Introduction to Shock

8/12/2019 Introduction to Shock

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Introduction to Shock

Is All

Shock Alike?

Barbie J. Barrett MD, FACEP

Associate Professor

Department of Surgery

Division of Emergency Medicine

Stanford University and Medical Center

Palo Alto, California U.S.A.


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Central Venous Pressure Training for MD


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RN Education on SCVO2


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Sepsis Class for

Paramedical Providers


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Shock is an imbalance between tissue oxygen

supply and demand, resulting in inadequate tissue

perfusion.

- Shock may be present in the face of a: high, low

or normal blood pressure

High or Low Cardiac Output (CO)High or Low Systemic Volume Resistance (SVR)

Definition


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Hypotension is a drop in systolic bloodpressure of > 40-50 mm HG from baseline.

Systolic < 90 mm HgMAP < 65 mm Hg

The Surv iv ing Sepsis Campaign recommends mainta in ing MAP at > 65.


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PERFUSIONis crucial

Normal blood

pressure maynot equate to

good flow


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ARDS Adult Respiratory Distress Syndrome

CA O2 Arterial Oxygen Content

CO Cardiac Output

EGDT Early Goal Directed Therapy

MAP Mean Arterial Pressure

MODS Multi-organ Dysfunction Syndrome

PAC Pulmonary Artery Catheter


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ScvO2 Central Venous Oxygen Saturation

SvO2 Mixed Venous Oxygen Saturation

SIRS Systemic Inflammatory ResponseSyndrome

SVR Systemic Vascular Resistance

TO2 Tissue Utilization of OxygenTO2crit Critical Oxygen Uptake to Supply

VO2 Ventilatory Oxygen Consumption


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Classification by Etiology

Hypovolemic

Hemorrhage

Serum/Plasma loss Drugs

Distributive

Anaphylactic

Neurogenic

Septic

Cardiogenic Myocardial

Dysrrhythmia

Congenital Heart

Disease (DuctDependent)

Obstructive Pneumothorax,

Tamponade,Dissection

Dissociative Heat, CO, Cyanide

Endocrine


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The Chain of Survival

EarlyDetectionEarly andRapidIntervention

ppropriateDispositionImprovedOutcomes


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Right Atrium (RA) or CVP

Indicates preload

Crude example of

fluid volume

Normal 28

mmHg


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Right Ventricle (RV)

Normal

systolic

1525

mmHg

Normal

diastolic

08

mmHg


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Pulmonary Artery (PA)

Normalsystolic 1525 mmHg

Normaldiastolic 8

15 mmHg PAD

correlateswith thefillingpressure ofthe left heart


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Pulmonary Capillary Wedge Pressure

(PCWP)

Sees what is

in front of it

left side of heart

Normal 812mmHg


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MortalitySeptic Shock 30% - 45% (1 month mortality)

Cardiogenic 60% - 90%

Hypovolemic 30% - 40%

Grater than 1 million cases of shock are seen in

Emergency Departments annually

EGDT = Early Goal Directed Therapy


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Oxygen supply and demand imbalance

Conversion from aerobic to anaerobicmetabolism

Lactic acidosis due to both appropriate andinappropriate response

Pathophysiology


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Cellular

Major third space fluid loss

Capillary Leak

Fluid & Electrolyte Imbalance

Diarrhea, Sweat, Vomit

Vasodilationdue to excessive activation of

macrophages, neutrophils

Pro inflammatory mediators

Prostanoids, Nitric Oxide

Kinins and Pyrogens


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Pathophysiology

Vascular Hyporeactivity

Adrenocortical Disruption

Decreased Response to Catecholamines

CardiacProfound Myocardial Depression

Excess Nitric Oxide Release of Myocardial Depressant Factors


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Pathophysiology

Resultant Systemic Physiology

-Cell Death-End Organ Dysfunction

MODS= Multiorgan Dysfunction Sydrome


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Identifying Acute Organ Dysfunctionas a Marker of Severe Sepsis

Cardiovascular:Tachycardia

Hypotension

Altered CVP +

PAOP

Renal:

OliguriaAnuria

CreatinineHematologic:

PlateletsPT/INR, aPTT

Protein C D-dimer

Hepatic:

Jaundice,

Liver

enzymes

Albumin

CNS:Altered

consciousness

Confusion

Respiratory:

Tachypnea

PaO2PaO2/FiO2

ratio

Metabolic: Metabolic acidosis

Lactate level Lactate clearance

Balk RA, Crit Care Clin, 2000-16.337.352Keipell RM Crit Care Nurs Clin North Am 2003-15.27.34


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Physiology

Characterized by three stages

Preshock (warm shock, compensated shock,

cryptogenic shock) Shock

End organ dysfunction


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Physiology

Compensated shock

Low preload shocktachycardia,

vasoconstriction, mildly decreased BP

Low afterload (distributive) shock

peripheral vasodilatation, hyperdynamic

state


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Pathophysiology

Shock

Initial signs of end organ dysfunction

Tachycardia Tachypnea

Metabolic acidosis

Oliguria Cool and clammy skin


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Physiology

End Organ Dysfunction

Progressive irreversible dysfunction

Oliguria or anuria Progressive acidosis, CO

Agitation, obtundation, coma

Patient death


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Shock Pathways

Distributive Cardiogenic Obstructive Hypovolemic

Decreased

SVR

Blood FlowMaldistribution

Shock

Decreased MAP

Low Cardiac Output

Myocardial

DysfunctionMyocardial

DamagePericardial

TamponadeHemorrhage

~%

Uncompensated

~%

Compensated Reduced

Systolic

FunctionHigh or Normal

Cardiac Output

Reduced

Filling

Reduced

Preload

DEATH


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Physical Examination

VitalsTemperature may be or normal.GeneralPale, Weak

HEENTDry Mucous Membranes, Pale Conjunctiva

NeckWeak or Absent Carotid Pulses

CardiovascularUsually Tachycardia

Late Bradycardia

ExceptionAthletes, Beta-blockers,

Intra-abdominal Hemorrhage

Hypoglycemia

Cardiovascular drugs


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RespiratoryTachypnea

Dead Space

Bronchospasm

Adult Respiratory Distress Syndrome (ARDS)Abdomen

ILEUSlow flow state

GI Bleed

Pancreatitis

Acute Cholecystitis

Mesenteric Ischemia


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Extremities Pulses

Look for effusions, tracks,

infections, septic joints, line infection,

SkinPale

Cyanosis

Acrocyanosis

DiaphoreticCapillary Refill

Altered Temperature


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GUGenitourinary (Trauma, Blood Loss)Oliguria

Polyuria

Neuro-

Altered Mental StatusCord Signs

Loss of cardiac sympathetic tone

Paralysis

Meningismus

Psyche

Agitation Obtundation


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Hypovolemic ShockHypovolemic Shock is an acute intravascular volume loss

Results from decreased preload

Etiology

Hemorrhage, Trauma,GI Bleed, and Ruptured Aneurysm

Fluid loss

Burns, Diabetic KetoacidosisDiabetic Insipidus, Vomiting, and

Diarrhea


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Cardiogenic Shock

Cardiogenic Shock is decreased cardiac

output (CO) despite adequate volume.

Cardiogenic Shock is the leading cause of

death in acute myocardial infarction.


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Cardiogenic Shock

Etiology

Myocardial Infarction

Cardiomyopathy

DysrhythmiaMechanical

CHF (Congestive Heart Failure)

Valve

Contusion

Extra cardiac (obstructive)


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Cardiogenic Shock

Artioventricular valves

Tricuspid and Mitral During diastole, the

valves serve as aconduit from atria toventricles

Semilunar Valves

Pulmonic and Aortic After the end ofsystole, highpressure drops withthe pulmonary arteryand aorta, causingretrograde flow thusfilling the aortic and

pulmonary cuspswith blood andsnapping them shut.

Aortic valve is thevalve mostfrequently replaced


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Cardiogenic Shock

Clinical features

Distended Neck VeinsWeak or Absent Pulse

Arrhythmia often Tachycardia

Pulsus Paradoxus (if tamponade)


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Distributive Shock

Distributive Shock is a metabolic derangement that impairs

cellular respiration, due to severe decrease in SVR

Vasodilation reduces after load.

May be found with cardiac output (CO).


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Infection

Other

Burns

Trauma

Pancreatiits

Fungemia

Parisitemia

Viremia

Other

SIRS

Bacteremia

SEPSIS`

Bone et al Chest 1992


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Bone RC et al. Chest 1992, 101:1644-1655

Sepsis: Defining a Disease Continuum

Septic Shock

Lactic Acid < 4


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Distributive Shock

Systemic Inflammation

Pancreatitis

BurnsBiliary

Toxic Shock Syndrome

Toxic Reactions (transfusion, drugs)

Do not confuse spinal shock with neurogenic shock.


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Distributive Shock

Anaphylaxis & Anaphylactoid (Know the difference)

Widespread vasodilatation due to release of histamine.

Endocrine

Addisonian

Myxedema

Anaphylactic Reaction


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Anaphylactic Reaction

vs

Anaphylactoid Reaction

Anaphylactic

Previous

exposer/sensitisation

Mediated by specific IgE

antibodies

Common reaction to

contrast media

Anaphylactoid

No prior exposure

necessary

No IgE antibody involved

Common reaction toinvenomations/insect, Nuts,

Shell fish, Pharmaceuticals,

Latex

Histamine known responsible agent for most of manifestations


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Anaphylaxis

Vasodilatation Increased vascular permeability

Bronchoconstriction

Increased mucus production Increased inflammatory mediators

recruitment to sites of antigen interaction


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Anaphylaxis

Immediate response

Cutaneous manifestations urticaria, erythema, pruritis, angioedema

Respiratory compromise stridor, wheezing, bronchorrhea, resp. distress

Circulatory collapse tachycardia, vasodilation, hypotension

Clinic Presentation


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Obstructive Shock

Obstructive Shock is extra cardiac obstruction to

blood flow.

Tension pneumothoraxCardiac tamponade

Pulmonary embolus

Aortic stenosis

Can two or three different types of shock exist in one patient?


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Dissociative Shock

Heat

Carbon MonoxideCyanide

Endocrine


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Evaluation

Simultaneous differential diagnosis thinking occurs in

tandem with your treatment.

Targeted History & Physical

What type(s) of shock am I dealing with?

Full Laboratory Protocols & Evaluation

What would you order? (dont forget pregnancy)What Cultures would you obtain?

E l ti


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Evaluation

Other Studies / Imaging

EKG = Electrocardiogram)

FAST = Focused Assessment with Sonography in Trauma

CT = Computerized Tomography

ECHO = Echocardiogram

LP = Lumbar Puncture (if appropriate)


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Evaluation

Monitoring

Vital signs including capnography

Urine output

CVP Central Venous PressureRectal probe

Arterial line

Pulmonary Artery (PA) catheterization

Suspected etiology will direct studies.


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Index of 2008Recommendations

Initial resuscitation (first 6hours)

Diagnosis

Antibiotic therapy

Source identification andcontrol

Fluid therapy

Vasopressors

Inotropic therapy

Steroids

Recombinant human activatedprotein C (rhAPC)

Blood productionadministration

Mechanical ventilation ofsepsisinduced acute lunginjury ALI/ARDS (acuterespiratory distress syndrome)

Sedation, analgesia, and

neuromuscular blockade in sepsis

Glucose control

Renal replacement

Bicarbonate therapy

Deep vein thrombosis (DVT)

prophylaxis Stress ulcer prophylaxis

Consideration for limitationof support

Dellinger RP, et al. Crit Care Med. 2008,36:296-327. (Updated 36:1394-1396)


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N Engl J Med 2001; 345(19):1368-1377

Early

Goal-Directed

Therapy


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Pearls and Pitfalls

There is no single test that is diagnostic for sepsis.

Young healthy patients may crash quickly due to theirabilities to compensate initially.

Obtain pregnancy testing on all females of child bearing age.

Dont miss tension pneumothorax.

Does the patient have a pneumothorax after your CVP(central venous pressure) line placement?

Precise diagnosis is often delayed but immediate treatment is

essential.

Dont miss cardiac tamponade in your cancer/dialysis patients.


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Pearls and Pitfalls

Isolated intracranial injuries do not cause shock.

Call for help.

Dont assume there is only one cause for shock.

Keep your code/resuscitation bay warm blood loss will

cause hypothermia.

Does the patient arrive with any preexisting lines that

may be infected.

Check and recheck lines, monitors and infusions

Up to 30% of shock patients can have adrenal insufficiency


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Is All Shock Alike?


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References

Dellinger R, Carlet JM, Masur H, et al. Surviving sepsis campaign

guidelines for management of severe sepsis and septic shock. CritCare Med 2004; 32(3): 858-873. Dellinger R, Levy M, Carlet J, et al. Surviving sepsis campaign:

International guidelines for management of severe sepsis and septicshock. Crit Care Med 2008;36(1):296-327.

Morris E, Light RB, Garber GE. Identifying patients with severe sepsiswho should not be treated with drotrecogin alfa (activated). Am JSurgery 2002; 184: 19S-24S.

Nguygen HB, Rivers EP, Knoblich BP, et al. Early lactate clearance isassociated with improved outcome in severe sepsis and septic shock.Crit Care Med 2004: 32(8): 1637-1642)

Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy inthe treatment of severe sepsis and septic shock. N Engl J Med2001;345(19):13681377.

Ruble, Cheryl RN, MICN, Alameida, Rich MD. Sepsis Workshop.

2011. Mills/Pensula Medical Center Sherwin RL, M.D. Shock. Wayne State University. July 18th 2006.Presentation

Tintinalli JE. TintinallisEmergency Medicine, A comprehensive StudyGuide 7thed. McGrawHill Med 2011. (165-182, 222-240, 1003-1014)

Vanhorebeek I, Van den Berghe G. The neuroendocrine response tocritical illness is a dynamic process. Crit Care Clin 2006; 22: 1-15.

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Introduction to Shock

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