Conventional cardiopulmonary resuscitation-induced refractory cardiac arrest due to latent left ventricular outflow tract obstruction due to a sigmoid septum: a case report

Patients with left ventricular outflow tract obstruction who do not exhibit a dynamic pressure gradient at rest, experience pressure gradient increases of ≥ 30 mmHg only during specific situations; this is called latent left ventricular outflow tract obstruction. It is provoked by increased cardiac contraction and preload and afterload depletion. There are a few reports of patients with it developing cardiac arrest. We present a case of latent left ventricular outflow tract obstruction in which the patient with a sigmoid septum experienced refractory pulseless electrical activity due to conventional advanced cardiac life support.

A 73-year-old Asian woman on escitalopram and lorazepam was transported to our hospital for chest and back pain with altered consciousness. On arrival, she was in shock and developed pulseless electrical activity. After initiation of conventional cardiopulmonary resuscitation according to adult advanced cardiovascular life support guidelines, she could not regain spontaneous circulation. She was ultimately resuscitated via venoarterial extracorporeal membrane oxygenation initiation. The only abnormal laboratory result at admission was anemia. Her hemodynamic status stabilized after red blood cell transfusion, and venoarterial extracorporeal membrane oxygenation was subsequently terminated. Transthoracic echocardiography showed a sigmoid septum; dobutamine-infused Doppler echocardiography revealed a significant outflow gradient, and continuous monitoring showed Brockenbrough–Braunwald sign, which confirmed a diagnosis of latent left ventricular outflow tract obstruction due to a sigmoid septum. As a result, carvedilol and verapamil were initiated. A follow-up dobutamine-infused Doppler echocardiography showed a reduction of outflow gradient, and she was discharged without any sequelae. Latent left ventricular outflow tract obstruction worsened due to increasing cardiac contraction and the depletion of preload and afterload. Depleted preload occurred due to dehydration and anemia, whereas depleted afterload occurred due to the prescribed drugs, which subsequently caused pulseless electrical activity. Moreover, β-stimulation from the adrenaline probably enhanced the hypercontractile state and caused refractory pulseless electrical activity in our case.

Patients with latent left ventricular outflow tract obstruction can progress to cardiogenic shock and pulseless electrical activity due to increased cardiac contraction and depletion of preload and afterload. We should consider the patient’s underlying conditions that induced pulseless electrical activity.