C h a p t e r 2 0
Heart Failure and Circulatory Shock
503
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.
Acute bleeding or other conditions
leading to decrease in blood volume
Heart
Increased heart rate
and cardiac contractility
Blood vessels
Vasoconstriction
of vessels in skin
and nonvital organs
Stimulation
of thirst
Posterior
pituitary
Stimulation of
ADH release
Kidney
Sodium and water
retention
Decreased urine output
Renin-angiotensin-
aldosterone mechanism
Adrenal cortex
Release of
aldosterone
Liver
Constriction of veins and
sinusoids with mobilization
of blood stored in liver
Compensatory mechanisms
Mechanisms to
maintain cardiovascular function
Mechanisms to
maintain blood volume
Hypothalamus
FIGURE 20-8.
Compensatory mechanisms used to maintain circulatory function and blood volume
in hypovolemic shock. ADH, antidiuretic hormone.
