Mechanism and Physiological Significance
A reduced heart rate is described as a negative chronotropic effect.
- Electrophysiological mechanism — deceleration of spontaneous diastolic depolarization across the membranes of pacemaker cells (P-cells) within the sinoatrial (SA) node.
- Prolonged diastole — results from shortened systole combined with overall rhythm slowing.
- Physiological significance — a prolonged diastole is critical because myocardial perfusion (coronary blood flow) occurs primarily during this phase. This ensures the restoration of cardiomyocyte energy stores. Consequently, the heart enters an "energy-conserving mode" with increased efficiency at a minimal oxygen demand.
Parameters and Criteria
- Physiological norm — a regular sinus rhythm with a heart rate below 60 beats per minute (typically 40–60 bpm at rest).
- Hemodynamically significant bradycardia — a clinical state requiring intervention, defined by a heart rate < 40 bpm and/or pauses exceeding 300 ms (clinically significant pauses typically exceed 3000 ms, or 3 seconds).
- Chronic heart failure therapy — a drop in heart rate below 50 bpm during $\beta$-blocker therapy is an indication to halve the dose (complete discontinuation is rarely required, only in cases of marked clinical worsening).
Etiology
A slowed heart rate can be a normal variant, the result of underlying pathology, or caused by external factors.
- Physiological norm — observed in healthy individuals, often mediated by increased vagal tone (vagotonia) coupled with decreased sympathetic nervous system activity.
- Pathological states — hypothyroidism (including pediatric cretinism, where bradycardia is accompanied by arterial hypotension); anorexia nervosa (accompanied by hypotension and hypothermia); hemorrhagic fever with renal syndrome (HFRS) during the oliguric phase (the onset of tachycardia during this phase is an unfavorable sign indicating myocardial damage and increased risk of complications).
- Fetal pathology — bradycardia serves as a risk factor for periventricular leukomalacia (alongside acidosis and hypotension).
- Iatrogenic (drug-induced) causes — administration of antiarrhythmic drugs, particularly amiodarone, and $\beta$-blockers.
- Intoxications — organophosphate poisoning (whose effects oppose those of atropine) and sedative overdose.
Clinical Significance and Management
When hemodynamically significant sinus bradycardia or atrioventricular (AV) block with an inadequate escape rhythm develops, the primary goal is hemodynamic stabilization.
- Mandatory actions — obtain a 12-lead ECG to rule out blocks and conduction abnormalities, review concurrent medications affecting heart rate, and identify the underlying cause of the rhythm slowing.
- First-line pharmacotherapy — intravenous administration of agents with a positive chronotropic effect. Atropine (0.6–1.0 mg) and epinephrine (adrenergic and dopaminergic agents) are utilized.
- Temporary cardiac pacing — indicated when atropine is ineffective and severe bradycardia persists. This involves temporary transvenous endocardial pacing.