Cardiogenic Shock

CARDIOGENIC SHOCK IS CAUSED BY A DECREASED
pumping ability of the heart that results in a shock-like
state with insufficient blood perfusion to organs and
tissues. During cardiogenic shock, systolic blood pressure is
less than 90 mmHg for greater than one hour and not
responsive to IV fluids. The cardiac index is less than
2.2 L/minute/m2, and the pulmonary capillary wedge pressure
is greater than 18 mmHg. Patients usually have
clouded consciousness and cold extremities.

I. CAUSES
Acute myocardial infarction is the most common cause of
cardiogenic shock. Other causes of cardiogenic shock are
given in Table 1. The complete occlusion of a coronary
artery by a clot causes death of an area of heart muscle that
is supplied by that blood vessel and its branches. If a very
large area of heart muscle is involved, the general pumping
capability of the heart is severely compromised. Because
dead myocardium cannot contract, blood cannot be
effectively ejected out of the left ventricle into the aorta
[see Fig. 1 in the chapter Anatomy of the Heart and
Circulation). Blood is held up in the lungs and fluid
accumulates in air sacs causing pulmonary edema which
results in severe shortness of breath. Because blood cannot
be ejected from the heart, the blood pressure falls
drastically. When more than 40% of the heart muscle is
involved, cardiogenic shock often occurs.

II. PATHOPHYSIOLOGY
In general terms shock is a clinical state in which target
organ–tissue perfusion is inadequate to supply vital substrates
and remove the metabolic waste. Inadequate cellular
oxygenation leads to marked generalized impairment of
cellular function and multiorgan failure.
The heart tries to contract more vigorously in the face of
this catastrophic event; the renin–angiotensin–aldosterone
system is activated and causes severe vasoconstriction
in an attempt to increase blood pressure (see Fig. 1 in
the chapter Angiotensin-Converting Enzyme Inhibitors/
Angiotensin Receptor Blockers), but over time the hypercontractility
of the heart ceases. This occurs because there
is utilization of glucose over fatty acids, loss of Krebs
cycle intermediates, and depletion of substrate required for
ATP production.

Figure 1 illustrates the pathophysiology of shock.
Because forward flow of blood is severely retarded, blood
returned to the heart from veins of the body and from the
lungs cannot be accommodated in a heart that is already
full of blood. Blood then backs up into the venous
circulation of the neck and in the lungs. This pressure of
blood returning to the heart is referred to as an increased
filling pressure (Fig. 1). It is easy to visualize that the shock
state may occur if there is no filling pressure as would
occur in severe dehydration or severe blood loss (i.e., the
tank has no gas).

Basically cardiogenic shock results from profound
reduction in cardiac output. This is usually caused by
marked reduction of left or right ventricular systolic function,
despite adequate ventricular filling pressures, and
there is a failure of compensatory vasoconstrictive mechanisms
that are overwhelmed by inappropriate vasodilation
in large, nonvital vascular beds. Thus this deprivescritical
areas like the heart ,brain, and kidney of perfusion.
Hochman points out that data from the shock trial and
registry indicate that cardiogenic shock is often not
simply due to extensive myocardial infarction with pump
failure, ‘‘but also involves inflammatory mediators. These
mediators induce nitric oxide synthase (iNOS) expression,
increasing nitric oxide (NO) and peroxynitrite levels,
resulting which results in further myocardial dysfunction
and failure of an appropriate peripheral circulatory
response.’’

III. MANAGEMENT
Most patients require an intra-aortic balloon pump and
IV vasopressor drugs to support blood perfusion to organs
and tissues. The opening of the obstructed artery using
balloon angioplasty with the insertion of stents has
improved survival. Because approximately 40% of cardiogenic
shock patients have occlusions in three coronary
arteries, emergency coronary artery bypass surgery is the
only measure that has improved survival in this group.
In the SHOCK trial, the overall 30-day mortality rate
was 47% in patients undergoing emergency revascularization
versus 56% in the medical stabilization group.
This improvement was maintained at the six-month
follow up.

IV. PERSPECTIVE AND RESEARCH
IMPLICATIONS
The incidence of cardiogenic shock will not decrease until
the main cause, which is obstruction to coronary arteries
by atheromatous plaque and thrombosis, is arrested.
Thrombolytic therapy is of little value and revascularization
with balloon angioplasty and coronary bypass surgery
can only be undertaken in special centers. The SHOCK
trial only studied 300 patients. More research is required
to assess if we could develop cardioactive agents to protect
the myocardium from necrosis during an occlusion of
a coronary artery.

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