Porth's Essentials of Pathophysiology, 4e

502

Circulatory Function

U N I T 5

• Adequate oxygenation • Normal circulating volume • No obstruction to flow

Normal

Impeded or obstructed flow Decreased volume

Pump failure

Mechanical obstruction

Massive vasodilation

Loss of intravascular volume

Hypovolemic

Cardiogenic

Obstructive

Distributive

FIGURE 20-7. Types of shock.

discussions of the manifestations of shock. Approximately 10% of the total blood volume can be lost or shifted without changing cardiac output or arterial pressure. The average blood donor loses approximately 500 mL or 10% of his or her blood without experiencing adverse effects. 6 However, as increasing amounts of blood (15% to 30% or 750 to 1500 mL) are removed, compensatory mecha- nisms are triggered. 50,51 The most immediate of these compensatory mechanisms are the sympathetic-mediated responses designed to maintain cardiac output and blood pressure (Fig. 20-8). Shortly after the onset of hemor- rhage or the loss of fluid volume, tachycardia, increased cardiac contractility, vasoconstriction, and other signs of sympathetic and adrenal medullary activity appear. The sympathetic vasoconstrictor response also mobi- lizes blood that has been stored in the venous side of the circulation as a means of increasing venous return to the heart. There is considerable capacity for blood storage in the large veins of the abdomen, and approxi- mately 350 mL of blood that can be mobilized in shock is stored in the liver. 6 Sympathetic stimulation does not initially cause constriction of the cerebral and coronary

vessels, and blood flow to the heart and brain is main- tained at essentially normal levels as long as the mean arterial pressure remains above 70 mm Hg. 6 Without (and, at times, despite) compensatory mechanisms to maintain cardiac output and blood pressure, the loss of vascular volume results in a rapid progression from the initial to the progressive, and finally to the irreversible stages of shock (more than 40% volume loss). 51 Compensatory mechanisms designed to restore blood volume (i.e., draw volume into the intravascular space) include absorption of fluid from the interstitial spaces, conservation of sodium and water by the kidneys, and thirst. Extracellular fluid is distributed between the inter- stitial spaces and the vascular compartment. When there is a loss of vascular volume, capillary pressures decrease and water is drawn into the vascular compartment from the interstitial spaces. The maintenance of vascular vol- ume is further enhanced by renally mediated humoral mechanisms that conserve fluid. A decrease in renal blood flow and glomerular filtration rate results in acti- vation of the renin-angiotensin-aldosterone mechanism, which produces an increase in sodium reabsorption by