Pacemaker syndrome

Pacemaker syndrome

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]

Overview

Pacemaker syndrome is a disease that represents the clinical consequences of suboptimal atrioventricular (AV) synchrony or AV dyssynchrony, regardless of the pacing mode, after the pacemaker plantation.. It is an iatrogenic disease that is often underdiagnosed. In general, the symptoms of the syndrome are a combination of decreased cardiac output, loss of atrial contribution to ventricular filling, loss of total peripheral resistance response, and nonphysiologic pressure waves.

Individuals with a low heart rate prior to pacemaker implantation are more at risk of developing pacemaker syndrome. Normally the first chamber of the heart (atrium) contracts as the second chamber (ventricle) is relaxed, allowing the ventricle to fill before it contracts and pumps blood out of the heart. When the timing between the two chambers goes out of synchronization, less blood is delivered on each beat. Patients who develop pacemaker syndrome may require adjustment of the pacemaker timing, or another lead fitted to regulate the timing of the chambers separately.

Historical Perspective

Pacemaker syndrome was first described in 1969 by Mitsui et al. as a collection of symptoms associated with right ventricular pacing. The name pacemaker syndrome was first coined by Erbel in 1979. Since its first discovery, there have been many definitions of pacemaker syndrome, and the understanding of the cause of pacemaker syndrome is still under investigation. In a general sense, pacemaker syndrome can be defined as the symptoms associated with right ventricular pacing relieved with the return of A-V and V-V synchrony.

Pathophysiology

The loss of physiologic timing of atrial and ventricular contractions, or sometimes called AV dyssynchrony, leads to different mechanisms of symptoms production. This altered ventricular contraction will decrease cardiac output, and in turn will lead to systemic hypotensive reflex response with varying symptoms.

Loss of Atrial Contraction

Inappropriate pacing in patients with decreased ventricular compliance, which may be caused by diseases such as hypertensive cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and aging, can result in loss of atrial contraction and significantly reduces cardiac output. Because in such cases the atrias are required to provide 50% of cardiac output, which normally provides only 15% - 25% of cardiac output.

Cannon A Waves

Main article: Cannon A waves

Atrial contraction against a closed tricuspid valve can cause pulsation in the neck and abdomen, headache, cough, and jaw pain.

Increased Atrial Pressure

Ventricular pacing is associated with elevated right and left atrial pressures, as well as elevated pulmonary venous and pulmonary arterial pressures, which can lead to symptomatic pulmonary and hepatic congestion.

Increased Production of Natriuretic Peptides

Main article: Atrial natriuretic peptide

Main article: Brain natriuretic peptide

Patients with pacemaker syndrome exhibit increased plasma levels of ANP. That's due to increase in left atrial pressure and left ventricular filling pressure, which is due to decreased cardiac output caused by dyssynchrony in atrial and ventricular contraction. ANP and BNP are potent arterial and venous vasodilators that can override carotid and aortic baroreceptor reflexes attempting to compensate for decreased blood pressure. Usually patients with cannon a waves have higher plasma levels of ANP than those without cannon a waves.

VA Conduction

A major cause of AV dyssynchrony is VA conduction. VA conduction, sometimes referred to as retrograde conduction, leads to delayed, nonphysiologic timing of atrial contraction in relation to ventricular contraction. Nevertheless, many conditions other than VA conduction promote AV dyssynchrony.

This will further decrease blood pressure, and secondary increase in ANP and BNP.

Epidemiology and Demographics

The reported incidence of pacemaker syndrome has ranged from 2% to 83%. The wide range of reported incidence is likely attributable to two factors which are the criteria used to define pacemaker syndrome and the therapy used to resolve that diagnosis.

Risk Factors

• In the pre-implantation period, two variables are predicted to predispose to the syndrome. First is low sinus rate, and second is a higher programmed lower rate limit. In post-implantation, an increased percentage of ventricular paced beats is the only variable that significantly predicts development of pacemaker syndrome.

• Patients with intact VA conduction are at greater risk for developing pacemaker syndrome. Around 90% of patients with preserved AV conduction have intact VA conduction, and about 30-40% of patients with complete AV block have preserved VA conduction. Intact VA conduction may not be apparent at the time of pacemaker implantation or even may develop at any time after implantation.

• Patients with noncompliant ventricles and diastolic dysfunction are particularly sensitive to loss of atrial contribution to ventricular filling, where that highly increase the chance of developing the syndrome. This includes patients with cardiomyopathy (hypertensive, hypertrophic, restrictive) and elderly individuals.

• Other factors correlated with development of pacemaker syndrome include decreased stroke volume, decreased cardiac output, and decreased left atrial total emptying fraction associated with ventricular pacing.

Natural History, Complications and Prognosis

Complications

Studies have shown that patients with pacemaker syndrome and/or with sick sinus syndrome are at higher risk of developing fatal complications that calls for the patients to be carefully monitored in the ICU. Complications include:

• Atrial fibrillation
• Thrombo-embolic events
• Heart failure

Diagnosis

Symptoms

No specific set of criteria has been developed for diagnosis of pacemaker syndrome. Most of the signs and symptoms of pacemaker syndrome are nonspecific, and many are prevalent in the elderly population at baseline. In the lab, pacemaker interrogation plays a crucial role in determining if the pacemaker mode had any contribution to symptoms.

Symptoms commonly documented in patients history, classified according to etiology:

• Neurological - Dizziness, near syncope, and confusion.

• Heart failure - Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and edema.

• Hypotension - Seizure, mental status change, diaphoresis, and signs of orthostatic hypotension and shock.

• Low cardiac output - Fatigue, weakness, dyspnea on exertion, lethargy, and lightheadedness.

• Hemodynamic - Pulsation in the neck and abdomen, choking sensation, jaw pain, right upper quadrant (RUQ) pain and headache.

• Heart rate related - Palpitations associated with arrhythmias

In particular, the examiner should look for the following in the physical examination, as these are frequent findings at the time of admission:

• Vital signs may reveal hypotension, tachycardia, tachypnea, or low oxygen saturation.

• Pulse amplitude may vary, and blood pressure may fluctuate.

• Look for neck vein distension and cannon waves in the neck veins.

• Lungs may exhibit crackles.

• Cardiac examination may reveal regurgitant murmurs and variability of heart sounds.

• Liver may be pulsatile, and the RUQ may be tender to palpation. Ascites may be present in severe cases.

• The lower extremities may be edematous.

• Neurologic examination may reveal confusion, dizziness, or altered mental status.

Physical Examination

Appearance of the Patient

• Diaphoretic

Vitals

Pulse

• Tachycardia]]

Blood Pressure

• Orthostatic hypotension

• Hypovolemic shock

Extremities

• Edema