A 79-year-old man was admitted with severe aortic stenosis. He suffered from chest discomfort on minimal exertion. His medical history included 5-times percutaneous coronary stent insertions for unstable angina, chronic obstructive pulmonary disease, atrial fibrillation, and atherosclerosis obliterans. Pre-procedural echocardiography showed severe aortic stenosis (severe thickened and calcified aortic valve, aortic valve area = 0.72 cm² , aortic annulus = 22 mm) and mild to moderate aortic regurgitation, moderate tricuspid regurgitation, both atrial enlargement, and concentric left ventricular hypertrophy. However, left ventricular systolic function (ejection fraction = 63%) and right ventricular systolic pressure (28 mmHg estimated by the maximal velocity of tricuspid regurgitation) were in normal range. The estimated logistic Euroscore of the patient was 29.8%. The cardiologists recommended transapical TAVI instead of conventional surgery because the patient was considered as the high-risk population.

After placing an invasive arterial catheter through a brachial artery, anesthesia was induced with intravenous midazolam, etomidate, and rocuronium. It was maintained with sevoflurane and a continuous infusion of remifentanil. A pulmonary artery catheter was placed through right internal jugular vein, and a transesophageal echocargiographic (TEE) probe was inserted. After a left anterior mini-thoracotomy, an angiocatheter was inserted through the apex of the left ventricle. A guidewire was passed through the aortic valve and arch, and the tip was positioned in the abdominal aorta for stability. Following the two times of rapid ventricular pacing (200 beats/min) for 10 seconds, the balloon valvuloplasty was performed. Norepinephrine (0.02-0.05 mcg/kg/min) was continuously infused for maintaining blood pressure and norepinephrine 5 mcg was successively injected twice prior to RVP for balloon valvuloplasty. From anesthetic induction to rapid ventricular pacing, the patient's vital signs were well maintained (systolic blood pressure, 90 to 144 mmHg; diastolic blood pressure, 46 to 70 mmHg; central venous pressure, 7 to 12 mmHg; mean pulmonary arterial pressure, 20 to 22 mmHg; and heart rate, 68 to 110 beats/min). In addition, the mean arterial pressure was also maintained at around 50 mmHg, during rapid ventricular pacing.

Following the balloon valvuloplasty with rapid ventricular pacing, the mean blood pressure dropped to below 40 mmHg and did not recover. At the same time, central venous and the mean pulmonary arterial pressures were raised up to 22 mmHg and 44 mmHg, respectively. TEE showed the severe global hypokinesia. Two minutes after a rapid ventricular pacing, ventricular fibrillation was developed. Several attempts of defibrillation failed to restore the sinus rhythm. Emergent extracorporeal membrane oxygenation (ECMO) device was initiated immediately, through femoral artery and vein. Coronary angiography showed normal coronary arterial flow. After starting the support by ECMO, the patient's hemodynamics became stable. A 26-mm Sapien transcatheter heart valve (Edward Lifesciences, Irvine, CA, USA) was deployed under the ECMO support. TEE and angiography showed merely minimal aortic regurgitation. The patient was transferred to an intensive care unit for further supportive care. However, regardless of the ECMO support and supportive medical treatments, he did not recover from the state of heart failure. Finally, he died from cardiogenic shock and heart failure on post-procedure day 4.

In this mortality case, we experienced an unexpected event of fatal hemodynamic collapse, which developed immediately after a rapid ventricular pacing, although the recommended anesthetic managements were applied. Previously, there has been a case report that described the severity of cardiovascular compromise after a valve implantation due to the coronary arterial occlusion [11]. However, in our case, coronary arterial blood flow was normal.

Generally, for TAVI procedure, similar general anesthetic technique for high risk conventional aortic valve replacement is recommended [12]. In addition, bolus administration of a vasopressor prior to, or immediately after, a rapid ventricular pacing has been suggested to maintain coronary perfusion pressure [2,12]. Continuous monitoring of TEE is also strongly recommended, and a hybrid operating room, which is able to initiate cardiopulmonary bypass or to convert into conventional surgery, is considered as the ideal place for the TAVI procedure [2,12]. Those recommendations were all achieved in this case. Therefore, we'd like to evaluate the possible causes of this fatal event.

First, transapical approach might be potentially harmful to the heart because it involves the introduction of a large catheter through the ventricular apex. An inevitable introduction of large-bore catheter during transapical TAVI could cause myocardial damage, followed by arrhythmia [5,13]. Second, we focused on the vague point of recommended anesthetic protocols for TAVI. Although an administration of a bolus vasopressor is generally advocated, the amount of vasopressor should be titrated optimally in these patients because a relatively small dose would lead to insufficient coronary perfusion during a rapid ventricular pacing, and too much would cause severe elevation in the pulmonary arterial pressure [14,15]. In addition, an increase in pulmonary arterial pressure would worsen the right ventricular contractility and cardiac output [14,15]. However, to our knowledge, there is no recommendation for the individual optimal dose of vasopressor during a rapid ventricular pacing essential to the TAVI procedure. Moreover, the "optimal" dose of vasopressor would likely be different in patients because of the individual variation. Additionally, cardiac output is absent during rapid ventricular pacing. Without cardiac output, it would be questionable whether it is possible to predict the appropriate amount of vasopressor for the adequate coronary perfusion, as well as to preserve the coronary flow merely by maintaining the mean arterial pressure of around 50 mmHg.

In conclusion, the anesthesiologists should keep in mind that the fatal hemodynamic collapse can develop after a rapid ventricular pacing, despite the strict adherence to currently-recommended anesthetic protocols. In addition, further studies would be recommended to find the individual optimal dose of vasopressor for more successful anesthetic management of TAVI procedure.