C h a p t e r 2 0
Heart Failure and Circulatory Shock
505
of the myocardium, and increasing coronary perfu-
sion.
56,58
Fluid volume must be regulated within a level
that optimizes the filling pressure and stroke volume.
Pulmonary edema and arrhythmias should be corrected
or prevented to increase stroke volume and decrease the
oxygen demands of the heart. Coronary artery perfu-
sion is increased by promoting coronary artery vasodi-
lation, increasing blood pressure, decreasing ventricular
wall tension, and decreasing intracardiac pressures.
Currently there are two therapeutic options for patients
with cardiogenic shock to support the circulation—
pharmacologic therapy and mechanical support.
The goal of pharmacologic treatment is to increase
cardiac contractility without increasing heart rate.
Dopamine, dobutamine and norepinephrine are the most
commonly used inotropic and vasopressor agents.
56,58,59
Dopamine is often the drug of choice because it acts both
as an inotrope as well as a vasoconstrictor. Dobutamine,
an inotropic agent with arterial vasodilator properties,
can be used in persons with less severe hypotension.
Catecholamines, such as norepinephrine, increase car-
diac contractility but also result in arterial constriction
and tachycardia, which worsens the imbalance between
myocardial oxygen supply and demand. Overall, these
drugs must be used with caution as they have been
associated with dysrhythmias, myocardial injury, and
increased mortality.
56,58
Mechanical support using an intra-aortic balloon
pump or extracorporeal membrane oxygenation can
help to increase systemic blood flow and stabilize the
patient.
60
The percutaneous intra-aortic balloon pump,
also referred to as counterpulsation, enhances coronary
and systemic perfusion yet decreases afterload and myo-
cardial oxygen demands.
56,60
The device, which pumps
in synchrony with the heart, consists of a balloon that
is inserted through a catheter into the descending aorta
(Fig. 20-9). The balloon is timed to inflate during ventric-
ular diastole and deflate just before ventricular systole.
Diastolic inflation creates a pressure wave in the ascend-
ing aorta that increases coronary artery blood flow and
a less intense wave in the lower aorta that enhances
organ perfusion. The abrupt balloon deflation at the
onset of systole results in a displacement of blood vol-
ume that lowers the resistance to ejection of blood from
the left ventricle. Thus, the heart’s pumping efficiency is
increased, myocardial oxygen supply is increased, and
myocardial oxygen consumption is decreased.
Obstructive Shock
The term obstructive shock describes circulatory shock
that results from mechanical obstruction of the flow of
blood through the central circulation (great veins, heart,
or lungs; see Fig. 20-7). It is also referred to as extra-
cardiac shock. Obstructive shock may be caused by a
number of conditions, including dissecting aortic aneu-
rysm, cardiac tamponade, pneumothorax, atrial myx-
oma, and evisceration of abdominal contents into the
thoracic cavity because of a ruptured hemidiaphragm.
6
The most frequent cause of obstructive shock is pulmo-
nary embolism.
The primary physiologic result of obstructive shock
is elevated right heart pressure due to right ventricular
dysfunction. Pressures are increased despite impaired
venous return to the heart. Signs of right ventricular
dysfunction occur, including elevation of CVP and jug-
ular venous distention. Treatment modalities focus on
correcting the cause of the disorder, frequently requir-
ing a procedure to remove or correct the obstruction;
for example, surgical interventions such as pulmonary
embolectomy, pericardiocentesis (i.e., removal of fluid
from the pericardial sac) for cardiac tamponade, or the
insertion of a chest tube for correction of a pneumo-
thorax or hemothorax. In severe or massive pulmonary
embolus, fibrinolytic drugs may be used to break down
the clots causing the obstruction. Once the obstruction
to blood flow is removed then normal blood flow can be
re-established.
Distributive Shock
Distributive or vasodilatory shock is characterized by
loss of blood vessel tone, enlargement of the periph-
eral vascular compartment, and displacement of the
vascular volume away from the heart and central cir-
culation.
61
In distributive shock, the capacity of the
vascular compartment expands to the extent that a
normal volume of blood does not fill the circulatory
system (see Fig. 20-7). Therefore, this type of shock
is also referred to as normo-volemic shock. There are
Left
subclavian
artery
Renal
arteries
Deflated
Inflated
Descending
aorta
Left
subclavian
artery
FIGURE 20-9.
Aortic balloon pump placed in the descending
aorta. (With permission from the Division of Cardiac Surgery;
Department of Surgery; Medical University Graz, Austria.)
