Case
A 58-year-old male with medical history of non-ischemic cardiomyopathy and American College of Cardiology / American Heart Association Stage D heart failure status post implantation of a HeartWare LVAD (HW-LVAD; Medtronic, Minneapolis, MN) as well as an ICD presented to the emergency room with multiple low-flow alarms over two days duration. On initial evaluation, the patient was awake and conversant with a mean arterial blood pressure (MAP) of 90mm of Hg, oxygen saturation of 97% on room air, and heart rate that could not be automatically determined on telemetry. His lungs were clear to auscultation and he had a normal LVAD hum over the precordium. His HW-LVAD interrogation displayed a flow rate of 2.9 liters/minute with multiple low-flow alarms (baseline flow rate of approximately 4 liters/minute) using a power of 3.8 watts at a speed of 2600 revolutions per minute (RPM). Flow waveform qualitatively appeared significantly dampened. Initial electrocardiogram (ECG) demonstrated disorganized rhythm (ECG 1) which was thought to be due to artifact from the LVAD, as it was markedly different from his prior ECGs. In order to confirm the underlying arrythmias, his ICD was interrogated, which was found to be at EOL and was unable to record any events. A bedside echocardiogram was performed, which showed rhythmic hypokinetic contraction of the left ventricle and regular opening and closing of the mitral valve (image 1, image 2). The apical 4-chamber view with perflutren lipid contrast (clip 1) and a parasternal long image without contrast (clip 2) also showed organized ventricular contractility. Therefore, emergent defibrillation was deferred as it was unclear whether the arrhythmia was atrial fibrillation (AF) distorted by artifact or ventricular fibrillation (VF) and because patient remained hemodynamically stable. Initial laboratory work was significant for serum creatinine of 2.7 mg/dL from baseline of 1.5-1.7 mcg/dL, potassium level of 4.9 mmol/L and magnesium level of 1.7 mg/dL. The patient received intravenous infusion of normal saline, cardiac electrophysiology was consulted, and the patient was admitted to the Intermediate Care Unit (IMC).
Subsequently low-flow alarms recurred without symptoms and MAP at that time remained preserved. Decreased flow rates were intermittently associated with loss of pulsatility on the LVAD monitor and drops in LVAD speed, concerning for suction events. His HW-LVAD speed was decreased to 2160 RPMs; however, due to persistence of low flow alarms and loss of pulsatility on the LVAD monitor, the patient was defibrillated at 200 J with subsequent conversion of irregular disorganized activity to normal sinus rhythm (ECG 2). Post defibrillation, his HW-LVAD flow rate improved to 3.5 liters/min along with restoration of baseline pulsatility. LVAD speed was increased back to 2600 RPMs, an intravenous amiodarone infusion was started, and the patient was transferred to the intensive care unit for closer monitoring. Subsequently, the patient underwent a ventricular tachycardia induction study which confirmed VF with successful defibrillation testing. His ICD generator was replaced.