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SHOCK
Classification and Approach
to Management
Anand Kumar, MD
Section of Critical Care Medicine
Section of Infectious Diseases
University of Manitoba, Winnipeg, Canada
UMDNJ-Robert Wood Johnson Medical School
Cooper Hospital, NJ
Slide 2
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 3
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 4
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 5
Shock Hemodynamics
CO
SVR
hypovolemic
cardiogenic
obstructive
afterload
preload
distributive
pre-resusc
post-resusc
Slide 6
PWP
EDV
Classification of Shock
Hypovolemic Cardiogenic Extracardiac Obstructive
(e.g. Hemorrhage)
Distributive
(e.g. septic)
(e.g. Myocardial
infarction)
Diastolic filling
Ventricular afterload
(e.g.
tension
(e.g.
massive pulmonary Preload
Myocardial damage
pneumothorax
embolus)
or
pericardial
tamponade)
( Diastolic
Diastolic filling
Systolic and diastolic
filling)
function
Diastolic function
Systolic function
Preload
CO = cardiac output; SVR = systemic vascular
resistance; MAP = mean arterial blood pressure;
MODS = multiple organ dysfunction syndrome.
( Systolic and
Diastolic function)
SVR
( CO)
CO
( SVR)
MAP
Shock
Kumar and Parrillo,
2001
Myocardial
depression
MODS
Slide 7
Maldistribution
of flow
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)
Slide 8
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
Slide 9
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%
Slide 10
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
Slide 11
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
Slide 12
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
Slide 13
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 14
Compensatory Responses to Shock
• Maximize cardiac performance
• Increase contractility
• Redistribute perfusion
• Optimize oxygen unloading
Kumar and Parrillo, 2001
Slide 15
hypovolemia
intravascular
volume
sepsis
myocardial dysfunction (e.g. MI)
cardiovascular obstruction (e.g. massive
PE)
venous
capacitance
venous pressure
cardiovascular stress
renal perfusion
circulatory shock ( MAP)
stretch receptors
baroreceptors
right atrial
aortic arch, carotid body
pulmonary artery
vascular chemoreceptors
carotid, aorta
medullary
hormonal sympathetic response
renal juxtaglomerular
chemoreceptor
epinepherine
apparatus
CNS
pituitary response
norepinephrine
renin/angiotensin
ACTH/ADH
neural
aldosterone
cortisol
cardiac contractility
aldosterone
Na/H2O retention
vasoconstriction
cardiac contractility
Kumar and Parrillo, 2001
Na retention
vasoconstriction
flow redistribution maintain cardiovascular
flow redistribution
catecholamine
Slide 16
responsiveness
ORGAN SYSTEM DYSFUNCTION
ORGAN SYSTEM
MANIFESTATIONS
CNS
Encephalopathy (ischemic or septic)
Cortical necrosis
Heart
Tachycardia, bradycardia
Supraventricular tachycardia
Ventricular ectopy
Myocardial ischemia
Myocardial depression
Pulmonary
Acute respiratory failure
Adult respiratory distress syndrome (ARDS)
Kidney
Prerenal failure
Acute tubular necrosis
GI
Ileus
Erosive gastritis
Pancreatitis
Acalculous cholecystitis
Colonic submucosal hemorrhage
Transluminal translocation of acteria/endotoxin
Kumar and Parrillo, 2001
Slide 17
Organ System Dysfunction
ORGAN SYSTEM
MANIFESTATIONS
Liver
Ischemic hepatitis
“Shock” liver
Intrahepatic cholestasis
Hematologic
Disseminated intravascular coagulation
Dilutional thrombocytopenia
Metabolic
Hyperglycemia
Glycogenolysis
Gluconeogenesis
Hypoglycemia (late)
Hypertriglyceridemia
Immune System
Gut barrier function depression
Cellular immune depression
Humoral immune depression
Kumar and Parrillo, 2001
Slide 18
Clinical Approach to Diagnosis and
Management
Shock Suspected
•
•
•
•
•
Hypotension
Tachycardia
Peripheral hypoperfusion
Oliguria
Encephalopathy
Slide 19
Diagnosis and Evaluation
• Clinical Signs
– primary diagnosis
– differential Dx
Slide 20
Diagnosis and Evaluation
• Laboratory
– Hgb, WBC, platelets
– PT/PTT
– Electrolytes, arterial blood gases
– BUN, Cr
– Ca, Mg
– serum lactate
– ECG
Slide 21
Clinical Approach to Diagnosis and
Management
• Initial Diagnostic Steps
• CXR
• abdominal views*
• CT scan abdomen or chest*
• echocardiogram*
• pulmonary perfusion scan*
Slide 22
Diagnosis and Evaluation
• Invasive Monitoring
– arterial pressure catheter
– CVP monitoring
– ScvO2
Slide 23
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)
Slide 24
Clinical Approach to Diagnosis
and Management
• Diagnosis Remains Undefined or Hemodynamic Status
Requires Repeated Fluid Challenges of Vasopressors
• Pulmonary Artery Catheterization
• Echocardiography
Slide 25
Diagnosis Using Pulmonary Artery
Catheterization
Diagnosis
Cardiogenic Shock
Pulmonary Artery
Occlusion Pressure
Cardiogenic shock
due to myocardial
dysfunction
Cardiogenic shock due
to a mechanical defect
Acute VSD
Cardiac
Output
Miscellaneous
Comments


Usually occurs with
evidence of extensive
myocardial infarction
(40% of LV infarcted),
severe cardiomyopathy,
or myocarditis.

LVCO 
and RVCO
>LVCO
Predominant shunt is
left to right, pulmonary
blood flow is greater
than systemic blood
flow: oxygen “step-up”
occurs at RV level.
Kumar and Parrillo, 2001
Slide 26
Diagnosis Using Pulmonary Artery
Catheterization
Diagnosis
Cardiogenic Shock
Pulmonary Artery
Occlusion Pressure
Acute mitral
regurgitation
Right ventricular
Extracardiac obstructive
forms of shock
Pericardial
tamponade

Cardiac
Output
Forward
CO
Normal or 


or
Slide 27
Kumar and Parrillo, 2001
Miscellaneous
Comments
V waves in pulmonary
artery occlusion
pressure tracing.
Elevated RA and RV
filling infarction
pressures with low or
normal pulmonary
artery occlusion
pressures.
RA mean, RV enddiastolic, pulmonary
artery occlusion mean
pressures are
elevated and within 5
mmHg of one another.
Diagnosis Using Pulmonary Artery
Catheterization
Pulmonary Artery
Diagnosis
Occlusion Pressure
Extracardiac obstructive
forms of shock
Massive pulmonary
Normal or 
embolism
Hypovolemic shock
Distributive forms
of shock
Septic shock
Anaphylactic
shock

Cardiac
Output

Miscellaneous
Comments
Usual finding is
elevated right-sided
pressures.

or normal
or normal
Slide 28
Kumar and Parrillo, 2001
 or normal,
rarely 
 or normal
Pre-resuscitation
cardiac output is
decreased
Clinical Approach to Diagnosis
and Management
Immediate 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.
Slide 29
Clinical Approach to Diagnosis and
Management
• Hypovolemic Shock
• Rapid replacement of blood, colloid orcrystalloid
• Identify source of blood or fluid loss
Slide 30
Clinical Approach to Diagnosis and
Management
• Cardiogenic Shock
• RV infarction
– fluid and inotropes with PA catheter monitoring
• Mechanical abnormality
Slide 31
Results of Current Therapy
Treatment
Strategy
In-hospital
Mortality Rate (%)
Inotropic support
+ Thrombolysis
+ IABP
+ CABG
+ PTCA if successful
if unsuccessful
90
80-90
80
50-60
50-60
80-90
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 32
Clinical Approach to Diagnosis
and Management
• Extracardiac Obstructive Shock
• Pericardial tamponade
Slide 33
Courtesy of David Hunter, MD
University of Minnesota
Slide 34
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 35
Fluid Therapy
• Crystalloids
• Colloids
• Packed red blood cells
• Infuse to physiologic endpoints
Slide 36
Relative Potency:
Vasopressors/Inotropes
Agent
Dose
CARDIAC
PERIPHERAL VASCULAR
Heart Contractility Vasoconstriction Vasodilation Dopaminergic
Rate
Dopamine
1-4 (m/k)/min
4-20 (mg/kg)/min
1+
2+
1+
2-3+
0
2-3+
1+
0
4+
2+
Norepi
2-20 mg/min
1+
2+
4+
0
0
Dobutamine
2-15 (mg/kg)/min 1-2+
3-4+
0
2+
0
Isoproterenol
1-5 mg/min
4+
4+
0
4+
0
Epinephrine
1-20 mg/min
4+
4+
4+
3+
0
Phenylephrine
20-200 mg/min
0
0
3+
0
0
Vasopressin
0.01-0.04 u/min
0
0
4+
0
0
Milrinone
37.5-75 mg/kg
bolus; then 0.3750.75 ug/kg/min
1+
3+
0
2+
0
Kumar and Parrillo, 2001
Slide 37
Conclusion
• This concludes the presentation.
Slide 38