failure of multiple organs and systems, and death (fig. 1).
Hypotension resulting from muscle mass loss may
cause hypoperfusion of still viable myocardial areas,
contributing to aggravation of the ventricular function. It is
estimated that a minimum loss of 40% of the left ventricular
mass is necessary for genesis of cardiogenic shock 17,18. The
loss of ventricular mass may be a consequence of a great
infarction in previously healthy patients, of small losses in
previously infarcted patients, or of large ischemic areas with
little necrosis in patients with advanced coronary atherosclerotic
disease 3. Compensatory mechanisms, such as the
activation of the autonomic nervous system and the reninangiotensin-
aldosterone system, promote increase in heart
rate, reflex vasoconstriction, sodium and water retention,
thus elevating the myocardial oxygen consumption 6,19.
The persistence of low cardiac output ends up accentuating
hypoxia, with accumulation of metabolites, acidosis, and
endothelial and cellular damage. This mechanism also
favors heart arrhythmias, which impair even more the
cardiac performance and may even lead to death. Failure of
multiple organs is the endpoint of this pathophysiological
situation.