Abstract
Reduced cardiac output during cross-clamping of the aorta has been attributed to the
increased afterload. A second mechanism involves reperfusion of the ischemic lower
torso. The author studied cardiac contractility during and following one hour of infrarenal
aortic cross-clamping. Methods: Ultrasonic crystals were implanted on the anterior
and posterior aspects of the left ventricle in 11 anesthetized dogs to measure the
external minor diameter. A pressure transducer was placed in the left ventricular,
and aortic and Swan-Ganz catheters were introduced. The animals were divided into
two groups: A Clamp group (n=6) sustaining one hour of infrarenal aortic cross-clamping,
and a Control group (n=5) who underwent a sham operator. Hemodynamic data were collected
during the one hour of cross-clamping and for the next two hours.
Results: Cardiac function did not change significantly at one and two hours following
removal of the clamp. Cardiac output decreased from 1.70±0.22 L/min at baseline to
1.30±0.14 and 1.19±0.10 at one and two hours, respectively, following removal of the
clamp. The end-systolic pressure-volume relationship (Emax) decreased from 29.7±6.3
mm Hg/mm at baseline to 18.1±3.6, 16.5±4.6, and 17.2±3.5 at thirty minutes, one hour,
and two hours, respectively, after declamping. The Control group showed no significant
changes in cardiovascular parameters at any time during the experiment. Conclusion:
Infrarenal aortic cross-clamping causes myocardial depression following declamping
but not during clamping.
