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.