Shock

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V.

Basic Principals
A. Characterized by hypoperfusion caused either by reduction in
cardiac output or effective circulating blood volume
Causes
A. Cardiogenic
B. Hypovolemic
C. Septic
Cardiogenic Shock
A. Defined
i. State where the heart has been damaged to the point where
it is unable to supply enough blood to the organs of the body
ii. Failure to pump blood causes a fall in blood pressure
iii. Organs begin to fail
B. Clinical examples
i. MI
ii. Ventricular rupture
iii. Arrythmia
iv. Cardiac tamponade
v. Pulmonary Embolism
Hypovolemic Shock
A. Defined
i. Loss of RBC mass and plasma from hemorrhage
ii. Loss of plasma volume alone due to extravascular fluid
seqesteration, or GI, urinary, and insensible losses
iii. Loss of more than 20% of blood volume result in shock
B. Pathogenesis
i. Decreased:
1. Cardiac output
2. Left ventricular end diastolic pressure
3. Mixed venous oxygen content
ii. Increased:
1. Peripheral vascular resistance
C. Clinical Features
i. Cold, clammy skin
ii. Hypotension
iii. Decreased urine output
iv. Hb level is not altered in early stages (due to equal loss of
RBC and plasma)
v. Increased anion gap: metabolic acidosis (due to increased
anaerobic glycolysis)
Septic Shock
A. Definition
i. Sepsis accompanied by hypotension that cannot be
corrected by the infusion of fluids
B. Etiology

i.
ii.
iii.
iv.
v.

VI.

Elderly patients with chronic diseases

Associated with AIDS
Widespread use of immunosuppressive drugs
Indwelling catheters and mechanical devices
Microbial: gram positive (s. aureus), gram negative (e. coli)
fungi (candida)
C. Inflammatory Response:
i. Microbial LPS engage innate immune receptors
ii. Triggers pro-inflammatory response (TLRs, PAMPs)
iii. Innate immunity activation leads to release of
1. TNF IL-1 IFN-y IL-12
iv. Upregulation of adhesion molecules
v. Complement cascade triggered
vi. Coagulation cascade activated via endothelial injury
vii. All these events form a pro-inflammatory state
D. Counter-Inflammatory
i. Seen in sepsis
ii. Shift from pro-inflammatory TH1 to anti-inflammatory TH2
iii. Explains immune suppressed states seen in some cases of
sepsis
Organs
A. Dysfunction
i. Systemic hypotension, interstitial edema, and small vessel
thrombosis decrease oxygen delivery to tissue
ii. High levels of cytokines and other mediators decreases
myocardial contractility
iii. Increased vascular permeability and endothelial injury lead
to Acute Respiratory Distress Syndrome (ARDS)
iv. Ultimately all these lead to multi-organ failure
B. Kidney
i. Acute tubular injury/necrosis
ii. Characterized by acute renal failure
iii. Two settings
1. Ischemia
2. Direct toxic injury
iv. Tubular epithelial cells are sensitive to ischemia (due to high
rate of oxygen consumption)
v. Morphology includes focal tubular epithelial necrosis,
occlusion of tubular lumen by casts
vi. Note: straight portion of the proximal renal tubule and the
ascending thick limb in the renal medulla are vulnerable
C. Acute Respiratory Distress Syndrome
i. Injury to pneumocytes and pulmonary endothelium
ii. Endothelial activation: circulating inflammatory mediators,
activation of adhesion molecules, procoagulant activity,
adhesion and extraversion of neutrophils

iii. Accumulation of Intralveolar Fluid: Leaky pulmonary

capillaries, damage and necrosis of Type 2 alveolar
pneumocytes, formation of hyaline membrane
D. Adrenal Waterhouse-Friderichsen Syndrome
i. Bacterial infection (Neisseria meningitides) leading to sepsis
ii. Rapidly progressive hypotension, disseminated intravascular
coagulation (DIC)
iii. Rapidly developing adrenocortical insufficiency associated
with massive bilateral adrenal hemorrhage
E. Septic Shock: Clinical Features
i. Hypotension
ii. Neurologic
iii. Weak rapid pulse
iv. Tachypnea (abnormal rapid breathing)
v. ARDS, renal insufficiency
vi. Coagulopathy complicates shock, leading to DIC
vii. Multiorgan failure