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Section of Critical Care MedicineSection of Infectious Diseases

University of Manitoba, Winnipeg, CanadaUMDNJ-Robert Wood Johnson Medical School

Cooper Hospital, NJ

Anand Kumar, MD

SHOCKClassification and Approach

to Management

Slide 3

Shock

• Cardiogenic Shock -a major component of the mortality associated with cardiovascular disease

• Hypovolemic Shock -the major contributor to early mortality from trauma

• Septic Shock -most common cause of death in American ICUs

Slide 4

Definition

• Kumar and Parrillo (1995): “the state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then if prolonged, to irreversible cellular injury”

Slide 5

Shock: Classification

• Hypovolemic Shock -due to decreased circulating blood volume

• Cardiogenic Shock -due to cardiac pump failure related to loss of myocardial contractility/functional myocardium or structural/mechanical failure

• Extra-cardiac Obstructive Shock -due to obstruction to flow in the cardiovascular circuit

• Distributive Shock -caused by loss of vasomotor control

Slide 6

Shock Hemodynamics

CO SVR PWP EDV

hypovolemic

cardiogenic

obstructive

afterloadpreload

distributive

pre-resuscpost-resusc

Slide 7

Classification of ShockHypovolemic Cardiogenic Extracardiac Obstructive Distributive

(e.g. Hemorrhage)

Preload

Diastolic filling

(e.g. Myocardial infarction)

Myocardial damage

Systolic and diastolicfunction

Diastolic filling(e.g. tension

pneumothoraxor pericardial tamponade)

Diastolic function Systolic function

Ventricular afterload(e.g. massive pulmonary

embolus) Preload

( Diastolic filling)

( Systolic andDiastolic function)

(e.g. septic)

Myocardialdepression

CO( SVR)

MAP

Shock

MODS

Maldistributionof flow

SVR( CO)

CO = cardiac output; SVR = systemic vascular resistance; MAP = mean arterial blood pressure; MODS = multiple organ dysfunction syndrome.

Kumar and Parrillo, 2001

Slide 8

Hypovolemic Shock

• degree of volume loss response

– 10% well tolerated (tachycardia)

– 20-25% failure of compensatory mechanisms (hypotension, orthostasis, decreased CO)

– >40% loss associated with overt shock (marked hypotension, decreased CO, lactic acidemia)

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Hypovolemic Shock

• rate of volume loss and pre-existing cardiac reserve response

• acute 1 L blood loss results in mild to moderate hypotension with decreased CVP and PWP

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Cardiogenic Shock

• #1 cause of in-hospital mortality from Q-wave MI

• requires at least 40% loss of functional myocardium

• usually involves left main or left anterior descending obstruction

• historically, incidence of cardiogenic shock post-Q wave MI has run 8-20%with mortality 70-90%

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Cardiogenic Shock

• mortality substantially better for cardiogenic shock due to surgically remediable lesions

– aortic valve failure

– papillary muscle rupture • ischemic form seen 3-7 days post-LAD territory infarct • v wave of > 10 mm often seen in PWP trace

– VSD (post-infarct, rarely traumatic)• post-infarct seen 3-7 days post-LAD occlusion• 5-10% oxygen saturation step-up

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Obstructive Shock

• rate of development of obstruction to blood flow response

– acute, massive PE involving 2 or more lobar arteries and 40-50% pulmonary bed can cause shock

– acute cardiac tamponade can occur with 150 mL fluid but over 2L can be well tolerated if slow accumulation

• similar variability based on presence of pre-existing cardiopulmonary disease

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Distributive Shock

• defining feature: loss of peripheral resistance

• dominantly septic shock, anaphylactic and neurogenic shock less common

• clinical form of shock with greatest contribution of other shock elements i.e., hypovolemia, cardiac failure

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Compensatory Responses to Shock

• Maintain mean circulatory pressure

• Volume

– Fluid redistribution to vascular space

– Decrease Renal losses

• Pressure

– Decreased venous capacitance

Kumar and Parrillo, 2001

Slide 15

Compensatory Responses to Shock

• Maximize cardiac performance

• Increase contractility

• Redistribute perfusion

• Optimize oxygen unloading

Kumar and Parrillo, 2001

Slide 16

hypovolemia

intravascularvolume

sepsis

venouscapacitance

venous pressure

myocardial dysfunction (e.g. MI)cardiovascular obstruction (e.g. massive PE)

renal perfusion

stretch receptorsright atrialpulmonary artery

renal juxtaglomerular apparatus

cardiac contractility vasoconstriction flow redistribution

sympathetic responsehormonal

epinepherinenorepinephrinerenin/angiotensinaldosterone

Na/H2O retention cardiac contractility vasoconstriction flow redistribution

cardiovascular stresscirculatory shock ( MAP)

baroreceptorsaortic arch, carotid body

vascular chemoreceptorscarotid, aortamedullary

chemoreceptorCNS pituitary response

neural ACTH/ADH

cortisolaldosterone

Na retentionmaintain cardiovascular catecholamine responsiveness

Kumar and Parrillo, 2001

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ORGAN SYSTEM DYSFUNCTION

CNS Encephalopathy (ischemic or septic)Cortical necrosis

Heart Tachycardia, bradycardiaSupraventricular tachycardiaVentricular ectopyMyocardial ischemiaMyocardial depression

Pulmonary Acute respiratory failureAdult respiratory distress syndrome (ARDS)

Kidney Prerenal failureAcute tubular necrosis

GI IleusErosive gastritisPancreatitisAcalculous cholecystitisColonic submucosal hemorrhageTransluminal translocation of acteria/endotoxin

ORGAN SYSTEM MANIFESTATIONS

Kumar and Parrillo, 2001

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Organ System Dysfunction

Liver Ischemic hepatitis“Shock” liverIntrahepatic cholestasis

Hematologic Disseminated intravascular coagulationDilutional thrombocytopenia

Metabolic HyperglycemiaGlycogenolysisGluconeogenesisHypoglycemia (late)Hypertriglyceridemia

Immune System Gut barrier function depressionCellular immune depressionHumoral immune depression

ORGAN SYSTEM MANIFESTATIONS

Kumar and Parrillo, 2001

Slide 19

Shock Suspected

• Hypotension• Tachycardia• Peripheral hypoperfusion• Oliguria• Encephalopathy

DIAGNOSTICTHERAPEUTIC

Clinical Approach to Diagnosis and Management

Slide 20

Diagnosis and Evaluation

• Clinical Signs

– primary diagnosis

– differential Dx

Slide 21

Diagnosis and Evaluation

• Laboratory

– Hgb, WBC, platelets

– PT/PTT

– Electrolytes, arterial blood gases

– BUN, Cr

– Ca, Mg

– serum lactate

– ECG

Slide 22

Clinical Approach to Diagnosis and Management

• Initial Diagnostic Steps

• CXR

• abdominal views*

• CT scan abdomen or chest*

• echocardiogram*

• pulmonary perfusion scan*

Slide 23

Diagnosis and Evaluation

• Invasive Monitoring

– arterial pressure catheter

– CVP monitoring

– ScvO2

Slide 24

Clinical Approach to Diagnosis and Management

• Admit to Intensive Care Unit (ICU)

• Venous access

• Central venous catheter

• Arterial catheter

• EKG monitoring

• Pulse oximetry

• Hemodynamic support (MAP <60 mmHg)

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Clinical Approach to Diagnosis and Management

• Diagnosis Remains Undefined or Hemodynamic Status Requires Repeated Fluid Challenges of Vasopressors

• Pulmonary Artery Catheterization

• Echocardiography

Slide 26

Diagnosis Using Pulmonary Artery Catheterization

Pulmonary Artery Cardiac Miscellaneous Diagnosis Occlusion Pressure Output Comments Cardiogenic Shock

Cardiogenic shock Usually occurs with due to myocardial evidence of extensive dysfunction myocardial infarction (40% of LV infarcted),

severe cardiomyopathy, or myocarditis.

Cardiogenic shock due to a mechanical defect

Acute VSD LVCO Predominant shunt is and RVCO left to right, pulmonary

>LVCO blood flow is greaterthan systemic bloodflow: oxygen “step-up”occurs at RV level.

Kumar and Parrillo, 2001

Slide 27

Diagnosis Using Pulmonary Artery Catheterization

Pulmonary Artery Cardiac Miscellaneous Diagnosis Occlusion Pressure Output Comments Cardiogenic Shock Acute mitral Forward V waves in pulmonary

regurgitation CO artery occlusion pressure tracing.

Right ventricular Normal or Elevated RA and RVfilling infarction

pressures with low or normal pulmonary artery occlusion pressures.

Extracardiac obstructive forms of shock

Pericardial or RA mean, RV end- tamponade diastolic, pulmonary artery occlusion mean

pressures are elevated and within 5 mmHg of one another.

Kumar and Parrillo, 2001

Slide 28

Diagnosis Using Pulmonary Artery Catheterization

Pulmonary Artery Cardiac Miscellaneous

Diagnosis Occlusion Pressure Output Comments Extracardiac obstructive forms of shock

Massive pulmonary Normal or Usual finding is embolism elevated right-sided

pressures.

Hypovolemic shock Distributive forms of shock

Septic shock or normal or normal, Pre-resuscitation rarely cardiac output

isAnaphylactic or normal or normal decreased shock

Kumar and Parrillo, 2001

Slide 29

Clinical Approach to Diagnosis and ManagementImmediate Goals in Shock

Hemodynamic support MAP >60mmHg PAOP = 12-18 mmHg Cardiac Index >2.2 L/min/m2

Maintain oxygen delivery Hemoglobin >9 g/dL Arterial saturation >92%

Supplemental oxygen and mechanical ventilation

Reversal of oxygen dysfunction Decreasing lactate (<2.2 mM/L) Maintain urine output Reverse encephalopathy Improving renal, liver function tests

MAP = mean arterial pressure; PAOP = pulmonary artery occlusion pressure.

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Clinical Approach to Diagnosis and Management

• Hypovolemic Shock

• Rapid replacement of blood, colloid orcrystalloid

• Identify source of blood or fluid loss

Slide 31

Clinical Approach to Diagnosis and Management

• Cardiogenic Shock

• RV infarction

– fluid and inotropes with PA catheter monitoring

• Mechanical abnormality

Slide 32

Results of Current Therapy

Inotropic support 90

+ Thrombolysis 80-90

+ IABP 80

+ CABG 50-60

+ PTCA if successful 50-60

if unsuccessful 80-90

Treatment In-hospital Strategy Mortality Rate (%)

From Klein L. W.: Intra-aortic balloon pumping. In Parrillo J.E., Bone R.C. (eds), Critical Care Medicine: Principles of diagnosis and management, St. Louis, 1995: Mosby.

Slide 33

Clinical Approach to Diagnosis and Management

• Extracardiac Obstructive Shock

• Pericardial tamponade

Slide 34

Courtesy of David Hunter, MDUniversity of Minnesota

Slide 35

Clinical Approach to Diagnosis and Management

• Distributive Shock

• Septic shock - Identify site of infection and drain, if possible

• Goals:

– SV02 >70%

– improving organ function

– decreasing lactate levels

Slide 36

Fluid Therapy

• Crystalloids

• Colloids

• Packed red blood cells

• Infuse to physiologic endpoints

Slide 37

Relative Potency: Vasopressors/Inotropes

CARDIAC PERIPHERAL VASCULAR

Agent Dose Heart Contractility Vasoconstriction Vasodilation Dopaminergic Rate Dopamine 1-4 (/k)/min 1+ 1+ 0 1+ 4+

4-20 (g/kg)/min 2+ 2-3+ 2-3+ 0 2+

Norepi 2-20 g/min 1+ 2+ 4+ 0 0

Dobutamine 2-15 (g/kg)/min 1-2+ 3-4+ 0 2+ 0

Isoproterenol 1-5 g/min 4+ 4+ 0 4+ 0

Epinephrine 1-20 g/min 4+ 4+ 4+ 3+ 0

Phenylephrine 20-200 g/min 0 0 3+ 0 0

Vasopressin 0.01-0.04 u/min 0 0 4+ 0 0

Milrinone 37.5-75 g/kg 1+ 3+ 0 2+ 0bolus; then 0.375-0.75 ug/kg/min

Kumar and Parrillo, 2001

Slide 38

Conclusion

• This concludes the presentation.