Anesth Analg 1999;89:531
© 1999 International Anesthesia Research Society
LETTERS TO THE EDITOR
Right Ventricular Response to Aortic Unclamping During Aneurysmectomy
Paul G. Loubser, MD
Baylor Anesthesiology Houston, TX 77030
Ueda et al.’s (1) concise demonstration of increased right ventricular (RV) afterload after aortic unclamping (AU) during abdominal aortic aneurysmectomy (AAA) focuses attention on an important phenomenon, particularly when a when a rapid infusion system (RIS®; Haemonetics, Braintree, MD) is used to correct hypovolemia. The rapid increase in preload produced by the RIS® may predispose patients to RV failure after AU. This is illustrated in a study recently conducted in 10 patients undergoing thoraco-AAA (2). Approximately 5 min after AU, mean pulmonary arterial pressure increased 9.8 ± 2.3 mm Hg, pulmonary vascular resistance increased 63.2 ± 14.4 dyne.s.cm-5, whereas RV stroke work index increased 4.5 ± 0.88 g · m-1 · m-2.
The etiology of this phenomenon is multifactorial. Ueda et al. (1) performed blood gas analyses in their study but did not report any specific data. In our study (2), blood gas analysis revealed a decreased pH (0.2 ± 0.4), decreased base excess (5.9 ± 1.7 mmol/L), and increased PaCO2 (19.4 ± 4.2 mm Hg) after AU, which suggests that combined metabolic and respiratory acidosis are contributory physiologic mechanisms.
Unfortunately, Ueda et al. (1) do not provide any practical clinical solutions to ameliorating this phenomenon after AU, such as using a pharmacological buffer that does not generate CO2 (tromethamine) or the temporary application of a selective pulmonary vasodilator (nitric oxide).
References
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Ueda N, Dohi S, Akamatsu S, et al. Pulmonary arterial and right ventricular responses to prophylactic albumin administration before aortic unclamping during abdominal aortic aneurysmectomy. Analg 1998;87:1020–6.[Abstract/Free Full Text]
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Loubser PG, Pundit M. Hemodynamic consequences of rapid volume replacement following aortic cross-clamp release using the R.I.S.® [abstract]. Anesth Analg 1998;86 (Suppl):46.
Response
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
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, 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.
Inhaled 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.
References
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Ueda N, Dohi S, Akamatsu S, et al. Pulmonary arterial and right ventricular responses to prophylactic albumin administration before aortic unclamping during abdominal aortic aneurysmectomy. Analg 1998;87:1020–6.
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Kaimura M, Nishiwaki K, Shimada Y. Rise in pulmonary arterial pressure following release of aortic crossclamp in abdominal aortic aneurysmectomy. Anesthesiology 1988;69:257–60.[Medline]
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Paterson IS, Klausner JM, Pugatch R. Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery. Ann Surg 1989;209:231–6.[Web of Science][Medline]
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Fratacci MD, Frostell CG, Chen TY, et al. Inhaled nitric oxide: a selective pulmonary vasodilator of heparin-protamine vasoconstriction in sheep. Anesthesiology 1991;75:990–9.[Web of Science][Medline]
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Pepke ZJ, Higenbottam TW, Dinh XA, et al. Inhaled nitric oxide as a cause of selective pulmonary vasodilation in pulmonary hypertension. Lancet 1991;339:11173–4.
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Rodriguez RM, Pearl RG. Pulmonary hypertension and major surgery. Anesth Analg 1998;87:812–5.[Free Full Text]
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McLean RF, Prielipp RC, Rosenthal MH, Pearl RG. Vasodilator therapy in microembolic porcine pulmonary hypertension. Anesth Analg 1990;71:35–41.[Abstract/Free Full Text]
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