PATHOGENESIS OF

CIRCULATORY SHOCK
• Imbalance between oxygen supply and oxygen requirements at
the cellular level.

• Cellular hypoxia results in impaired cellular function and may

progress to irreversible organ damage and death.

• The causes of circulatory shock classically are divided into four

general types : cardiogenic, hypovolemic, and distributive.
• Cardiogenic shock results from heart disorders that cause
inadequate cardiac output despite sufficient vascular volume.

• Obstructive shock develops when circulatory blockage disrupts

cardiac output.

• Hypovolemic shock associated with loss of blood volume as a

result of haemorrhage or excessive loss of extracellular fluids
• Distributive shock is characterized by a greatly expanded
vascular space because of inappropriate vasodilation.

• Anaphylactic, neurogenic, and septic are forms of distributive

shock.

• Each type of shock has certain unique features, but all are
associated with impaired tissue oxygenation that can progress to
refractory shock and organ failure.
IMPAIRED TISSUE OXYGENATION
CARDIOGENIC SHOCK
• Severe dysfunction of the left, right, or both ventricles that
results in adequate cardiac pumping.
• Most common cause of cardiogenic shock is myocardial
infarction which leads to dysfunction or loss of left ventricular
myocardium.
• The low cardiac output state is associated with a high left
ventricular diastolic filling pressure (preload).
• High left ventricular preload leads to movement of fluid from
the pulmonary vascular beds into the pulmonary interstitial
space, which initially results in interstitial pulmonary edema and
later in alveolar pulmonary edema.
OBSTRUCTIVE SHOCK
• Obstructive shock occurs due to impairment of ventricular filling
during diastole due to some external pressure on the heart.
Decreased ventricular filling leads to reduced cardiac output.
• Causes :
Pericardial cardiac tamponade: bleeding into the
pericardium with external pressure on the heart.
Pulmonary embolism: embolus formation occurs in the
pulmonary vein so that no blood reaches to left heart.
Tension pneumothorax: progressive build-up of air within
the pleural space, usually due to a lung laceration which
allows air to escape into the pleural space but not to return.
HYPOVOLEMIC SHOCK
 Decreased
Decreased Decreased
intravascular
preload cardiac output
volume

Decreased
Hypoxic cell tissue hypotension
injury perfusion

Progressive shock
• Circulatory volume deficits may be the result of internal or
external losses.

• Internal losses can result from internal haemorrhage ,fracture of

long bones, or leakage of fluid into the interstitial spaces.

• External loses can result from external haemorrhage , burns,

sever vomiting and diarrhoea, or diuresis
 DISTRIBUTIVE SHOCK

 ANAPHYLACTIC SHOCK
NEUROGENIC SHOCK
SEPTIC SHOCK
ANAPHYLACTIC SHOCK
• Massive peripheral dilatation

• Blood volume maybe normal but the sudden enlargement of vascular

space causes blood to pool in the periphery. In some cases, there is also
leakage of fluid from the bloodstream into the interstitial spaces.

• Cardiac preload drops

• Decrease in cardiac output

NEUROGENIC SHOCK
• Often transitory

• Depression of vasomotor center in the medulla or from

interruption of sympathetic nerve fibres in the spinal cord.

• Causes :
• Brain trauma
• Spinal cord injury
• High spinal anesthesia
• Drug overdose
• Interruption of neural pathway for the baroreceptor reflex

• Loss of sympathetic tone in vasculature

• Profound peripheral vasodilation of both arterioles and veins

• Peripheral pooling of blood and hypotension

• Decreased venous return to the heart leads to decreased cardiac

output and hypotension
SEPTIC SHOCK
• Most cases of septic shock are caused by gram-positive
bacteria, followed by endotoxin-producing gram-negative
bacteria, although fungal infections are an increasingly
prevalent cause of septic shock.

• Toxins produced by pathogens cause an immune response;

in gram-negative bacteria these are endotoxins, which are
bacterial membrane lipopolysaccharides(lps).
 SYSTEMIC INFLAMMATORY RESPONSE
SYNDROME (SIRS)
• A characteristic of septic shock and often fatal

• An exaggerated, generalised manifestation of a local inflammatory reaction

• A hypermetabolic state characterised by two or more signs of systemic

inflammation (fever, tachycardia, tachypnea, leukocytosis or leukopenia)

• Leads to organ dysfunction and hypotension

 MOLECULAR PATHOGENESIS OF SIRS
• the massive inflammatory reaction results from systemic release
of cytokines (TNF, IL-1, IL-6, and platelet-activating factor [PAF];
> 30 endogenous mediators of SIRS)

• the most potent stimulus of TNF release: LPS

• other stimulus: toxin-1; enterotoxin; antigens of mycobacteria,

fungi, parasites, and viruses; products of complement activation
•Direct toxic effects of TNF on endothelial cells:
–compromising membrane permeability
–inducing cell apoptosis
•Indirect effects of TNF
–initiating a cascade of other mediators that amplify its deleterious
effects
–promoting adhesion of PMN leukocytes to endothelial surfaces
–activating extrinsic coagulation pathway
•TNF stimulates release of IL-1,IL-6, PAF, and other
eicosanoids that may mediate tissue injury
•TNF increases expression of adhesion molecules:
intercellular adhesion molecules (ICAMS); vascular cell
adhesion molecules (VCAMS); p-selectin; and endothelial-
leukocyte adhesion molecules (ELAMS) on endothelial
surfaces, promoting leukocyte adhesion and leukostasis
REFERENCE
• PATHOPHYSIOLOGY ,COPSTEAD BANASIK ,
FIFTH EDITION,2013