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CardiothoracicAnesthesia
VOL 4, NO 6, SUPPL 5
Management
DECEMBER 1990
of Surgical
Introduction
N 1908, WHEN the symptoms of the low cardiac output syndrome were first described,
little was known about the underlying pathophysiology of congestive heart failure. Since then,
ongoing research has led to better understanding
of the etiology of this disorder and the discovery
of many treatment approaches for the management of the decreased myocardial function that
is observed in this syndrome.
In the cardiac surgical patient, the operative
procedure itself may cause the low cardiac output
syndrome, particularly in patients with poor
ventricular function. Following cardiac surgery,
a direct myocardial insult can occur, which decreases contractility. Cardiac output then decreases and dysrhythmias may result. Contractility is reduced further, filling pressures increase,
and perfusion pressure decreases, further perpetuating the downward spiral of the low cardiac
output syndrome. An appropriate management
strategy needs to be developed to prevent this
downward spiral. The classic pharmacological
management tool has been inotropes.
The ideal pharmacological agent would
improve cardiac output by altering preload, afterload, and contractility without triggering
tachycardia or dysrhythmias or increasing myocardial oxygen consumption. Catecholamines,
which stimulate /3,- and &-receptors and often
cu-receptors, alter contractility but may cause
dysrhythmias and increases in heart rate and
myocardial oxygen consumption. This result may
further compromise the balance of myocardial
oxygen supply and demand and further exacerbate ventricular dysfunction.
The phosphodiesterase-III (PDE-III) inhib-
No 6, SuppI
(December), 1990: p 1
Jerrold H. Levy, MD