TCHP Education Consortium€¦ · 7:45 - 8:45 a.m. Introduction to Hemodynamic Monitoring Brett...

Hemodynamics, Shock, and Infection in Critical Care

November 12th, 2015 7:30 a.m. to 4:00 p.m.

Hennepin County Medical Center - Shapiro Building, Lower Level –

Room SL.180

Description/Purpose Statement Health care professionals entering into critical care can be intimidated by the complexity of patients in the ICU. It is vital that the care giver understands hemodynamics and how failure of the normal regulatory mechanisms in the body can lead to rapid and profound shock. The purpose of this class is to understand the principles behind hemodynamics and to look at the causes, symptoms, and types of shock. Assessment and management of patients with hemodynamic problems and shock will be addressed. Target Audience/Prerequisite This class was designed for the novice critical care or telemetry nurse who has already attended the Cardiovascular Critical Care and Neurological Critical Care classes.

Pre-requisite It is highly recommended that you attend the Cardiovascular Critical Care and Neurological Critical Care classes prior to attending this class.

Before You Come to Class You must complete the Understanding Adult Hemodynamics Primer and the Shock and Infection in Critical Care Primer. Please bring your primer post-tests to class with you for processing.

Schedule 7:30 - 7:45 a.m. Registration 7:45 - 8:45 a.m. Introduction to Hemodynamic Monitoring Brett Fladager 8:45 - 9:00 a.m. Break 9:00 - 11:00 a.m. Pressure Monitoring (CVP), Arterial Line Monitoring, Minimally-Invasive

Pressure Monitoring (FloTrac) Brett Fladager

11:00 a.m.– 12:15 p.m. Overview of Shock, Hypovolemic Shock and Cardiogenic shock review Trent Heather 12:15 – 1:00 p.m. Lunch 1:00 – 2:30 p.m. Infection in the ICU Environment and Sepsis and Septic Shock Trent Heather 2:30 - 2:45 p.m. Break 2:45 – 3:30 p.m. Neurogenic Shock Review and Anaphylactic Shock Trent Heather 3:30 - 4:00 p.m. Putting It All Together Trent Heather

For attending this class, you are eligible to receive:

8.4* or 7.00** contact hours (see below)

Criteria for successful completion: All participants must attend the program and complete verification and evaluation forms to receive contact hours. If you are an ANCC certified nurse, you must attend the ENTIRE activity to receive contact hours and complete the application process with TCHP. The Twin Cities Health Professionals Education Consortium is an approved provider of continuing nursing education by the Wisconsin Nurses Association, an accredited approver by the American Nurses Credentialing Center's Commission on Accreditation.

If you complete the primer for this class, you are eligible to receive an

additional:

2.0* or 1.66** contact hours (see below) per primer

Criteria for successful completion for all: You must read the primer, complete the post-test and evaluation, and submit it to TCHP for processing. If you are an ANCC certified nurse, you must complete the application process with TCHP.

*Denotes contact hours used for renewing licensure with the MN Board of Nursing or other Board that uses a 50 min/contact hour formula. These contact hours will be issued unless you request contact hours that comply with the ANCC formula. **Denotes contact hours used for renewing Nursing Certification with ANCC or other organization that uses the formula of 60 min/contact hour. You must request these contact hours if you need them.

Continued on next page

You must print out your own course materials! None will be available at the class. Click on the link below to access:

www.tchpeducation.com/coursebooks/coursebooks_main.htm If the link does not work, copy and paste the link (web page address) into your internet browser. Available 1 week prior to class.

TCHP Education Consortium

http://www.tchpeducation.com/coursebooks/coursebooks_main.htm

Please Read! • Check the attached map for directions to the class and assistance with parking. • Certificates of attendance will be distributed at the end of the day. • You should dress in layers to accommodate fluctuations in room temperature. • Food, beverages, and parking costs are your responsibility. • If you are unable to attend after registering, please notify the Education Department at your hospital or TCHP at 612-873-2225. • In the case of bad weather, call the TCHP office at 612-873-2225 and check the answering message to see if a class has been cancelled. If a class

has been cancelled, the message will be posted by 5:30 a.m. on the day of the program. • More complete class information is available on the TCHP website at www.tchpeducation.com.

http://www.tchpeducation.com/

Finding the Shapiro (SL180) Conference Room at HCMC 701 South 8th Street, Minneapolis, MN 55401

Finding the classroom from Outside the Building:

Enter the main entrance of HCMC Blue building from South 8th Street (directly across the street from

the Parkside Professional Building). Once inside the door, take a right and head towards the information desk. Turn left and go past the gift shop and coffee stand to the open stairway on your right. Take the stairs to the lower level. Turn to your right at the bottom of the stairs. *Take a right at the first hallway, just past the vending area. The Shapiro (SL180) conference room will be on your right

Finding the classroom from the Hospital/Allied Ramp: Take the ramp elevators to the lower level. Follow the signs to the hospital. Follow the hallway past the stairway. Follow directions above from *.

Driving Directions to HCMC:

From the Northeast:

Take 35W south to Exit 17C (Washington Avenue). Turn right onto Washington. Follow

Washington Avenue to Chicago Avenue and turn left. Take a left onto 9th street. Turn left

again to enter the Allied Ramp. Take the ramp elevator to the lower level and follow the

instructions above.*

From the Northwest: Take I-94 east to exit 230 (4th Street). Follow 4th Street through

downtown to Chicago Avenue and turn right onto Chicago Avenue. Follow Chicago to 9th

Street and turn left. Turn left again to enter the Allied Ramp. Take the ramp elevators to

the lower level and follow the instructions above.*

From the East: Take I-94 W to exit 234B (5th Street). Follow 5th Street around the Dome;

turn left on Chicago Avenue. Follow Chicago to 9th Street and turn left. Turn left again to

Downtown

East/Metrodome Light Rail Station

Hospital/ Allied Parking Ramp

B Building

Main Entrance

Traffic flow patterns in this area are changing –

please follow detour signs.

http://www.metrotransit.org/rail/stations/04_metrodome.asp



enter the Allied Ramp. Take the ramp elevators to the lower level and follow the

instructions on the previous page.*

From the South: Take 35W North to exit 16A (downtown exit). Take 5th Avenue exit;

follow 5th Avenue to 8th Street and turn right. Turn right on Chicago Avenue and in one

block, turn left on 9th Street. Take a left to enter the Allied Ramp. Take the ramp elevators

to the lower level and follow the instructions on the previous page.*

From the West: Take 394 east to exit 9B (6th Street). Follow 6th Street to Chicago

Avenue; turn right onto Chicago. Take Chicago Avenue to 9th Street and turn left. Turn left

again to enter the Allied Ramp. Take the ramp elevators to the lower level and follow the

directions on the previous page.*

Public transportation is another options for getting downtown. For bus schedules and

information, go to www.metrotransit.org. Light Rail Transit to HCMC: HCMC is located at

the corner of Park Ave. and 6th Street, conveniently located just 1-1/2 blocks south of the

Downtown East/Metrodome station of the Light Rail Transit line. Light Rail information is

available at www.metrotransit.org/rail/index.asp.

Parking:

There are various options for parking around HCMC, but we suggest you park in the

Hospital/Allied Ramp. Directions and maps guide you to and from this ramp. Meters are

available around the hospital and vary in price. Check www.mplsparking.com for rates. Parking rates are subject to change without notice, but the current cost of park in the Allied ramp is $11.00. (cash or credit using the payment kiosk as you exit). The program coordinator will have a limited number of discount coupons for the Hospital/Allied Ramp available for $6.00. You must pay with cash or check in the exact amount for the discount coupon—change is not available.

-

Visit www.hcmc.org for

more maps and directions.

E = Hospital/

Allied Ramp

(*parking lot

entrance)

3 = HCMC, Blue

Building

E = Hospital/

Allied Ramp

(*parking lot

entrance)

3 = HCMC, Blue

Building

Visit www.hcmc.org for

more maps and directions.

http://www.metrotransit.org/

http://www.metrotransit.org/rail/index.asp

http://www.mplsparking.com/

http://www.hcmc.org/

http://www.hcmc.org/

Understanding Adult Hemodynamics

© 11/2005 TCHP Education Consortium. Revised 2014

This educational activity expires December 31, 2017.

All rights reserved. Copying, electronically transmitting or sharing without permission is forbidden.


This home study is pre-reading for a class.

Please complete this activity and bring your post-test and evaluation to class with you.


©TCHP Education Consortium, 10/2005; 2014 edition

Page 1

Understanding Adult

Hemodynamics

Introduction/Purpose Statement

Aristotle started investigating it in the 4th

century

B.C.; Galen in the 2nd

century A.D. continued to

investigate it. The heart, blood vessels, and concepts

of hemodynamics were intriguing to Harvey,

Malpighi and van Leeuwenhoek in the 1600's. So

what exactly is hemodynamics? Heme means

"blood", and dynamus means "movement," so

hemodynamic means the movement of blood.

We care about the movement of blood, and monitor

it, because how the blood moves through the body

will determine how the tissues are replenished with

oxygen and nutrients and are able to excrete end-

products of metabolism.

The purpose of this home study program is to give a

brief introduction to hemodynamic monitoring - how

we do it, what the numbers mean, and how we can

optimize the movement of blood in the body. You’ll

also learn about a variety of pharmacologic strategies

that are used to improve cardiac output.

CV Surgery Class

All patients undergoing cardiovascular surgery

will have some sort of hemodynamic monitoring.

If you are unfamiliar with hemodynamic

monitoring, you should read this primer to be

able to understand content presented in the CV

Surgery class.

Hemodynamic Monitoring Class

This primer was developed to give you a starting

point in learning how to manage patients with

hemodynamic monitoring. This primer can be

used as either a stand-alone educational activity

or as an introduction to the "Hemodynamic

Monitoring" class.

Synthesizing Key Element of Critical Care

This primer will give you a reference point for

applying pharmacologic agents to effect change

in hemodynamic parameters. It is important to

have a good understanding of this primer prior to

attending the Synthesis of Key Elements of

Critical Care class.

If you are taking multiple classes, please note

that this primer only needs to be completed once.

Target Audience

This home study was designed for the novice critical

care or telemetry nurse; however, other health care

professionals are invited to complete this packet.

Content Objectives

1. Identify non-invasive indicators of hemodynamic

status.

2. List three indications for invasive hemodynamic

monitoring.

3. Describe the relationships among preload,

contractility, compliance, afterload, and cardiac

output.

4. Describe pharmacologic strategies that

manipulate heart rate, preload, contractility, and

afterload to improve cardiac output.

Disclosures

In accordance with ANCC requirements governing

approved providers of education, the following

disclosures are being made to you prior to the

beginning of this educational activity:

Requirements for successful completion of

this educational activity:

In order to successfully complete this activity

you must read the home study, complete the

post-test and evaluation, and submit them for to

TCHP for processing.

Conflicts of Interest

It is the policy of the Twin Cities Health

Professionals Education Consortium to provide

balance, independence, and objectivity in all

educational activities sponsored by TCHP.

Anyone participating in the planning, writing,

reviewing, or editing of this program are

expected to disclose to TCHP any real or

apparent relationships of a personal,

professional, or financial nature. There are no



Page 2

conflicts of interest that have been disclosed to

the TCHP Education Consortium.

Expiration Date for this Activity:

As required by ANCC, this continuing education

activity must carry an expiration date. The last

day that post tests will be accepted for this

edition is December 31, 2017—your envelope

must be postmarked on or before that day.

Planning Committee/Editors*

*Linda Checky, BSN, RN, MBA, Program Manager

for TCHP Education Consortium.

*Lynn Duane, MSN, RN, Assistant Program

Manager for TCHP Education Consortium.

Sharon Stanke, DNP, MSN, RN, Nursing Instructor

in Critical Care, Minneapolis VA Health Care

System.

Authors

Karen Poor, MN, RN, Former Program Manager for

the TCHP Education Consortium.

Sharon Stanke, DNP, MSN, RN, Nursing Instructor

in Critical Care, Minneapolis VA Health Care

System.

Content Experts

Denise Rogich, PharmD, Pharmacist at the

Minneapolis VA Medical Center.

*Sharon Stanke, DNP, MSN, RN, Nursing

Instructor in Critical Care, Minneapolis VA Health

Care System.

Carrie Wenner, PharmD, Pharmacist at the

Minneapolis VA Medical Center.

*Denotes reviewer of the current edition

Contact Hour Information

For completing

this Home Study and evaluation,

you are eligible

to receive:

2.0* or 1.66** contact hours (see

below)

Criteria for successful

completion: You must read the

home study packet, complete the

post-test and evaluation, and

submit them to TCHP for

processing.

The Twin Cities Health Professionals

Education Consortium is an approved

provider of continuing nursing

education by the Wisconsin Nurses

Association, an accredited approver

by the American Nurses Credentialing

Center’s Commission on

Accreditation.

*Denotes contact hours used for renewing licensure with the MN

Board of Nursing or other Board that uses a 50 min/contact hour formula. These contact hours will be issued unless you request

contact hours that comply with the ANCC formula.

**Denotes contact hours used for renewing Nursing Certification with ANCC or other organization that uses the formula of 60

min/contact hour. You must request these contact hours on the

evaluation form if you need them.

Please see the last page of the packet before the post-

test for information on submitting your post-test and

evaluation for contact hours.



Page 3

The Concepts of Hemodynamics

The end-all and be-all of hemodynamic monitoring is

the cardiac output. The cardiac output (CO) is the

amount of blood ejected from the ventricle in one

minute. This amount of blood is adequate to supply

the body tissues with oxygenated blood.

Normally, the cardiac output is between

4-8 liters of blood every minute.

Imagine an organ the size of your fist

pumping out 2-4 Coke bottles of blood

every minute!

Two components multiply to make the cardiac

output: the heart rate and the stroke volume.

CO = HR x SV Of course, different sized folks need different

amounts of blood circulating. An 80-pound little old

lady needs less blood than a 350-pound linebacker,

right? To even things out a little bit, there is a

calculation called the "cardiac index."

The cardiac index (CI) is the cardiac output adjusted

for body surface area. CI should be between 2.5 - 4.2

liters of blood per minute per square meter of surface

area.

Heart rate The first component of the

cardiac output is the heart

rate. The heart rate and

stroke volume should

work like a teeter-totter.

If one goes up, the other

should go down, and vice

versa. This is the concept

of the compensatory

heart rate.

The most common change in the heart rate to

compensate is for it to go faster (become

tachycardic) because of low stroke volume or

increased tissue oxygen needs.

Causes of compensatory tachycardia are:

Hypovolemia from dehydration, bleeding,

loss of fluid

Low blood pressure

Anxiety, fear, pain, and anger cause the

sympathetic nervous system to release

endogenous and exogenous catecholamines

Fever

Exercise

There are limitations to the compensation that

tachycardia can provide: heart rates above 180

beats/min in a normal heart, or above 120 in a

diseased heart, are too fast to compensate. If the

stroke volume continues to decline, the heart rate can

only increase so much to balance cardiac output.

On the other hand, the heart can go more slowly

(become bradycardic) to compensate for a high

cardiac output or high blood pressure. This can be

seen with seasoned athletes with "strong pumps,"

who often have heart rates in the 40's-60's at rest.

Beyond the compensatory tachy- or brady-cardias,

there are those rhythms that hurt the hemodynamic

state of the patient.

Sinus tachycardias that are > 180 in the normal heart

or > 120 in the diseased heart are not compensatory

anymore because the heart can't fill adequately with

blood to pump out. Other dysrhythmias have the

same problem, but an additional one: they lose 20%

of their cardiac output because their atria are not

contracting in sync with the ventricles. These

rhythms are:

Atrial tachycardia

Uncontrolled atrial flutter/atrial fibrillation

Junctional tachycardia

SVT

Ventricular tachycardia

Bradycardias that present problems to the

hemodynamic standing of the patient are:

Junctional rhythm

2nd

degree AV block, type II

3rd

degree AV block

Idioventricular rhythm

What can cause these kinds of bradycardias? The

most common causes are:

Myocardial infarction

Vagal stimulation (bearing down)



Page 4

Beta blocking and calcium channel blocking

agents

Stroke volume The stroke volume is the amount of blood

ejected with each ventricular contraction.

Kinda makes sense, doesn't it? The

amount of blood per beat X the number

of beats in a minute is the amount of

blood that leaves the heart every minute

(also known as Cardiac Output or CO).

Three main factors determine stroke volume:

contractility, preload, and afterload.

Contractility Contractility is the force and velocity with

which ventricular ejection occurs,

independent of the effects of preload and

afterload. Huh? Think of contractility as

the "squeeze." Remember “squeeze” when

we get to pharmacology as it is synonymous with

“intrope.”

Contractility increases (the heart squeezes harder)

from:

The fight or flight response from fear,

anxiety, stress, pain, hypovolemia

Exercise

The bad thing about increased contractility is that

although it increases stroke volume, it will also

increase the demand of oxygen by the heart (MVO2).

This can be hazardous in someone with heart disease.

The prime example: the guy who has the heart attack

while shoveling snow -- all the exercise increased his

heart rate and his contractility and his heart couldn't

handle the extra work.

Decreased contractility decreases stroke volume and

MVO2. The causes might be:

hypoxia

hypercapnia

metabolic acidosis

hyperkalemia

hypocalcemia

myocardial infarction

cardiac surgery

Preload Preload is the amount of blood

in a ventricle before it contracts.

It's the "gas in the tank."

Preload is also known as "filling

pressures."

Preload is determined by:

1. The total circulating blood volume: how much

blood is actually in the blood vessels?

2. The distribution of vascular volume: where is

the blood and fluid? In the blood vessels, in the

cells, or in the "3rd

space?"

3. Atrial systole: are the atria contracting in sync

with the ventricles? If they are not, there is a

decrease in preload by 20%.

There is a theory that helps to explain how preload

and contractility are related: the Frank Starling Law.

This is what it says --

Imagine that you have a

rubber band in your hands

that you are stretching. If

you stretch out the rubber

band out about three inches, it will contract back

pretty well.

Now imagine that you stretch out

your rubber band just an inch or so.

What will happen now? It won't

contract back very fast or with very

much force. This is what happens when a person

becomes hypovolemic - they don't have a lot of

stretch, so they don't have a lot of squeeze.

Next, if you stretch out your rubber band six-eight

inches, it will contract back more strongly and faster.

This is the

principle

behind a

fluid challenge or fluid flush. If you give someone a

little fluid to stretch their heart, they should squeeze

back harder.



Page 5

The last idea in the Frank-Starling Law is that you

can overstretch the heart - by filling it so full of fluid

that the muscle fibers can't contract back well if at all.

This is what happens in congestive heart failure.

Compliance Compliance is part of the stroke

volume determination. It refers

to the distensibility of the

ventricular myocardium - or its

ability to stretch. People with

normal compliance have hearts

that are able to stretch with

volume loads - for example,

you would do fine if you chugged a 20 ounce glass of

water on a hot day - your heart would be able to

accommodate that change.

People who have increased compliance, though, run

the risk of overstretching and not being able to

contract back well. Conditions that have increased

compliance are:

Congestive heart failure

Dilated cardiomyopathy

On the flip side, people with decreased myocardial

compliance don't stretch well to accommodate

changes in load. People who have:

a myocardial infarction,

a stunned myocardium from surgery or

trauma, or

restrictive cardiomyopathy

may all have difficulty handling increased loads of

fluid.

Afterload The last concept is afterload. Afterload is how

hard the heart (either the right or the left side)

has to push to get the blood out. Afterload is

also thought of as the resistance to flow or how

clamped the blood vessels are.

Afterload is determined by:

The compliance of the aorta

Mass/viscosity of blood: how thick or thin it

is

Vascular resistance: whether the blood

vessels are constricted or dilated

Oxygen level: hypoxemia will cause

vasoconstriction

Monitoring hemodynamics the old fashioned way

Long before there were monitors, cables, and lines,

health care providers had to look, listen, and feel the

patient to determine their hemodynamic status.

Because all tissues are dependent on oxygenated

blood, a deficiency in delivery will affect each organ

system.

The "first things to go" when the blood circulation is

not what it should be are the skin and the gut.

Indicators of diminished blood supply to these organs

are:

Cool, clammy skin

Pale, ashen, or cyanotic skin color

Diminished bowel sounds

Diarrhea or constipation

Increased NG tube drainage

The "second things to go" are the kidneys and lungs.

Failure to get blood to these organs has much more

serious consequences:

Increased respiratory rate and effort

Shortness of breath

Decreased PaO2 on ABG or decreased SaO2

Crackles in the lungs from heart failure

Decreased urine output

Increased urine concentration

Elevated BUN/creatinine/potassium

Finally, the brain and the heart are very greedy for

oxygenated blood. They are the first and last organs

to be perfused. When they fail, indicators may be:

Decreased or altered level of consciousness

Disorientation

Slowly reacting pupils

Chest pain/pressure



Page 6

Tachy or brady-dysrhythmias, ectopy

ST segment elevation

Monitoring Using Tools

Why do we sometimes choose to use invasive lines

instead of monitoring the patient in non-invasive

ways?

Well, our patients are not always straight-forward,

textbook cases. They are complicated and complex

and can be difficult to diagnose. Secondly, invasive

monitoring can help determine what kinds of

treatment should be started, as well as evaluating how

well the treatment is working. And last, treatment for

another problem may affect how the blood circulates;

invasive line monitoring can also measure those

effects.

There are four types of invasive lines:

1. Arterial line

2. CVP

3. Pulmonary artery catheter

4. Left atrial line (rarely used)

Of course, not everyone who is admitted to an ICU

needs to have invasive arterial lines. Virtually all

post-open heart surgery patients, however, will have

at least an arterial line, if not a PA or CVP line in too.

There are certain conditions where invasive

monitoring is quite helpful:

Complicated MI

Unstable MI with drug titration

CHF/pulmonary edema

Multisystem failure/ shock

High risk cardiac patient for surgery or

procedure

High risk OB

Respiratory failure

The Arterial Line The arterial line transmits a systolic and diastolic

pressure through a system that turns the pressure into

an electrical waveform and a number. In short, the

arterial line gives us a blood pressure. In cardiac

surgery patients, the mean arterial pressure is

followed, with a desired MAP between 60-80 mmHg.

However, the arterial line blood pressure is not the

same as a cuff pressure. There appears to be

differences between direct (arterial) and indirect non-

invasive (cuff) readings measuring systolic blood

pressure during hypotension. The mean blood

pressure from both techniques is considered a more

reliable means of assessing prognosis and is the

preferred metric to use for diagnosis and treatment

decisions in the ICU.1

Note that an arm cuff

pressure

is more likely to under-estimate MAP/blood pressure

than to over-estimate it.2

The Pulmonary Artery Catheter The pulmonary artery (PA) catheter is also known as

the Swan Ganz catheter. It will directly measure

three different pressures and is used to obtain the

cardiac output, contractility, and afterload

information.

The PA catheter is floated through a major vein into

the superior or inferior vena cava. From there, it is

floated through the heart and into the pulmonary

artery. It has a pressure sensor in the right atrium and

another one in at the distal end of the catheter to

measure the pulmonary artery pressure. When the

balloon at the end of the catheter is inflated,

pulmonary capillary wedge pressure is obtained to

give information about the left side of the heart.

Right atrial pressure

The right atrial pressure (RAP) measures the venous

return to the right heart. It is a right heart preload

measurement.



Page 7

The RAP is essentially the same pressure that is

obtained with a CVP on a triple lumen catheter.

Normally, the RAP will be between 2 and 6 mm Hg.

It can be increased in:

Fluid overload

Cardiac tamponade

Right heart dysfunction

Pulmonary problems

The RAP is decreased with:

Dehydration/volume loss

Venodilation

Right ventricular pressure This pressure is not documented routinely, as it

should only be seen during the passage of the catheter

on insertion and removal. The normal value for RV

pressure is 20-30 systolic/0-5 diastolic.

Pulmonary artery pressure The pulmonary artery pressure (PAP) is measured at

the distal end of the catheter. The normal values for

PAP are 20-30 systolic (PAS)/10-20 diastolic (PAD).

Increased pressures are found in:

Atrial or septal defects

Pulmonary hypertension

LV failure

Mitral stenosis

Pulmonary capillary obstructive pressure (PAOP)

Often called the "wedge," this pressure is obtained

when the balloon on the end of the PA catheter is

inflated. This blocks off all pressures from the right

side of the heart, allowing the pressure sensor at the

tip of the catheter to see, indirectly, the pressures on

the left side of the heart. It is a left heart preload

measurement.

Normally, the PAOP is between 8 and 12 mm Hg. It

is increased in:

Fluid overload

Mitral valve stenosis

Aortic stenosis or regurgitation

LV failure

Constrictive pericarditis or tamponade

The PAOP is decreased with:

Hypovolemia

Vasodilation

The diastolic number of the PA pressure is often used

instead of the PAOP, particularly in cardiac surgery

patients. The PAD is always higher (by 1-4 mm Hg)

than the PAOP, but is a close approximation.

Cardiac Output

The cardiac output can be measured by using the PA

catheter. When the procedure has been finished, the

computer will generate a bunch of numbers. You

will first gather your direct readings of PAP, RA, and

PAOP, and measure the CO. You can then obtain the

rest of the hemodynamic picture using computer

generated values based on mathematical formulas.

Here are the numbers with the normal values and

what they measure:

Cardiac output: 4-8 L/min

Cardiac index: 2.5 - 4.0 L/min/m2 (keep > 2.1)

Stroke volume: 60-100 ml/beat Contractility

Systemic vascular resistance (SVR): 800-1200

dynes/s/cm-5

Left heart afterload

Pulmonary vascular resistance (PVR): 50-150

dynes/s/cm-5

Right heart afterload

The direct measurements from the PA catheter give

information on the preload status of the heart.

RAP: 2-6 Hg Right heart preload

PAOP: 8-12 mm Hg Left heart preload



Page 8

Manipulation of Cardiac Output

Well, okay, now we've got all of these numbers -

what do we do with them? Here's the overall idea:

We want to get blood to the tissues without

beating the heart to death.

To optimize cardiac output, we need to optimize each

of the components of cardiac output - the heart rate,

preload, contractility, and afterload. Here are the

strategies for the different components.

Heart rate If the patient is in a non-compensatory

tachycardia, such as atrial fibrillation,

atrial flutter, supraventricular

tachycardia (SVT), or paroxysmal

atrial tachycardia (PAT), the first interventions are

usually pharmacological:

Beta blocking agents: such as atenolol,

metoprolol, propranolol, sotalol, or esmolol

Calcium channel blockers, such as diltiazem

and verapamil

Adenosine

Amiodarone

If drugs don't work, or the patient is unstable,

synchronized cardioversion is the treatment of

choice.

Ventricular tachycardia is another non-compensatory

tachycardia that should be treated immediately. If

the patient is stable, lidocaine or amiodarone are the

drugs of choice. A second line drug is procainamide.

If drugs don't convert the v-tach, or if the patient is

unstable, he/she is cardioverted.

Bradycardia is a bit more straight forward. If the

heart rate is too slow to support the cardiac output, it

needs to speed up. The drug of choice is atropine.

Epinephrine and dopamine may also be tried.

Usually, though, if atropine doesn't work, the patient

is either put on a transcutaneous pacemaker or has a

transvenous pacemaker placed.

Contractility If low contractility is the problem, the interventions

take two paths: either to increase the stretch or to

increase the strength.

Increasing the stretch goes right back to the Frank

Starling Law - if you stretch further, you should

contract back better. Crystalloids, such as normal

saline, lactated Ringers, or D5NS, will stay in the

vascular space and will stretch the myocardium.

Colloids, such as albumin, Dextran, Hespan, fresh

frozen plasma, or packed RBC's, are also used.

Colloids are preferable in situations where there is

edema, as they will act to pull fluid out of the "3rd

space" and put it back into the vasculature.

Increasing the strength should start with fixing what's

causing the decreased squeeze, such as

correcting hypoxia, hypercapnia, and

electrolyte imbalances. The squeeze

can also be increased by giving positive

inotropic drugs, like moderate dose

dopamine, dobutamine, epinephrine, or milrinone

(see page 4 to review squeeze/contractility/inotrope).

Sometimes the problem is that the contractility is too

high - the heart is squeezing harder than it has to.

Because increased contractility increases the

myocardial oxygen consumption, angina or MI may

result. Drugs are used to decrease contractility:

Beta blockers - atenolol, labetalol,

metoprolol, propranolol, sotalol, timolol

Calcium channel blockers - diltiazem,

felodipine, nicardipine, nifedipine,

verapamil

Preload Problems with preload fall

into two categories: there's

too much or there's too

little. If there is too much

preload, furosemide or

other diuretics are the first

choice to "unload" the heart. Renal dose dopamine

(2-5 mcg/kg/min) may be given (you may see this

given in practice, however, this practice is not

evidence-based). In special cases, dialysis may be

indicated to remove excess fluid from the body.



Page 9

If there is not enough preload, it's simple - give some!

The rule of thumb is to replace like-for-like. If they

lost blood, give them PRBC's. If they've had diarrhea

and vomiting for a week, give them crystalloids.

Most cardiac surgery patients are kept on the high

end of preload with a RAP of 10 mm Hg and a PAOP

of 15 mm Hg.

Afterload

Just like preload, afterload can either be too

high or too low. If the afterload is too high - an

SVR > 1200, the heart is working really hard to

pump out its blood. Drugs are the first choice to

decrease a high SVR:

Nitroglycerin IV

Nitroprusside IV

If the patient is more stable, calcium channel

blockers: diltiazem, felodipine, nicardipine,

nifedipine, verapamil

If pharmacologic management isn't doing the trick,

an intra-aortic balloon may be inserted. The IABP

helps to decrease SVR by deflating the balloon just

before ventricular contraction, creating almost a

"vacutainer" effect that allows the heart move blood

through the system with much less effort.

On the flip side, the SVR can be too low. A really

low SVR indicates venous pooling, in which case, the

preload drops. Vasoconstricting drugs can do the

trick to increase SVR:

Norepinephrine (Levophed®)

Phenylephrine (Neosynephrine®)

Algorithm of Treatment

Please see the algorithm on the next page for

recommended treatments to optimize cardiac output.



Page 10

Cardiac Output/Cardiac Index

Decreased

Contractility (SV, RVSWI, LVSWI)

Preload (RAP, PAOP)

Afterload (SVR, PVR)

High Low High Low High Low

Beta Blockade

Calcium

channel

blockade

Positive Inotropes:

•dobutamine

•dopamine

•milrinone

•digoxin

Dilators:

•nitroglycerin

•nitroprusside

•milrinone

•alpha and

calcium

channel

blockers

Diuretics:

•furosemide

•bumetanide

•ethacrynic acid

•mannitol

Volume:

•colloids

•crystalloids

•blood

•hetastarch

Dysrhythmia

control:

•drugs

•pacemaker

•AICD

Dilators:

•nitroglycerin

•nitroprusside

•milrinone

•alpha and

calcium

channel

blockers

IABP

increase

augmentation

Pressors:

•epinephrine

•norepinephrine

•dopamine

•neosynephrine

IABP

decrease

augmentation


© TCHP Education Consortium 10/ 2005; 2014 edition

Page 11

Introduction Now let’s take a look at the medications that are used

to manipulate cardiac output. First data is gathered to

determine what aspects of the cardiac output need

adjustment. Patient history, physical assessment, vital

signs, and key hemodynamic parameters from the PA

catheter all contribute to the assessment data. Once

we’ve determined what the problems are, we are

ready to determine which vasoactive drugs will

benefit our patient. Remember, the primary goal is

to optimize cardiac output/index. To do that, we

need to optimize each of the components of cardiac

output - the heart rate, preload, contractility, and

afterload. In order to choose the appropriate

medication, we need to keep in mind the

physiological response that these medications

produce and to titrate those effects using the MAP

and SV.

Let’s review a few relevant terms before we continue

to discuss individual medications.

Inotropic: affects contractility

A positive effect increases contractility

A negative effect decreases contractility

Chronotropic: affects the heart rate

A positive effect increases the heart rate

A negative effect decreases heart rate

Dromotropic: affects conductivity

The hemodynamic effects of vasoactive drugs occur

as a result of their interactions with receptors in the

heart and vascular system. These receptors are:

Alpha-receptors:

Are located in the blood vessels and cause

vasoconstriction in most vessels, especially

the arterioles.

Increase afterload by causing peripheral

vasoconstriction and increasing blood

pressure.

Beta 1 receptors:

Are located in the heart.

Have inotropic, chronotropic, and

dromotropic effects.

Because of their inotropic, chronotropic, and

dromotropic effects, stimulation of the Beta 1

receptors increases contractility and heart rate,

thus increasing cardiac output.

Beta 2 receptors:

Are located in the bronchial and vascular

smooth muscles.

Cause bronchodilation, and vasodilatation.

Reduce afterload.

Dopaminergic receptors:

Are located in the renal and mesenteric

artery bed.

Dilate renal and mesenteric arteries.

Reduce preload by inducing diuresis

/natriuresis.

According to the algorithm on page 8, preload is one

of the three factors affecting cardiac output. When

preload is too high (i.e., high RAP and PAOP),

medications are used to reduce the preload.

Medications that are used to reduce preload are

diuretics and vasodilators.

Furosemide (Lasix®) and Bumetanide (Bumex®)

Lasix®

and Bumex®

are diuretics that act on the loop

of Henle in the kidney. These medications decrease

the preload by increasing urine output, thus reducing

the work of the heart. They are used for acute

pulmonary edema, CHF, peripheral edema, and HTN.

Monitor serum electrolytes such as potassium closely

because potassium is depleted as the patient diureses.



Page 12

Expected Hemodynamic Outcome

for Lasix®

and Bumex®

Heart

rate

Preload

(RA,PAOP, PAD)

Contrac-

tility

Afterload

(SVR)

Blood

pressure

Dopamine: Renal-Dose and Low-Dose Renal-dose dopamine is used in clinical practice from

time to time. Current evidence does not support renal

dose dopamine as effective. However, the practice

persists due to the following beliefs:

Dopamine will cause different vasoactive

effects depending on the dose infused. At

low doses, dopamine stimulates the

dopaminergic receptors in the arteries

located in the kidneys, abdomen, heart and

brain.

The vasodilatation of renal and mesenteric

arteries will cause an increase in urine

output and results in a decreased preload.

Renal-dose and low-dose dopamine are rarely used,

but the effects are listed below.

Renal-dose dopamine is used for patients who have a

high preload or low urine output. This often occurs

in patients with CHF.

Receptors stimulated by

renal and low-dose dopamine

Alpha

(Vaso-constriction)

Beta 1

(Heart rate and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal dilation )

Renal-dose dopamine is generally considered to be in

the range of approximately 0.5-2mcg/kg/min.

When further reduction in preload is needed,

dopamine may be titrated up into the “low dose”

range. Low dose dopamine is approximately 2-

5mcg/kg/min. and is titrated by 1-2 mcg/kg/min

every 5-10 min. Low dose dopamine will have little

to no effect on the heart rate or blood pressure.

Expected hemodynamic outcome

for renal and low dose dopamine

Heart

rate

Preload

(RA,PAOP,

PAD)

Contractility Afterload

(SVR)

Blood

pressure

Vasodilators are used to reduce afterload and, to a

somewhat lesser extent, reduces preload. Reducing

afterload decreases the amount of squeeze needed to

circulate blood, conserving myocardial O2

consumption. Reducing preload involves getting rid

of excess fluid in the system. This decreases the

amount of blood in the right atrium prior to

contraction of the atria during the cardiac cycle. The

two medications discussed here are nitroprusside and

nitroglycerine.

Nitroprusside or Nipride Nipride is used for hypertensive emergencies to

reduce blood pressure.

Nipride relaxes the arterial and venous smooth

muscles causing vasodilatation thus decreasing

afterload. The primary effect is arterial

vasodilatation. This is a very potent medication and

can quickly drop the BP and the SVR (afterload).

Monitor closely when making any dose changes.

This medication works very quickly, which means

when you start the medication there are immediate

effects. The half-life is so short that when you stop

the medication its effects are gone.

The dosage range is 0.5 to 5 mcg/kg/min. and the

average dose is 2 mcg/kg/min. Start nipride at

0.5mcg /kg/min and titrate by 0.25-0.5 mcg/kg/min

every 2 min to achieve the desired parameters

determined by the physician. Nipride may be titrated

to B/P or SVR.

Use a volumetric infusion pump to administer this

medication. Nipride may be infused in a peripheral

IV. As a vasodilator, nipride will not cause tissue

damage upon infiltration as can occur with

vasopressors such as dopamine.

Do not flush or bolus in the IV site of nipride because

the blood pressure will drop immediately. Nipride

tends to deteriorate in the presence of light. To

protect nipride from light, the container should be

covered with foil, or another opaque material and



Page 13

discarded after 12 hours. An arterial line is beneficial

for continuously monitoring the blood pressure.

At high doses or with long term therapy (>72 hours),

nipride converts to thiocyanate and may result in

cyanide toxicity. Do not exceed 10mcg/kg/min. for

longer than 10 minutes or it will increase the risk for

cyanide toxicity. If infused at this high of a rate it

must be turned off because of the potential for

cyanide toxicity.

One of the risks associated with nipride

administration is a precipitous drop in blood pressure.

Sometimes dopamine is needed to keep the blood

pressure in a therapeutic range, while providing

afterload reduction.

Expected hemodynamic outcome for nipride

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Nitroglycerin Nitroglycerin is used for patients with angina and

hypertension.

This medication is a venodilator; dilating the venous

system. When the veins are dilated blood moves

more easily through the system, reducing the pressure

needed to circulate the blood around. Coronary

perfusion will increase, and both preload and

afterload will decrease.

Nitroglycerin may be infused in a peripheral IV. Use

a volumetric infusion pump. The usual dosage starts

at 5-10 mcg/min. The range is 10-200 mcg /min.

Titrate nitroglycerine by 10 mcg every 5 minutes to

achieve the goal blood pressure or relief of chest

pain.

The dosage of nitroglycerin may also be based on the

patient’s weight. The normal range is 0.5 –1.5 mcg

/kg/min. Titrate by 0.1 –0.2 mcg /kg every 5

minutes.

It is common to have complaints of a headache

because of the dilation happening in the cerebral

vasculature. Acetaminophen is usually effective for

headaches caused by nitroglycerine.

Expected hemodynamic outcome for Nitroglycerin

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Contractility or “squeeze” is the third component that

affects cardiac output. Drugs that have beta 1 effects

increase the contractility o the heart.

Dobutamine

Dobutamine is used for patients experiencing heart

failure, cardiogenic shock, and sometimes following

cardiac surgery for patients requiring intravenous

inotropic support.

Receptors stimulated by dobutamine

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation)

Minimal

Dobutamine increases cardiac contractility (a positive

inotropic effect) because of the beta 1 effect of the

medication. By increasing the squeeze of the heart or

contractility, it will help to increase the blood

pressure and cardiac output.

These same beta 1 effects also increase heart rate and

may lead to an increased myocardial oxygen demand

due to tachycardia.

Dobutamine also has beta 2 effects which cause

vasodilation, resulting in a decrease in afterload /

systemic vascular resistance. Dobutamine may also

decrease PAOP or preload to the L side of the heart.

The usual dosage is 2.5 to 20 mcg/kg/min. Start at 2

mcg/kg/min. Titrate dobutamine by 1-2 mcg/kg/min

every 5- 10 minutes to obtain the desired MAP and

SV.

Dobutamine should be infused in a central line

because it does have some alpha (vasoconstrictive)



Page 14

effects. There may be tissue necrosis if infiltration

occurs. Use a volumetric infusion pump. An arterial

line is beneficial for continuously monitoring the

blood pressure.

Expected hemodynamic outcome for dobutamine

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Milrinone (Primacor®) Milrinone is used for low cardiac output due to poor

contractility. This is commonly seen in patients with

acute, decompensated right heart failure. Milrinone is

a good medication for CHF as a short-term therapy.

Receptors stimulated by milrinone

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

none none none none

Milrinone is a good medication for improving

contractility but the mechanism of action is different

than the medications we have already discussed. It

does not stimulate the alpha or beta cells. Milrinone

increases the cyclic-AMP concentrations in the cell

which improves contractility and vasodilatation

(afterload reduction).

While milrinone increases contractility and decreases

afterload, it has minimal effect on the heart rate. This

means that it increases cardiac output without an

increase in heart rate or oxygen consumption.

Recommended dosage is a 50 mcg/kg load over 10

minutes, followed by a maintenance dose of 0.375 to

0.75 mcg/kg/min. The dose will vary depending on

renal function. Use a volumetric infusion pump and

monitor MAP and SV. Because milrinone does not

cause vasoconstriction, it may be infused

peripherally.

Expected hemodynamic outcome for milrinone

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Dopamine: Medium-Dose The medium-dose range is about 5-10 mcg/kg/min.

When the dose of dopamine is increased the beta 1

and 2 receptors are stimulated causing an increase in

heart rate, contractility and, to a lesser extent,

vasodilatation.

A medium dose of dopamine is used to achieve a

positive inotropic effect in patients with heart failure.

Heart rate also increases. When used in this fashion,

the effects are similar to dobutamine. Monitor MAP

and SV.

Receptors stimulated by medium-dose dopamine

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

Expected hemodynamic outcome for

medium-dose dopamine

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Many times critically ill patients have problems with

low blood pressure. To ensure that all the body’s

organs are being perfused properly, it is necessary to

keep the blood pressure in an acceptable range.

Vasopressors are used to increase the blood pressure

by constricting the arterial blood vessels. Constricting



Page 15

the vascular system also increases the afterload and

cardiac output. Vasopressors are used to manage

such situations as severe hypotension and cardiac

arrest.

In general, all vasoactive medications should be

given in a central IV port. If a vasoconstrictor

infiltrates, tissue necrosis may occur. If this happens,

notify the physician immediately. The recommended

treatment is Phentolamine, infiltrated subcutaneously

at the extravasation site.

Vasoconstrictors clamp down or shunt blood away

from the periphery in order to give blood to the more

important organs and systems. Monitor the

circulation to the extremities as part of your routine

assessments. Dusky and/or mottled extremities that

are cool or cold to the touch can occur with

peripheral vasoconstriction. There are times when the

need to maintain BP outweighs the need to maintain

good circulation to the extremities. The physician

will try to balance these needs as much as possible.

Use a volumetric infusion pump. An arterial line is

beneficial for continuously monitoring the blood

pressure.

Dopamine: High-dose (10-20 mcg/kg/min) High-dose dopamine is reserved for the treatment of

severe hypotension that is not related to

hypovolemia.

Receptors stimulated by high-dose dopamine

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

In high doses, dopamine stimulates the alpha-

receptors causing vasoconstriction. This effect tends

to override the other effects that occur at lower doses

(including the vasodilator effect).

When high-dose dopamine clamps down on the blood

vessels, internal organs are not perfused as well and

the “renal effect” is lost; urine output may decrease.

Systemic vascular resistance increases and the

amount of squeeze needed to circulate the blood also

increases. Couple that with an increase in heart rate

and it is easy to see why there is also an increase of

myocardial oxygen demand.

A dopamine infusion is usually started at 5

mcg/kg/min and is titrated at 1-2 mcg/kg/min. every

5-15 minutes until adequate results are achieved.

When you are administering high doses of dopamine,

you may want to consider using norepinephrine

(Levophed®

) in addition to dopamine, or as an

alternative.

Expected hemodynamic outcome for

high-dose dopamine

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Norepinephrine (Levophed®)

Levophed®

is used for profound hypotension caused

by such conditions as myocardial infarction,

septicemia, transfusion reactions and drug reactions.

Receptors stimulated by Levophed®

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

Minimal

Levophed®

is a potent vasoconstrictor used to

increase blood pressure. The primary effects are

alpha-adrenergic effects, resulting in

vasoconstriction. Used mainly for pressor effects

indicated in severe hypotension secondary to low

peripheral resistance.

When using Levophed®

, always correct hypovolemia

first. Vasoconstriction when the “tank” is dry will

not increase blood pressure. Levophed is an

especially good medication for septic shock.

The loading dose for Levophed®

is 8-12 mcg/min.,

followed by a maintenance dose of 2-4 mcg/min. The

therapeutic dosage range is 2-12 mcg/min. Titrate by



Page 16

1-2 mcg every 5-10 minutes to achieve the desired

effect.

Levophed®

has the potential to cause end-organ renal

damage with prolonged use due to vasoconstriction.

Because of the possibility of causing extreme

hypertension, monitor vital signs closely.

Expected hemodynamic outcome for Levophed®

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Phenylephrine (Neosynephrine®) Phenylephrine is used in the management of

hypotension caused by shock, anesthesia or

hypersensitivity reactions to drugs.

Receptors stimulated by phenylephrine

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

Phenylephrine has a powerful effect on the alpha-

receptors causing potent vasoconstriction, although it

is not as potent as Levophed®

. phenylephrine

completely lacks the chronotropic and inotropic

effects on the heart.

The usual dose of phenylephrine starts at 100-180

mcg/min then decreases to 40-60 mcg/min once

stabilized. The usual dose range is 20-200 mcg/min.

Like Levophed®

, phenylephrine also has the

possibility of causing end organ damage with

prolonged use due to vasoconstriction.

Expected hemodynamic outcome for phenylephrine

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Epinephrine (Adrenaline)

Epinephrine is naturally occurring hormone secreted

by the adrenal glands. A sympathomimetic, it

imitates almost all the actions of the sympathetic

nervous system (the “fight or flight” response). This

medication is commonly used intravenously during

cardiac arrest, and as an infusion for severe

hypotension.

Receptors stimulated by epinephrine

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

Epinephrine has mixed effects on the receptors of the

sympathetic nervous system. It stimulates alpha, beta

1 and beta 2 receptors.

The results of alpha stimulation are vasoconstriction

and an increase in blood pressure. An increase in

contractility and heart rate occur as a consequence of

beta 1 stimulation. Myocardial oxygen demand is

increased as a result.

The usual dose is 1-8 mcg/min. or 0.01-0.05

ug/kg/min. Titrate epinephrine by 1mcg/min or 0.01

mcg/kg every 5 minutes. Monitor blood pressure

every 5 minutes.

Expected hemodynamic outcome for epinephrine

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure



Page 17

Vasopressin (Pitressin®) Vasopressin is most commonly used for vasodilator

shock, GI bleeding, and organ donor management.

Receptors stimulated by vasopressin

Alpha

(Vaso-

constriction)

Beta 1

(Heart rate

and

contractility)

Beta 2

(Vaso-

dilatation)

Dopaminergic

(Renal

dilation )

Other

none none none none

Vasopressin is a naturally occurring anti-diuretic

hormone most commonly used in the treatment of

diabetes insipidus. The hormone is released in the

presence of a low blood volume and has direct effect

on V1 vascular smooth muscles receptors causing

constriction. When vasopressin is administered at

higher doses, vasoconstrictive effects occur due to

vasopressin’s action on vasopressin receptors.

The usual dosage is quite low, at about 0.04 units

/min. with the usual dosage range of 0.01-0.1

units/min. Vasopressin is not usually titrated; rather

it is left at a set dose. Vasopressin at a set dose allows

for active titration and weaning of catecholamine

drips using MAP as a guide.

Higher doses have been used with GI Bleeding,

although there is some evidence that the higher dose

may increase mortality.

Be careful in the transcription and administration of

this medication. Because of the small dosages,

decimal point errors are common when orders are

written and transcribed. A single decimal point

mistake results in a dose that is TEN TIMES what

was intended.

Expected hemodynamic outcome for vasopressin

Heart

rate

Preload

(RA,

PAOP,

PAD)


(SVR)

Blood

pressure

Now let’s take a look at the different medications you

will use to manage your patient’s hemodynamic

status. Please fill in your answers in the spaces

provided. Compare your answers to those at the end

of the case studies.

Case 1:

Bob has an Anterior Wall Myocardial Infarction (AWMI) with sustained hypotension SBP < 85 and a low cardiac output due to poor contractility. There is an elevated preload to the left side of the heart (PAOP: pulmonary artery wedge), and an elevated afterload (SVR: systemic vascular resistance).

In order to manage Bob’s hemodynamics each component should be addressed.

Bob’s preload is elevated In order to optimize Bob’s preload you may want to use a.________.

Bob also has an elevated afterload (SVR).

In order to reduce the resistance the heart has to work against, afterload reducers or ________are a good choice.

In order to help Bob with the low contractility, a _______ _______medication would be beneficial.

Case 2 Your next patient, Joe, is admitted with a necrotic bowel. He has a fever of 39.8º C and a WBC of 26,000. His cardiac output is very high (9.6 L /min) and his B/P is very low: 68/ 40. His afterload or SVR is low: 480.

In order to maintain adequate arterial pressure and organ perfusion ____________are needed.

Answers: (Case 1) diuretic, vasodilators, positive inotropic. (Case 2) vasoconstrictors or pressors



Page 18

Summary

Understanding the concepts behind hemodynamics

can help you plan, implement, and evaluate your

interventions when working with patients who have

disturbances in their hemodynamic status. Every set

of numbers needs to be compared to your physical

examination of the patient and interventions are

planned accordingly. It takes continued monitoring

and intervention adjustment to maintain an optimal

outcome for the patient. We hope that this program

gave you some knowledge about hemodynamics:

Why and how we do hemodynamic monitoring, and

common vasoactive medications used in critically ill

patients.

References

1. Lehman, L., et.al., (July 2013). Methods of Blood

Pressure Measurement in the ICU, Crit Care Med.

Jan 2013; 41(1): 34–40. Manuscript available online:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3724

452/

2. Lakhal, K, et.al. (2012). Noninvasive monitoring

of blood pressure in the critically ill: Reliability

according to the cuff site (arm, thigh, or ankle). Crit

Care Med, 40: 1207-1213.

Bibliography

Gahart, B. and Nazareno, A. (2013). 2013

Intravenous Medication, 29th

ed. Elsevier, Inc., St.

Louis, MO. ISBN: 978-0323-08481-9.

Hitner, H. and Nagle, B. (2012). Pharmacology, 5th

ed. McGrawHill Publishing, Inc., NY. ISBN: 978-0-

07-352086-5.

You have received this packet as pre-reading to

prepare you for attending a TCHP class. If you have

paid to attend the class, the cost of this home study is

covered by your course tuition. Please fill out the

attached post-test and evaluation and bring them with

you to class. The program coordinator will process

your post-test for contact hours and return it to you

with a certificate of completion.

If you are unable to complete the post-test and

evaluation prior to class, you can mail it in later to

TCHP or complete it on the TCHP website at

www.tchpeducation.com under home studies.

To mail it in:

HCMC – TCHP Office

701 Park Avenue – Mail Code SL

Minneapolis, MN 55415*

Please make a copy of your post-test prior to mailing

as it will not be returned to you. Paid participants

may request contact hours for this home study

without a processing charge up to 3 months after you

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*Please check the TCHP website for updates to our

address: www.tchpeducation.com

http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=23269127

http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=23269127

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3724452/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3724452/




Page 19

Post- Test: Understanding Adult

Hemodynamics Please print all information clearly and sign the verification

statement. If you wish to submit your post-test

electronically (preferred method), please access it from


1. Name (please print legal name above)

2. Birth date (required)

Format: 01/03/1999 M M D D Y Y Y Y

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Hospitals must use work email)

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6. Which of the following may be indicators of a

compromised hemodynamic status?

a) Shortness of breath

b) Chest pain

c) Disorientation

d) Increased urine output

e) Increased NG tube drainage

List 3 conditions in which invasive monitoring would

be helpful.

7. ____________________

8. ____________________

9. ____________________

10. Components that make up cardiac output are:

a) Heart rate x preload

b) Stroke volume x afterload

c) Stroke volume x heart rate

d) Heart rate x contractility

11. Cardiac index refers to:

a) Cardiac output adjusted for body surface

area

b) Classification of system for MIs

c) Cardiac vessel disease

d) Both B & C

12. All of the following are main factors for stroke

volume except:

a) Contractility

b) Heart rate

c) Afterload

d) Preload

13. Afterload is determined by

a) Compliance of the aorta

b) How thick or thin the blood is

c) SVR

d) Both A & B

e) All of the above

14. The RAP is:

a) Decreased with volume loss

b) Preload to the heart

c) Normally between 2-6 mm Hg

d) All of the above

15. Which of the following is used to increase

preload?

a) Giving volume

b) Using vasodilators

c) Using vasopressors

Match the medication to the action below:

16. ____ Epinephrine

17. ____ Medium-dose dopamine

18. ____ Nitroprusside

19. ____ Nitroglycerin

20. ____ Levophed®

a) Reduces BP

b) Venodilator

c) Increases contractility

d) Vasoconstrictor

e) Alpha, beta 1 & 2 stimulant

Expiration date: The last day that post tests will be

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envelope must be postmarked on or before that day.




Page 20

Evaluation: Understanding Adult Hemodynamics Please complete the evaluation form below by placing an “X” in the box that best fits your evaluation of this

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1. Identify non-invasive indicators of hemodynamic

status.

2. List three indications for invasive hemodynamic

monitoring.

3. Describe the relationships among preload, contractility,

compliance, afterload, and cardiac output.

4. Describe pharmacologic strategies that manipulate

heart rate, preload, contractility, and afterload to

improve cardiac output.

5. The teaching / learning resources were effective.

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12. Describe how you plan to incorporate the knowledge gained in this home study into your practice (indicate

all that apply):

___This information has made me more knowledgeable about my practice.

___I feel that I will be more skilled at assessing and managing patients with hemodynamic problems.

___I will use this information to educate my patients.

___I will use this information to educate my colleagues.



Page 21

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Expiration date: December 31, 2017

Shock and Infection in Critical Care Primer

© 2000 TCHP Education Consortium. Revised 2007, 2015

This educational activity expires April 30, 2018. All rights reserved. Copying, electronic transmission and sharing without permission is forbidden.


This home study is pre-reading for a class.

Please complete this activity and bring your

post-test and evaluation to class with you.

Cardiovascular Critical Care Primer

© 2000 TCHP Education Consortium; 2014 edition

Page 1

Introduction

Introduction/Purpose Statement Failure of the normal regulatory mechanisms in the body

can lead to rapid and profound shock. The purpose of this

home study is to review the pathophysiology of

cardiogenic, hypovolemic, anaphylactic, and neurogenic

shock. A brief review of sepsis and septic shock is also

covered.

Target Audience This home study was designed for the novice critical care

or telemetry nurse; however, other health care

professionals are invited to complete this packet.

Content Objectives 1. List the classifications of shock.

2. List the functions of the cell and the microcirculation.

3. Describe the stages of shock.

4. Describe three major mechanisms put into action to

compensate for shock.

5. Define terms related to shock.

Requirements for successful completion of this

educational activity: In order to successfully complete this activity you must

read the home study, complete the post-test and

evaluation, and submit them for processing.

Conflicts of Interest It is the policy of the Twin Cities Health Professionals

Education Consortium to provide balance, independence,

and objectivity in all educational activities sponsored by

TCHP. Anyone participating in the planning, writing,

reviewing, or editing of this program are expected to

disclose to TCHP any real or apparent relationships of a

personal, professional, or financial nature. There are no

conflicts of interest that have been disclosed to the TCHP

Education Consortium.

Expiration Date for this Activity:

As required by ANCC, this continuing education activity

must carry an expiration date. The last day that post tests

will be accepted for this edition is April 30, 2018—your

envelope must be postmarked on or before that day.

Planning Committee/Editors*

*Linda Checky, BSN, RN, MBA, Program Manager for

TCHP Education Consortium.

*Lynn Duane, MSN, RN, Assistant Program Manager

for TCHP Education Consortium.

Trent Heather, BSN, BA, Clinical Care Supervisor,

SICU, Hennepin County Medical Center.

Author Karen Poor, MN, RN, Former Program Manager, TCHP

Education Consortium

Content Experts *Trent Heather, BSN, BA, Clinical Care Supervisor,


Lynelle Scullard, BSN, RN, CCRN, Nurse Manager,


*Denotes reviewer of current edition

Contact Hour Information

For completing

this Home Study and evaluation,

you are eligible

to receive:

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information that follows)

Criteria for successful

completion: You must read the

home study packet, complete the

post-test and evaluation and

submit them to TCHP for

processing.

The Twin Cities Health Professionals

Education Consortium is an approved

provider of continuing nursing

education by the Wisconsin Nurses

Association, an accredited approver

by the American Nurses Credentialing

Center’s Commission on

Accreditation.

*Denotes contact hours used for renewing licensure with the MN Board

of Nursing or other Board that uses a 50 min/contact hour formula.

These contact hours will be issued unless you request contact hours that comply with the ANCC formula.

**Denotes contact hours used for renewing Nursing Certification with

ANCC or other organization that uses the formula of 60 min/contact hour. You must request these contact hours on the evaluation form if

you need them.

Please see the last page of the packet before the post-test

for information on submitting your post-test and

evaluation for contact hours.



Page 2

An Overview of Shock

Definition

Shock is a state of inadequate perfusion relative to tissue

demands.

Classification

The integrity of the circulatory system is dependent on:

(a) efficient cardiac pump, (b) an adequate blood volume,

and (c) a healthy vascular bed. The loss of any one of

these three essential components leads to one of the three

major classes of shock:

Cardiogenic: loss of an efficient cardiac pump

Hypovolemic: inadequate blood volume

Distributive (neurogenic, anaphylactic, and septic):

an unhealthy vascular bed

The cascading events of shock begin with inadequate

oxygen transport and cellular dysfunction, which proceed

to tissue and vascular disturbances, and end with organ

dysfunction or failure.

Oxygen Transport

Oxygen transport has two components: oxygen delivery

(DO2) and oxygen utilization /consumption (VO2).

Oxygen delivery (DO2) is the product of cardiac output

and arterial oxygen content. Calculation of the arterial

oxygen content depends on (1) the hemoglobin content of

blood, (2) the oxygen saturation of hemoglobin, and (3)

the amount of oxygen bound to hemoglobin. Changes in

any of these three factors and/or changes in cardiac output

alters oxygen delivery to tissues.

Normally, systemic oxygen delivery is five times greater

than oxygen consumption. In other words, 20 percent of

DO2 is absorbed (VO2), while 80 percent of DO2 remains

in returning venous blood. The body adjusts to maintain

this ratio; usually by increasing or decreasing cardiac

output.

Tissue oxygen utilization cannot be directly measured;

however, the calculation of VO2 infers utilization and

serves as a guide to the adequacy of tissue perfusion and

cellular metabolism. Factors that determine VO2 are: (1)

DO2, (2) state of microcirculation, and (3) cellular milieu.

Other components that affect carried and released oxygen

are pH, temperature and CO2. This relationship can be

mapped with the oxyhemoglobin dissociation curve.

Life at the Cellular Level

The cell is the unit, or building block, of all living things.

The cell has several structures that are vital for

functioning:

1. Cell membrane: a barrier with selective

permeability between plasma and interstitial fluid

that allows interchanges to occur between the cell

and its environment. When damaged, it becomes

permeable to almost anything.

2. Nucleus: controls the biochemical reactions; site of

cellular reproduction.

3. Cytoplasm: the protoplasm within the cell but

outside of the nucleus; site of most cellular activity.

4. Organelles: specialized metabolic machinery of the

cell that produce and store protein, detoxify contents,

aid in phagocytosis, and provide cellular energy.

Cellular metabolism refers to all chemical and energy

transformations that occur in the body, including anabolic

and catabolic reactions. Carbohydrates, proteins, and fats

are oxidized, producing CO2, H2O, heat, and chemical

energy. This oxidation (catabolism) is a complex, slow

process which liberates energy (ATP) in small, usable

amounts.

The Microcirculation

The term microcirculation is used to describe a group of

blood vessels within the tissues that acts as an

independent organ unit in regulating blood supply to the

tissues. The functions of the microcirculation are to:

Deliver nutrients to, and remove wastes from,

cells

Adjust blood flow in response to tissue

metabolic needs

Maintain intravascular/interstitial osmotic

equilibrium

The portion of the vascular bed lying between the

arterioles and the venules is considered the

microcirculation. There are no distinct boundaries

between the divisions, and the arrangement and

distribution differ from tissue to tissue depending on

architecture and function.

The artery has a strong, smooth muscle wall, and directs

blood to capillary beds and controls pressure of the blood

delivered to those beds. Arterioles are referred to as

“resistance vessels.” Adjustments to the blood flow, and

therefore, tissue perfusion pressure, is made by the

sympathetic innervation and vasomotor influences.



Page 3

The arteries branch into the metarterioles, and from there

into the pre-capillary sphincters. The capillaries at the

end of the arterial system form a junction with the venous

system.

It is in the capillary system that nutrients, oxygen and

waste products are exchanged from the arterial side to the

venous side. Once that process is complete, the blood

exists into the venules and finally the veins.

The microcirculation is controlled by the metabolites

from surrounding tissues. These metabolites have an

intrinsic capacity to regulate blood flow to compensate for

changes in the perfusion pressure and metabolic needs.

There is a delicate balance between blood flow and tissue

demand that is maintained by the (1) autonomic nervous

system (modulates vascular tone), (2) humoral, (3)

chemical, and (4) metabolic influences.

Moment to moment redistribution of blood flow through

the microcirculation is known as autoregulation.

Actively metabolizing cells release local mediators such

as K+, H

+ ion, CO2, and lactic acid, causing local

vasodilatation in order to deliver greater blood flow to

vascular beds with higher metabolic activity.

Pathophysiology of Shock: Initial Stage

This is the stage in which there are (theoretically) cellular

changes in response to shock. There are also no clinical

signs or symptoms except elevated lactate levels.

In the initial stage of shock, the cell switches from aerobic

metabolism to anaerobic metabolism, which causes

decreased energy production and increased lactic acid

levels. Diminished blood flow to the microcirculation

reduces oxygen delivery and sequesters metabolic by-

products, thereby reducing oxygen delivery and

utilization. The cell metabolism suffers, and the cell

begins to deteriorate.

Compensatory Stage of Shock

The homeostatic compensatory mechanisms of the body

are activated by decreased cardiac output. Compensation

is mediated through neural, hormonal, and chemical

changes.

Neural Compensation

Baroceptors located in the aorta and carotid bodies sense

a decrease in the blood pressure. Messages are sent to the

medullary vasomotor center that stimulates the

sympathetic nervous system. The SNS uses the

endogenous catecholamines (epinephrine and

norepinephrine), which are released from the adrenal

medulla, to:

1. Constrict the blood vessels in the skin, GI tract and

kidneys

2. Dilate the blood vessels in the skeletal muscles and

coronary arteries

3. Sweat

4. Increase the heart rate and contractility

5. Increase the rate and depth of breathing

6. Dilate the pupils

Hormonal Compensation

Mediated through the sympathetic nervous system,

humoral compensation begins. The anterior pituitary

releases ACTH, which causes a release of

mineralocortocoids and glucocorticoids. The

mineralocorticoids balance the sodium and water levels.

The glucocorticoids regulate the metabolic function of the

body through the stress response. Cortisol sensitizes the

muscle of the arteriole to the effects of catecholamines.

The posterior pituitary releases ADH, causing

vasoconstriction and renal retention of water.

The kidneys, which are flow dependent, also sense the

decreased blood pressure. The kidneys release renin in

response, which then stimulates the angiotensin and

aldosterone systems. These hormones cause:

Retention of sodium and water

Increased blood volume in the major blood

vessels because of water retention and

vasoconstriction of the smaller blood vessels

Decreased urine volume and sodium excretion

Increased potassium excretion and increased

urine osmolarity

Chemical Compensation

Hypoxemia and cellular hypoxia cause an increase in

respiratory depth and rate. The acid-base balance is

disturbed with the “blowing off” of CO2, which leads to

respiratory alkalosis. The combination of hypoxemia and

alkalosis adversely affects the level of consciousness.



Page 4

Progressive Stage of Shock

In this stage of shock, previously helpful compensatory

responses are no longer effective. Severe hypoperfusion

to all organ systems causes multi-organ dysfunction

syndrome (multi-system organ failure). The

microcirculation loses the ability to autoregulate blood

flow, leading to decreased blood volume returning to the

central blood vessels. This causes further organ

hypoperfusion.

Refractory Stage of Shock

This final and irreversible stage reflects the very last part

of a patient’s life. The cellular and organ destruction has

been so severe that death is inevitable.

Essential versus Non-essential Organs

The body long ago developed a priority list for scant

amounts of blood. On the top of the list:

Brain

Heart

Lungs

These organs will receive the most blood possible during

shock through stimulation of the beta receptors, which

causes vasodilation.

The other organs of the body, such as the skin and gut,

have primarily alpha-receptors, which when stimulated

cause vasoconstriction. They are considered to be “non-

essential organs.”

Organ-Specific Effects of Shock

Brain - Essential Organ

Beta adrenergic stimulation dilates cerebral vessels to

attempt to maintain enough flow for a MAP of 50. Late

in shock, the vasomotor center fails to recognize and

respond to sympathetic stimulation. Early symptoms of

hypoperfusion are irritability and agitation, replaced by

unresponsiveness in late stages.

Heart - Essential Organ

In all forms of shock except cardiogenic shock, the

myocardium experiences a protective flow.

Autoregulation maintains coronary flow as long as arterial

pressure does not fall below 70 mm/Hg. The

deterioration of heart function makes shock irreversible.

All other organs are considered biologically

expendable.

Skeletal Muscle, Fat, Skin

Vasoconstriction from alpha receptor stimulation results

in muscle weakness, cramping, and fatigue. The skin

becomes cool; its color ashen to cyanotic. The potential

for skin breakdown is enormous.

Kidneys

The low blood pressure is seen as a decreased glomerular

filtration rate (GFR) by the kidney. In order to increase

flow, the kidneys activate the renin-angiotensin-

aldosterone compensatory mechanism. Metabolic

acidosis created by cellular increases of lactic acid is

perpetuated by the kidneys’ inability to break down and

excrete lactic acid.

Lungs

Hyperpnea occurs as a compensatory response to

sympathetic stimulation, hypoxia, and metabolic acidosis.

The increased respiratory rate increases pulmonary

muscle oxygen consumption. Coupled with primary

damage from centrally mediated chemicals to pulmonary

capillary endothelial cells, increased capillary

permeability results in interstitial and intra-alveolar

edema and decreased pulmonary compliance. Resultant

decreased ventilation and impeded gas exchange further

decrease oxygen delivery to cells.

Mesentery

In early stages of shock, there is a marked decrease in

blood flow to the gut manifested by nausea, vomiting, and

hypoactive bowel sounds. Later, intestinal damage and

necrosis by digestive enzymes cause damage to the

protective mucosal barrier. Bacteria and toxins are

released into the bloodstream. Hypoperfusion to the

intestines also enhances the formation and absorption of

endotoxins released from native gram negative bacteria.

When released, these endotoxins cause extensive vascular

dilatation, greatly increasing cellular metabolism despite

inadequate oxygen and nutrients to cells.

Liver

The liver filters and detoxifies drugs, metabolites, and

coagulation products. The liver also stores glucose as

glycogen. The metabolic rate of the liver is very high

with consumption of large quantities of oxygen and

nutrients. In shock, the catecholamines stimulate liver

activity. Glucose is made available to the cells, which are

unable to use it, resulting in hyperglycemia. Hepatic

ischemia results in a decrease in its metabolic and



Page 5

detoxification functions. Loss of clotting factors induce

coagulopathies such as DIC.

Pancreas

Shock induces the release of amylase and lipase into the

circulation. A chemical called myocardial depressant

factor (MDF), released from the pancreas, decreases

myocardial contractility.

Cardiogenic Shock

Cardiogenic shock is caused by inadequate myocardial

contractility from acute myocardial infarction, coronary

artery disease, or mechanical factors (valvular

regurgitation, low output syndrome, arrhythmias).

Pathophysiology of Cardiogenic Shock

In cardiogenic shock, the left ventricle has been injured in

some way, leading to impaired pumping.

Decreased tissue perfusion

Decreased BP

Decreased C.O

Decreased S.V .

Pulmonary interstitial edema

Intra-alveolar edema

Increased pulmonary

capillary pressure

Increased pulmonary

venous pressure

IncreasedLAP

Elevated left ventricular

filling pressure

Inadequate systolic emptying

Impaired pumping ability

of the left ventricle

Because the pumping is ineffective, less blood is pushed

out with each heartbeat, leading to a decreased stroke

volume*. The heart rate increases to compensate for a

low cardiac output and blood pressure, but will eventually

be insufficient to compensate for the decreased stroke

volume. The tissues begin to be inadequately perfused.

The impaired pumping also leads to less blood being

pushed from the ventricle during systole. The left

ventricle gradually fills with more and more blood,

causing an elevated pressure within the LV and left

atrium. This pressure “backs up” into the pulmonary

vasculature, causing an increased pulmonary capillary

pressure.

* Stroke volume = the amount of blood pumped out of the left

ventricle with each contraction.

Hypovolemic Shock

In hypovolemic shock, there is a critical depletion of

intravascular volume from hemorrhage (most common),

plasma loss due to burns, dehydration, traumatic shock

due to blood loss and major tissue damage.

Pathophysiology of Hypovolemic Shock

The pathophysiologic process of hypovolemic shock is

straight-forward. Blood and/or fluids have left the body,

causing a decreased amount of volume in the blood

vessels.

Inadequate tissue perfusion

Decreased cardiac output

Decreased stroke volume

Decreased ventricular filling

Decreased venous return

Decreased intravascular volume

Venous return is decreased because of the lack of fluid in

the vascular space, causing decreased ventricular filling.

The ventricles do not have as much blood as normal to

pump out, so the stroke volume is decreased.



Page 6

The heart rate will increase to compensate for the

diminished stroke volume and resulting poor cardiac

output and blood pressure. Eventually, if the fluid or

blood loss continues, the heart rate will not be able to

compensate for the decreased stroke volume.

The end result of hypovolemic shock is inadequate tissue

perfusion.

Neurogenic Shock

Neurogenic shock is caused by the loss of sympathetic

control (tone) of resistance vessels, resulting in the

massive dilatation of arterioles and venules. Neurogenic

shock can be caused by general or spinal anesthesia,

spinal cord injury, pain, and anxiety.

Pathophysiology of Neurogenic Shock

Tissue perfusion

Cardiac output

Stroke volume

Venous return

Venous dilation

Peripheral vascular

resistance

Arteriolar dilation

Massive vasodilation

Loss of sympathetic tone

In neurogenic shock, there has been an insult to the

nervous system so that impulses from the sympathetic

nervous system (the fight or flight response) cannot

maintain normal vascular tone or stimulate

vasoconstriction.

The lack of SNS stimulation causes a massive venous and

arterial vasodilation. On the venous side, blood pools in

the distensible veins and does not return to the larger

veins. Because of this pooling, there is a diminished

amount of blood that returns to the heart. Stroke volume,

cardiac output, and blood pressure all fall.

On the arterial side, there is decreased peripheral vascular

resistance, which actually helps the heart to pump with

less energy. The drawback is that with decreased

peripheral pressure, there is not the driving force to get

blood, oxygen, and nutrients to the cells. This also causes

a small degree of arterial blood pooling, which decreases

the amount of blood returning to the heart.



Page 7

Anaphylactic Shock

Shock due to the severe allergic antigen-antibody reaction

to substances such as drugs, contrast media, blood

products, or insect or animal venom is called anaphylactic

shock. Food products such as seafood, nuts, peanuts,

peanut butter, and MSG can also cause anaphylactic

shock.

Pathophysiology of Anaphylactic Shock

Venous & arterial dilation

Massive

vasodilation

Interstitial edema

Relative hypovolemia

Capillary

permeability

Release of vaso-

active mediators

Antigen-antibody reaction

Activation of

sensitized antibodies

Exposure to antigen

The immune system goes “haywire” in anaphylactic

shock in an extreme allergic reaction. At some point, the

individual is exposed to the substance and develops

antibodies against it. On subsequent exposure to the

substance (the antigen), these antibodies will aggressively

bind to the antigen, forming an antigen-antibody complex.

This complex causes the release of chemicals that cause

vasodilation (in particular, histamine).

Both veins and arteries vasodilate, leading to decreased

blood returning to the heart. The capillaries become

permeable to nearly everything, allowing fluids, proteins,

and sometimes blood to pass through into the interstitial

space. This causes massive interstitial edema. The

vasodilation and fluid sequestration in the interstitium

causes a relative hypovolemia.

Septic Shock

Sepsis is a condition that occurs in many critically ill

patients. Sepsis is the systemic response to infection.

Many types of organisms can cause sepsis, including

gram-negative bacteria, gram-positive bacteria, and fungi.

The infections can occur anywhere in the body; urinary

tract infections are probably the most common cause of

sepsis. Septic shock is said to occur when the sepsis has

progressed to the point where it is affecting many organ

systems.

Pathophysiology of Septic Shock

The immune and inflammatory response begins to try to

combat the organism that is causing an infection. The

body releases multiple chemicals into the blood stream,

including cytokines, vasodilators, complement factors,

and free radicals. In septic shock, this response is not

adequate to eliminate the infection and actually causes

increased damage. The organism itself also releases

substances called endotoxins or exotoxins, which further

harm the organs and tissues.

The combination of these chemicals and toxins cause: (1)

peripheral vasodilation – interstitial edema and decreased

blood return to the heart, and (2) decreased ability of the

cells and tissues to take up oxygen and nutrients.

The heart tries harder and harder to get oxygen and

nutrients to the cells by increasing the heart rate and

contractility initially, sometimes driving the cardiac

output twice to three times its normal amount.

Eventually, however, the immune response and

compensatory mechanisms may not enough to combat the

infection and resulting cellular destruction. The patient

may develop multi-organ dysfunction syndrome (MODS);

AKA multi-system organ failure (MSOF).

Conclusion

Patients with a wide variety of problems can develop

shock. Knowing the underlying pathophysiology may

help guide you in assessing and managing the care of the

patient with cardiogenic, hypovolemia, and distributive

types of shock.

Resources

1. Dellinger, R. (2013). Surviving sepsis campaign:

International guidelines for management of severe

sepsis and septic shock: 2012. Critical Care Medicine

www.ccmjournal.org, 41(2), 580-637.

2. Sonneville, R. (2013). Understanding brain

dysfunction in sepsis. Annals of Intensive Care,

3(15), 1-11.

http://www.ccmjournal.org/



Page 8

Recommended Reading

1. Alspach, J.G. (2006) AACN Core Curriculum for

Critical Care Nursing. 6th

ed. Philadelphia: Elsevier.

2. Seidel HM, Ball JW, Dains JE et al, eds. (2010)

Mosby's Guide to Physical Examination, 7th

ed. St.

Louis: Mosby, Inc.

3. Stillwell, S. (2006). Mosby’s Critical Care Nursing

Reference. 4th

ed. St. Louis, Mo: Mosby/Elsevier.

4. Cheever K.H. & Hinkle J.L. (2013) Brunner &

Suddarth's Textbook of Medical-Surgical Nursing,

13th

ed. Philadelphia: Lippincott William and

Wilkins.

5. Wiegand, D.J.L. & Carlson, K.K. (eds.) (2011).

AACN Procedure Manual for Critical Care. 6th

ed.

Philadelphia: Elsevier.

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Page 1

Shock & Infection in Critical Care Primer Post-Test

Please print all information clearly and sign the

verification statement. If you wish to submit your

post-test electronically (preferred method), please

access it from www.tchpeducation.com under home

studies.

1. Name (please print legal name above)

2. Birth date

(required)

Format: 01/03/1999 M M D D Y Y Y Y

3. Email:

(Required to return your certificate of completion to you—TCHP Hospitals must use work email)

4. Where do you work? (example: HCMC, MVAHCS,

MVH, etc.). Enter N/A if you are not employed

Hospital Unit

5. Personal verification of successful completion of

this educational activity (required):

I verify that I have read this home study and have

completed the post-test and evaluation.

Signature

6) The sympathetic nervous system will do all of

the following actions in response to a low

cardiac output except:

a) increase cardiac rate and contractility

b) constrict the pupils

c) dilate blood vessels in the skeletal muscles

and coronary arteries

d) sweat

7) In the initial stage of shock, all of the following

are true except:

a) The cell switches from aerobic to anaerobic

metabolism, which increases lactic acid

levels

b) Blood flow is diminished to the

microcirculation resulting in reduced oxygen

delivery and utilization

c) ADH is released, causing vasoconstriction

d) Cells begin to deteriorate

8) Which organ is considered essential in relation to

blood supply in the shock states?

a) gastrointestinal tract

b) kidneys

c) heart

d) lungs

9) The two pathophysiologic processes that occur in

cardiogenic shock are:

a) anoxia and decreased tissue perfusion

b) decreased stroke volume and inadequate

systolic emptying

c) low cardiac output and high urine output

d) pulmonary edema and decreased stroke

volume

10) What is the most common cause of hypovolemic

shock?

a) dehydration

b) burns

c) hemorrhage

d) vomiting

11) The massive vasodilation that occurs in

neurogenic shock results in:

a) venous dilation

b) arteriolar dilation

c) decreased cardiac output

d) all of the above

12) What of the following will NOT cause

anaphylactic shock?

a) a first bee sting

b) blood products

c) peanut butter

d) contrast media

13) The most common causal agent of septic shock

is:

a) upper respiratory infection

b) urinary tract infection

c) central line infection

d) none of the above

Expiration date: The last day that post tests will

be accepted for this edition is April 30, 2018—

your envelope must be postmarked on or before

that day.




Page 2

Evaluation: Shock and Infection Critical Care Primer

Please complete the evaluation form below by placing an “X” in the box that best fits your evaluation of this

educational activity. Completion of this form is required to successfully complete the activity and be awarded

contact hours.

At the end of this home study program, I am able to: Strongly

Agree

Agree Neutral Disagree Strongly

Disagree

1. List the classifications of shock.

2. List the functions of the cell and the microcirculation.

3. Describe the stages of shock.

4. Describe three major mechanisms put into action to

compensate for shock.

5. Define terms related to shock.

6. The teaching / learning resources were effective.

If not, please comment:

The following were disclosed in writing prior to, or at the start of, this educational activity

(please refer to the first 2 pages of the booklet).

Yes No

7. Notice of requirements for successful completion, including purpose and objectives

8. Conflict of interest

9. Expiration Date for Awarding Contact Hours

10. Did you, as a participant, notice any bias in this educational activity that was not previously

disclosed? If yes, please describe the nature of the bias:

11. How long did it take you to read this home study and complete the post test and evaluation:

______hours and ______minutes.

12. Did you feel that the number of contact hours offered for this educational activity was appropriate for the

amount of time you spent on it?

____Yes

____No, more contact hours should have been offered

____No, fewer contact hours should have been offered.

13. Describe how you plan to incorporate the knowledge gained in this home study into your practice (indicate

all that apply):

___This information has made me more knowledgeable about my practice. ___I feel that I will be more skilled at assessing and managing patients experiencing shock and infection.

___I have a better understanding of the tests, procedures, and precautions to use with this type of

patient.

___I will use this information to educate my patients.

___I will use this information to educate my colleagues.

___I do not plan to integrate any of this information into my practice (please explain)

Other/answer explanation:______________________________________________

Expiration date: April 30, 2018


2000 TCHP Education Consortium; 2015 edition

Page 3

14. What best describes your reason for completing this home study? (select all that apply):

___It was assigned pre-reading for a class I am taking.

___I wanted to learn more about caring for patients experiencing shock and infection.

___I needed contact hours.

Other: ________________________________________________________________

15. Do you think there is a continued need to have this home study available?

___Yes, this information will continue to be relevant.

___No, this information is no longer relevant.

___Don’t know.

___It depends. (please specify):_____________________________________________

If you are an ANCC-certified nurse* or need contact hours based on a 60 min/contact hour formula, fill out the

information below. Please note that you will receive a follow up survey via email to track how you are using the

information presented in this packet in your professional practice 3-6 months from now.

Name:

Email:

*Certified nurses renew their certification (CCRN, PCCN, etc.) with the organization that manages their

certification. Most nurses are not certified and renew licensure with their state Board of Nursing.

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