504
U N I T 5
Circulatory Function
As shock progresses, the respirations become rapid
and deep to compensate for the increased production
of acid and decreased availability of oxygen. Decreased
intravascular volume results in decreased venous return
to the heart and a decreased central venous pressure
(CVP). The pulse becomes weak and thready, indicat-
ing vasoconstriction and reduced filling of the vascular
compartment. When shock becomes severe, the periph-
eral veins may collapse. Sympathetic stimulation leads
to intense vasoconstriction of the skin vessels, which
results in cool and mottled skin. In hemorrhagic shock,
the loss of red blood cells results in pallor of the skin
and mucous membranes.
Urine output decreases very quickly in hypovolemic
shock. Compensatory mechanisms decrease renal blood
flow as a means of diverting blood flow to the heart
and brain. Oliguria of 20 mL/hour or less indicates
inadequate renal perfusion. Continuous measurement
of urine output is essential for assessing the circulatory
and volume status of the person in shock and monitor-
ing the response to fluid replacement.
Restlessness, agitation, and apprehension are com-
mon in early shock because of increased sympathetic
outflow and increased levels of epinephrine. As the
shock progresses and blood flow to the brain decreases,
restlessness is replaced by altered arousal and menta-
tion. Loss of consciousness and coma may occur if the
person does not receive or respond to treatment.
Treatment.
The treatment of hypovolemic shock is
directed toward correcting or controlling the underlying
cause (replacing or shifting volume) and improving tis-
sue perfusion. Ongoing loss of blood must be corrected,
such as in surgery. Oxygen is administered to increase
oxygen delivery to the tissues. Medications usually are
administered intravenously. Frequent measurements
of heart rate and cardiac rhythm, blood pressure, and
urine output are used to assess the severity of circulatory
compromise and to monitor treatment.
Restoration of vascular volume can be accomplished
through intravenous administration of fluids, blood and
blood products.
52
The crystalloids (e.g., isotonic saline
and Ringer lactate) are readily available and effective,
at least temporarily. Colloids or plasma volume expand-
ers (e.g., pentastarch and colloidal albumin) have a
high molecular weight, do not necessitate blood typ-
ing, and remain in the vascular space for longer periods
than crystalloids such as dextrose and saline, but are
considerably more expensive.
52,53
Blood or blood prod-
ucts (packed or frozen red cells) are administered based
on hematocrit and hemodynamic findings. Fluids and
blood are best administered based on volume indicators
such as CVP and urine output.
Vasoactive medications are agents capable of con-
stricting or dilating blood vessels. Considerable con-
troversy exists about the advantages or disadvantages
related to the use of these drugs. As a general rule,
vasoconstrictor agents are not used as a primary form
of therapy in hypovolemic shock, and may be detrimen-
tal.
54
Replacing volume is the first priority but vaso-
pressor and inotropic agents may be used as an adjunct
to help restore tissue perfusion and normalize cellular
metabolism. These agents are given only when volume
deficits have been corrected yet hypotension persists.
Cardiogenic Shock
Cardiogenic shock occurs when the heart fails to pump
blood sufficiently to meet the body’s demands (see
Fig. 20-7). Clinically, it is defined as decreased cardiac
output, hypotension, hypoperfusion, and indications of
tissue hypoxia despite an adequate intravascular vol-
ume.
55,56
Cardiogenic shock most commonly occurs from
an acute myocardial infarction,
57
but may also occur
from non-ischemic causes including myocardial contu-
sion, acute mitral valve regurgitation due to papillary
muscle rupture, sustained arrhythmias, severe dilated
cardiomyopathy, and cardiac surgery. Cardiogenic
shock can also occur with other types of shock because
of inadequate coronary blood flow. Approximately 3%
to 6% of the patients with ST elevation MI (STEMI)
develop cardiogenic shock despite receiving reperfusion
therapy (see Chapter 19).
55–57
Most patients who die of
cardiogenic shock have had extensive damage to the left
ventricle because of a recent infarct or reinfarction.
Regardless of cause, in persons with cardiogenic shock
there is failure to eject blood from the heart, hypoten-
sion, and inadequate cardiac output. Compensatory neu-
rohumoral responses take place, which include activation
of the sympathetic and renin-angiotensin systems lead-
ing to vasoconstriction, tachycardia, and fluid retention.
Increased systemic vascular resistance often contributes to
the deterioration of cardiac function by increasing after-
load or the resistance to ventricular systole. Preload, the
filling pressure, also is increased as blood returning to the
heart is added to blood that previously was not pumped
forward, resulting in an increase in end-systolic ventricu-
lar volume. Increased resistance to ventricular systole (i.e.,
afterload) combined with decreased myocardial contrac-
tility causes an increase in end-systolic ventricular volume
and preload, further complicating cardiac status.
Manifestations.
The signs and symptoms of cardio-
genic shock are consistent with those of end-stage heart
failure. The lips, nail beds, and skin may become cya-
notic because of stagnation of blood flow and increased
extraction of oxygen from the hemoglobin as it passes
through the capillary bed. Mean arterial and systolic
blood pressures decrease due to poor stroke volume,
and there is a narrow pulse pressure and near-normal
diastolic blood pressure because of arterial vasoconstric-
tion. Urine output decreases because of lower renal per-
fusion pressures and the increased release of aldosterone.
Elevated preload is reflected in a rise in CVP and pul-
monary capillary wedge pressure of at least 15 mm Hg.
Neurologic changes, such as alterations in cognition or
consciousness, may occur because of low cardiac output
and poor cerebral perfusion.
Treatment.
Treatment of cardiogenic shock requires
striking a precarious balance between improving car-
diac output, reducing the workload and oxygen needs
