Etiopathogenesis of Shock or Acute Circulatory Failure

In this article, we will discuss the Etiopathogenesis of Shock or Acute Circulatory Failure. So, let’s get started.

Etiopathogenesis

Adequate organ perfusion, depends on arterial pressure which is determined by cardiac output and peripheral vascular resistance. Normally when cardiac output falls systemic peripheral resistance rises to maintain a systemic pressure to perfuse vital organs. Cardiac output is a product of stroke volume and heart rate. The stroke volume is dependent on preload, afterload and myocardial contractility. Hence, organ perfusion may be compromised by a decrease in cardiac output or its maldistribution. However, when mean arterial pressure falls to <60 mmHg organ dysfunction occurs.

Vascular resistance is proportional to length of vessel and viscosity of blood and inversely proportional to fourth power of the radius of the vessel, therefore, cross-sectional area of the vessel is major determinant of vessel resistance. Vascular resistance is regulated by arterial tone which depends on neural (sympathetic) system, hormonal (adrenal) mechanisms and intrinsic or local factors (a variety of vasoconstrictor, e.g. endothelial-II, angiotensin II) and oxygen free radicals and vasodilators, e.g. endothelial derived relaxation factor eicosanoids, etc. The balance between vasoconstrictive and vasodilatory factors determine the local perfusion.

Microcirculatory failure is critical in pathogenesis of shock. Normal blood supply to an organ does not guarantee the fulfillment of adequate metabolic demands of all segments of that organ. Adhesion of leukocytes and platelets to the damaged or activated endothelium causes occlusion of microvasculature, activation of coagulation cascade and fibrin deposition (microthrombi) also contribute to vessel occlusion. Shunting of blood and decrease deformability of RBCs through vessel are also contributory factors for microcirculatory failure.

Microvascular flow depends on the balance between colloid osmotic pressure and capillary hydrostatic pressure, which, in turn determines the balance between intravascular and extravascular fluid. Sympathetic stimulation decreases the capillary hydrostatic pressure by constricting the precapillary resistance vessels, results in movement of fluid from the extravascular compartment to intravascular compartment. As severe tissue hypoxia and acidosis supervene, then this sympathetically mediated responses are overcome by metabolic vasodilatation and this response along with vasoconstriction can cause extravasation of fluid into interstitial space resulting in reduction of effective circulatory volume. In addition, circulating toxins, adhesions of activated leukocytes can increase capillary permeability and further increase the tissue edema. This process is increased by furter loss of plasma proteins into the interstitium resulting in reduction of colloid osmotic pressure, intravascular volume and tissue perfusion.

The causes of acute circulatory failure are divided into two groups:

(i) Those associated with low central venous pressure such as hypovolemic shock, anaphylaxis and septic shock.(ii) Those associated with raised central venous pressure such as cardiogenic shock, pulmonary embolism and cardiac tamponade.

Central venous pressure measurement before and during management of shock is mandatory.

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