Highlights & Basics
- Sinus bradycardia is any heart rhythm slower than 50 bpm, even if transient, owing to sinus node dysfunction and/or atrioventricular (AV) conduction abnormalities.
- Causes include intrinsic sinus node, AV nodal, and His-Purkinje disease, or extrinsic influences, which may be reversible.
- Common symptoms include syncope, fatigue, and dizziness; however, the patient may be asymptomatic.
- Evaluation involves determining the association of symptoms with heart rate and an assessment of underlying cardiovascular conditions. A 12-lead ECG and/or a heart monitor are the diagnostic tests of choice.
- Patients with a reversible cause may not require long-term therapy; however, patients with nonreversible causes may require an implantable pacemaker with or without a defibrillator. Urgent treatment may include temporary pacing and drug interventions.
- Potentially life-threatening complications, including cardiovascular collapse and death, may occur.
Quick Reference
History & Exam
Key Factors
pulse rate <50 bpm
age >70 years
use of known causative medications
presence of known underlying cause
dizziness/lightheadedness
syncope
fatigue
exercise intolerance
shortness of breath
cannon a-waves in jugular venous pulse
jugular venous distension
Other Factors
increased intracranial pressure
abnormal heart sounds
abdominal or lower extremity edema
hypotension
mental status changes
pallor
extremities cool to touch
hypothermia
chest pain
rashes
thyroid goiter
Diagnostics Tests
1st Tests to Order
12-lead ECG
Holter monitoring
event monitor/mobile cardiac telemetry
exercise testing
carotid sinus massage
echocardiogram
thyroid function tests
basic metabolic panel
arterial blood gas
cardiac biomarkers
serum digoxin level
serum creatinine
Other Tests to consider
implantable-loop recorder
tilt-table testing
Lyme titers
electrophysiology testing
nocturnal pulse oximetry or overnight polysomnography
Treatment Options
acute
hemodynamically unstable
pharmacotherapy
temporary pacing
hemodynamically stable: sinus node dysfunction
reversible cause: asymptomatic or mild symptoms
reversible cause: severe symptoms
nonreversible cause: asymptomatic or mild symptoms
nonreversible cause: severe symptoms
Definition
Classifications
Clinical classification
Bradycardia classification
- Sinus bradycardia: heart rate <50 bpm. It can be a normal finding, especially during rest or sleep, or can be abnormal and symptomatic.[4] It is common in athletes, as they often have high resting vagal tone.
- Sinus nodal pauses/arrest: episodic, abrupt termination of sinus rhythm generally lasting >3 seconds. Episodes can last >30 seconds. There can be hemodynamic collapse, acute drop in blood pressure, and/or loss of consciousness. The term sinus arrest is used generally for long sinus node pauses (i.e., >5 seconds). Paroxysmal sinus arrest or bradycardia can be due to intense vagal discharge.[5]
- Sinus nodal exit block: sinus node continues to activate but electrical activation is delayed and blocked either completely or incompletely between the sinus node and the atria. There can be various levels of block (e.g., complete or intermittent block).[6]
- Tachycardia-bradycardia syndrome: occurs when there are episodic periods of tachycardia (usually atrial flutter, atrial fibrillation, or atrial tachycardia), followed by termination of the tachycardia leading to sinus arrest or long sinus pauses, followed by sinus bradycardia.[7]
- Chronotropic incompetence: a form of bradycardia in which the sinus rate does not accelerate appropriately with exercise. Although there are no standardized criteria for diagnosing chronotropic incompetence, it is generally defined as failure to reach 85% of the age-predicted maximal heart rate (defined as 220 minus the patient's age in years), or the inability to reach 80% of the heart rate reserve (computed as the change in heart rate from rest to peak exercise divided by the difference of the resting HR and the age-predicted maximal HR), on a dynamic exercise test.[8]
- Sinus node dysfunction (SND): historically known as sick sinus syndrome; a general term describing bradycardia presumed to be caused by sinus node disease manifesting as one of the above abnormalities. There is evidence of slowing of sinus node function. Although this is generally not due to autonomic abnormalities, they can contribute. The exact cause is unknown, but it is thought that degenerative fibrosis of the cardiac conduction fibers and surrounding atrial myocardium from factors such as long-standing hypertension, valvular disease, coronary artery disease, atrial arrhythmias, congestive heart failure, or increasing age contribute. The incidence of SND increases with age. SND accounts for nearly half of the pacemaker implantations in the United States. Some patients have marked bradycardia owing to SND only after medications that slow the sinus node are initiated. It has been associated with atrioventricular (AV) nodal conduction abnormalities and a high risk of systemic embolism.[9] [10] [11] [12]
- First-degree AV block: delay in AV conduction, such that the PR interval is >0.2 seconds. During first-degree AV block, there is one-to-one conduction but there is delay in AV nodal conduction.[13] It is not necessarily associated with bradycardia but it may be associated with higher degrees of AV block and subsequent bradycardia or sinus node dysfunction.
- Second-degree AV block: periodic failure of conduction from the atria to the ventricles. This assumes that the atrial rate is regular. A blocked premature atrial beat is not second-degree AV block. There are different types:
- Mobitz I: grouped beating with a constant PP interval, lengthening in the PR interval, and changing (usually shortening) RR intervals with the cycle ending with a P-wave and not followed by a QRS complex. As the PR interval gradually prolongs, the RR interval tends to stay the same or shorten.[14] This is also called Wenckebach AV block.
- Mobitz II: associated with single nonconducted P-waves with a constant PP interval and constant PR intervals (no change in the PR >0.025 seconds).[15]
- 2:1 block: only one PR interval to examine before the blocked P-wave and 2 P-waves for every QRS complex. In most cases, it will change to Mobitz I or II. If there is an associated bundle branch block along with a normal PR interval, this suggests block in the His-Purkinje system.
- High-degree AV block: more than one sequentially blocked P-wave.[16]
- Third-degree AV block: occurs when there are no conducted impulses from the atria to the ventricles. This is also called complete AV block. This may occur with regular atrial activity without conduction or with an atrial tachyarrhythmia.
- Paroxysmal AV block: normal AV nodal conduction followed by sudden block of AV conduction associated with a long pause and multiple blocked P-waves, with subsequent resumption of AV conduction. This can be related to underlying AV nodal or His-Purkinje conduction anomalies or to abrupt parasympathetic activation causing block in AV nodal conduction. In the latter instance, there is often slowing in sinus activation.
- Vagotonic AV block: slowing of the sinus node with prolongation of the PR interval followed by AV block owing to transient abrupt increase in parasympathetic tone.
- Congenital complete heart block: usually associated with a narrow QRS complex escape rhythm arising in the AV node.
- Ectopic atrial rhythm: originates from atrial structures other than the sinus node during sinus bradycardia or sinus arrest.
- Junctional rhythm: escape rhythm when there is bradycardia or arrest of sinus node or atrial activation. Activation of the junction may occur with or without AV block.[17]
- Ventricular rhythm: an escape rhythm from the ventricles when there is AV block or sinus bradycardia.
- Atrial and ventricular activation occur from different pacemakers. Ventricular activation may be from junctional or infranodal automaticity. AV dissociation can occur in the presence of intact AV conduction, especially when rates of the pacemaker, either junctional or ventricular, exceed the atrial rate.
- The atria and ventricles do not activate in a synchronous fashion but beat independent of each other. Usually, the ventricular rate is the same as or faster than the atrial rate. When the atrial rate is faster and the atria and ventricles are beating independently, complete heart block is present.
- AV dissociation can be complete or incomplete. When incomplete, some P-waves conduct and capture the ventricles but, if they do not, it is complete. Complete AV dissociation mimics AV block and has to do with P-wave timing in relation to independent ventricular activation.
- There are two types:
- Isorhythmic: when the atrial rate is the same (or nearly the same) as the ventricular rate but the P-wave is not conducted
- Interference: when P-waves and QRS rates are similar but, occasionally, the atria conduct to the ventricles.
Vignette
Common Vignette 1
Common Vignette 2
Other Presentations
Epidemiology
Etiology
- Intrinsic causes are the result of fibrous changes of the nodal tissue. Intrinsic causes are vast and include idiopathic degenerative processes (e.g., aging), congenital or genetic abnormalities, valvular disease, direct tissue damage (e.g., hypoxia, surgical trauma [surgical aortic and tricuspid valve repair/replacement, transcatheter aortic valve replacement]), tissue inflammation or infiltration (e.g., sarcoidosis, amyloidosis, hemochromatosis), infections (e.g., typhoid fever, diphtheria, tuberculosis, toxoplasmosis, rheumatic fever, viral myocarditis, Lyme disease), autoimmune or collagen vascular diseases (e.g., lupus erythematosus, connective tissue disease), or abnormal autonomic effects.[18]
- Extrinsic causes include exposure to toxins (e.g., lead, black widow spider venom, or tricyclic antidepressant overdose), drugs (e.g., digoxin, beta-blockers, calcium-channel blockers, ivabradine, or class I or III anti-arrhythmic drugs), electrolyte abnormalities (e.g., hyperkalemia, acidemia), or environmental insults (e.g., hypothermia).[3] [19] [20] [21] Additionally, situations that cause high (intense) vagal tone (activation) (increased parasympathetic input to the sinus node) can result in bradycardia. These include vomiting, coughing, glottis stimulation, micturition, and defecation. Iatrogenic causes include vagal nerve stimulators. Carotid sinus hypersensitivity and neurocardiogenic syncope could also lead to bradycardia. Some causes, such as hypothyroidism, electrolyte disorders, and those that are drug-induced, are reversible. Inferior wall myocardial infarction and increased intracranial pressure can also cause various types of bradycardia (i.e., Cushing reflex).
Pathophysiology
Images
ECG showing sinus pause
ECG showing tachy-brady syndrome
ECG showing tachy-brady syndrome
ECG showing tachy-brady syndrome
ECG showing tachy-brady syndrome
ECG showing first-degree atrioventricular (AV) block
ECG showing Mobitz I (Wenckebach) second-degree atrioventricular (AV) block
ECG showing Mobitz I (Wenckebach) second-degree atrioventricular (AV) block
ECG showing Mobitz I (Wenckebach) second-degree atrioventricular (AV) block during acute inferior wall myocardial infarction
ECG showing Mobitz II second-degree atrioventricular (AV) block
ECG showing Mobitz II second-degree atrioventricular (AV) block
ECG showing 2:1 atrioventricular (AV) block
ECG showing 2:1 atrioventricular (AV) block
ECG showing complete atrioventricular (AV) block
ECG showing complete atrioventricular (AV) block
ECG showing complete atrioventricular (AV) block with ventricular escape
ECG showing complete atrioventricular (AV) block with ventricular escape
ECG showing complete atrioventricular (AV) block with junctional escape
ECG showing junctional rhythm
ECG showing interference atrioventricular (AV) dissociation
ECG showing interference atrioventricular (AV) dissociation
Diagnostic Approach
History
Physical exam
ECG
- Sinus bradycardia: regular P-wave followed by QRS at a rate of <50 bpm; ambulatory ECG monitoring is helpful to correlate symptoms with heart rate.[42]
- Sinus nodal pauses or arrest: long RR cycle length, which is longer than the RR interval of the underlying sinus rhythm.Image
- Sinus nodal exit block: an absent P-wave and prolongation of the RR cycle length, usually twice the underlying sinus RR interval.
- Tachycardia-bradycardia syndrome: episodic periods of tachycardia (usually atrial flutter, atrial fibrillation, or atrial tachycardia), followed by termination of the tachycardia leading to sinus arrest or long sinus pauses, followed by sinus bradycardia.Images
- Second-degree AV block:
- 2:1 AV block: only one PR interval to examine before the blocked P-wave and 2 P-waves for every QRS complex. Block can be at the level of the AV node or the His-Purkinje system. If the QRS is narrow, the level of the block is probably in the AV node (which is more benign). If the QRS is wide (owing to bundle branch block or other conduction delay), block in the AV node is still most common but block in the His-Purkinje system is more frequent than when the QRS complex is narrow.Images
- High-degree: more than one sequentially blocked P-wave. Block can be at the level of the AV node or the His-Purkinje system, as is the case with 2:1 AV block.
- Third-degree AV block: occurs when there are no conducted impulses from the atria to the ventricles. There is no consistent PR relationship. It may occur with ventricular or junctional escape rhythm.Images
- Paroxysmal AV block: normal AV nodal conduction followed by sudden block of AV conduction associated with a long pause and multiple blocked P-waves, with subsequent resumption of AV conduction. This may begin with an ectopic impulse.
- Vagotonic AV block: slowing of the sinus node with prolongation of the PR interval followed by AV block owing to transient abrupt increase in parasympathetic tone.
- Congenital complete heart block: usually associated with a narrow QRS complex escape rhythm arising in the AV node.
- Escape rhythms may also occur in AV block, such as atrial (abnormal P-wave and decreased PR interval), junctional (above the bundle of His, produces a rate of approximately 40 to 60 bpm and narrow QRS complexes), and ventricular rhythms (below the bundle of His, produces a slower rate of 20 to 40 bpm and wide QRS complexes).Image
- Isorhythmic: when the atrial rate is the same (or nearly the same) as the ventricular rate but the P-wave is not conducted
- Interference: when P-waves and QRS rates are similar but, occasionally, the atria conduct to the ventricles.Images
Laboratory investigations
Other initial investigations
- Asymptomatic bradycardia and pauses (especially nocturnal) are not uncommon in the normal heart and are probably nondiagnostic.
- Shows sinus pauses, sinus arrest, second- or third-degree AV block, or severe sinus bradycardia with symptoms. First-degree AV block or Mobitz type I AV block may be noted while patients are asleep owing to high vagal tone.
- May be used if severe sinus node dysfunction (e.g., sinus exit block, sinus pauses, sinus arrest, or tachy-brady syndrome) is suspected but cannot be documented.
- May help distinguish the location of the block (i.e., AV node versus His-Purkinje system) in 2:1 and high-degree AV block. A long-monitored strip should be run because 2:1 AV block is unlikely to persist. The other forms of AV block (Mobitz I or II) should then become apparent. Monitoring while the patient does some form of exertion (e.g., arm exercise, standing, and walking) may also help to demonstrate the level of block. Block at the level of the AV node should improve with the adrenergic stimulation, but block below the AV node in the His-Purkinje system may worsen as AV nodal conduction improves and increases the frequency of inputs to the His-Purkinje system.
- Widely used in the diagnosis of symptomatic bradycardia and can be worn for up to 30 days.
- Earlier designs were patient-triggered and so relied on the patient being able to recognize his or her symptoms and activate the monitor in a timely manner. This issue has been corrected by newer-generation monitors with auto-triggering capability.
- Smartphone event monitors convert cardiac electric signal to an ultrasound FM sound signal, which is then demodulated to a digital ECG tracing. The ECG is generated in real time and can also be stored and instantaneously transmitted to a secure server for further analysis.
- Photoplethysmographic-based smart devices (e.g., watches) may also be used.
- Shows sinus pauses, sinus arrest, second- or third-degree AV block, or severe sinus bradycardia with symptoms. May be used if severe sinus node dysfunction (e.g., sinus exit block, sinus pauses, sinus arrest, or tachy-brady syndrome) is suspected but cannot be documented. Particularly useful in diagnosing Mobitz I AV block.
- A subnormal increase in heart rate after exercise (chronotropic incompetence) can be useful in diagnosing sinus node dysfunction.[43] [45] However, sensitivity and specificity are unclear and the results obtained may not be reproducible.[46] Even so, exercise-induced AV block, even if asymptomatic, can be significant and suggests disease of the His-Purkinje system.
- Identifying symptoms owing to sinus bradycardia can be difficult; however, exercise testing can be useful to help determine sinus node dysfunction as the cause of symptoms.
- Useful in determining level of block in second-degree AV block.
- Useful for exercise-induced symptoms where AV block is suspected.
- Performed during continuous ECG monitoring (after evaluating for the presence of carotid bruit by direct auscultation) in the evaluation of carotid sinus hypersensitivity, which causes symptomatic bradycardia and is associated with sinus node dysfunction.[42]
- Diagnostic yield of carotid sinus massage can be increased by performing this during head-up tilting.[47]
- A pause of >3 seconds with symptoms is indicative of a cardio-inhibitory response from carotid sinus hypersensitivity.
- Can help diagnose Mobitz I and II AV block; it will accentuate Wenckebach in the AV node but will have an opposite effect if the block is below the His bundle.
- May help distinguish the location of the block (i.e., AV node versus His-Purkinje system) in 2:1 and high-degree AV block. It may improve block in the His-Purkinje system by slowing the sinus and AV nodal inputs to the His-Purkinje system, enabling the His-Purkinje system longer in which to recover between inputs.
- Care should be taken when performing this maneuver and evaluation for carotid bruit should be performed before it is attempted.
- Although it provides no direct diagnostic role for bradycardia, it provides valuable information regarding underlying heart disease that can influence management and decision making. Patients with significantly reduced left ventricular systolic function may have underlying obstructive coronary artery disease and should be considered for either noninvasive testing (such as myocardial perfusion imaging) or invasive testing (coronary angiography) based on the index of clinical suspicion. This is particularly important in the presence of left bundle branch block or right bundle branch block and left anterior hemiblock in association with symptomatic bradycardia (e.g., syncope). These patients are more likely to develop bradycardia particularly due to AV block. Patients who are found to have significantly reduced left ventricular systolic function should be referred for an implantable cardioverter defibrillator (ICD) if clinically appropriate.[42]
Further investigations
- A subcutaneous monitoring device used for the detection of cardiac arrhythmias. Typically implanted under local anesthesia in the left parasternal or pectoral region. Small devices can be inserted by a qualified physician using an injection approach, and can be used for monitoring for up to 3 years.
- Also useful to rule out bradyarrhythmia as a cause of symptoms by identifying normal sinus rhythm at the time of a symptom event of interest.
- May show sinus pauses, sinus arrest, second- or third-degree AV block, or severe sinus bradycardia with symptoms. May be used if severe sinus node dysfunction (e.g., sinus exit block, sinus pauses, sinus arrest, or tachy-brady syndrome) is suspected but cannot be documented. It is particularly useful in diagnosing Mobitz I AV block.
- Used to evaluate adequacy of the autonomic system, especially when there is suspicion of neurocardiogenic syncope with a paroxysmal drop in heart rate due to vagal activation.[42]
- A commonly used method is head-upright tilting, which causes dependent venous pooling and thereby provokes the autonomic response.
- Recommended when symptoms cannot be correlated clearly and when significant bradyarrhythmias are suspected based on presentation and other clinical information but cannot be diagnosed by noninvasive modalities.[42]
- Electrophysiologic measurements of sinus node function serve only as an adjunct to clinical and noninvasive parameters because these tests are based on assumptions that limit their validity and clinical utility.
- There is little utility for electrophysiology testing in already documented second- and third-degree AV block. Testing can be useful in patients with AV block and no clear symptom association; in patients with symptoms of bradycardia in whom AV block is suspected but not documented; and when the site of AV block cannot be determined reliably by surface tracings.
- May be used if severe sinus node dysfunction (e.g., sinus exit block, sinus pauses, sinus arrest, tachy-brady syndrome) is suspected but cannot be documented.
- Atrial pacing at progressively shorter cycle lengths during an electrophysiology study can manifest Mobitz type I in subjects with normal or abnormal AV node conduction.
- Useful to demonstrate the location of the block (i.e., AV node versus His-Purkinje system) in 2:1 and high-degree AV block.
- Useful for patients with symptoms suspicious for SDB, including daytime somnolence, multiple night-time awakenings, morning headaches, loud snoring, and dry mouth on awakening.
- Prior to pacemaker placement, patients with risk factors for SDB should be evaluated with polysomnography. In one small study, eight patients with asymptomatic bradyarrhythmias were referred for pacemaker evaluation; seven of the patients had bradyarrhythmias only at night or during the day while asleep.[54] Patients with symptoms suggestive of sleep apnea were referred for overnight polysomnography studies that were all positive for obstructive sleep apnea. Treatment for sleep apnea led to reduced sleep apnea symptoms and continued asymptomatic nocturnal bradyarrhythmias without pacemaker therapy after a 22-month follow-up. Therefore, it is paramount to screen patients for sleep apnea when presenting with nocturnal bradycardia before pacemaker placement. This is especially true when asymptomatic nocturnal bradycardias are noted on inpatient overnight cardiac monitoring, or home-based smartphone or watch sleep monitoring apps.
- Particularly in patients with nocturnal bradyarrhythmias or conduction disturbances that are asymptomatic, treatment of obstructive sleep apnea may prevent progression to symptomatic conduction delays.
Risk Factors
History & Exam
Tests
Differential Diagnosis
Differentiating Signs/Symptoms
- Post premature ventricular contraction (PVC) potentiation not present during sinus rhythm without PVCs.
- Cannon a-waves seen in the jugular venous pulse.
Differentiating Tests
- ECG and rhythm strip correlated with pulse show a premature ventricular beat after each normal beat.
Differentiating Signs/Symptoms
- Nonperfused ventricular ectopy causing apparent sinus bradycardia.
- Patients are usually asymptomatic.
- Cannon a-waves may be seen in the jugular venous pulse.
Differentiating Tests
- ECG and rhythm strip correlated with pulse. Specific ECG findings depend on the cause. However, ventricular beats occur earlier than normal.
Atrial fibrillation
Differentiating Signs/Symptoms
- Apical versus peripheral pulse.
- Irregular pulse rate.
Differentiating Tests
- ECG shows absent P waves, presence of fibrillatory waves, and irregular QRS complexes. A rhythm strip may be useful.
Differentiating Signs/Symptoms
- Atrial rate is fast but the ventricular rate is slow.
Differentiating Tests
- ECG shows slight notching on preceding T-wave.
Ventricular tachycardia
Differentiating Signs/Symptoms
- A-waves, variable S1, and variable pulse seen in jugular venous pressure.
Differentiating Tests
- ECG shows atrioventricular (AV) dissociation with capture and fusion.
Cardiac tamponade
Differentiating Signs/Symptoms
- Muffled heart sounds.
- Sinus tachycardia.
- Pulsus paradoxus (usually <10 mmHg).
- Elevated jugular venous pressure.
Differentiating Tests
- ECG shows low voltage QRS or total electrical alternans.
- Echocardiogram shows large pericardial effusion or chamber collapse and respiratory variation of ventricular filling.
Screening
Treatment Approach
Hemodynamically unstable patients
Hemodynamically stable patients: general approach
- The first letter designates the chamber that is paced (O is none; A is atrium; V is ventricle; D is dual chamber).
- The second letter is the chamber in which sensing occurs (O is none; A is atrium; V is ventricle; D is dual chamber).
- The third letter is the response to sensed event (O is none; I is inhibition; T is triggered; D is both inhibition and triggering).
- The fourth letter usually refers to the rate response (R).
- The fifth letter refers to antitachycardia capabilities and is not used commonly.
Hemodynamically stable: sinus node dysfunction
- In patients with sinus node dysfunction owing to a reversible or isolated cause (e.g., specific medication, electrolyte disorder, or vasovagal event, such as a blood draw), the underlying cause should be addressed (e.g., stopping responsible drug, correction of electrolyte abnormality, regulation of thyroid dysfunction). Theophylline may be used in selected patients with mild symptoms, such as predominantly exertional dizziness and/or fatigue.[57] [58]
- Acute treatment is needed if there are severe symptoms or sequelae, including syncope, near-syncope, hypotension, marked fatigue, or ventricular arrhythmias (including torsades de pointes). In patients with a nonreversible cause, the role of pharmacotherapy is limited and permanent pacing is the treatment of choice. In patients with a reversible cause, temporary pacing is needed and underlying causes should be corrected.
- Atrial-based (AAI), ventricle-based (VVI), and dual chamber (DDD) pacing modes are all useful in correcting bradycardia caused by sinus node dysfunction, although the optimal pacing mode remains controversial. Nonetheless, growing evidence indicates that AAI, which avoids pacing of the ventricle, is associated with a relatively lower risk of atrial fibrillation and heart failure.[59] Because patients with sinus node disease are at risk of the development of AV block or atrial fibrillation, DDD pacemakers incorporating algorithms that enable the minimization of right ventricular pacing (functional AAI pacing) are preferred over the single-lead AAI system.[60] [61]
- Patients need to be evaluated for possible ICD placement. This can be accomplished by imaging (echocardiography, or less commonly, cardiac computed tomography or cardiac magnetic resonance imaging) to assess left ventricular systolic function. If new left ventricular systolic dysfunction is identified during evaluation of a patient with bradycardia, exclusion of underlying structural heart disease and coronary artery disease should be done prior to permanent device implantation.
- Accumulating evidence suggests that right ventricular pacing in patients with systolic left ventricular dysfunction may be associated with an increased risk of atrial fibrillation, worsening heart failure, and mortality secondary to left ventricular desynchronization. Therefore, pacing of the ventricle should be avoided in patients who do not need it.[59] [62] Dual-chamber pacemakers incorporating algorithms that enable the minimization of ventricular pacing (functional AAI pacing) are preferred in these patients.[63]
Hemodynamically stable: acquired AV block
- Permanent pacing is indicated only when any of the following are present: high-grade AV block, Mobitz type II second-degree AV block, third-degree AV block, or evidence of infranodal block that is not caused by a physiologic mechanism or reversible cause, regardless of symptoms. In addition, patients who underwent catheter ablation of the AV junction; or those who develop persistent AV block after surgical or transcutaneous implantation of aortic or mitral valve prostheses, or after surgical myectomy or alcohol septal ablation for hypertrophic cardiomyopathy; and those with certain specific neuromuscular diseases (e.g., myotonic dystrophy type 1 or Kearns-Sayre syndrome) and infiltrative cardiomyopathies (sarcoidosis, amyloidosis) with any of the above AV conduction abnormalities, should undergo permanent pacemaker implantation.[11] [42]
- In addition to symptomatic patients who fall into one of the above categories, patients with persistent atrial fibrillation and symptomatic bradycardia, and patients with symptomatic bradycardia who need to be on rate-lowering medications for long-term guideline-directed management of another cardiac condition (e.g. coronary artery disease, systolic congestive heart failure), should be referred for permanent pacemaker implantation.[11]
- VVI, DDD, or atrial synchronous-ventricular inhibited (VDD) pacing modes are useful in correcting bradycardia caused by AV block. Although the optimal pacing mode remains controversial, modes that preserve atrioventricular synchrony (VDD or DDD) are preferred.
- Among patients who have a clear indication for permanent pacemaker implantation, moderate to severe left ventricular systolic dysfunction (estimated left ventricular ejection fraction between 36% and 50%), and a high (>40%) expected burden of ventricular pacing, one should consider the use of cardiac resynchronization therapy or biventricular pacemaker implantation, or consider implantation of a His-bundle pacemaker system.[11]
- Patients with symptomatic bradycardia in whom the level of AV block is at the level of the AV node (supra-Hisian AV block) should be considered for a His-bundle lead-based dual chamber pacemaker instead of a conventional right ventricular lead-based dual chamber pacemaker, to reduce the long-term deleterious effects of chronic right ventricular pacing.
- Permanent pacing is the only available therapeutic modality for persistent acquired AV block that is a result of nonreversible causes.
- As a general rule, all symptomatic patients with AV block require permanent pacing regardless of the specific type or anatomic level of AV block.
- VVI, DDD, and VDD pacing modes are useful in correcting bradycardia caused by AV block. Although the optimal pacing mode remains controversial, modes that preserve atrioventricular synchrony (VDD or DDD) are preferred.
- Patients need to be evaluated for possible ICD placement.
- Accumulating evidence suggests that right ventricular pacing in patients with systolic left ventricular dysfunction may be associated with an increased risk of atrial fibrillation, worsening heart failure, and mortality secondary to left ventricular desynchronization. Therefore, pacing of the ventricle should be avoided in patients with preserved AV conduction.[59] [62] Cardiac resynchronization therapy (biventricular pacing) was superior to right ventricular pacing in reducing a composite of all-cause mortality, heart failure hospitalization, and left ventricular end systolic volume in patients with left ventricular ejection fraction <50%; New York Heart Association (NYHA) class I, II, or III; and >40% right ventricular pacing (e.g., patients with AV block).[64] Whether the same results apply to patients with bradycardia and normal ejection fraction requiring >40% right ventricular pacing remains unclear.
Hemodynamically stable: congenital complete AV block
- Patients need to be evaluated for possible ICD placement.
- Accumulating evidence suggests that right ventricular pacing in patients with systolic left ventricular dysfunction may be associated with increased risk of atrial fibrillation, worsening heart failure, and mortality secondary to left ventricular desynchronization. Therefore, pacing of the ventricle should be avoided in patients with preserved AV conduction.[59] [62]
- Cardiac resynchronization therapy (biventricular pacing) was superior to right ventricular pacing in reducing a composite of all-cause mortality, heart failure hospitalization, and left ventricular end systolic volume in patients with left ventricular ejection fraction <50%; NYHA class I, II, or III; and >40% right ventricular pacing (e.g., patients with AV block).[64] Current guidelines recommend that either biventricular pacing or His-bundle pacing should be preferred over right ventricular pacing for patients with a left ventricular ejection fraction between 36% and 50% and AV block, who have an indication for permanent pacing and are expected to require ventricular pacing >40% of the time to reduce the risk of developing systolic heart failure.[11] Whether the same results apply to patients with bradycardia and normal ejection fraction requiring >40% right ventricular pacing remains unclear.
Hemodynamically stable: vagally mediated bradycardia
- Pacing may be indicated for patients with recurrent symptoms who demonstrate a hyperactive response to carotid sinus massage (defined as ventricular asystolic pause of >3 seconds), are thought to have symptoms owing to hypersensitive carotid sinus, and have no other explainable cause for syncope.
- Patients without these indications do not require treatment.
- The initial approach is usually based on education and lifestyle modification regardless of the intrinsic autonomic mechanism underlying syncopal events. The main aspects of this approach include:
- Identification and avoidance of precipitating factors
- Measures to be taken during impending events, such as lying down, elevation of legs, and tensing maneuvers
- Adequate fluid and salt intake.
- Data documenting specific therapy for vasovagal syncope are sparse. Multiple drugs with different mechanisms have been used with no or little documented benefit.[65] [66] Isolated studies demonstrating benefit of medical therapies, including fluoxetine, have been published.[67] European guidelines state that fludrocortisone should be considered in young patients with orthostatic vasovagal syncope with low-to-normal arterial blood pressure, while midodrine should be considered in patients with vasovagal syncope and orthostatic symptoms. Beta-blocking agents are not generally indicated for the management of neurocardiogenic syncope.[68]
- Use of permanent pacing should be reserved for patients with recurrent severe episodes of syncope refractory to medical therapy who have significant asystolic episodes documented during clinical events. In such patients, dual-chamber permanent pacing with rate-drop response or closed loop stimulation should be the preferred pacing mode.[69] [70]
- Heart-rate response observed during tilt-table testing may not correlate with that during clinical events and should be used with caution for the selection of patients who may or may not benefit from pacing.
- When pacing is considered for neurocardiogenic syncope, the DDD pacing mode is considered to be the preferred pacing mode. The value of programmable pacemaker features such as rate-drop response (during which the rate increases abruptly if a gradual slowing is seen), or closed loop stimulation (during which pacing rate increases if there is evidence of changes in local impedance that may reflect changes in right ventricular contractility by a proprietary algorithm), may be beneficial.[65] [66]
Hemodynamically stable: bradycardia associated with neurologic disorders
- Bradycardia in patients with neurologic disorders can be acute (e.g., Cushing reflex associated with increased intracranial pressure) or chronic. In many situations, the bradycardia may be transient, and clinical monitoring of the bradycardia may be preferable. However, after elimination of reversible causes of bradycardia in these patients, permanent pacing may be needed in a small proportion of patients with neurologic disorders.
- In patients with epilepsy associated with severe symptomatic bradycardia (ictal bradycardia) that is not controlled with anticonvulsants, permanent pacing is a reasonable treatment option for reducing the severity of symptoms.[11]
- Patients diagnosed with myotonic dystrophy type 1 or Kearns-Sayre syndrome, who have evidence of second-degree atrioventricular block, third-degree atrioventricular block, or an abnormal electrophysiology study (H-V interval of greater than or equal to 70 ms), should be referred for pacemaker (or ICD if there is concomitant systolic dysfunction) implantation regardless of symptoms, if meaningful survival of more than 1 year is expected.[11] [42]
- Patients with traumatic spinal cord injury (above the sixth thoracic vertebra level) can have episodes of profound bradycardia in response to painful or noxious stimuli, due to impaired sympathetic innervation and autonomic dysreflexia. These episodes usually resolve over time and with elimination of noxious stimuli, and conservative measures and watchful waiting for resolution of symptomatic bradycardia is preferable.[11]
Treatment Options
hemodynamically unstable
pharmacotherapy
Primary Options
- atropine
0.5 to 1 mg intravenously as a bolus, repeat every 3-5 minutes as needed, maximum 3 mg total dose
- atropine
Secondary Options
- epinephrine (adrenaline)
2-10 micrograms/min intravenous infusion initially, titrate rate according to response
- epinephrine (adrenaline)
- dobutamine
0.5 to 1 micrograms/kg/min intravenous infusion initially, titrate rate according to response, maximum 20-40 micrograms/kg/min
- dobutamine
- aminophylline
consult specialist for guidance on dose
- aminophylline
- theophylline
consult specialist for guidance on dose
- theophylline
Comments
- In patients with systemic hypotension, signs of cerebral hypoperfusion, progressive heart failure, angina, or life-threatening ventricular tachyarrhythmia, medical therapy should be started immediately until temporary cardiac pacing is initiated.
- The most common medications used to increase ventricular rate are intravenous atropine and epinephrine. All drugs are only marginally effective in providing sustained chronotropic support. Dobutamine can also be considered, especially when there is evidence of concomitant systolic heart failure.
- Atropine should not be used in patients who have had a heart transplant or have acute spinal cord injury; use theophylline or aminophylline instead.[41]
- Their efficacy is limited to patients with sinus node dysfunction or conduction abnormalities at the level of the atrioventricular (AV) node. However, patients with infranodal conduction system disease may demonstrate further worsening bradycardia.
- Address underlying cause where one can be identified (e.g., prescription drug toxicity).
temporary pacing
Comments
- Patients who are not responsive to medical therapy require prompt temporary pacing. The two most commonly used modes of temporary pacing are transcutaneous and transvenous.
- Transcutaneous pacing can be applied rapidly through external adhesive electrodes. However, this pacing modality usually serves as a bridge to transvenous pacing because it causes painful skeletal muscle stimulation and usually requires sedation. Furthermore, the efficacy of transcutaneous pacing to provide stable ventricular capture is limited to 78% to 94%.[55] [56] It can be used as a sole temporary pacing modality to provide backup in some patients with transient, infrequent, and short-lived episodes of bradycardia until a reversible cause is corrected or a permanent pacemaker is implanted.
- Transvenous pacing is the most secure and effective modality for patients who require continuous temporary pacing. The temporary pacing lead is usually placed in the right ventricle or, rarely, in the right atrium or both chambers using one of the central veins (femoral, subclavian, or internal jugular). A mechanical prosthetic tricuspid valve is a contraindication to right ventricular pacing. Complications are common (up to 20%) and relate most commonly to venous access, infection, thromboembolism, heart perforation, or lead dislodgement. Ideally, pacing should not exceed more than a few days because of the incremental risk of infection.[55] [56]
hemodynamically stable: sinus node dysfunction
reversible cause: asymptomatic or mild symptoms
treatment of underlying cause
Comments
- For mild symptoms when sinus node dysfunction is a result of a reversible or isolated cause (e.g., specific medication, electrolyte disorder, or vasovagal event, such as a blood draw), hospitalization is usually unnecessary.
- Underlying cause should be addressed (e.g., ceasing drug treatment, administration of electrolytes, or correction of thyroid dysfunction).
theophylline
reversible cause: severe symptoms
treatment of underlying cause + temporary pacing
Comments
- Temporary pacing is needed if there are severe symptoms or sequelae, including syncope, near-syncope, hypotension, marked fatigue, or ventricular arrhythmias (including torsades de pointes).
- Underlying causes should be corrected and include specific medication, electrolyte disorder, vasovagal events, and thyroid dysfunction.
- Atrial-based (AAI), ventricle-based (VVI), and dual chamber (DDD) pacing modes are all useful in correcting bradycardia caused by sinus node dysfunction, although the optimal pacing mode remains controversial. Nonetheless, growing evidence indicates that AAI, which avoids pacing of the ventricle, is associated with a relatively lower risk of atrial fibrillation and heart failure.[41] [59]
- Accumulating evidence suggests that right ventricular pacing in patients with systolic left ventricular dysfunction may be associated with an increased risk of atrial fibrillation, worsening heart failure, and mortality secondary to left ventricular desynchronization. Therefore, pacing of the ventricle should be avoided.[59] [62] Dual-chamber pacemakers incorporating algorithms that enable the minimization of ventricular pacing (functional AAI pacing) are preferred in patients with systolic left ventricular dysfunction.[63]
nonreversible cause: asymptomatic or mild symptoms
reassurance
Comments
- No specific treatment is required, and patients can be reassured about their condition.
nonreversible cause: severe symptoms
permanent pacing
Comments
- Acute treatment is needed if there are severe symptoms or sequelae, including syncope, near-syncope, hypotension, marked fatigue, or ventricular arrhythmias (including torsades de pointes). The role of pharmacotherapy is limited in this situation, and permanent pacing is the treatment of choice.
- Atrial-based (AAI), ventricle-based (VVI), and dual chamber (DDD) pacing modes are all useful in correcting bradycardia caused by sinus node dysfunction, although the optimal pacing mode remains controversial. Nonetheless, growing evidence indicates that AAI, which avoids pacing of the ventricle, is associated with a relatively lower risk of atrial fibrillation and heart failure.[41] [59]
- Accumulating evidence suggests that right ventricular pacing in patients with systolic left ventricular dysfunction may be associated with an increased risk of atrial fibrillation, worsening heart failure, and mortality secondary to left ventricular desynchronization. Therefore, pacing of the ventricle should be avoided.[59] [62] Dual-chamber pacemakers incorporating algorithms that enable the minimization of ventricular pacing (functional AAI pacing) are preferred in patients with systolic left ventricular dysfunction.[63]
- If patients have indications for permanent pacing, but also have indications for an implantable cardioverter defibrillator (ICD) such as systolic left ventricular dysfunction, they need to be evaluated for possible placement of an ICD with pacing capabilities.
hemodynamically stable: acquired atrioventricular block
reversible cause: asymptomatic without indications for pacing
treatment of underlying cause
Comments
- The underlying cause should be addressed (e.g., ceasing drug treatment, administration of electrolytes, or correction of thyroid dysfunction).
reversible cause: symptomatic or indications for pacing
treatment of underlying cause + temporary pacing
Comments
- The underlying cause should be addressed (e.g., ceasing drug treatment, administration of electrolytes, or correction of thyroid dysfunction).
- Pacing is indicated when any of the following is present: high-grade atrioventricular (AV) block, Mobitz type II second-degree AV block, third-degree AV block, or evidence of infranodal block that is not caused by a physiologic mechanism or reversible cause, regardless of symptoms. In addition, patients who underwent catheter ablation of the AV junction; or those who develop persistent AV block after surgical or transcutaneous implantation of aortic or mitral valve prostheses, or after surgical myectomy or alcohol septal ablation for hypertrophic cardiomyopathy; and those with certain specific neuromuscular diseases (e.g., myotonic dystrophy type 1 or Kearns-Sayre syndrome) and infiltrative cardiomyopathies (sarcoidosis, amyloidosis) with any of the above AV conduction abnormalities, should undergo permanent pacemaker implantation.[41]
- Additionally, patients with persistent atrial fibrillation and symptomatic bradycardia, and patients with symptomatic bradycardia who need to be on rate-lowering medications for long-term guideline-directed management of another cardiac condition (e.g., coronary artery disease, systolic congestive heart failure), should be referred for permanent pacemaker implantation.[41]
- Ventricle-based (VVI), dual chamber (DDD), and atrial synchronous-ventricular inhibited (VDD) pacing modes are useful in correcting bradycardia caused by AV block. Although the optimal pacing mode remains controversial, modes that preserve atrioventricular synchrony (VDD or DDD) are preferred.
- Consider the use of a biventricular pacemaker or a His-bundle pacemaker system in patients who need pacing and have a left ventricular ejection fraction of 36% to 50%, and a high (>40%) expected burden of ventricular pacing.
- Symptomatic bradycardia in patients in whom the level of AV block is at the level of the AV node should be considered for a His-bundle lead-based dual chamber pacemaker.
nonreversible cause: asymptomatic without indications for pacing
reassurance
Comments
- Pacing is indicated when any of the following is present: high-grade atrioventricular (AV) block, Mobitz type II second-degree AV block, third-degree AV block, or evidence of infranodal block that is not caused by a physiologic mechanism or reversible cause, regardless of symptoms. In addition, patients who underwent catheter ablation of the AV junction; or those who develop persistent AV block after surgical or transcutaneous implantation of aortic or mitral valve prostheses, or after surgical myectomy or alcohol septal ablation for hypertrophic cardiomyopathy; and those with certain specific neuromuscular diseases (e.g., myotonic dystrophy type 1 or Kearns-Sayre syndrome) and infiltrative cardiomyopathies (sarcoidosis, amyloidosis) with any of the above AV conduction abnormalities, should undergo permanent pacemaker implantation.[41]
- If these indications are absent and the patient is asymptomatic, no specific treatment is required and the patient can be reassured.
nonreversible cause: symptomatic or indications for pacing
permanent pacing
Comments
- Pacing is indicated when any of the following is present: high-grade atrioventricular (AV) block, Mobitz type II second-degree AV block, third-degree AV block, or evidence of infranodal block that is not caused by a physiologic mechanism or reversible cause, regardless of symptoms. In addition, patients who underwent catheter ablation of the AV junction; or those who develop persistent AV block after surgical or transcutaneous implantation of aortic or mitral valve prostheses, or after surgical myectomy or alcohol septal ablation for hypertrophic cardiomyopathy; and those with certain specific neuromuscular diseases (e.g., myotonic dystrophy type 1 or Kearns-Sayre syndrome) and infiltrative cardiomyopathies (sarcoidosis, amyloidosis) with any of the above AV conduction abnormalities, should undergo permanent pacemaker implantation.[41]
- Additionally, patients with persistent atrial fibrillation and symptomatic bradycardia, and patients with symptomatic bradycardia who need to be on rate-lowering medications for long-term guideline-directed management of another cardiac condition (e.g., coronary artery disease, systolic congestive heart failure), should be referred for permanent pacemaker implantation.[41]
- As a general rule, all symptomatic patients with AV block require permanent pacing regardless of the specific type or anatomic level of AV block. Permanent pacing is the only available therapeutic modality for persistent acquired AV block as a result of nonreversible causes.
- Ventricle-based (VVI), dual chamber (DDD), and atrial synchronous-ventricular inhibited (VDD) pacing modes are useful in correcting bradycardia caused by AV block. Although the optimal pacing mode remains controversial, modes that preserve atrioventricular synchrony (VDD or DDD) are preferred.
- Consider the use of a biventricular pacemaker or a His-bundle pacemaker system in patients who need pacing and have a left ventricular ejection fraction of 36% to 50%, and a high (>40%) expected burden of ventricular pacing.
- Symptomatic bradycardia in patients in whom the level of AV block is at the level of the AV node should be considered for a His-bundle lead-based dual chamber pacemaker.
- Accumulating evidence suggests that right ventricular pacing in patients with systolic left ventricular dysfunction may be associated with increased risk of atrial fibrillation, worsening heart failure, and mortality secondary to left ventricular desynchronization. Therefore, pacing of the ventricle should be avoided in patients with preserved AV conduction.[59] [62]
- If patients have indications for permanent pacing, but also have indications for an implantable cardioverter defibrillator (ICD) such as systolic left ventricular dysfunction, they need to be evaluated for possible placement of an ICD with pacing capabilities.
hemodynamically stable: congenital atrioventricular block
asymptomatic without indications for pacing
reassurance
Comments
- Indications for pacing include wide QRS escape rhythm, complex ventricular arrhythmia, or impaired systolic left ventricular function. Although not agreed on universally, pacing should also be considered strongly in asymptomatic patients with ventricular escape rhythm of <50 bpm or prolonged ventricular pauses. If these indications are absent, no specific treatment is required and the patient can be reassured.
- Some data suggest that early institution of pacing in asymptomatic patients may improve survival. However, whether or not all asymptomatic patients with congenital atrioventricular block require permanent pacemaker implantation remains controversial.
symptomatic or indications for pacing
permanent pacing
Comments
- There is a general consensus that permanent pacing is indicated for all symptomatic patients or for asymptomatic patients with any of the following: wide QRS escape rhythm, complex ventricular arrhythmia, a mean daytime heart rate of <50 bpm, or impaired systolic left ventricular function.
- In addition, patients with adult congenital heart disease (ACHD) who have significant atrioventricular (AV) conduction abnormalities (high-grade AV block, Mobitz II second-degree AV block, or third-degree AV block that is not expected to resolve) should undergo permanent pacemaker implantation, and pacemaker algorithms that reduce the risk of atrial arrhythmias should be incorporated in these devices.[41]
- Although not agreed on universally, pacing should be considered strongly in asymptomatic patients with ventricular escape rhythm of <50 bpm or prolonged ventricular pauses.
- Pacing modes that preserve atrioventricular synchrony (atrial synchronous-ventricular inhibited [VDD] or dual chamber [DDD]) are usually used.
- If patients have indications for permanent pacing, but also have indications for an implantable cardioverter defibrillator (ICD) such as systolic left ventricular dysfunction, they need to be evaluated for possible placement of an ICD with pacing capabilities.
hemodynamically stable: vagally mediated bradycardia
carotid hypersensitivity syndrome
permanent pacing
Comments
- Pacing may be indicated for patients with recurrent symptoms who demonstrate a hyperactive response to carotid sinus massage (defined as ventricular asystolic pause of >3 seconds), are thought to have symptoms owing to hypersensitive carotid sinus, and have no other explainable cause for syncope.
neurocardiogenic or vasovagal syncope
lifestyle modifications
Comments
- Initial approach is usually based on education and lifestyle modification, regardless of the intrinsic autonomic mechanism underlying syncopal events.
- The main aspects of this approach include: identification and avoidance of precipitating factors; measures to be taken during impending events, such as lying down, elevation of legs, and tensing maneuvers; adequate fluid and salt intake.
pharmacotherapy
Primary Options
- fludrocortisone
0.1 to 0.2 mg orally once daily
- fludrocortisone
- midodrine
2.5 to 10 mg orally three times daily
- midodrine
- fluoxetine
20 mg orally once daily
- fluoxetine
Comments
- The role of medication is limited.
- Medical therapy is usually considered in patients who do not respond to lifestyle modifications. The choice of the drug is made on an individual basis.
- The most commonly used drugs are fludrocortisone, midodrine, and selective serotonin-reuptake inhibitors (SSRIs).
- European guidelines state that fludrocortisone should be considered in young patients with orthostatic vasovagal syncope with low-to-normal arterial blood pressure, while midodrine should be considered in patients with vasovagal syncope and orthostatic symptoms.[68]
permanent pacing
Comments
- Pacing is reserved for patients with recurrent severe episodes of syncope refractory to medical therapy who have significant bradycardia documented during clinical events.
- Heart-rate response observed during tilt-table testing may not correlate with that during clinical events and should be used with caution for the selection of patients who may or may not benefit from pacing.
- When pacing is considered for neurocardiogenic syncope, the dual chamber (DDD) pacing mode is considered to be the preferred pacing mode. The value of programmable pacemaker features such as rate-drop response (during which the rate increases abruptly if a gradual slowing is seen), or closed loop stimulation (during which pacing rate increases if there is evidence of changes in local impedance that may reflect changes in right ventricular contractility by a proprietary algorithm), may be beneficial.[65] [66]
hemodynamically stable: bradycardia associated with neurologic disorders
consider permanent pacing
Comments
- Bradycardia can be acute (e.g., Cushing reflex) or chronic. In many situations, the bradycardia may be transient. First, identify and eliminate reversible causes. Watchful waiting for spontaneous resolutions is reasonable. Permanent pacing may be needed in a small proportion of patients.
- In patients with epilepsy associated with severe symptomatic bradycardia (ictal bradycardia) that are not controlled with anti-epileptic medications, permanent pacing is a reasonable treatment option for reducing the severity of symptoms.[41]
- Patients diagnosed with myotonic dystrophy type 1 or Kearns-Sayre syndrome, who have evidence of second-degree atrioventricular (AV) block, third-degree AV block, or an abnormal electrophysiology study (H-V interval of ≥70 ms), should be referred for pacemaker (or implantable cardioverter defibrillator [ICD] if there is concomitant systolic dysfunction) implantation regardless of symptoms, if meaningful survival of more than 1 year is expected.[41]
- Patients with traumatic spinal cord injury (above the sixth thoracic vertebra level) can have episodes of profound bradycardia in response to painful or noxious stimuli. These episodes usually resolve over time and with elimination of noxious stimuli, and conservative measures and watchful waiting for resolution of symptomatic bradycardia is preferable.[41]
Emerging Tx
Alternative pacing systems
Prevention
Secondary Prevention
Follow-Up Overview
Prognosis
Monitoring
- Do not need regular follow-up. May monitor themselves as outpatients and notify their doctors only when they develop cardinal symptoms.
- Symptomatic patients should be seen by a physician, preferably a cardiologist, as soon as possible, with appropriate testing undertaken to establish the degree and mechanism of bradycardia and whether symptoms are secondary to the rhythm.
- Follow-up at this point depends on the type of diagnostic modality used. For example, if the patient has an event monitor, the follow-up should happen at the end of 30 days or before this if a patient transmission demonstrates a concerning rhythm correlating with symptoms.
- Similarly, if a patient has an implantable-loop recorder, he or she should be followed up if a symptomatic episode occurred that caused the patient to activate the device. Routine follow-up in patients with implantable-loop recorders can be every 3 to 6 months for the battery life of the device (i.e., usually 18-24 months).
- A cardiologist, preferably an electrophysiologist, must follow patients after a pacemaker has been implanted.
- The initial follow-up should be 1 week after implant to assess the pocket and incision site for possible infection.
- 2-month follow-up must occur after pacemaker implantation and then yearly thereafter.
- The reason for frequent yearly follow-up is to assess the device for lead function and battery life, and to review any events that were recorded by the device.
Complications
Citations
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Key Articles
Referenced Articles
Guidelines
Treatment
Summary
Updated comprehensive guidelines for appropriate use of pacemakers and implantable cardioverter-defibrillators (ICD), including clinical indications for pacing and ICD, selection of optimal device and pacing mode, cost, and follow-up.Published by
American College of Cardiology, American Heart Association, Heart Rhythm Society
Published
2018
Summary
Evidence-based recommendations regarding resuscitation and emergency cardiac care.Published by
American Heart Association
Published
2020
Summary
Guidance on the management of adult and pediatric patients with suspected syncope.Published by
American College of Cardiology, American Heart Association, Heart Rhythm Society
Published
2017
Summary
Recommendations on pacemaker device and mode selection.Published by
American College of Cardiology; American Heart Association; Heart Rhythm Society
Published
2012
Summary
European guidelines that include treatment recommendations for underlying causes of bradycardia.Published by
European Society of Cardiology
Published
2018
Summary
Guidelines advocating classification of bradyarrhythmias according to mechanism rather than etiology, for the selection of patients for permanent cardiac pacing therapy.Published by
European Society of Cardiology; European Heart Rhythm Association
Published
2021