C h a p t e r 2 0
Heart Failure and Circulatory Shock
501
the cellular and extracellular compartments, and lim-
ited amounts of ATP are produced. Without sufficient
energy production, normal cell function cannot be main-
tained. The Na
+
/K
+
-ATPase membrane pump function
is impaired, resulting in intracellular accumulation of
sodium and loss of potassium. The increase in intracel-
lular sodium results in cellular edema and increased cell
membrane permeability. Mitochondrial activity becomes
severely depressed and lysosomal membranes may rup-
ture, resulting in the release of enzymes that cause fur-
ther cellular destruction. This is followed by cell death
and the release of intracellular contents into the extra-
cellular space. The extent of the cell injury and organ
dysfunction is primarily determined by the degree and
duration of the shock state.
Compensatory Mechanisms
The clinical manifestations of shock are at least partly
due to the body’s compensatory responses to hypoperfu-
sion. The most immediate of the compensatory mecha-
nisms are those of the sympathetic nervous system and
the renin-angiotensin mechanism, which maintain car-
diac output and blood pressure. Often blood is shunted
from the kidneys to other vital organs.
The sympathetic nervous system provides important
reflexive mechanisms that are essential to the support of
the circulatory system during shock, particularly hypo-
volemic shock.
6
These reflexes increase heart rate and
stimulate constriction of blood vessels throughout the
body. There are two types of adrenergic receptors for the
sympathetic nervous system: alpha (
α
) and beta (
β
). The
β
receptors which are further divided into subtypes
β
1
and
β
2
receptors. Stimulation of the
α
receptors causes vaso-
constriction; stimulation of
β
1
receptors cause an increase
in heart rate and force of myocardial contraction; and
of
β
2
receptors, vasodilation of the skeletal muscle beds
and relaxation of the bronchioles. In shock, there is an
increase in sympathetic outflow that results in increased
epinephrine and norepinephrine release and activation of
both
α
and
β
receptors (Chapter 34). Thus, increases in
heart rate and vasoconstriction occur in most types of
shock (cardiac output = stroke × heart rate). The arteri-
oles constrict in most parts of the systemic circulation,
thereby increasing the peripheral vascular resistance, and
the veins and venous reservoirs constrict, thereby helping
to maintain adequate venous return to the heart.
There also is an increase in renin release, leading to
an increase in angiotensin II, which augments vasocon-
striction and leads to an aldosterone-mediated increase
in sodium and water retention by the kidneys. In addi-
tion, there is a local release of vasoconstrictors as well
as norepinephrine, angiotensin II, vasopressin, and
endothelin, which contribute to arterial and venous
vasoconstriction.
The compensatory mechanisms that the body recruits
cannot be sustained over the long term and become det-
rimental when the shock state is prolonged. This intense
vasoconstriction causes a decrease in tissue perfusion
and insufficient supply of oxygen. Cellular metabolism
is impaired, vasoactive inflammatory mediators such as
histamine are released, production of oxygen free radi-
cals is increased, and excessive lactic acid and hydrogen
ions result in intracellular acidity and accompanying
metabolic acidosis.
6
Each of these factors promotes
cellular dysfunction or death. If circulatory function is
reestablished, whether the shock is irreversible or if the
patient will survive is determined largely at the cellular
level regardless of the type of shock.
Types of Shock
In general, shock states are distinguished by clinical signs
and symptoms, history, and physical exam. Circulatory
shock can be caused by a decrease in blood volume
(hypovolemic shock), an alteration in cardiac function,
obstruction of blood flow through the circulatory sys-
tem (obstructive shock), or excessive vasodilation with
maldistribution of blood flow (distributive shock). The
main types of shock are summarized in Chart 20-1 and
depicted in Figure 20-7.
Hypovolemic Shock
Hypovolemic shock occurs when there is an acute
loss of 15% or more of the circulating blood volume.
The decrease may be caused by a loss of whole blood,
plasma, extracellular fluid or excessive dehydration
(Chart 20-1). Hypovolemic shock also can result from
an internal hemorrhage or from third-space losses, when
extracellular fluid is shifted from the vascular compart-
ment to the interstitial space.
Hypovolemic shock, which has been the most widely
studied type of shock, is often used as a prototype in
CHART 20-1
Classification of Circulatory Shock
Hypovolemic
Loss of whole blood
Loss of plasma
Loss of extracellular fluid
Cardiogenic
Myocardial damage (myocardial infarction, contusion)
Sustained arrhythmias
Acute valve damage, ventricular septal defect
Cardiac surgery
Obstructive
Inability of the heart to fill properly (cardiac
tamponade)
Obstruction to outflow from the heart (pulmonary
embolus, cardiac myxoma, pneumothorax, or
dissecting aneurysm)
Distributive
Loss of sympathetic vasomotor tone (neurogenic
shock)
Presence of vasodilating substances in the blood
(anaphylactic shock)
Presence of inflammatory mediators (septic shock)
