A 65-year-old male who complained of dyspnea was diagnosed with hypertrophy based on X-ray findings and was hospitalized emergently for an acute heart failure. His past medical history included hypertension and 8 years of hemodialysis treatment due to chronic kidney disease (stage 5GD) by unknown causes. His height and weight were 176 cm and 55 kg, respectively. His laboratory data were abnormal as follows: C-reactive protein, 1.84 mg/dl; N-terminal pro-brain natriuretic peptide, > 35,000 pg/ml; troponin T, 0.111 ng/ml; BUN, 58.2 mg/dl; and Cr, 9.2 mg/dl. Cardiothoracic ratio was 63% based on chest X-ray with butterfly shadow. Electrocardiogram indicated a sinus rhythm, a heart rate of 101 bpm, and a QS pattern in V2–3. Transthoracic echo showed the following findings: ejection fraction (EF), 59%; left ventricular internal dimension in diastole/systole (LVDd/Ds), 57/30 mm; interventricular septum thickness, 20 mm; posterior LV wall thickness, 15 mm; diameter of left atrium, 56 mm; LV mass index, 201 g/m2; aortic valve pressure gradient, 104/54 mmHg (max/mean); aortic valve area, 0.54 cm2; and aortic regurgitation mild, mitral regurgitation mild, and tricuspid regurgitation mild (pressure gradient, 27 mmHg). The patient’s coronary angiography result indicated stenosis of left anterior descending branch #6, 75%, and left circumflex coronary artery #11, 75%, and computed tomography revealed left-sided pleural effusion. Finally, he was diagnosed with aortic valve stenosis (AS) and angina pectoris, and it was decided to perform elective surgery of aortic valve replacement (AVR) and cardiac artery bypass.
After the initiation of CPB and aortic clamping, cardiac arrest was induced immediately after cardioplegia infusion and maintained with 500–700 ml infusion every 30 min. Left internal thoracic artery–left anterior descending branch (LITA–LAD) and saphenous vein–right coronary artery (SVG–RCA) anastomoses and AVR (Magna EaseTM 23 mm) were performed. When the aortic forceps were declamped at 13:57 (marked “A” in Fig. 1), VF occurred immediately as shown in Fig. 1 (anesthetic record). Several attempts of EC with lidocaine (100 and 50 mg) and landiolol (2.5–15 mg) and three times of administrations of nifekalant (5–15 mg) were temporarily effective at 14:12–25 (marked “B”), and the patient ECG suggested sinus rhythm with premature ventricular counts. However, the sinus rhythm and VT occurred alternatively, and the rhythm subsequently changed to torsades de pointes (TdP), which might have occurred because of the overdose of nifekalant at around 14:55 (marked “C”). Therefore, we administered 2 g of magnesium sulfate followed by amiodarone three times, reaching a total of 450 mg (each dose of 150 mg), and initiated continuous infusion at 50 mg/h (c.f. Fig. 1). We also initiated the pacemaker (VVI setting) and IABP at 14:50 and 15:16 (marked “D” and “E”), respectively.
All these procedures appeared to be effective at terminating the VT and subsequently succeeded in weaning from CPB. Thus, the situation with the sinus rhythm was sustained until the end of surgery. During this period, we also took caution to maintain normothermia with no electrolyte imbalance. The flow of the two bypass grafts was assessed using a flowmeter, i.e., LITA–LAD, 50 ml/min, and SVG–RCA, 9 ml/min. Transesophageal echocardiography revealed only diffuse hypokinesis with approximately 20% of EF just after aortic declamping, which gradually improved toward the weaning of CPB to approximately 30% of EF. After admission to the intensive care unit (ICU), the patient showed no VF or VT under the continuous infusion of amiodarone (50 mg/h), and the IABP was withdrawn on postoperative day (POD) 1 and extubated on POD 2. The patient was discharged from the ICU on POD 3 and from the hospital on POD 12 without any complication.