Bradycardia

Introduction

  • Bradyarrhythmia is defined as a HR<60bpm.
  • The etiology of bradyarrhythmia is numerous and can be associated with physiological or pathological states.
  • The level of disturbance in the cardiac conduction system responsible for the bradyarrhythmia is an important marker of prognosis and dictates the management strategy.
  • Surface ECG is an invaluable tool in the diagnosis of bradyarrhythmia.
  • Chronic therapy with permanent pacemaker is indicated in certain cases.

Clinical Features

  • Clinical presentation varies in severity depending on the degree of cardiac output compromise.
    • Can be asymptomatic, and only incidentally appreciated on the ECG.
    • Can represent normal physiological adaptations to intense exercise.
  • Common symptoms: Fatigue, exercise intolerance, dyspnea, anginal pain, pre-syncope, syncope
    • Palpitations can be experienced in tachycardia-bradycardia syndrome.

Anatomy of the Conduction System

  • Impulses generated in the SA propagate through the atria and reach the AV node through specialized internodal pathways.
  • The AV node then conducts incoming impulses to the rapid His-Purkinje system, allowing for the initiation of ventricular depolarization.
  • Sinus beats originates from sinoatrial node (automatic focus)
  • Located at the junction of SVC and RA.
  • Blood supply to the SA node is from the sinoatrial node artery.
    • Sinoatrial node artery arises from right coronary artery (55%), left circumflex (35%) or is dual supplied by both (10%)
  • Serves as the electrical connection between atria and ventricles and modulates incoming impulses from the SA node.
  • Can serve as a subsidiary pacemaker.
  • Blood supply to the AV node is from the AV nodal artery.
    • AV nodal artery arises from posterior descending artery (80%), left circumflex (10%) or dual supplied by both (10%)
    • Also receives collateral blood supply from left anterior descending artery (relatively less susceptible to ischemia)
  • Conduct impulse to the ventricular myocardium.
  • The left bundle branch gives rise to anterior fascicle and posterior fascicle.
  • Relatively less influenced by the autonomic nervous system compared to SA and AV node.
  • Blood supply from both the AV nodal artery and septal perforators of LAD.
    • Anterior fascicle = blood supply only from septal perforators of LAD.
    • Posterior fascicle = blood supply from both septal perforators of LAD and PDA.

Etiology

  • Etiologies are divided into intrinsic (pathophysiological processes inherent to the conduction system) or extrinsic (external processes influences the function of an intact conduction system).
  • Cardiomyopathy (ischemic or nonischemic)
  • Congenital heart disease
  • Idiopathic degenerative fibrosis
    • Lenegre disease
    • Lev disease
  • Infection/Inflammatory
    • Chagas disease
    • Diphtheria
    • Infectious endocarditis
    • Lyme disease
    • Tuberculosis
    • Measles
    • Mumps
    • Toxoplasmosis
    • Sarcoidosis
    • Myocarditis
  • Infiltrative disease
    • Amyloidosis
    • Hemochromatosis
    • Lymphoma
  • Ischemia/Infarction
  • Collagen vascular disease
    • Rheumatoid arthritis
    • Scleroderma
    • SLE
    • Polymyositis
  • Surgical or procedural trauma
    • Cardiac ablation or catheterization
    • Congenital heart disease repair
    • Valve replacement
    • Myomectomies
    • Radiation
  • Neuromyopathic disorders

*Table is reproduced in part from the 2018 ACC/AHA/HRS Guidelines on the Evaluation and Management of Patients with Bradycardia and Cardiac Conduction Delay.

  • Autonomic perturbation:
    • Carotid sinus hypersensitivity
    • Vasovagal syncope
    • Situational syncope (cough, defecation, glottic stimulation, micturition, vomiting)
    • Excessive vagal tone
    • Conditioned athletes (normal)
  • Sleep
  • Metabolic
    • Hyper/hypokalemia
    • Acidosis
    • Hypoxia
    • Hypothermia
    • Hypothyroidism
    • Addison’s disease
  • Drugs
    • Beta-blockers, CCB, digoxin, antiarrhythmic drugs, sympatholytic agents (e.g., clonidine), lithium, amitriptyline, phenytoin, prednisone
  • Increased intracranial pressure
  • Sepsis

*Table is reproduced in part from the 2018 ACC/AHA/HRS Guidelines on the Evaluation and Management of Patients with Bradycardia and Cardiac Conduction Delay.

Electrocardiographic Features

Sinus Node Dysfunction

  • Sinus bradycardia: Sinus rate <50bpm, with P-waves upright in leads I, II and aVL and negative in aVR
  • Sinus pause: >3seconds between consecutive sinus node depolarizations.
  • Sinus arrest: Complete failure of impulse formation in the SA node. Absence of atrial depolarization on ECG (no sinus P-waves)
  • Sinoatrial exit block: Failure of normal sinus impulse to conduct to the atria due to delay in conduction within or around the SA node.
  • Chronotropic incompetence: Inadequate ↑ in HR in response to increased demand.
    • Resting ECG will be normal. Exercise testing will reveal blunted HR response (failure to achieve HR 100-120bpm at max. effort, or plateau at <70-80% of max HR at peak effort)
  • Tachycardia-bradycardia syndrome: Alternating periods of bradyarrhythmia with tachyarrhythmia
    • Can manifest as prolonged pause or asystole at termination of atrial tachyarrhythmia.
  • Carotid sinus hypersensitivity: >3second pause in response to carotid massage.
    • ECG manifestation similar to sinus arrest, pause or exist block.
  • Sinus arrhythmias: Phasic variation in underlying sinus cycle length with no change in P-wave morphology or PR interval.
    • P-wave morphology and axis will be different from normal sinus P-waves depending on the location of the ectopic focus.

Atrioventricular Conduction System Abnormalities:

  • This section needs to be rewritten 1-2 bullets per entity I didnt include the bundle branch part in this topic
  • First degree AV block: All atrial impulses are conducted to the ventricular, producing a regular ventricular response.
    • PR interval >200msec
    • PR interval can rarely exceed P-P interval resulting in “skipped P-wave phenomenon.”
    • Can be the result of conduction delay to AV node or in His-Purkinje system.
      • QRS complex of normal duration and contour would suggest conduction delay originating in AV node.
      • First-degree AV block with concomitant BBB would suggest infranodal delay.
    • Second degree AV block: Some atrial impulses are blocked from reaching the ventricle.
      • Non-conducted P-waves can be preceded by a fixed or lengthening PR interval.
      • Mobitz type I: Progressive prolongation in the PR interval before blocked P-wave.
        • Typical features of Wenckebach:
          • Progressive prolongation of PR interval in Wenckebach cycle.
          • R-R interval progressively shortens as a result of the decreasing increment in PR interval prolongation over the Wenckebach cycle.
            • Greatest increment in conduction time is seen in 2nd beat of the Wenckebach.
          • PR interval after the block tends to be shorter than the one preceding the block.
          • Duration of the pause is less than twice the R-R interval of the preceding conducted beats.
          • Group beating pattern.
        • If QRS complex is narrow, Wenckebach block is almost always in AV node.
      • Mobitz type II: PR interval remains constant prior to blocked P-wave.
        • The PR interval can be normal or prolonged.
        • RP-PR reciprocity (like that seen in Wenckebach) is absent.
        • Mobitz type II block almost always localizes below AV node.
        • Intra-Hisian block can result in Mobitz type II block with narrow QRS complex.
      • 2:1 AV block: Every second atrial impulse fails to conduct to the ventricle. Cannot be classified into type I or II readily (cannot discern a PR pattern from only one preceding conducted beat).
        • Certain features can suggest location of block:
          • Narrow complex QRS: The block is likely intranodal.
          • Very long PR interval of conducted beat (>300msec) would suggest AV nodal block whereas shorter preceding PR interval (<160msec) would suggest intra-Hisian or infra-Hisian block.
          • Exercise, atropine, or isoproterenol would be expected to improve AV nodal block and worsen His-Purkinje block. Carotid sinus massage would improve conduction in His-Purkinje block but worsen it in AV block. (See table below)
        • High-grade AV block: Two or more consecutive P-waves fail to conduct.
          • The location of the block can be at the AV node or with HPS.
        • Third degree AV block: No atrial impulses are conducted to the ventricle (AV dissociation).
          • Marching P-waves with continuously changing PR interval.
          • Underlying regular ventricular rhythm.
          • Atrial rate is always faster than the ventricular rate.
          • Location of the block is typically at HPS in acquired complete heart block and at the AV node in most congenital third-degree AV block (this is associated with narrow junctional escape rhythm that is responsive to exercise or atropine).

Approach to Evaluation

Step 1: Patients with suspected bradyarrhythmia or conduction disorder should have a comprehensive history and physical examination (Class I) and ECG (Class I) completed. Blood work may be indicated depending on the suspected etiology (Class IIa)

AHA 2018 - Evaluation of bradycardia and conduction disease algorithm

History:

  • Determine the timing, severity, duration, and frequency of symptoms.
  • Ask about triggers and alleviating factors.
  • Establishing the relationship between the symptoms and the associated triggers can help narrow the differential.
    • Potential associated factors: positional change, prolonged standing, emotional or physical stress, medication, food, micturition, defection, and tight collars.
  • Past history of cardiac disease or cardiovascular risk factors may suggest intrinsic pathology of the conduction system.
  • Thorough review of medications (both prescription and over the counter)

Physical Exam:

  • Orthostatic vitals can help determine the presence of autonomic dysfunction and suggest a diagnosis.
  • Look for evidence of adequate perfusion (mental status, capillary refill and temperature at extremities, urine output etc.)
  • Look for evidence of underlying heart disease or systemic disease (See Etiology Table)
  • Correlate the pulse with auscultated heart sounds.
    • In some arrhythmias (ventricular or atrial bigeminy), the premature beat may not generate enough stroke volume to be palpated at the periphery and may be mistaken for bradycardia.
  • Carotid sinus massage if suspecting carotid hypersensitivity syndrome (if not contraindicated, i.e. no ipsilateral carotid bruit).
    • This should be done in both supine and upright position, while on BP and ECG monitor
  • NOTE: Bradycardic patients can be normo-tensive but still be in shock.

ECG: Seen ECG features

  • If exercise related symptoms, consider exercise ECG.
  • If symptoms are infrequent, consider extended cardiac rhythm monitoring (See non-invasive testing)

If SND, AV block or conduction disorder suggested by initial evaluation proceed to the appropriate next step.

Step 2a: Evidence of sinus node dysfunction

  • Identify reversible etiology and treat (Class I).
  • Can consider echocardiography if structural heart disease is suspected.
  • Additional investigations include exercise ECG or ambulatory ECG.

NOTE: electrophysiological testing should not be completed primarily for the evaluation of sinus node function; if being completed for other reasons, it may be helpful to evaluate the sinus node as part of the study (Class IIb)

AHA 2018: Initial evaluation of suspected or documented SND algorithm

Step 2b: Evidence of AV nodal block

  • Identify reversible etiology and treat (Class I)
  • If initial evaluation indicates Mobitz type II second degree block, advanced AV block or complete AV block then complete a TTE (Class I)
  • Additional investigations include echocardiography and advanced imaging, exercise ECG testing, ambulatory ECG, and electrophysiology study (if other investigation are inconclusive).
AHA 2018: Initial evaluation of suspected atrioventricular block algorithm

Step 2c: Evidence of conduction disorder

  • Identify reversible etiology and treat (Class I)
  • If LBBB identified, complete a TTE (Class I)
  • If symptomatic, consider ambulatory ECG monitoring (Class I), if that is nondiagnostic then consider electrophysiology study (Class IIa).
  • If there is a high suspicion for structural disease, complete advanced imaging as indicated.
AHA 2018 - Evaluation of bradycardia and conduction disease algorithm

Diagnostic Testing

Non-invasive:

  • ECG: Monitoring period depends on the frequency of the symptoms and suspected arrhythmia. Ambulatory monitoring for 24-48 hours is usually sufficient if a 12-lead ECG is nondiagnostic. Sometimes extended periods of monitoring with an event recorder may be required (for up to a period of 4 weeks). In cases where the arrhythmia is extremely infrequent, implantable cardiac loop recorders can be used (monitor for months to years).

Device

Description

Recording duration

Holter monitor

External device with leads worn constantly, that continuously records ECG.

24-72 hours

Event monitor

External device the stores recorded ECG only when triggered by patient (i.e., during awake symptomatic event). 

Weeks

External loop recorder

External device, that is worn constantly for the recording period. Can be patient-activated or auto-triggered. Has memory loop capabilities (will store recording immediately preceding and after the triggered event)

Weeks

Implantable loop recorder

Subcutaneously implanted device. Operates similar to the external loop recorder

Months to years

  • Autonomic maneuvers:
    • Carotid sinus massage: If no contraindications exist, pressure can be applied to one carotid sinus. A positive response is present if a ≥3 second pause and/or ≥50mmgHg drop occur with the massage.
    • Tilt table testing: Head-up tilt-table testing can be used to differential syncopal episodes caused by SND from those mediated by autonomic abnormalities.
    • Pharmacological testing: Pharmacological blockade of autonomic influence on the heart can be used to ascertain the intrinsic heart rate (this would reflect the sinus node rate and help assess degree of intrinsic dysfunction).
      • Both propranolol (0.2mg/kg) and atropine (0.04mg/kg) are given
      • The normal intrinsic heart rate = 118.1 – (0.57 x Age)
    • Maneuvers in AV block:
 

AV node

Infranodal

Vagal maneuvers

Worsen conduction

Does not affect conduction

Beta-blockers

Worsens conduction

Does not affect conduction

Atropine

Improves conduction

May worsen conduction

Isoproterenol

Improves conduction

May worsen conduction

Exercise

Improves conduction

May worsen conduction

Invasive Testing

  • Electrophysiological testing can help evaluate the function of the SA node, as well as determine the level of block in patients with AV block or other conduction blocks.

Approach to Management:

Hemodynamically Unstable Patient:

  1. Follow ACLS Algorithm (Link algorithm)
  2. Administer atropine 0.5mg IV q3-5 minutes for a total dose of 3mg.
    1. NOTE: atropine would not be effective in transplanted (i.e., denervated) hearts.
  3. Initiate temporary cardiac pacing: (see below for indication for temporary pacing)
    1. Transcutaneous OR
    2. Transvenous
  4. Consider administrating ONE of the following chronotropic agents if the patient remains symptomatic despite atropine, and temporary pacing is not available or is unsuccessful.
    • Epinephrine 2-10 mcg/min IV infusion titrate to effect.
      • Usual dose is 0.1-0.5 mcg/kg/min.
    • Dopamine 2-20mcg/kg/min IV infusion, can titrate to a maximum of 50mcg/kg/min for response (note that doses >20mcg/kg/min may increase the risk of tachyarrhythmias)
    • Isoproterenol 2-10mcg/min continuous IV infusion, titrate to response.

If drug toxicity is suspected, use the appropriate antidote.  See table.

AHA 2018: Acute Medical Management of Bradycardia Attributable to SND or Atrioventricular Block

Sinus Node Dysfunction:

  • If patient is hemodynamically unstable (see above).
  • If the patient is hemodynamically stable:
    • Identify and treat reversible etiology.
      • Drugs, autonomic imbalance, ischemia, metabolic abnormalities, etc. (See Etiology)
    • In patients with no reversible causes, where symptoms correlate to bradycardia, PPM is indicated (Class I)
    • In patients who experience drug-induced bradycardia, where the drugs benefits outweigh discontinuation, a PPM is indicated Class I)
    • Oral theophylline can be considered (Class IIb) in patients who do not want a PPM or if symptom-correlation of the bradycardia is likely but uncertain.
  • Note on Permanent Pacemaker in SND:
    • If patients have normal AV nodal conduction system (and not expected to experience disease), or have reasons to avoid an RV lead then single chamber atrial pacing would be indicated in select patients (Class I).
    • In patients with concurrent AV nodal disease, dual chamber pacing (Class I) would be indicated, the AV interval can be extended to minimize ventricular pacing (Class IIa).
    • Physiological pacing is preferred in patients who require frequent pacing (maintaining AV synchrony, minimizing RV pacing).
AHA 2018: Chronic SND management algorithm

Atrioventricular Block:

  • If patient is hemodynamically unstable (see above).
  • If the patient is hemodynamically stable:
    • Identify and treat reversible causes. (See Etiology)
    • Refer to guideline below for indication for PPM in AV block.
    • Special scenarios:
      • In Mobitz type I block, where QRS is wide (suggesting infranodal disease), PPM may be indicated especially if HV interval is prolonged on His-bundle electrocardiogram.
      • Mobitz type II block:
        • If associated with AMI, temporary pacing may be needed (this should be avoided in inferior infarct, as there is risk of RV perforation and the block is usually only transient) – in addition to revascularization.
        • If associated with Lyme carditis, pacing is usually not required. The conduction block usually improves within 1-6 weeks. Some patients may have persistent high-grade AV block which would require pacing.
AHA 2018: Management of bradycardia or pauses attributable to chronic atrioventricular block algorithm

This section needs to be shorted and pared down to only discuss relevant to IM. Rest can be in tables

Summary of Indications for Permanent Pacemaker in Bradyarrhythmia:

Class I indications:

  • Symptomatic bradycardia of irreversible etiology (if determined to be the cause of symptoms)
    • If the symptomatic bradycardia is caused by necessary guideline-directed medical therapy, then PPM insertion would still be a Class I indication.
  • Mobitz type II second degree, high-grade or third-degree AV block of irreversible etiology (even in the absence of symptoms)
  • Alternating BBB
  • Syncope and BBB, if evidence of disease in the HPS on EP study.

Summary for Indication for Temporary Pacing in Bradyarrhythmia:

  • Temporary pacing (transcutaneous, transvenous or epicardial) may be indicated as a temporizing measure in patient with medically refractory symptomatic or hemodynamically unstable bradycardia, until the bradycardia resolves, or a permanent pacemaker is inserted.

Summary of Indications for Permanent Pacemaker in Bradyarrhythmias:

Reproduced form the 2018 ACC/AHA/HRS Guidelines on the Evaluation and Management of Patients with Bradycardia and Cardiac Conduction Delay

  • Sinus Node Dysfunction (SND):
    • Class I Indications:
      • Symptoms directly attributable to SND.
      • Symptomatic sinus bradycardia secondary to guideline-directed management and therapy, where no alternative treatment exists, and continuation of therapy is clinically necessary.
    • Class IIa Indications:
      • Tachy-brady syndrome with symptoms attributable to bradycardia.
      • Symptomatic chronotropic incompetence.
    • Class III Indications:
      • Asymptomatic sinus bradycardia or sinus pauses secondary to physiologically elevated parasympathetic tone.
      • Sleep-related sinus bradycardia or transient sinus pauses during sleep.
      • Asymptomatic SND or if symptoms have been documented to occur in the absence of bradycardia or chronotropic incompetence.
    • Atrioventricular Block:
      • Class I Indications:
        • Symptomatic AV block in patients with known reversible cause, in whom the AV block does not resolve despite treatment of underlying cause.
        • Mobitz type II second-degree AV block, high-grade AV block or third-degree AV block not attributable to reversible or physiological cause.
        • Neuromuscular disease with conduction disorders with evidence of second-degree AV block, third-degree AV block or HV interval ≥70msec, regardless of symptoms if meaningful survival > 1 year expected (with addition of defibrillator as necessary).
        • Permanent AF with symptomatic bradycardia.
        • Symptomatic AV block as a consequence of guideline-directed management and therapy for which no alternative therapy exists and continuation of treatment is clinically necessary.
      • Class IIa Indications:
        • Symptomatic second- or third-degree AV block, on chronic stable doses of medically necessary beta-blockers or antiarrhythmics, PPM is reasonable without further observation for reversibility.
        • Mobitz type II second-degree, high-grade AV block or third-degree AV block associated with infiltrative cardiomyopathy (cardiac sarcoidosis, amyloidosis) if meaningful survival > 1 year is expected (with addition of defibrillator if necessary).
        • Lamin A/C gene mutations (Limb-girdle and Emery-Dreifuss muscular dystrophy) with PR interval > 240 msec and LBBB, if meaning survival >1 year is expected (with addition of defibrillator if necessary).
        • Marked first-degree or Mobitz type I second-degree AV block where symptoms are clearly attributable to AV block.
      • Class IIb Indications:
        • Symptomatic second- or third-degree AV block associated with thyroid function abnormalities but without clinical myxedema, PPM can be considered without further observation for reversibility.
        • Neuromuscular disease with PR interval > 240msec, a QRS duration > 120 msec, or fascicular block if meaningful survival > 1 year expected (with addition of defibrillator if necessary).
      • Class III Indications:
        • First-degree AV block or Mobitz type I second-degree or 2:1 AV block believed to be at the level of AV node with symptoms that DO NOT correspond temporally to AV block.
        • Asymptomatic first-degree AV block or Mobitz type I second-degree AV block or 2:1 AV block believed to be at the level of the AV node.
        • Acute AV block attributable to known reversible nonrecurrent cause, with complete resolution of AV block with treatment of underlying cause.
        • Asymptomatic vagally mediated AV block.
      • Conduction Disorders (with 1:1 AV conduction):
        • Class I Indications:
          • Syncope and BBB, in patients who have HV interval ≥70msec or evidence of infranodal block at EP study.
          • Alternating BBB.
        • Class IIa Indications:
          • Patients with Kearns-Sayre syndrome and conduction disorder, if meaningful survival > 1 year expected (with addition of defibrillator if necessary)
        • Class IIb Indications:
          • Patients with Anderson-Fabry disease and QRS prolongation >110msec if meaningful survival > 1 year expected (with addition of defibrillator if necessary)
          • Heart failure with mildly to moderately reduced EF (36-50%), and LBBB (QRS≥150msec), CRT may be considered.
        • Class III Indications:
          • Asymptomatic isolated conduction disease and 1:1 AV conduction.
        • Post-Surgery:
          • Class I Indications:
            • New postoperative SND or AV block associated with persistent symptoms or hemodynamic instability, that does not resolve after isolated coronary artery bypass surgery or after surgery for AF or after aortic valve replacement or after mitral valve repair or replacement, or tricuspid valve surgery. PPM is recommended before discharge.
            • New AV block after transcatheter aortic valve replacement associated with symptoms or hemodynamic instability that does not resolve. PPM is recommended before discharge.
            • Mobitz type II second-degree AV block, high-grade AV block or persistent complete AV block after alcohol septal ablation or surgical myomectomy.
          • Class IIb Indications:
            • New persistent LBBB after transcatheter aortic valve replacement.
          • Adults Congenital Heart Disease:
            • Class I Indications:
              • Symptomatic SND or chronotropic incompetence, atrial based PPM is recommended.
              • Symptomatic bradycardia related to AV block.
              • Congenital complete AV block with any symptomatic bradycardia, wide QRS escape rhythm, mean daytime HR<50bpm, complex ventricular ectopy or ventricular dysfunction.
              • Postoperative second-degree Mobitz type II atrioventricular block, high-grade atrioventricular block, or third-degree atrioventricular block that is not expected to resolve.
              • Asymptomatic congenital complete AV block.
            • Class III Indications:
              • If venous to systemic intracardiac shunts present, placement of endocardial pacing leads is potentially harmful.
            • Acute MI:
              • Class I Indications:
                • Patients presenting with an acute MI with Mobitz type II second-degree AV block, high-grade AV block, alternating bundle-branch block, or third-degree AV block (persistent or infranodal), permanent pacing is indicated after a waiting period.
              • Class III Indications:
                • Acute MI and transient AV block that resolves.
                • Acute MI with new BBB or isolated fascicular block in absence of second or third-degree AV block.
              • Epilepsy:
                • Class IIa Indications:
                  • Patients with epilepsy associated with severe symptomatic bradycardia (ictal bradycardia), where antiepileptic medications are ineffective.

Further Reading

  • DeGuzman, M., Rahimtoola, S.H. (1983). What is the role of pacemakers in patients with coronary artery disease and conduction abnormalities?. Cardiovasc Clin. 13:191-207.
  • Walsh, E. P., Alexander, M. E., & Cecchin, F. (2006). Electrocardiography and Introduction to Electrophysiologic Techniques. Nadas’ Pediatric Cardiology, 145–181
  • Issa, Z. F., Miller, J. M., & Zipes, D. P. (2019). Clinical Arrhythmology and Electrophysiology. Philadelphia, PA: Elsevier.
  • Kusumoto, F. M., Schoenfeld, M. H., Barrett, C., Edgerton, J. R., Ellenbogen, K. A., Gold, M. R. et al. (2019). 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. In Circulation (Vol. 140)
  • Epstein, A. E., Dimarco, J. P., Ellenbogen, K. A., Estes, N. M., Freedman, R. A., Gettes, L. S., et al. (2008). ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: Executive Summary. Journal of the American College of Cardiology, 51(21);2085-2105.

Authors

  • Authors: Drs. Yehia Fanous (MD, FRCPC, Internal Medicine Resident), Atul Jaidka (MD, FRCPC, Cardiology Fellow), 
  • Staff Reviewer: Pending (MD, FRCPC[Cardiology])
  • Copy Editor: Pending 
  • Last Updated: February 25, 2021
  • Comments or questions please email feedback@cardioguide.ca
Print Friendly, PDF & Email