Section Progress
0% Complete

Indications for pacemaker implantation

Bradyarrhythmia is the main indication for the implantation of a pacemaker. When considering a permanent pacemaker for bradyarrhythmia, it is important to distinguish persistent, reversible and intermittent bradycardia. The pathophysiology and prognosis differ for these entities. Note that the terms bradyarrhythmia and bradycardia are used interchangeably throughout this chapter.

Intermittent bradycardia

The following conditions may cause intermittent bradycardia:

Causes of persisting bradycardia

Reversible causes of bradycardia

Reversible causes of bradycardia must always be excluded before initiating an investigation. Table 1 presents the most common reversible causes of bradycardia.

Table 1. Reversible causes of bradycardia.

DrugsBeta-blockers. Calcium antagonists. Digoxin (digitalis). Ivabradin. Class IA, IC and III antiarrhythmics. Tricyclic antidepressants*. Lithium. Cholinesterase inhibitors. Methyldopa. Reserpine. Clonidine.
ConditionsMyocardial ischemia, myocardial infarction (can cause permanent bradycardia, particularly anterior infarctions). Viral myocarditis. Lyme disease. Rheumatic fever. Endocarditis. Heart surgery (can cause permanent bradycardia). Hypothyroidism. Medullar lesion. Increased intracranial pressure. General hypoxia.
Autonomic nervous systemNeurocardiogenic syncope. Carotid Sinus Hypersensitivity.
Electrolyte disturbancesHypokalemia. Hyperkalemia. Hypercalcemia.
Benign causesWell-trained athletes display bradycardia at rest. Bradycardia during sleep is considered normal.
* Tricyclic antidepressants: amitriptyline, amoxapine, desipramine, (Norpramin), doxepin, imipramine (Tofranil), nortriptyline (Pamelor), protriptyline, Trimipramine.

If a reversible cause of bradycardia is suspected, management should be targeted at that cause. With regards to medications, the clinical need must be reconsidered if bradycardia is a side-effect of the medication. Often, the medication must be continued despite the emergence of bradycardia (e.g beta-blockers in heart failure), which means that the pacemaker is indicated in order to continue treatment with that medication.

It should be noted that the development of AV block upon instigation of beta-blockers suggests concealed conduction disturbance in the AV system. Thus, beta-blockers can reveal people at risk of future AV blocks. A normal functioning AV node should not develop AV block when treated with beta-blockers.

Persisting bradycardia

AV block

AV-blockDefinitionIndication for pacing
AV block IPR interval ≥0.22 sRarely
AV block II, type 1 (Wencheback block)PR interval is gradually prolonged until one atrial impulse (P-wave) is blocked in the AV node.Generally not.
AV block II, type 2Some atrial impulses (P-waves) are blocked, but PR interval is constant.Yes.
AV block IIINo atrial impulses reach the ventricles. Asystole occurs if an escape rhythm is not established.Yes

In AV block II and AV block III, atrial impulses do not reach the ventricles. This may lead to bradycardia, particularly in AV block III. Fortunately, other cardiac structures also exhibit automaticity and these structures may establish an escape rhythm during high-degree AV blocks. The potential consequences of high-degree AV-block are as follows:

Pacemaker is indicated in AV block II and AV block III, including in asymptomatic individuals. With regards to AV block I, pacing is indicated if symptoms of hemodynamic compromise exist; this is generally related to extreme prolongation in PR interval (>0.3 seconds), which results in atrioventricular (AV) desynchronization. This implies that atrial and ventricular activation is not synchronized, such that the atria contracts against closed valves, which affects ventricular filling. The indication for pacing is further strengthened if AV block I is accompanied by wide QRS complexes, since this indicates (this indicates that the conduction defect is located bilaterally in the bundle branches, which is associated with a high risk of developing AV block II or AV block III.

The risk of progression to AV block III is substantially higher for type 2 AV block II, as compared with type 1 AV block II. This is due to the fact that in type 1 AV block II (Wencheback block), the block is generally located in the AV node or the bundle of His, whereas in type 2 AV block II, the block is usually located distal to the bundle of His. Conduction defects distal to the bundle of His have a worse prognosis. The risk of progression to AV block III is particularly high if there is simultaneous bundle branch block or fascicular block. Nevertheless, type 1 AV block II (Wencheback block) requires pacing if the patient has significant symptoms that are assumably caused by the AV block.

Sinus node dysfunction (SND)

SND includes the following conditions:

Pacemaker must be considered in all these conditions, despite the low risk of asystole. The low risk of asystole is explained by the fact that (1) there are several latent pacemakers downstream of the sinus node and (2) AV conduction is not affected by sinus node dysfunction. Indeed, mortality in sinus node dysfunction is comparable to peers without sinus node dysfunction. The purpose of pacing is, therefore, to improve functional capacity, alleviate symptoms, prevent syncope and allow drug therapy that reduces heart rate (beta-blockers, ivabradine, calcium antagonists, etc.).

Sinus bradycardia indicates pacing if symptomatic (at rest or during physical activity). It is important to establish an association between the bradycardia and the symptoms since the pacemaker adds little to no benefit unless symptoms are caused by bradycardia. Asymptomatic sinus bradycardia is not an indication of pacing.

The diagnosis of chronotropic incompetence is established by means of exercise stress testing. If stress testing reveals chronotropic incompetence and it is judged to limit exercise capacity, then pacing is indicated.

In summary, symptomatic sinus node dysfunction is an indication for pacing.

Other causes of bradycardia

Carotid sinus hypersensitivity is an exaggerated response to carotid sinus baroreceptor stimulation, which results in bradycardia upon stimulation of the carotid sinus baroreceptor. This may lead to transient syncope.

Neurocardiogenic syncope is caused by a drastic downregulation of sympathetic activity and a simultaneous parasympathetic surge, which results in bradycardia and hypotension. Neurocardiogenic syncope may be triggered by emotional stress, coughing, defecation, change of body position. Vasovagal syncope is also included in this group.

Ablation and heart surgery are iatrogenic causes of bradycardia. Both interventions may cause transient or permanent damage to the conduction system.

Carotid sinus hypersensitivity and neurocardiogenic (vasovagal) syncope may require pacemaker if symptoms are pronounced and recurring. Bradycardia due to ablation or cardiac surgery typically requires a pacemaker.

Intraventricular conduction defects

Intraventricular conduction defects may require pacing in the following situations:

Other indications for pacemaker

Pacemaker in management of arrhythmias

Anti-tachycardia pacing (ATP)

Pacemakers may be used to detect and treat supraventricular arrhythmias by means of overdrive pacing, which implies that the pacemaker fires pulses with higher frequency than the arrhythmia, which extinguishes the arrhythmia. This is referred to as anti-tachycardia pacing.

Some pacing devices are equipped with a defibrillator, which is used to treat ventricular arrhythmias. Such devices are referred to as ICD (Intracardiac Cardioverter Defibrillator). ICD is indicated in patients with a high risk of ventricular arrhythmias.


Evidence-based Cardiovascular Medicine.

Peer-Reviewed Courses.

Trusted by experts worldwide.

Join our newsletter and get a free ECG Pocket Guide

ECG pocket guide

Start learning now