Pacemaker syndrome is a phenomenon associated with suboptimal atrioventricular (AV) synchrony that leads to loss of atrial “kick”.
Pacemaker syndrome can occur in any implantable device, but is most commonly seen in the setting of a single chamber device with ventricular sensing and pacing lead. Since there is no atrial sensing lead to guide the ventricle, the ventricle contracts at the programmed rate regardless of the timing of atrial contraction. This leads to loss of AV synchrony which leads to a loss in stroke volume and cardiac output.
Neurologic: Fatigue, memory loss, confusion, and often transient blackouts
Cardiovascular: Exertional dyspnea, orthopnea, palpitations, a decrease in exercise capacity, syncope
Neck vein distension and cannon wave in JVP tracing
Precordial examination may reveal regurgitant murmurs and variability in the intensity of first heart sound
Pulsatile liver and ascites may be present in severe cases
Lower extremity edema
Neurologic examination may reveal confusion, dizziness, or altered mental status
pacing spikes with adequate capture but no relation/synchrony between P waves and QRS complexes
ECG 1A Patient with dual chamber pacemaker without any pathological signs and symptoms
ECG 1B The same patient with atrial capture loss. In this case, pacemaker ventricular stimulation became dissociated from atrial depolarization, leading to AV dyssynchrony and symptoms of Pacemaker syndrome.
upgrade to a dual chamber device is necessary for single-chamber pacemakers
switching to DDD or VDD modes in a dual chamber device
if loss of capture in atrial lead is documented, increase the voltage/duration of atrial stimulation to restore atrial capture, or change from bipolar to unipolar setting
if the patient has LV dysfunction and low EF, then a CRT will be the preferred device for implantation/up-gradation