Definition of Shock

A clinical syndrome that occurs when acute

circulatory failure with inadequate or
inappropriately distributed tissue perfusion
results in failure to meet metabolic demands
causing generalized cellular hypoxia with or
without lactic acidosis
Categories of Shock
Hypovolemic
Reduction in circulating blood volume
Hemorrhage, plasma loss (burns/ascites), or extracellular fluid loss
(ketoacidosis/trauma)
Cardiogenic
Severe heart failure (MI, acute mitral regurgitation)
Obstructive
Circulatory obstruction (embolism/tamponade)
Septic
Infection or septicemia
Vasodilation, arteriovenous shunting and capillary damage cause
hypotension and maldistribution of blood flow
Categories of Shock, cont
Anaphylactic
Due to allergen-induced vaosdilation
Bee sting, peanut allergy, food allergies
Neurogenic
Follows high spinal trauma (above T6)
Interrupts sympathetic outflow causing
vasodilation, hypothermia, and bradycardia which
can be severe if vagal (parasympathetic)
stimulation is unopposed
Clinical Features
Depend on the underlying cause of the shock
and the severity
General features
Hypotension (systolic <100)
Tachycardia (>100)
Tachypnea (>30)
Oliguria (<30 ml/hr)
Drowsiness/confusion/agitation
Clinical Features, cont
Cold, clammy shock
Hypovolemic, cardiogenic, obstructive, and late shock
Cold peripheries from skin vasoconstriction, weak pulses,
evidence of low CO (oliguria, cyanosis, confusion)
Warm, dilated shock
Early septic and anaphylactic
Warm peripheries from skin vasodilation, bounding pulses,
high CO, flushed skin
Pathophysiology
Infection, trauma, allergens, hypoxia activate
endothelial cells and white cells releasing
interleukins and tumor necrosis factor
This results in an inflammatory response and a
thrombolytic response
The coagulation cascade is started and fibrin clots
form
The capillary is now inflamed and occluded
This damages the organ the capillary is in and
reduces oxygen delivery to that organ, furthering the
damage
Investigations
Labs: routine blood tests (eg-CBC), ABGs, lactic
acid levels, cardiac enzymes, blood type/cross
match
Vital signs: temperature, RR, SaO2, UO
Hemodynamics: continuous BP, CVP, EKGmay
also need CO, SVR, PCWP, SvO2 depending on
severity
Radiology: CXR
Microbiology: blood, sputum, and urine cultures
Assessment
Clinical features, SVR, and CVP define the cause of shock
CVP
CVP is reduced
Hypovolemic or anaphylactic
CVP is high
Cardiogenic or obstructive
CVP can be low, normal, or high with septic shock
SVR
SVR is high
Cardiogenic with vasoconstriction (cold, clammy shock)
SVR is low
Septic with vasodilation (warm, dilated shock)

Assessment, cont
Hypovolemic Shock
Low CVP/PCWP + low CO + high SVR
Cardiogenic Shock
High CVP/PCWP + low CO + high SVR
Septic Shock
Low CVP/PCWP + high CO + low SVR
Complications
Circulatory failure with tissue hypoxia leads
to multi-organ failure including ARDS, SIRS,
acute renal failure, GI ulceration
Eventually refractory shock with irreversible
tissue damage occurs leading to death
Multi-organ Failure
Brain: coma, intracerebral bleed
Lungs: ARDS
Heart: MI
Liver: failure
Kidneys: failure
GI: mucosal damage
Blood vessels: DIC, hemorrhagic purpura, bleeding
at injection and line insertion sites
Skin/extremities: ischemia, gangrene

Management
Mortality increases if shock lasts more than
an hour (the golden hour)
Try to correct the underlying cause of the
shock, reverse the tissue oxygen debt, and
prevent organ damage
Management, cont
Identify and treat the cause of the shock
Correct hypoxemia
Use supplemental oxygen
Intubate and ventilate (obtunded patients have a
high risk of aspiration)
Ventilatory support reduces the WOB, improves
cardiac function, and increases tissue oxygen
delivery
Management, cont
Resuscitation
Fluid resuscitation
Hypovolemia with low CVP/PCWP requires fluid
replacement
Cardiogenic shock with high CVP/PCWP needs fluid
restriction
At the onset of septic shock, fluid replacment is essential
but later fluid restriction may be needed to avoid
pulmonary edema
Management, cont
Inotropic support
Indicated when hypotension (MAP <60) or tissue
hypoxemia persist despite adequate fluid replacement or
when fluid is contraindicated
Type of inotrope depends on the cause of the shock
With warm shock, the CO is high but vasodilation may
cause hypotension, inadequate tissue perfusion, and organ
hypoxianorepinephrine increases SVR restoring the BP
and tissue perfusion
With cold shock, the CO is low due to poor myocardial
contractility and SVR is high from sympathetic
vasoconstrictiondobutamine increases contractility and
reduces SVR

Management, cont
Correct acidosis
Remove circulatory obstructions
Thrombolysis for pulmonary emboli (TPA,
Streptokinase)
Drainage of cardiac tamponade/pneumothorax
Correction of DIC to prevent microcirculatory
obstruction