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Cardiac Pacemakers


L. Brent Mitchell

, MD, Libin Cardiovascular Institute of Alberta, University of Calgary

Last full review/revision Jan 2021| Content last modified Jan 2021

The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic drugs, cardioversion-defibrillation, implantable cardioverter-defibrillators (ICDs), pacemakers (and a special form of pacing, cardiac resynchronization therapy), catheter ablation, surgery, or a combination, is used.

Pacemakers sense electrical events and respond when necessary by delivering electrical stimuli to the heart. Permanent pacemaker leads are placed via thoracotomy or transvenously, but some temporary emergency pacemaker leads can be placed on the chest wall.

Indications for pacemaker placement

Indications for pacemaker placement are numerous (see table) but generally involve symptomatic bradycardia or high-grade atrioventricular block (AV block). Some tachyarrhythmias may be terminated by overdrive pacing with a brief period of pacing at a faster rate; the pacemaker is then slowed to the desired rate. Nevertheless, ventricular tachyarrhythmias are better treated with devices that can cardiovert and defibrillate as well as pace (implantable cardioverter-defibrillators).

Indications for Permanent Pacemakers


Indicated (Established by Evidence or Expert Opinion)

Possibly Indicated and Supported by Bulk of Evidence or Expert Opinion

Possibly Indicated But Less Well Supported by Evidence or Expert Opinion

Not Indicated or Harmful

Sinus node dysfunction*

Symptomatic bradycardia with symptoms directly correlated to bradycardia

Symptomatic bradycardia due to essential drugs (alternatives contraindicated)

Symptomatic bradycardia in patients with tachy-brady syndrome and symptoms attributable to bradycardia

Symptomatic chronotropic incompetence (heart rate cannot meet physiologic demands)

Asymptomatic bradycardia

Symptoms consistent with bradycardia but clearly shown not to be associated with it

Symptomatic bradycardia due to nonessential drugs

Sleep-related bradycardia

AV block*

Any acquired high-grade, 3rd-degree, or 2nd-degree type II AV block regardless of symptoms and that is not attributable to reversible or physiologic causes

Symptomatic AV block that does not resolve despite treatment of potential causes

Third-degree or 2nd-degree AV block, or HV interval of ≥70 ms in patients with neuromuscular diseases associated with conduction abnormalities (eg, myotonic dystrophy) regardless of symptoms

Symptomatic bradycardia in patients with atrial fibrillation

Symptomatic AV block due to essential drugs which cannot be discontinued

2nd-degree type II, 3rd-degree, or high-grade AV block in patients with an infiltrative cardiomyopathy (eg cardiac sarcoidosis or amyloidosis) and life expectancy > 1 year

PR interval > 240 milliseconds and left bundle branch block in patients with lamin A/C gene mutations (including limb-girdle and Emery Dreifuss muscular dystrophies) and life expectancy > 1 year

1st-degree or 2nd-degree Type I AV block with symptoms that are clearly attributable to the AV block

Symptomatic 2nd-degree or 3rd-degree AV block due to due to thyroid function abnormalities without observing for reversibility

PR interval > 240 milliseconds, QRS duration > 120 milliseconds, or fascicular block, in patients with neuromuscular diseases associated with conduction abnormalities (eg, myotonic dystrophy) if life expectancy > 1 year

1st-degree AV block, type I 2nd-degree AV block or 2:1 AV block at the AV node level in patients who are asymptomatic

1st-degree AV block, type I 2nd-degree AV block or 2:1 AV block at the AV node level, in patients with symptoms that are not attributable to the AV block

AV block expected to resolve or unlikely to recur (eg, due to drug toxicity or Lyme disease or occurring asymptomatically during transient increases in vagal tone)


Sustained, pause-dependent VT (including torsades de pointe VT)

High-risk patients with congenital long QT syndrome

Symptomatic recurrent SVT reproducibly terminated by pacing when ablation and/or drugs fail (except when there is an accessory AV connection capable of high-frequency antegrade conduction)

Prevention of symptomatic, recurrent atrial fibrillation refractory to drugs when sinus node dysfunction coexists

Frequent or complex ventricular ectopy without sustained VT when long QT syndrome is absent

Torsades de pointes VT with reversible causes

Prevention of AF in patients without another indication for pacing

After acute myocardial infarction*

Persistent 2nd-degree type II, high-grade or 3rd-degree AV block



Transient AV block

Acquired BBB or fascicular block without 2nd- or 3rd-degree AV block

Fascicular and bundle branch block*

Syncope in patients with an HV interval of ≥ 70 millisecond or evidence of infranodal block at electrophysiology study

Alternating BBB

Fascicular and bundle branch block in patients with Kearns-Sayre syndrome if life expectancy is > 1 year

QRS prolongation > 110 millisecond in patients with Anderson-Fabry disease

In patients with heart failure and LVEF 36-50% and LBBB (QRS ≥ 150 milliseconds) as part of cardiac resynchronization therapy (CRT) if life expectancy is > 1 year

Fascicular and bundle branch block with 1:1 AV conduction in asymptomatic patients

Congenital heart disorders

Advanced 2nd- or 3rd-degree AV block causing symptomatic bradycardia, ventricular dysfunction, or low cardiac output

Sinus node dysfunction correlated with symptoms during age-inappropriate bradycardia

Postoperative high-grade 2nd- or 3rd-degree AV block that is not expected to resolve or that persists ≥ 7 days after surgery

Congenital 3rd-degree AV block with a wide QRS escape rhythm, complex ventricular ectopy, or ventricular dysfunction

Congenital 3rd-degree AV block in infants with a ventricular rate of < 55 beats/min or with a congenital heart disorder and a ventricular rate of < 70 beats/minute

Sustained pause-dependent VT, with or without prolonged QT, when pacing has been documented as effective

Congenital heart disorder and sinus bradycardia to prevent recurrent episodes of intra-atrial reentrant tachycardia

Congenital 3rd-degree AV block persisting after age 1 year if average heart rate is < 50 beats/minute, ventricular rate pauses abruptly for 2 or 3 times the basic cycle length, or symptoms due to chronotropic incompetence occur

Asymptomatic sinus bradycardia in children with a complex congenital heart disorder and resting heart rate of < 40 beats/minute or pauses in ventricular rate of > 3 seconds

Patients with a congenital heart disorder and impaired hemodynamics due to sinus bradycardia or loss of AV synchrony

Unexplained syncope in patients who have had congenital heart disorder surgery that was complicated by transient 3rd-degree AV block with residual fascicular block

Transient postoperative 3rd-degree AV block that converts to sinus rhythm with residual bifascicular block

Congenital 3rd-degree AV block in asymptomatic infants, children, adolescents, or young adults with an acceptable ventricular rate, a narrow QRS complex, and normal ventricular function

Asymptomatic sinus bradycardia after biventricular repair of a congenital heart disorder and resting heart rate of < 40 beats/minute or pauses in ventricular rate of > 3 seconds

Transient postoperative AV block when AV conduction returns to normal

Asymptomatic postoperative bifascicular block with or without 1st-degree AV block and without prior transient 3rd-degree AV block

Asymptomatic type I 2nd-degree AV block

Asymptomatic sinus bradycardia when the longest RR interval is < 3 seconds and minimum heart rate is > 40 beats/minute

Hypersensitive carotid sinus syndrome and neurocardiogenic syncope†

Recurrent syncope due to spontaneously occurring carotid sinus stimulation or to carotid sinus pressure that induces asystole of > 3 seconds

Recurrent syncope without obvious triggering events and with a hypersensitive cardioinhibitory response (ie, carotid sinus pressure induces asystole of > 3 seconds)

Significantly symptomatic neurocardiogenic syncope associated with bradycardia documented clinically or during tilt-table testing

Hyperactive cardioinhibitory response to carotid sinus stimulation without symptoms or with vague symptoms (eg, dizziness, light-headedness)

Situational vasovagal syncope that can be averted by avoidance

Post cardiac transplantation

Inappropriate or symptomatic bradycardia that is persistent or expected to persist

Other established indications for permanent pacing


Prolonged or recurrent relative bradycardia limiting rehabilitation or discharge after postoperative recovery

Syncope after transplantation even when bradyarrhythmia has not been demonstrated


Hypertrophic cardiomyopathy

Same as established indications for sinus node dysfunction or AV block


Medically refractory, symptomatic hypertrophic cardiomyopathy when resting or induced LV outflow is significantly obstructed

Asymptomatic or medically controlled hypertrophic cardiomyopathy

Symptomatic hypertrophic cardiomyopathy with no evidence of LV outflow obstruction

Cardiac resynchronization therapy (CRT) for patients with severe systolic heart failure

CRT (with or without an ICD) for patients with LVEF ≤ 35%, LBBB, QRS duration ≥ 0.15 second, sinus rhythm, and NYHA class II, class III, or ambulatory class IV heart failure symptoms during optimal medical therapy

CRT (with or without an ICD) for patients with LVEF ≤ 35%, sinus rhythm, LBBB, QRS duration 0.12–0.149 second, and NYHA class II, class III, or ambulatory class IV heart failure symptoms during optimal medical therapy

CRT for patients with LVEF ≤ 35%, sinus rhythm, non-LBBB, QRS duration ≥ 0.15 second, and NYHA class III or ambulatory class IV heart failure symptoms during optimal medical therapy

CRT for patients with LVEF ≤ 35% in AF who otherwise meet criteria for CRT, and AV node ablation or pharmacologic therapy will allow near 100% ventricular pacing

CRT for patients with LVEF ≤ 35% who are undergoing new or replacement device with anticipated > 40% ventricular pacing

LVEF ≤ 30% caused by ischemic heart disease) in sinus rhythm, QRS duration ≥ 0.15 second, and NYHA class I heart failure symptoms during optimal medical therapy

LVEF ≤ 35%, sinus rhythm, non-LBBB, QRS duration 0.12–0.149 second, and NYHA class III or ambulatory class IV heart failure symptoms during optimal medical therapy

LVEF ≤ 35%, sinus rhythm, non-LBBB, QRS duration ≥ 0.15 second, and NYHA class II heart failure symptoms during optimal medical therapy

NYHA class I or II heart failure symptoms and non-LBBB QRS pattern with QRS duration < 0.15 second

Comorbidity and/or frailty that will limit survival with good functional status to < 1 year

AF = atrial fibrillation; AV = atrioventricular; BBB = bundle branch block; EF = ejection fraction; HV interval = interval from the start of the HIS signal to the beginning of the 1st ventricular signal; ICD = implantable cardioverter-defibrillator; LBBB = left bundle branch block; LV = left ventricular; NYHA = New York Heart Association; SVT = supraventricular tachycardia; VT = ventricular tachycardia.

Note: Indications described in the above table are based on guidelines in the following footnotes:

* Adapted from Kusumoto FM, Schoenfeld MH, Barrett C, et al: 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. J Am Coll Cardiol 2018, 25701; DOI: 10.1016/j.jacc.2018.10.044

† Adapted from Epstein AE, DiMarco JP, Ellenbogen KA, et al: 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 Guidelines for device-based therapy of cardiac rhythm abnormalities. Circulation 117(21):e350–e408, 2008 and Circulation 127(3):e283–e352, 2013

Types of cardiac pacemakers

Types of pacemakers are designated by 3 to 5 letters (see table Pacemaker Codes), representing which cardiac chambers are paced, which chambers are sensed, how the pacemaker responds to a sensed event (inhibits or triggers pacing), whether it can increase heart rate during exercise (rate-modulating), and whether pacing is multisite (in both atria, both ventricles, or more than one pacing lead in a single chamber). For example, a VVIR pacemaker paces (V) and senses (V) events in the ventricle, inhibits pacing in response to sensed event (I), and can increase its rate during exercise (R).

VVI and DDD pacemakers are the devices most commonly used. They offer equivalent survival benefits. Compared with VVI pacemakers, physiologic pacemakers (AAI, DDD, VDD) appear to reduce risk of atrial fibrillation (AF) and heart failure and slightly improve quality of life.

Advances in pacemaker design include lower-energy circuitry, new battery designs, and corticosteroid-eluting leads (which reduce pacing threshold), all of which increase pacemaker longevity. Mode switching refers to an automatic change in the mode of pacing in response to sensed events (eg, from DDDR to VVIR during AF). Leadless ventricular pacemakers that consist of a combined impulse generator and lead that are entirely contained within the right ventricle have recently been introduced. They are placed transvenously using specially designed delivery systems and are retained in the right ventricle by screws or tines. The leadless pacemakers currently in use are about 1 mL in size, 2 grams in weight, and are of VVI or VVIR configuration.

Examples of Pacemaker Codes*






Chamber Paced

Chamber Sensed

Response to Sensed Event

Rate Modulation

Multisite Pacing

A = Atrium

A = Atrium

O = None

O = Not programmable

O = None

V = Ventricle

V = Ventricle

I = Inhibits pacemaker

A = Atrium

D = Dual (both)

D = Dual (both)

T = Triggers pacemaker to stimulate ventricles

R =Rate-modulated

V = Ventricle

D = Dual (both): For events sensed in ventricles, inhibits; for events sensed in atria, triggers

D = Dual (both)

* The pacemaker code is defined by 3 to 5 letters (here defined by positions I to V). Any one of the letters may be used for each particular position. For example, in position I, the letter code may be A, V or D. In position III, the letter code may be O, I, T, or D and so on.

Complications of pacemaker use

Pacemakers may malfunction by

  • Oversensing events
  • Undersensing events
  • Failing to pace
  • Failing to capture
  • Pacing at an abnormal rate

Tachycardias are an especially common complication. Rate-modulating pacemakers may increase stimuli in response to vibration, muscle activity, or voltage induced by magnetic fields during magnetic resonance imaging. In pacemaker-mediated tachycardia, a normally functioning dual-chamber pacemaker senses a ventricular premature or paced beat transmitted to the atrium (ie, through the AV node or a retrograde-conducting accessory pathway), which triggers ventricular stimulation in a rapid, repeating cycle.

Additional complications associated with normally functioning devices include cross-talk inhibition, in which sensing of the atrial pacing impulse by the ventricular channel of a dual-chamber pacemaker leads to inhibition of ventricular pacing, and pacemaker syndrome, in which AV asynchrony induced by ventricular pacing causes fluctuating, vague cerebral (eg, light-headedness), cervical (eg, neck pulsations), or respiratory (eg, dyspnea) symptoms. Pacemaker syndrome is managed by restoring AV synchrony by atrial pacing (AAI), single-lead atrial sensing ventricular pacing (VDD), or dual-chamber pacing (DDD), most commonly the latter.

Environmental interference comes from electromagnetic sources such as surgical electrocautery and MRI, although MRI may be safe when the pacemaker generator and leads are not inside the magnet. Cellular telephones and electronic security devices are a potential source of interference; telephones should not be placed close to the device but are not a problem when used normally for talking. Walking through metal detectors does not cause pacemaker malfunction as long as patients do not linger.

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