Myocardial depression following declamping of the infrarenal aortic cross-clamp

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.