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Acute pulmonary edema after percutaneous balloon valvuloplasty for pulmonary valve stenosis.

A 66-year-old man was scheduled for percutaneous balloon valvuloplasty of pulmonary valvular stenosis under general anesthesia in the cardiac catheterization laboratory. The patient had a significant history of cardiorespiratory disease. In 1944, his family physician detected a heart murmur, and in 1955, the patient was referred to a cardiologist and told he had “a narrowed valve.” The patient was then lost to follow-up, and his old hospital records were lost. The patient claimed to have been asymptomatic until he sustained an inferior myocardial infarction in 1999 and was referred to this hospital for further investigations. On admission, the patient admitted to smoking 15 cigarettes per day until his myocardial infarction, and his exercise tolerance was reduced to less than 500 meters during the last few years. His medications were aspirin and atenolol. On examination, the patient was noted to be cyanotic, had clubbing of the fingers, had a raised jugular venous pressure, and had bilateral basal crepitations on chest auscultation. The patient had a soft ejection systolic murmur with a normal second heart sound, and there was no right ventricular heave. Further investigations revealed polycythemia (hemoglobin, 19 g/dL; hematocrit, 57.3%), mild renal impairment (serum creatinine, 143 mmol/ L), and arterial blood gases and lung function testing as shown in Tables 1 and 2. A chest radiograph was normal, and a 12-lead electrocardiogram showed T-wave inversion in leads I through III and no evidence of right ventricular hypertrophy. At cardiac catheterization, the patient was found to have moderate left ventricular dysfunction, with a mild stenosis of the left anterior descending coronary artery and complete occlusion of the dominant right coronary artery. There was a severe pulmonary valve stenosis with a peak-to-peak systolic gradient of 90 mmHg (Fig 1). A small atrioseptal defect or patent foramen ovale was noted and confirmed with transesophageal echocardiography. Transesophageal echocardiography did not show any evidence of right or left ventricular dysfunction, and left ventricular ejection fraction was calculated to be 60%. Oxygen saturations and pressure measurements are shown in Tables 3 and 4. It was decided that the pulmonary stenosis should be treated by percutaneous balloon valvuloplasty. Standard anesthetic monitoring was applied, including a 5‐lead electrocardiogram and direct arterial blood pressure measurement via a 20G radial artery catheter inserted under local anesthesia. Pulse oximetry in air showed a saturation (SpO2) of 92%. After preoxygenation (SpO2 increased to 100%), anesthetic induction consisted of fentanyl, 100 g; etomidate, 16 mg; and vecuronium, 8 mg. After endotracheal intubation, the lungs were ventilated with oxygen, air, and isoflurane, 0.8% to 1.4%, for maintenance of anesthesia. The right internal jugular vein was cannulated with 2 long 14G catheters for monitoring of central venous pressure and easy administration of drugs. During the procedure, 1000 mL of lactated Ringer’s solution was infused. Anesthesia was uneventful, and the angiographic findings compared well with the previous measurements. Balloon pulmonary valvotomy using a 25 mm 40 mm balloon resulted in the peak-to-peak gradient falling to 12 mmHg (Figs 2 and 3, Table 5). The patient’s other cardiovascular parameters were unchanged, and PaO2 improved immediately to 9.65 kPa. The procedure time was 15 minutes. The small atrial septal defect was of little or no significance, and no further procedures were carried out. Neuromuscular blockade was reversed with glycopyrrolate, 500 g, and neostigmine, 2.5 mg, and the patient’s lungs were ventilated with oxygen until adequate spontaneous ventilation was restored and the patient’s trachea could be extubated. Total anesthetic time was 45 minutes. The patient was transferred to the postanesthesia care unit to await transfer to the ward. Within 5 minutes of admission to the postanesthesia care unit, the patient developed a tachycardia (120 beats/min), his respiratory rate increased to 30 breaths/min, and SpO2 decreased to 85%, despite supplemental oxygen by facemask.