# Cardiac Arrest During the Medical Management of Left Ventricular Outflow Tract Obstruction Following the Transcatheter Aortic Valve Implantation

## TL;DR

A patient experienced cardiac arrest after treatment for a heart condition following a valve implant, highlighting risks of using drugs that reduce heart contractility.

## Contribution

Highlights the risk of cardiac arrest from excessive negative inotropic therapy in managing post-TAVI left ventricular outflow tract obstruction.

## Key findings

- Excessive negative inotropic effects may cause cardiac arrest despite improving left ventricular outflow tract obstruction.
- Refractory hypotension improved with adrenaline, dobutamine, and phenylephrine after cardiac arrest.
- Hemodynamic stability was achieved without further need for negative inotropes.

## Abstract

Systolic anterior motion of the mitral valve and left ventricular outflow tract obstruction are complications following transcatheter aortic valve implantation and can lead to hemodynamic collapse. Medical management for those complications is usually centered on a reduction in left ventricular contractility with negative inotropes. An 88-year-old woman underwent transcatheter aortic valve implantation for severe aortic stenosis. Hemodynamic collapse and exacerbation of mitral regurgitation occurred immediately after valve implantation. For suspected left ventricular outflow tract obstruction, medical management centered on negative inotropes was performed. Hemodynamics and left ventricular outflow tract obstruction improved over time; however, the oxygen supply-demand imbalance progressed. On postoperative day 5, the patient suddenly went into pulseless electrical activity. Cardiopulmonary resuscitation was performed for three minutes, resulting in the return of spontaneous circulation. Subsequent refractory hypotension and oxygen supply-demand imbalance improved with continuous infusion of adrenaline, dobutamine, and phenylephrine. Her hemodynamics remained stable after she was weaned off the pressor infusions, and negative inotropes were not required again. In summary, the cause of cardiac arrest was possibly due to excessive negative inotropic effects even though the effects contributed to improvement of left ventricular outflow tract obstruction. Anesthesiologists and intensivists should recognize the risk of cardiac arrest induced by negative inotropic effects and use negative inotropes with rigorous hemodynamic monitoring, even when left ventricular outflow tract obstruction is treated effectively.