Porth's Essentials of Pathophysiology, 4e

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Heart Failure and Circulatory Shock

C h a p t e r 2 0

Acute bleeding or other conditions leading to decrease in blood volume

Compensatory mechanisms

Mechanisms to maintain cardiovascular function

Mechanisms to maintain blood volume

Hypothalamus

Liver

Heart

Stimulation of thirst

Posterior pituitary

Constriction of veins and sinusoids with mobilization of blood stored in liver

Increased heart rate and cardiac contractility

Stimulation of ADH release

Renin-angiotensin- aldosterone mechanism

Adrenal cortex

Kidney

Blood vessels

Release of aldosterone

Vasoconstriction of vessels in skin and nonvital organs

Sodium and water retention

Decreased urine output

FIGURE 20-8. Compensatory mechanisms used to maintain circulatory function and blood volume in hypovolemic shock. ADH, antidiuretic hormone.

the kidneys. The decrease in blood volume also stim- ulates centers in the hypothalamus that regulate anti- diuretic hormone (ADH) release and thirst. Antidiuretic hormone, also known as vasopressin, constricts the peripheral arteries and veins and greatly increases water retention by the kidneys. Although the mechanism of ADH is more sensitive to changes in serum osmolality, a decrease of 10% to 15% in blood volume serves as a strong stimulus for ADH and thirst. 6 During the early or initial stages of hypovolemic shock, vasoconstriction decreases the size of the vascu- lar compartment and increases systemic vascular resis- tance. This response usually is all that is needed when the injury is slight and blood loss is minimal (e.g., 10% or less). As hypovolemic shock progresses, vasoconstric- tion of the blood vessels that supply the skin, skeletal muscles, kidneys, and abdominal organs becomes more severe, with a further decrease in blood flow and conver- sion to anaerobic metabolism resulting in cellular injury. Manifestations. The signs and symptoms of hypo- volemic shock depend on its severity and are closely related to low peripheral blood flow and excessive sympathetic stimulation. They include thirst, increased heart rate, cool and clammy skin, decreased arterial

blood pressure, oliguria (decreased urine output), and changes in mentation. 50,51 Laboratory tests of hemo- globin and hematocrit provide information regarding the severity of blood loss or hemoconcentration due to dehydration. Serum lactate levels and arterial pH provide information about the severity of acidosis due to anaerobic metabolism. 52 Early signs of hypovolemic shock include tachycar- dia, peripheral vasoconstriction, and a slight increase or decrease in blood pressure, as the body tries to maintain cardiac output despite the decrease in stroke volume. Thirst is an early symptom in hypovolemic shock. In moderate to severe shock arterial blood pressure is decreased. However, controversy exists over the value of blood pressure measurements in the early diagnosis and management of shock. This is because compensatory mechanisms tend to preserve blood pressure until shock is relatively far advanced. 51 Furthermore, a normal arte- rial pressure does not ensure adequate tissue perfusion and oxygenation of vital organs at the cellular level. This does not imply that blood pressure should not be closely monitored in patients at risk for development of shock, but it does indicate the need for other assessment measures.