Bradyarrhythmias

Overview

Definition

Bradyarrhythmia:

• Heart rate < 60/min
• Caused by dysfunction in conduction at the level of the sinus node, atrioventricular (AV) node, or His/Purkinje system

Anatomy

• Conduction system:
  • Sinoatrial (SA) node:
    • Cluster of cells near the junction of the right atrium and the superior vena cava
    • “Natural pacemaker”: initiates electrical impulses to stimulate contraction
  • AV node:
    • Sits near the coronary sinus on the interatrial septum
    • Receives the impulses from the SA node
    • Slows electrical impulse from the SA node (AV nodal delay) to allow atrial ejection of blood before ventricular contraction
  • Bundle of His: connects impulses from the AV node to the ventricles
  • Bundle branches: 
    • Conducts impulses through the interventricular system
    • Goes to right and left
  • Purkinje fibers: depolarize the ventricles
• Innervation: 
  • Parasympathetic: reduces sinus node automaticity (↓ heart rate)
  • Sympathetic: increases sinus node automaticity (↑ heart rate)

Physiology

Sequential events of a cardiac cycle:

1. SA node initiates impulse. P wave: 
   • Atrial depolarization  
   • Atrial contraction
2. PR segment:
   • Impulse reaches AV node.
   • Impulse passes to the His bundle. 
3. QRS complex: 
   • Atrial repolarization (masked by QRS complex) 
   • Depolarization of ventricles
   • Ventricular contraction
4. ST segment: completion of ventricular depolarization
5. T wave: repolarization of ventricles
6. Completion of repolarization

Epidemiology and Etiology

Epidemiology

• Incidence increases with age, commonly at > 70 years of age.
• Sinus node dysfunction and high-grade atrioventricular block are the most common indications for permanent pacemaker placement.

Etiology

Intrinsic causes:

• Aging: number-1 primary cause (degeneration of the conduction system and pacemaker cells)
• Heart failure
• Ischemic heart disease (e.g., myocardial infarction)
• Congenital heart disease
• Infiltrative cardiac disorders (e.g., sarcoidosis, amyloidosis, hemochromatosis)
• Post-radiation fibrosis
• Ischemic fibrosis
• Ion channel dysfunction
• Autonomic dysfunction
• Inflammatory cardiac disorders (Chagas disease, Lyme disease, myocarditis)

Extrinsic causes:

• Medications: 
  • Most common extrinsic cause
  • Beta blockers, calcium channel blockers (CCBs), digoxin, anti-arrhythmics, acetylcholinesterase inhibitors (AchEIs), lithium, sympatholytics, ivabradine
• Hypothyroidism
• Hyperkalemia, hypokalemia
• Hypothermia
• Neonatal lupus: congenital heart block due to transplacental transfer of antibodies (anti-Ro, anti-La)
• Surgery (transcatheter aortic valve implantation, radiofrequency ablation, transcoronary ablation of septal hypertrophy)
• Obstructive sleep apnea
• Central nervous system (CNS) conditions (intracranial hypertension)
• Increased vagal activity (e.g., carotid sinus stimulation, vomiting, coughing, Valsalva maneuver)

Bradyarrhythmia Due to Sinus Node Dysfunction

Sinus (sinoatrial) node dysfunction (SND)

• Also called sick sinus syndrome
• Non-physiologic sinus rate of < 50/min and/or sinus pauses > 3 sec
• ECG changes and clinical symptoms are both present.
• ECG findings alone do not indicate SND (e.g., highly conditioned athletes).

Pathophysiology

• Defect in cardiac impulse formation (automaticity) and/or conduction from the SA node
• Often secondary to senescence of SA node (sinus node fibrosis)
• SA node is unable to generate a heart rate sufficient for the physiologic needs of the individual.

Types

• Sinus bradycardia: 
  • Sinus rhythm with a heart rate < 60/min 
  • SA node sends out electrical impulse at a regular interval.
  • ECG: 
    • P wave is followed by a QRS complex.
    • Normal PR interval
• Sinus arrest or pause:
  • Disorder of automaticity
  • Sinus node fails to generate an impulse.
  • ECG: 
    • Missing P wave, QRS complex, and T wave → pause generated
    • Length of pause has no relation to length of sinus cycle length.
  • Sinus pause < 3 sec: can be seen in normal individuals
  • AV node and lower conduction system become the pacemaker and an escape rhythm is produced.
  • No escape rhythm or long pauses (> 3 sec) → symptoms (syncope, dizziness)
• Sinoatrial exit block (SA block): 
  • Disorder of conduction
  • SA node depolarizes, but there is a failure in the signal transmission to the rest of the atria. 
  • ECG: 
    • Absence of P wave on the ECG
    • Distinguishing feature from sinus arrest: Length of the SA block is a multiple of the P-P interval before the pause.
• Tachycardia-bradycardia syndrome: episodes of alternating tachycardia and bradycardia

Bradyarrhythmia Due to Atrioventricular Block

Atrioventricular block

• Conduction defect (from atrium to ventricle)
• Can be transient or permanent
• Physiologic AV block: from enhanced vagal tone (e.g., athletes, sleep, carotid sinus massage, carotid sinus hypersensitivity syndrome)

Pathophysiology

• Delay or interruption in the electrical conduction between the atria and the ventricles 
• Due to either anatomical or functional impairment

Types

• 1st-degree AV block:
  • Delayed conduction from atrium to ventricle, without interruption
  • Regular QRS complexes
  • Can be physiologic
  • Often asymptomatic and diagnosed by ECG
  • ECG: PR interval > 0.2 sec or > 200 msec (normal: 0.12–0.20 sec)
• 2nd-degree AV block:
  • Incomplete AV block: There is intermittent atria-to-ventricle conduction.
  • Mobitz type 1 (Wenckebach):
    • Atrial impulses do not reach the ventricles.
    • Impairment usually within the AV node
    • Can be physiologic in young and highly conditioned athletes
    • Often asymptomatic
    • ECG:
      • PR interval progressively and predictably lengthens.
      • Non-conducted P wave → “dropped” QRS complex
    • Mnemonic: “Longer, longer, longer, drop! This must be a Wenckebach!”
  • Mobitz type 2:
    • Impairment distal to the AV node (His bundle and bundle branches)
    • Higher risk to progress to 3rd-degree AV block
    • Can be associated with hemodynamic instability
    • ECG:
      • Consistent unchanging PR intervals
      • Abrupt failure of P wave conduction: “dropped” QRS complex
      • QRS complex is “dropped” unpredictably without PR interval lengthening.
• 2nd-degree AV block, high grade:
  • 2 or more consecutively blocked P waves
  • Compared with 3rd-degree AV block, there is some relationship between P and QRS waves, indicating some degree of AV conduction.
• 3rd-degree (complete) AV block:
  • Complete disconnection of electrical pathways between the atria and the ventricular system
  • Associated with hemodynamic instability
  • ECG: 
    • No relationship between the P waves and QRS complexes
    • Variable PR interval
    • QRS, P-P, and R-R intervals are constant.

Clinical Presentation

Symptoms are related to bradyarrhythmia, causing low cardiac output:

• Chest pain
• Fatigue
• Syncope, presyncope
• Hypotension 
• Shortness of breath
• Dizziness, light-headedness
• Confusion, cognitive slowing (from cerebral hypoperfusion)
• Chronotropic incompetence from sinoatrial node dysfunction: inability to increase heart rate response to increased demand or activity

Diagnosis

Diagnostic cardiac tests

• ECG: best diagnostic test for patients with bradyarrhythmia
• Holter monitor:
  • Continuous recording up to 2 weeks with symptom-rhythm correlation done with patient diary
  • Detects frequently occurring events and symptoms 
• Loop recorder: 
  • Type of event recorder with continuous recording and storage of rhythm data over weeks
  • Provides recording before, during, and after the event
  • Can be an external or implantable recorder
• Post-event recorder:
  • Monitoring starts when a patient’s symptoms commence.
  • Dependent on patient activating the device 
• Mobile cardiac outpatient telemetry: 
  • Mobile or real-time monitors that provide recording up to 30 days
  • Continuous analysis of ECG with real-time transmission of cardiac event to the attending cardiac unit
• Electrophysiologic study (EPS): In AV blocks, EPS helps in determining the level of block and rhythm at risk for complete heart block.
• Exercise stress test:
  • Can exclude myocardial ischemia
  • Detects chronotropic incompetence
• Pharmacologic challenge with atropine or isoproterenol:
  • Use of medication to increase sinus rate
  • Rate increase of < 25% or rate < 90/min considered abnormal
  • Rarely used 

Additional cardiac tests

• Echocardiography:
  • Evaluates left ventricular function 
  • Helps detect infiltrative disorders
• Cardiac magnetic resonance: for diagnostic evaluation of cardiomyopathy that can produce arrhythmias

Laboratory tests

• Metabolic panel
• Thyroid function tests
• Serologic testing for Lyme disease if suspected (AV conduction block: most common objective finding of Lyme carditis)

Polysomnography

• Sleep-disordered breathing: a common cause of nocturnal bradyarrhythmia
• Sleep apnea: associated with bradycardia and AV blocks

Management

General management

Assess hemodynamic stability of the patient with bradyarrhythmia:

• Hemodynamically unstable patients:
  • 1st-line: atropine 0.5 mg IV bolus (repeat dose up to 3 mg)
  • Persistent instability: 
    • Transcutaneous pacing (initial option to stabilize patient; limited by inconsistent myocardial capture)
    • Followed by transvenous pacing
  • If with hypotension: dopamine, epinephrine, or isoproterenol
  • Once stable, proceed with management as with hemodynamically stable patients.
• Hemodynamically stable patients:
  • Search for reversible causes.
  • Treat the cause accordingly.
  • Permanent pacemaker placement: persistent symptoms with no cause found

Specific considerations

• Stable, asymptomatic conditions do not require treatment:
  • Sinus bradycardia
  • 1st-degree heart block 
  • 2nd-degree heart block Mobitz type 1 
• Reversible causes do not require a permanent pacemaker:
  • Correct electrolyte disturbances (e.g., hyperkalemia).
  • Treat infections and underlying disease.
  • Remove causative medications. 
• Indications for permanent pacemaker placement:
  • Symptomatic sinus node dysfunction (e.g., chronotropic incompetence, frequent sinus pauses with symptoms)
  • Symptomatic sinus bradycardia that results from a required medication for a medical condition
  • Complete heart block
  • High-grade AV block
  • 2nd-degree AV block Mobitz 2 
  • 2nd-degree AV block Mobitz 1 if symptomatic or block is at intra- or infra-His levels
  • 1st-degree AV block with hemodynamic compromise
  • AV conduction blocks in certain conditions:
    • Neuromuscular disease
    • Infiltrative cardiomyopathies (e.g., sarcoidosis)
    • Lamin A/C gene mutation–related cardiomyopathy
    • Symptomatic AV block due to reversible cause but AV block persists

Clinical Relevance

Potential etiologies of conduction deficits:

• Lyme disease: a disease that is caused by an infection with Borrelia burgdorferi. Lyme carditis commonly presents with atrioventricular block within 1–2 months of infection. Diagnosis is by ECG and positive Lyme serologic testing. Patients with symptomatic AV block are treated with intravenous (IV) antibiotics (ceftriaxone). Asymptomatic patients with 1st-degree AV block are treated with oral antibiotics (doxycycline, amoxicillin, cefuroxime). Resolution of AV block is expected with treatment.
• Sarcoidosis: a multisystem disease characterized by non-caseating granulomas in the affected organs. In cardiac sarcoidosis, the ventricular myocardium is most commonly affected. Atrioventricular block is the most frequent presentation. Work-up includes ECG, cardiac magnetic resonance imaging, and endomyocardial biopsy if necessary. Immunosuppressive therapy is part of the management. When complete heart block or high-grade conduction disease is present, a permanent pacemaker is indicated.
• Hyperkalemia: serum potassium level of  > 5.5 mEq/L. Cardiac manifestations usually occur when potassium concentration reaches ≥ 7 mEq/L. Hyperkalemia with cardiac abnormalities is a medical emergency. Electrocardiogram findings include peaked T waves, advanced AV block, sinus bradycardia, and sinus arrest. Rapidly acting therapies including intravenous calcium, insulin, and glucose are given along with potassium-removing agents.
• Myocardial infarction: refers to ischemia of the myocardial tissue due to obstruction of the coronary arteries. Myocardial infarction is usually accompanied by an increase in cardiac enzymes, typical ECG changes, and chest pain. Conduction abnormalities can occur in myocardial infarction. Atrioventricular blocks can be addressed with temporary cardiac pacing while the patient is stabilized. Arrhythmias can resolve with treatment of the ischemia but persistence would require pacemaker placement.
• Obstructive sleep apnea (OSA): a disorder characterized by recurrent obstruction of the upper airway during sleep, which causes hypoxia and fragmented sleep. Individuals with obstructive sleep apnea have been found to have sinus bradycardia, sinus pauses, and atrioventricular block. Positive airway pressure (PAP) therapy helps improve arrhythmias in patients with OSA.
• Beta blockers: a group of medications used in the treatment of hypertension, ischemic heart disease, migraine headaches, and heart failure. Bradycardia and hypotension are the most common presentation of beta-blocker overdose. Under cardiac monitoring, severely symptomatic patients are given fluid resuscitation and IV atropine. Additional treatments given to counter the cardiotoxic effects include IV glucagon, IV calcium salts, insulin with glucose, and vasopressors.