London, UK
EditorPatients with long standing mitral valve disease are at risk of developing pulmonary hypertension, which may be a particular problem perioperatively at the time of cardiac surgery. As a phosphodiesterase type 5 pathway inhibitor, sildenafil may selectively reduce the pulmonary vascular resistance and thus have an important role to play in the management of this condition. We recently managed two patients who developed acute right ventricular dysfunction associated with systemic hypotension at the time of cardiac surgery (one at anaesthetic induction, one intraoperatively). Both responded favourably to nasogastric sildenafil therapy, with a significant reduction in pulmonary vascular resistance and improved haemodynamics.
The first patient was a 64-yr-old male who had had previous coronary artery bypass grafting and developed severe mitral regurgitation secondary to bacterial endocarditis. At right heart catheterization immediately before surgery, his pulmonary artery pressure (PAP) was 85/36 mm Hg (mean 58 mm Hg) and mean capillary wedge pressure (PCWP) was 32 mm Hg. Anaesthetic induction was achieved with propofol, pancuronium and alfentanil.
Bypass grafts were performed with mitral annuloplasty and quadrangular repair using cardiopulmonary bypass and intermittent fibrillation without a cross clamp. Immediate postoperative transoesophageal echocardiogram revealed minimal mitral regurgitation. An intra-aortic balloon pump was inserted before weaning off cardiopulmonary bypass. Immediately after coming off bypass, his systolic blood pressure fell to 70 mm Hg and norepinephrine, milrinone and epinephrine were prescribed. His right heart measurements were not significantly changed with a PAP of 80/42 mm Hg (mean 58 mm Hg) and a PCWP of 32 mm Hg. As we have had encouraging experience managing patients with other forms of pulmonary hypertension using sildenafil, and given some encouraging reports in the literature, we prescribed sildenafil 50 mg nasogastrically. Within 1 h, the PA pressure had fallen to 46/21 mm Hg (mean 29 mm Hg) with a mean PCWP of 18 mm Hg. The patient made an uneventful recovery and sildenafil 50 mg tds was continued for 6 weeks after surgery.
The second patient was a 65-yr-old male who had a tissue aortic valve replacement 18 yr previously and who subsequently developed severe aortic and mild to moderate mitral valve regurgitation with two vessel coronary artery disease. Redo aortic valve replacement and coronary artery bypass surgery was performed. Preoperative right heart catheterization showed a PAP of 78/20 mm Hg (mean 48 mm Hg) and mean PCWP of 24 mm Hg. Anaesthetic induction was achieved with propofol, pancuronium and alfentanil.
The PA pressure rose acutely on induction to 90 mm Hg accompanied by systemic hypotension. He remained hypotensive in spite of mechanical ventilatory support epinephrine and milrinone and a frusemide infusion was added. In view of persisting hypotension of 70/40 mm Hg with a systolic PAP of 8090 mm Hg sildenafil 50 mg was given nasogastrically. Within 30 min, the systolic PAP fell to 50 mm Hg, and the systemic systolic pressure rose to 100 mm Hg. Successful surgical intervention was performed. Sildenafil 50 mg tds nasogastrically, and subsequently orally, was continued for 6 weeks after surgery, and he made an uneventful recovery.
Pulmonary hypertension represents a significant risk to general anaesthesia and surgical intervention. Mitral valve disease is a recognized cause of pulmonary hypertension and induction of anaesthesia in these patients can sometimes produce cardiovascular collapse. In addition, myocardial insults can occur as a consequence of: stunning or reperfusion injury; the effects of cardiopulmonary bypass and myocardial handling; and acute changes in ventricular pressures and in end diastolic volume after valve surgery. Sildenafil causes selective inhibition of phosphodiesterase type 5 pathways and, as these pathways are largely confined to the lung and urological tract, sildenafil offers a therapeutic potential in the management of patients with pulmonary hypertension by causing selective vasodilatation.1 2 Some benefit has been shown using inhaled nitric oxide in managing patients with pulmonary hypertension associated with mitral valve disease.3 Given the pharmacological properties of nitric oxide and sildenafil, it is possible that these drugs could be synergistic. Sildenafil potentiates the effects of pulmonary cyclic guanosine monophosphate and enhances the vasodilatory effects of this pathway. In our patients who both had preoperative pulmonary hypertension and mitral valve disease, one deteriorated acutely at anaesthetic induction and the other immediately after coming off bypass. Given our background favourable experience with sildenafil in managing other patients with pulmonary hypertension, we prescribed it for both patients and each demonstrated a significant reduction in pulmonary vascular resistance with a rise in systemic blood pressure after its administration nasogastrically. We therefore suggest that sildenafil be considered for the management of selected patients with pulmonary hypertension who develop right ventricular dysfunction at induction or during cardiac surgery.
B. P. Madden
A. Sheth
T. B. L. Ho
J. E. S. Park
R. R. Kanagasabay
London, UK
References
1 Maxey TS, Smith CD, Kern JA, et al. Beneficial effects of inhaled mitric oxide in adult cardiac surgical patients. Ann Thorac Surg 2002; 73: 52932
2 Michelakis E, Tymchak W, Lien D, Webster L, Hashimoto K, Archer S. Oral sildenafil is an effective and specific pulmonary vasodilator in patients with pulmonary arterial hypertension: comparison with inhaled nitric oxide. Circulation 2002; 105: 2398403
3 Bhatia S, Frantz RP, Severson CJ, Durst LA, McGoon MD. Immediate and long-term hemodynamic and clinical effects of Sildenafil in patients with pulmonary arterial hypertension receiving vasodilator therapy. Mayo Clin Proc 2003; 78: 120713[ISI][Medline]