8Part I / Introduction
ischemia, which can then further impair its pumping performance. Timely treatment
should therefore be directed at interrupting the vicious cycle by maintaining the coro-
nary perfusion pressure, thereby ensuring continued cardiac viability. Measures
required may include urgent coronary revascularization to salvage threatened viable
myocardium, mechanical circulatory support, control of bradyarrhythmia or tach-
yarrhythmia, removal and counteraction of negative inotropic effects, and correction
of metabolic derangement.
PATHOPHYSIOLOGY OF CARDIOGENIC SHOCK
There is more information about the pathophysiology of cardiogenic shock than can
be included in this chapter. Therefore, this chapter is necessarily selective and includes
only information that is directly relevant to the diagnosis and treatment of cardiogenic
shock in clinical practice.
Cardiac and Extracardiac Determinants
When diagnosing cardiogenic shock, it is important to determine whether the pre-
sentation of shock is truly cardiogenic. Central cardiac factors need to be distin-
guished from peripheral and extracardiac factors. The presentation of shock in a
coronary care unit does not necessarily preclude the occurrence of shock from other
causes than the heart, such as hypovolemic (absolute or relative) shock, septicemic or
anaphylactic shock, or shock secondary to a massive pulmonary embolism. It is also
possible that more than one type of shock can be present concurrently. Nevertheless,
because the heart is not the sole determinant of circulatory collapse, the central con-
tribution of cardiac function and its inadequacy must be considered in relation to the
state of the peripheries, including the vasculature, gas exchange, blood constituents,
and volume.
Other compounding factors such as intercurrent infection, anemia, hypoxia (sec-
ondary to respiratory diseases), hypothermia, hyperpyrexia, dysthyroidism, thiamine
deficiency, Addisonian crisis, or other systemic disorders may play a role. Prompt
recognition and identification of these compounding factors are necessary before
appropriate correction of these defects can be instituted. Drugs with myocardial
depressant actions or hypotensive agents (e.g., morphine, diamorphine, β-blockers,
arterial vasodilators, streptokinase) may be precipitating or contributory factors toward
the onset of shock. Prompt recognition, withdrawal, or counteraction of such harmful
effects of drugs may alter the nature and course of shock.
Etiology and Sequence of Events
In true cardiogenic shock, the initiating event occurs in the heart. Most clinicians
associate it with myocardial infarction, although the etiology of cardiogenic shock can
be the result of any defect in the heart, be it affecting the myocardial function (e.g.,
ischemia, infarction, stunning, contusion, arrhythmia, heart block, myocarditis), or the
integrity of valves (e.g., chordal or papillary muscle rupture, acute regurgitation in
endocarditis), or the integrity of cardiac structures (e.g., acute ventricular septal defect
[VSD], acute tamponade). Urgent measures should be put in place to deal with these
lesions, but while the definitive procedures are being planned and arranged, it is crucial
to deal with the hemodynamic and metabolic consequences of the shock.
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