What causes bradycardia (low heart rate)?

What Causes a Low Heart Rate (Bradycardia)

Bradycardia results from two primary mechanisms: sinus node dysfunction (SND) or atrioventricular (AV) conduction block, though hypoxemia, medications, and reversible metabolic conditions are critical causes that must be identified first. 1

Immediate Life-Threatening Causes to Rule Out First

• Hypoxemia is a common cause of bradycardia and should be assessed immediately by evaluating work of breathing and pulse oximetry. 1
• Severe hypothermia (body temperature <30°C/86°F) causes profound depression of both heart rate and respiratory rate through direct CNS and cardiovascular effects—patients may appear clinically dead but are potentially salvageable with aggressive rewarming. 2
• Cushing's triad (bradycardia, hypertension, irregular respirations) indicates critically elevated intracranial pressure requiring immediate intervention. 2

Medication-Induced Bradycardia

Beta-blockers and calcium channel blockers are the most common drug-related causes of bradycardia. 3, 4

• Beta-blockers cause bradycardia by blocking sympathetic stimulation to the heart. 3
• Non-dihydropyridine calcium channel blockers (verapamil, diltiazem) slow AV nodal conduction and decrease heart rate. 3
• Drug discontinuation resolves bradycardia in 60% of cases, though 26% persist despite withdrawal and may require permanent pacing. 4
• Other medications causing bradycardia include: digitalis glycosides, antiarrhythmics (amiodarone, propafenone, quinidine, sotalol), and multiple chemotherapeutic agents (cisplatin, paclitaxel, 5-fluorouracil). 1, 2, 3
• Opioids and sedatives cause simultaneous respiratory and cardiac depression through CNS effects. 2

Sinus Node Dysfunction (SND)

SND encompasses multiple electrocardiographic manifestations, all reflecting impaired sinus node automaticity or conduction. 1

Specific forms include:

• Sinus bradycardia: Sinus rate <50 bpm. 1
• Sinoatrial exit block: Blocked conduction between sinus node and atrial tissue, manifesting as "group beating" or sinus pauses. 1
• Sinus pause: Sinus node depolarizes >3 seconds after last atrial depolarization. 1
• Sinus node arrest: Complete absence of sinus node depolarization. 1
• Tachycardia-bradycardia syndrome: Alternating periods of atrial tachyarrhythmias with sinus bradycardia or pauses when tachycardia terminates. 1
• Chronotropic incompetence: Inability to increase heart rate appropriately with activity (failure to attain 80% of expected heart rate reserve during exercise). 1

Atrioventricular (AV) Conduction Block

AV blocks result from medications, electrolyte disturbances, or structural problems from acute myocardial infarction or other myocardial diseases. 1

• First-degree AV block: PR interval >200 ms with 1:1 conduction—generally benign and requires no treatment. 1
• Second-degree AV block, Mobitz type I: Block at the AV node level—often transient and asymptomatic. 1
• Second-degree AV block, Mobitz type II: Block below the AV node within the His-Purkinje system—often symptomatic with potential to progress to complete heart block, especially in acute MI. 1
• Third-degree (complete) AV block: No impulses pass between atria and ventricles—can be permanent or transient depending on underlying cause. 1

Vagally-Mediated Bradycardia

Increased parasympathetic tone can cause physiologic bradycardia in specific situations. 1

• In newborns: Bradycardia during feeding, sleep, or defecation represents normal increased vagal tone and requires no intervention if heart rate remains >60 bpm without signs of poor perfusion. 2, 5
• Vasovagal syncope: Sudden increase in parasympathetic tone causes bradycardia (usually sinus slowing or arrest, sometimes with AV block). 1
• Vagally-mediated AV block during sleep can be recognized by concomitant sinus node slowing (P-P prolongation) and is often asymptomatic. 1

Other Causes

• Acute myocardial infarction can cause structural damage leading to conduction abnormalities. 1
• Electrolyte disturbances (particularly hyperkalemia) can impair conduction. 1
• Carotid sinus hypersensitivity produces reflex bradycardia. 6
• Vagal paraganglioma or neck masses involving vagus nerves can cause significant bradycardia. 2

Critical Clinical Pitfall

A heart rate <50 bpm may be physiologically normal for some patients (especially trained athletes), while a rate >50 bpm may be inadequate for others. 1 The key is determining whether bradycardia is symptomatic (causing syncope, presyncope, dizziness, heart failure symptoms, or confusional states from cerebral hypoperfusion) or hemodynamically significant (causing acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or shock). 1

Do not pronounce death in hypothermic patients before rewarming unless obvious signs of death (rigor mortis, nonsurvivable trauma) are present. 2