Can you explain bradycardia, its classifications (sinus bradycardia, sick‑sinus syndrome, atrioventricular block types I, II, III, junctional bradycardia, ventricular escape rhythm), causes, clinical presentation, diagnosis, and management?

Bradycardia: Comprehensive Overview

Definition and Classification

Bradycardia is defined as a heart rate below 50 beats per minute when clinically significant, and is broadly classified into two main categories: sinus node dysfunction (SND) and atrioventricular (AV) block. 1, 2

Sinus Node Dysfunction (SND)

SND encompasses multiple distinct electrocardiographic manifestations related to disorders of impulse formation 2:

• Sinus bradycardia: Sinus rate <50 bpm with normal P-wave morphology 1, 2
• Ectopic atrial bradycardia: Atrial depolarization from a pacemaker other than the sinus node with rate <50 bpm 1, 2
• Sinoatrial exit block: Blocked conduction between the sinus node and adjacent atrial tissue, manifesting as "group beating" of atrial depolarization and sinus pauses 1, 2
• Sinus pause: Sinus node depolarizes >3 seconds after the last atrial depolarization 1, 2
• Sinus node arrest: No evidence of sinus node depolarization for prolonged periods 1, 2
• Tachycardia-bradycardia syndrome: Sinus bradycardia, ectopic atrial bradycardia, or sinus pause alternating with periods of abnormal atrial tachycardia, atrial flutter, or atrial fibrillation 1
• Chronotropic incompetence: Failure to reach 80% of expected heart rate reserve during exercise (calculated as [220 - age] minus resting heart rate) 1, 2
• Isorhythmic dissociation: Atrial depolarization slower than ventricular depolarization from an AV nodal, His bundle, or ventricular site 1

Atrioventricular (AV) Block

AV block represents impaired conduction through the AV node or His-Purkinje system 1:

• First-degree AV block: P waves with 1:1 AV conduction and PR interval >200 ms (technically AV delay, not true block) 1
• Second-degree AV block - Mobitz Type I (Wenckebach): P waves with constant rate (<100 bpm) showing periodic single nonconducted P wave with progressively lengthening PR intervals before the dropped beat 1
• Second-degree AV block - Mobitz Type II: P waves with constant rate (<100 bpm) with periodic single nonconducted P wave where conducted beats have constant PR intervals 1
• 2:1 AV block: Every other P wave conducts to the ventricles 1
• Advanced or high-grade second-degree AV block: Two or more consecutive nonconducted P waves 1
• Third-degree (complete) AV block: Complete failure of atrial impulses to conduct to the ventricles with independent atrial and ventricular rhythms 1

Subsidiary Escape Rhythms

When higher pacemakers fail, subsidiary pacemakers may emerge 1:

• Junctional rhythm: Escape rhythm originating from the AV junction, typically 40-60 bpm 1
• Ventricular escape rhythm: Escape rhythm from the ventricles, typically <40 bpm with wide QRS complexes 1

Causes of Bradycardia

Intrinsic Cardiac Causes

• Degenerative fibrosis: The most common cause of bradycardia in elderly patients, representing age-related degeneration of the conduction system 2
• Ischemic heart disease: Particularly inferior myocardial infarction affecting the AV node blood supply 2
• Infiltrative diseases: Sarcoidosis, amyloidosis, hemochromatosis affecting conduction tissue 1
• Inflammatory conditions: Myocarditis, Lyme disease, rheumatic fever 1
• Congenital heart disease: Structural abnormalities affecting conduction pathways 1

Extrinsic and Reversible Causes

Identifying reversible causes is critical before considering permanent pacing 2:

• Medications: Beta-blockers, calcium channel blockers (diltiazem, verapamil), digoxin, antiarrhythmic drugs (amiodarone, sotalol), and ivabradine 2
• Metabolic disorders: Hypothyroidism (screen with thyroid function tests), hyperkalemia, hypomagnesemia 2
• Hypoxemia: A common and immediately reversible cause requiring urgent assessment 2
• Obstructive sleep apnea: Should be screened if bradycardia occurs during sleep or risk factors are present 2
• Increased vagal tone: Can occur in athletes, during sleep, or with vasovagal episodes 1

Physiologic Bradycardia

Sinus bradycardia is a normal physiologic finding in trained athletes, who commonly have resting heart rates of 40-50 bpm while awake and may have sleeping rates as low as 30 bpm with sinus pauses >2 seconds 1. This reflects increased vagal tone and adaptive changes from athletic conditioning 1.

Clinical Manifestations

Symptomatic Bradycardia

Symptomatic bradycardia is defined as documented bradyarrhythmia directly causing syncope, presyncope, transient dizziness, lightheadedness, heart failure symptoms, or confusional states from cerebral hypoperfusion attributable to slow heart rate 1, 3.

The clinical presentation varies widely depending on 1:

• Electrophysiologic manifestations (type of bradycardia)
• Ventricular rate and duration of pauses
• Whether the abnormality is fixed or intermittent
• Underlying medical conditions
• Concurrent medications

Timing-Dependent Symptoms

Vagally mediated AV block occurring during sleep when parasympathetic tone is increased may be asymptomatic, recognized by concomitant sinus node slowing (P-P prolongation) 1. Conversely, sudden increases in parasympathetic tone with vasovagal syncope can cause symptomatic bradycardia 1.

Asymptomatic Bradycardia

Asymptomatic sinus bradycardia, even with rates as low as 37-40 bpm, requires no treatment and has a benign prognosis 2. Many patients with first-degree AV block or Mobitz Type I second-degree AV block remain asymptomatic 1.

Diagnosis

Key Diagnostic Principle

The key determinant for treatment is not the absolute heart rate number, but rather the correlation between bradycardia and symptoms 2, 3. A slow heart rate may be physiologically normal for some patients, while a heart rate >50 bpm may be inadequate for others 3.

Electrocardiographic Evaluation

The 12-lead ECG is essential for identifying 1:

• Type of bradycardia (sinus vs. AV block vs. escape rhythm)
• Degree of AV block
• QRS morphology (narrow vs. wide, suggesting level of block)
• Presence of conduction tissue disease (bundle branch blocks, fascicular blocks)

Ambulatory Monitoring

24-hour Holter monitoring or event recorders are critical for 1:

• Documenting symptom-rhythm correlation
• Identifying intermittent bradyarrhythmias
• Assessing nocturnal bradycardia patterns
• Evaluating chronotropic response

Exercise Testing

Exercise testing helps assess 1:

• Resolution of bradycardia with increased sympathetic tone
• Chronotropic competence
• Exercise-induced AV block (rare but concerning)

Distinguishing Physiologic from Pathologic Bradycardia

In athletes, bradycardia can be confirmed as physiologic by demonstrating: (1) absence of symptoms such as dizziness or syncope; (2) heart rate normalizes during exercise with preservation of maximal heart rate; and (3) bradycardia reverses with training reduction or discontinuation 1.

First-degree AV block and Mobitz Type I second-degree AV block in athletes are confirmed as physiologic if they resolve with hyperventilation or exercise 1.

Evaluation for Reversible Causes

Before considering permanent pacing, systematically evaluate 2:

• Medication review (beta-blockers, calcium channel blockers, digoxin, antiarrhythmics)
• Thyroid function tests
• Electrolytes (potassium, magnesium)
• Oxygenation status
• Sleep study if obstructive sleep apnea suspected

Management

General Management Principles

Intervention is warranted only when bradycardia is symptomatic or likely to progress to a life-threatening condition 3. Treating asymptomatic bradycardia based solely on heart rate is not indicated 2, 3.

Acute Management

For hemodynamically unstable symptomatic bradycardia 1:

• Atropine 0.5-1 mg IV (may be ineffective for infranodal block)
• Temporary pacing (transcutaneous or transvenous)
• Catecholamines (dopamine, epinephrine) if pacing unavailable

Management of Reversible Causes

Failing to identify reversible causes before considering permanent pacing is a common pitfall 2:

• Discontinue or reduce offending medications if possible
• Correct metabolic abnormalities (thyroid replacement, electrolyte correction)
• Treat hypoxemia
• Manage obstructive sleep apnea

Permanent Pacemaker Indications

Class I Indications (Definite)

Permanent pacing is indicated for 1:

• Symptomatic sinus node dysfunction with documented bradycardia causing symptoms
• Third-degree (complete) AV block with symptomatic bradycardia
• Second-degree Mobitz Type II AV block (even if asymptomatic, due to risk of progression)
• Bifascicular block with intermittent complete heart block and symptomatic bradycardia

Class II Indications (Reasonable)

Permanent pacing may be considered for 1:

• Sinus node dysfunction with heart rates <40 bpm when clear symptom-bradycardia association not documented but symptoms consistent with bradycardia present
• Bifascicular or trifascicular block with syncope when complete heart block not proven but other causes excluded
• Markedly prolonged HV interval (>100 ms) on electrophysiology study

Class III Indications (Not Indicated)

Permanent pacing is NOT indicated for 1, 2, 3:

• Asymptomatic sinus node dysfunction, even with heart rate <40 bpm
• Asymptomatic first-degree AV block
• Asymptomatic Mobitz Type I (Wenckebach) second-degree AV block
• Bradycardia clearly documented not to be associated with symptoms
• Bradycardia due to reversible causes (medications, metabolic disorders)

Special Considerations

Athletes

First-degree AV block and Mobitz Type I second-degree AV block are common in trained athletes (present in 35% and 10% respectively) and require no intervention if they resolve with exercise 1. However, Mobitz Type II and third-degree AV block are rare in athletes and require careful diagnostic evaluation 1.

Tachycardia-Bradycardia Syndrome

Patients with tachycardia-bradycardia syndrome often require both permanent pacing and antiarrhythmic medications to control tachyarrhythmias 1.

Common Pitfalls and Caveats

• Do not implant permanent pacemakers for asymptomatic bradycardia regardless of heart rate 2, 3
• Always exclude reversible causes (medications, thyroid, electrolytes, hypoxemia) before permanent pacing 2
• Recognize that nonspecific symptoms like fatigue are multifactorial and difficult to correlate with modest bradycardia 1
• In vasovagal syncope, bradycardia is often accompanied by significant vasodepressor effect, making pacing alone insufficient 1
• Mobitz Type II and third-degree AV block warrant careful evaluation even in athletes, as these are rarely physiologic 1
• Temporary pacing may be necessary while treating reversible causes in hemodynamically stable patients, avoiding unnecessary permanent pacemaker implantation 1