What is bradycardia?

What is Bradycardia?

Bradycardia is a heart rate below 50-60 beats per minute that may be either physiologic (normal) or pathologic (disease-related), with clinical significance determined entirely by whether it produces symptoms such as syncope, presyncope, dizziness, fatigue, heart failure, or confusion from inadequate cerebral perfusion. 1

Core Definition and Heart Rate Thresholds

• Bradycardia is generally defined as a heart rate below 50 beats per minute, though some guidelines use 60 bpm as the cutoff 1, 2
• The absolute heart rate number alone does not determine pathology—a slow heart rate may be physiologically normal for some patients (especially athletes), while a heart rate above 50 bpm may be inadequate for others depending on metabolic demands 1, 3, 4
• Symptomatic bradycardia specifically refers to a documented bradyarrhythmia directly responsible for clinical manifestations including syncope, near-syncope, transient dizziness, lightheadedness, confusional states from cerebral hypoperfusion, fatigue, exercise intolerance, or congestive heart failure 1, 3

Major Categories of Bradycardia

Sinus Node Dysfunction (SND)

• Sinus bradycardia: Sinus rate <50 bpm with normal P-wave morphology 1
• Sinus pause/arrest: Absence of sinus node depolarization for >3 seconds after the last atrial depolarization 1
• Sinoatrial exit block: Blocked conduction between sinus node and atrial tissue, manifesting as "group beating" or sinus pauses 1
• Chronotropic incompetence: Inability to increase heart rate appropriately with activity, typically defined as failure to attain 80% of expected heart rate reserve during exercise 1
• Tachycardia-bradycardia syndrome: Alternating periods of bradycardia with atrial tachycardia, atrial flutter, or atrial fibrillation, often with prolonged sinus pause when tachycardia terminates 1

Atrioventricular (AV) Block

• First-degree AV block: PR interval >200 ms with 1:1 conduction (technically AV delay, not true block—generally benign) 1, 5
• Second-degree AV block, Mobitz Type I (Wenckebach): Progressive PR prolongation before a nonconducted P wave, typically nodal level block 1
• Second-degree AV block, Mobitz Type II: Sudden nonconducted P waves with constant PR intervals before and after—indicates infranodal disease and often requires pacing 1, 5
• 2:1 AV block: Every other P wave conducts, location of block uncertain without further testing 1
• Advanced/high-grade AV block: ≥2 consecutive nonconducted P waves with evidence of some AV conduction 1
• Third-degree (complete) AV block: No evidence of AV conduction, with atria and ventricles beating independently 1

Critical Distinction: Physiologic vs. Pathologic Bradycardia

Physiologic Bradycardia (Normal)

• Occurs in highly trained athletes, during sleep, and in young healthy individuals due to increased vagal tone 1, 3, 4
• Resting heart rates of 40-50 bpm while awake and as low as 30 bpm during sleep are normal in trained athletes 4
• Key distinguishing features: Complete absence of symptoms, appropriate heart rate increase with exercise or physiologic demands, and reversibility with deconditioning 4
• First-degree AV block and Mobitz Type I second-degree AV block are common in athletes (35% and 10% respectively) and do not require treatment if asymptomatic 4
• Caution must be exercised not to confuse physiological sinus bradycardia with pathological bradyarrhythmias 1

Pathologic Bradycardia (Disease)

• Produces symptoms directly attributable to the slow heart rate 1, 3
• Definite correlation of symptoms with bradyarrhythmia is required to fulfill criteria for symptomatic bradycardia 1
• May result from intrinsic cardiac disease, medications (beta-blockers, calcium channel blockers, digoxin, antiarrhythmics), acute myocardial infarction, electrolyte abnormalities, hypothyroidism, or increased intracranial pressure 1, 6

Clinical Manifestations Requiring Assessment

Cardinal Symptoms

• Syncope or presyncope—the most debilitating symptoms, particularly when resulting in trauma due to sudden, unpredictable nature 3, 5
• Transient dizziness or lightheadedness from cerebral hypoperfusion 1, 3
• Fatigue and exercise intolerance—common but less specific symptoms 1, 5
• Confusional states or altered mental status from inadequate cerebral perfusion 1, 3, 5
• Heart failure symptoms: Dyspnea on exertion, pulmonary edema, jugular venous distension 1, 3, 5
• Ischemic chest discomfort (angina) when bradycardia reduces coronary perfusion 5, 6

Signs of Hemodynamic Compromise

• Hypotension (systolic BP <90 mmHg, cool extremities, delayed capillary refill) 5
• Shock with end-organ hypoperfusion 5
• Acute heart failure with pulmonary edema 5

When Treatment is Indicated vs. Not Indicated

Treatment IS Indicated

• Intervention is warranted only when bradycardia is symptomatic or likely to progress to a life-threatening condition 3
• Specific indications include: Bradycardia associated with hypotension, myocardial ischemia, escape ventricular arrhythmias, altered mental status, or inadequate cardiac output for metabolic demands 5
• Permanent pacemaker implantation is reasonable for symptomatic bradycardia that persists after excluding reversible causes 1, 5

Treatment is NOT Indicated

• Asymptomatic bradycardia, even with heart rates as low as 30-40 bpm, requires no treatment 3, 5, 4
• Permanent pacemaker implantation is not indicated for asymptomatic sinus node dysfunction or physiologic bradycardia 3, 4
• There is no established minimum heart rate below which treatment is indicated—correlation between symptoms and bradycardia is the key determinant for therapy 5
• The universal application of pacing therapy to treat a specific heart rate cannot be recommended except in specific circumstances 1

Common Causes and Mechanisms

Intrinsic Cardiac Disease

• Primary disturbance of cardiac automaticity and/or conduction accounts for approximately 49% of cases presenting to emergency departments 6
• Congenital third-degree AV block, particularly with wide QRS escape rhythm or ventricular dysfunction 1
• Post-cardiac surgery AV block that persists >7 days is unlikely to resolve and typically requires permanent pacing 1

Medication-Related

• Adverse drug effects account for approximately 21% of emergency presentations with compromising bradycardia 6
• Common culprits: Beta-blockers, calcium channel blockers (verapamil, diltiazem), digoxin, antiarrhythmic drugs, and ivabradine 1, 5
• Digoxin toxicity produces characteristic enhanced atrial, junctional, or ventricular automaticity combined with AV block 1

Acute Myocardial Infarction

• Accounts for approximately 14% of emergency bradycardia presentations 6
• Autonomic derangements during acute MI are common, with bradycardia more frequent in inferior MI due to vagal stimulation 1
• Persistent infranodal conduction impairment indicates more severe myocardial injury and worse prognosis, often requiring consideration of pacemaker with defibrillator capacity if LVEF is reduced 1

Reversible Causes

• Electrolyte abnormalities (particularly hyperkalemia) account for approximately 4% of cases 6
• Hypothyroidism 5
• Increased intracranial pressure (Cushing's reflex) 1
• Drug toxicity or intoxication (6% of emergency presentations) 6

Acute Management Approach

Immediate Pharmacologic Therapy

• Atropine 0.5 mg IV every 3-5 minutes to maximum 3 mg is first-line therapy for symptomatic bradycardia 5, 7
• Doses less than 0.5 mg may paradoxically slow heart rate 5, 7
• Atropine is most effective for sinus bradycardia and AV nodal blocks, but less effective for infranodal blocks with wide-complex escape rhythms 5
• Critical warning: Atropine can exacerbate block in patients with infranodal conduction disease and is potentially harmful in this setting 1
• Aminophylline/theophylline may be considered if atropine is ineffective, though data are limited 1

Temporary Pacing

• Transcutaneous pacing is reasonable for symptomatic bradycardia unresponsive to atropine and serves as a bridge to transvenous pacing if needed 5
• Approximately 20% of patients presenting with compromising bradycardia require temporary emergency pacing for initial stabilization 6
• In acute MI with conduction abnormalities, early and unnecessary pacing should be avoided as recovery of conduction frequently occurs, and pacemaker complications (including death) range from 3-7% 1

Observation Alone

• In one large registry, 39% of patients with compromising bradycardia had symptoms resolve with bed rest alone 6

Long-Term Management and Prognosis

• Permanent pacemaker implantation is ultimately required in approximately 50% of patients presenting with compromising bradycardia 6
• 30-day mortality for patients presenting with compromising bradycardia is approximately 5% 6
• Asymptomatic sinus bradycardia has a benign prognosis and does not affect survival—natural history does not warrant prophylactic intervention 5
• Age alone is not a contraindication to pacing if symptomatic and reversible causes are excluded, though frailty, comorbidities, functional status, life expectancy, and quality of life priorities must be considered through goals of care discussions 5