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Ann Thorac Surg 1996;61:1051-1052
© 1996 The Society of Thoracic Surgeons
Department of Surgery, Harvard Medical School and Massachusetts General Hospital, Boston, Massachusetts
The study by Fullerton and associates [1] published in this issue of The Annals represents a significant step forward in the management of right heart failure. This clinical problem has vexed cardiac surgeons for decades, initially in the setting of operations for advanced mitral valve disease, after embolectomy for acute pulmonary embolism, and after certain operations for congenital heart disease. In recent decades, right heart failure has been recognized as a significant source of morbidity and mortality after heart transplantation, and after the institution of left ventricular mechanical assistance. Techniques to manage this often difficult problem can greatly benefit these clinical areas.
The traditional therapeutic strategies for managing right heart failure have focused on the use of various agents that decrease pulmonary vascular resistance and therefore, right heart afterload. However, until recently, vasodilator agents used to treat right heart failure were nonspecific; that is, agents such as tolazoline, nitroprusside, or nitroglycerin dilate not only the pulmonary vascular bed, but also the systemic vascular bed. Very early studies have suggested a possible relationship between systemic hemodynamics and right heart performance [2]. As an extension of these early studies, my colleagues and I showed previously that right heart performance is directly related to systemic pressure, and that the mechanism may involve the perfusion of the right ventricular (RV) free wall. With increasing RV afterload, failure occurs and is associated with ischemia of the RV free wall; by increasing systemic pressure, ischemia and failure can be reversed, suggesting that ischemia be the mechanism of failure in RV overload [3]. Increased RV afterload and preload can further complicate matters by impeding the circulation to the RV free wall [4].
The determinants of RV function and the mechanisms involved in RV failure are undoubtedly more complex. Subsequent studies have shown that the relationship between left and right heart hemodynamics is influenced by the pericardium: in systems with a closed pericardium, left heart hemodynamics have much more profound effect on right heart performance as compared with systems with an open pericardium [5], suggesting the role of ventricular interaction or ventricular septal shift as determinants of maximal RV function.
Because of these findings, two important principles have emerged in the management of right heart failure: (1) RV afterload must be reduced and (2) systemic pressure must be maintained or increased. Traditional therapies using nonspecific vasodilators are often ineffective for managing RV failure because in addition to decreasing RV afterload, they decrease systemic pressure and, therefore, reduce maximal RV performance. An early strategy that has been devised to meet these physiologic goals involves the use of prostaglandin E1 infusion into the right side of the circulation to decrease RV afterload, with its effects on the systemic circulation counterbalanced by left-sided infusion of norepinephrine [6]. Although this strategy is useful in some circumstances, it requires considerable titration to achieve the desired physiologic effects; therefore, many find this technique cumbersome.
A significant advance in managing pulmonary hypertension was the discovery that inhaled nitric oxide can profoundly and selectively dilate the pulmonary circulation [7]. Because of its efficacy, this agent has been used for the treatment of pulmonary hypertension and RV failure in a variety of clinical settings. The selectivity of this agent often results not only in decreased RV afterload, but also in an increase in RV (and hence cardiac) output, which can result in increased systemic pressure, thus augmenting RV performance by a second mechanism. However, this agent is an unstable gas that is most readily administered to intubated patients. Dependence and withdrawal phenomena have been observed after prolonged use, making weaning from this agent sometimes challenging. The need to scavenge exhaled gas remains a significant issue. For these reasons, many have found use of this agent cumbersome or difficult.
The application of adenosine by Fullerton and associates for the treatment of postoperative pulmonary hypertension represents a significant advance in the treatment of RV failure. They showed that central venous infusion of adenosine at a dose of 50 µg•kg-1•min-1 can produce substantial decreases in pulmonary vascular resistance and an increase in cardiac output without diminishing systemic hemodynamics. Thus, they have achieved RV afterload reduction while maintaining an important determinant of maximal RV function: systemic perfusion pressure. They demonstrated acute efficacy similar to that observed with nitric oxide inhalation without the administration limitations imposed by an inhaled agent. Although Fullerton and associates have not addressed the issues of prolonged infusion, tachyphylaxis, and withdrawal, their acute findings suggest that adenosine may be an ideal agent for managing right heart failure after heart operations.
Footnotes
Address reprint requests to Dr Vlahakes, Department of Surgery, Massachusetts General Hospital, EDR105, Boston, MA 02114-2696.
References
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 Y. Jeon, J. H. Ryu, Y. J. Lim, C. S. Kim, J.-H. Bahk, S. Z. Yoon, and J. Y. Choi Comparative hemodynamic effects of vasopressin and norepinephrine after milrinone-induced hypotension in off-pump coronary artery bypass surgical patients. Eur. J. Cardiothorac. Surg., June 1, 2006; 29(6): 952 - 956. [Abstract] [Full Text] [PDF]
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