Key result
LV failure due to myocardial contractile and load imbalance primarily drives acute pulmonary edema.
Describes the mechanism of acute pulmonary edema secondary to congestive left ventricular failure as an imbalance between myocardial contractile strength and load.
Emphasizes load reduction in acute pulmonary edema management; confirms classic mechanism but leaves open needs for targeted intervention trials.
Acute pulmonary edema is a disorder in which L there is sudden and relatively rapid transudation of fluid from the pulmonary capillary bed into the alveolar spaces. Whereas left ventricular failure is the usual cause of acute pulmonary edema, it also occurs after a variety of noncardiac disturbances, such as inhalation of irritating gases, pulmonary embolism, and intracranial hemorrhage. Instances of acute pulmonary edema secondary to disorders of atrial and ventricular rhythm or to mechanical interference with pulmonary venous drainage (mitral stenosis, stenosis of pulmonary veins) represent special conditions. This communication is concerned primarily with pulmonary edema secondary to congestive left ventricular failure.1-3 Mechanism The fundamental disorder in acute pulmonary edema is failure of the left ventricle to serve as an effective pump, due to imbalance between myocardial contractile strength and myocardial load. Such an imbalance is, in turn, related to a loss or damage of myocardial contractile units.
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George E. Burch (1969) conducted a review in Acute pulmonary edema. Acute pulmonary edema is primarily caused by left ventricular failure due to an imbalance between myocardial contractile strength and load.
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