The Annals of Thoracic Surgery, Vol 29, 42-48, Copyright © 1980 by The Society of Thoracic Surgeons
Extended evaluation of effects of anoxia on ventricular performance and compliance
FH Levine, JG Copeland, DB Melvin and EB Stinson
Eight dogs were prepared by implanting a left ventricular pressure
transducer, aortic flow probe, and endocardial ultrasound crystals across
the maximum transverse left ventricular diameter. In an unanesthetized
state, the dogs were evaluated at rest and with acute volume loading, both
before ischemic cardiac arrest and sequentially (2, 4, 6, 12, 24, and 48
hours) after 20 minutes of arrest during normothermic cardiopulmonary
bypass. At a left ventricular end- diastolic diameter comparable to
preoperative levels, left ventricular systolic pressure, heart rate, and
rate of rise of left ventricular pressure were not changed, but at 2 to 6
hours there was a significant decrease in cardiac output (p less than
0.01), left ventricular stroke work (p less than 0.01), ejection fraction
(p less than 0.05), maximum rate of systolic diameter shortening (p less
than 0.05), and circumferential fiber shortening (p less than 0.05). They
gradually returned to control levels by 24 hours postoperatively. Left
ventricular compliance, as measured by left ventricular end-diastolic
pressure at a set end-diastolic diameter and by left ventricular diastolic
pressure/diameter, was reduced at 2 hours (p less than 0.01) and gradually
returned to control values at 48 hours. Thus, reversible myocardial injury
due to anoxia is associated with both decreased contractility and
compliance, with resultant depressed left ventricular performance for 24 to
48 hours after injury.
