have ever wantedto do.
What about your job as a nurse makes you happy?
Seeing my patients make progress and recovermakes me happy. The patients I care for are burnvictims and they are very close to death. When thesepatients take a turn for the better by just openingtheir eyes for the first time in the unit, it is nothingshort of a miracle. As a nurse, I can be a changeagent and I can bring hope to the hopeless, deliverhealing to the resistant, encourage and teach thenoncompliant, and see miracles happen at the bed-side. This is why I am so excited about my job.
Tell us about an extraordinary experienceyou’ve had as a critical care nurse.
I cared for a very ill, severely burned, and heav-ily sedated patient for months. While caring for her,I used to get close to her ear and whisper, “You cando it. I’m here for you. I’m praying for you.” Sheslowly improved and one day, when she was able tosit up in bed, she said, “Thank you for encouragingme. I heard everything you said.” It felt incredibleto find out that she heard me all those times when Iwhispered reassuring words to her. To be able to
Jacqueline Kramer, RN, isa staff nurse in the ICU/Burn Unitat Detroit Receiving Hospital inDetroit, Michigan.
©2015 American Association of Critical-Care Nurses doi:http://dx.doi.org/10.4037/ccn2015150
92 CriticalCareNurse Vol 35, No. 1, FEBRUARY 2015 www.ccnonline.org
I Am a Critical Care Nurse features the extraordinaryin a critical care nurse’s ordinary experiences. To befeatured in this department, contact Critical Care Nursevia e-mail at [email protected].
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