Right Ventricular Response to Aortic Unclamping During Aneurysmectomy

In Response: Dr. Loubser correctly pointed out our important omission in our Discussion [1] as to the etiology of increased right ventricular (RV) afterload after aortic unclamping (XU) during anesthesia and surgery for patients undergoing aneurysmectomy (AAA). The etiology is multifactorial, and it has been speculated that the cause of this phenomenon is due to desaturated pulmonary artery blood [2], thormboxane A2 by the ischemia during the cross-clamping period [3]. Both the pulmonary return of venous blood associated with metabolic and respiratory acidosis (which could have occurred during the cross-clamping) may be one of the factors for developing pulmonary hypertension and RV afterload after XU. As shown in Table 1, we measured a series of arterial blood gas tensions and pH, and serum electrolytes and glucose for all patients studied. However, although a significant decrease in pH, increase in PCO2, decrease in HCO3-, and some increase in serum potassium concentration were present in our patients, because of relatively small changes, it is unlikely that the acidosis after XU is a main factor in this phenomenon.Table 1: Arterial Blood Gas Tensions and pHInhaled nitric oxide (NO) has been reported to be effective in reducing pulmonary hypertension without causing systemic vasodilation [4,5]. However, Rodriguez and Pearl [6] reported a case in which nitroglycerin was more effective than NO in treating pulmonary hypertension in a patient with AAA. We have had several patients in whom IV administration of prostaglandin E1 could ameliorate this increase in pulmonary arterial pressure after XU. Although prostaglandin E1, nitroglycerin, and sodium nitroprusside similarly produce a 30% reduction in mean systemic arterial pressure, prostaglandin E1 caused an equivalent amount of pulmonary and systemic vasodilation, as expressed by the pulmonary vascular resistance to systemic vascular resistance ratio, and nitroglycerin and sodium nitroprusside significantly increased the pulmonary vascular resistance to systemic vascular resistance ratio [7]. Thus, we believe that prostaglandin E1 may be a choice for this phenomenon, in which significant pulmonary hypertension could occur, associated with systemic hypotension after XU in AAA surgery. Norio Ueda, MD Shuji Dohi, MD Shigeru Akamatsu, MD Department of Anesthesiology and Critical Care Medicine; Gifu University School of Medicine; Gifu 500-8705, Japan