PATHOPHYSIOLOGY OF HYPOVOLEMIC SHOCK
Shock is a complex and dynamic process involving many compensatory mechanisms. An
initiating cause results in a decreased intravascular volume. As a result of the decreased
intravascular volume, venous return and ventricular filling (preload) is decreased. Decreased
ventricular filling leads to decreased stroke volume and decreased cardiac output. The end
result is inadequate tissue perfusion and oxygen delivery.
Decreased cardiac output and hypotension cause a baroreceptor mediated sympathoadrenal
reflex, which activates the patient’s compensatory mechanisms to help maintain perfusion.
There is a release of norepinephrine, epinephrine, and cortisol from the adrenal gland.
Epinephrine and norepinephrine cause an increase in heart rate and contractility, arteriolar
constriction that increases systemic vascular resistance and redirects blood flow to the heart
and brain and away from skin, muscle, kidneys and gastrointestinal tract. Cortisol enhances
the effects of the catecholamines on arterioles. Sodium and water is conserved due to reninangiotensin
/ aldosterone activation, causing an increased intravascular volume.