CORRESPONDENCE
Venous Return after Cross-Clamping To the Editor: In response to the letter to the editor entitled “Venous Return after Cross-Clamping” (Ann Thorac Surg 33:418, 1982), we have not encountered massive venous return with cardiac distention in coronary bypass surgery, as observed by Dr. Theman and his colleagues. We have, however, seen ventricular dilatation in coronary revascularization patients who have some degree of unrecognized aortic insufficiency at the time of cross-clamp removal. This occurs if the heart slows, fibrillates, or is unable to cope with the amount of blood returning to the left ventricular cavity. Left ventricular dilatation can prevent pulmonary venous drainage, if substantial, into the left ventricular cavity, thereby increasing pulmonary artery pressure with subsequent right ventricular distention from undrained coronary or other venous return. We doubt the explanation of venous return offered by the authors. If true, the phenomenon should occur with much greater frequency, since the operation is done in the same way in thousands of patients. However, this complication has not been reported as occurring with any frequency, so we doubt that the mechanism exists. In support of our proposition that unrecognized aortic insufficiency was the real problem in the patients mentioned in Dr. Theman’s letter is the fact that he and his co-workers could resolve the massive venous return by left ventricular venting, which would, of course, help prevent left ventricular distention. Most cardiologists do not do an aortic root injection during coronary angiography, and a moderate degree of aortic insufficiency can go undetected prior to institution of cardiopulmonary bypass. Even then, this insufficiency may be missed and can cause problems once the aortic cross-clamp is removed, before the heart is able to contract and adequately evacuate the left ventricle. This could result in a serious problem only if the left ventricle is not vented in coronary revascularization procedures. We are eager to read alternative responses from other surgeons.
John H . Rousou, M . D . Richard M . Engelman, M . D . Cardiac Surgery Department Baystate Medical Center 759 Chestnut St Springfield, M A 01 107
To the Editor: I have encountered two instances of the condition described by Theman and associates-perhaps with a 331
lesser degree of ventricular distention, since the right ventricle did not rupture. In the first patient, a small venous line air lock that had been overlooked enabled flows to continue at a rate close to 3 L/min. Blood appeared to be accumulating in the right atrium and ventricle at the time the aorta was unclamped. The heart was not beating during this period (nonvented), and the exclusion clamp had been applied for construction of the proximal anastomoses. The problem was corrected as the heart began to beat and the air lock became evident. In the second patient, what appeared to be right atrial and ventricular distention occurred to a severe degree when the aorta was unclamped and an exclusion clamp applied to a rather short ascending aorta. The distention, I think, was related to the clamp impinging on the aortic valve, with some degree of aortic insufficiency created by distortion of the aorta in a heart that was recovering from cardioplegic arrest and had not resumed beating. After sinus rhythm was established, right ventricular distention still occured despite venous drainage. This was corrected when the exclusion clamp was removed. I have not encountered this situation since the introduction of a single period of aortic cross-clamping for construction of all distal and proximal anastomoses in coronary surgery. Tomas Antonio Salerno, M . D . , F.R.C.S.(C) Department of Surgery Royal Victoria Hospital 687 Pine Ave W Montreal, PQ, Canada
To the Editor: We read with interest the letter from Theman and colleagues describing their experience with massive cardiac distention following release of the aortic cross-clamp. We believe we have a more mechanistic explanation of the problem. A modest fall in aortic pressure is normal after this maneuver, because the coronary vascular bed with the attendant reactive hyperemia that occurs even after cardiac arrest, is restored to the perfusion circuit. The authors postulate that in certain patients the aortic arch baroreceptors are “supersensitive” to this decrease in perfusion pressure and respond with severe venoconstriction. Because perfusion flow rate is increased to 2.6 L/min/m2 to facilitate rewarming at this time, the authors implicate massive system venous return overwhelming the capacity of the venous cannula as an etiological factor in cardiac distention. Over the past year, we have noted a similar phenomenon in some patients undergoing coronary revascularization, but we think the problem is due to augmented coronary sinus flow that cannot be