Tachycardia & Bradycardia

Heart rate is a number. Rhythm is a mechanism. These are not the same clinical question, and conflating them leads to mismanagement.

Tachycardia is a heart rate above 100 beats per minute. Bradycardia is a heart rate below 60 beats per minute. Both are findings — not diagnoses. The clinical work is determining what is driving the rate and whether the rate itself requires treatment.

A heart rate of 115 in a patient with sepsis, pain, fever, or volume depletion is physiologic compensation. The rate is appropriate to the clinical state. Treating the number without treating the cause is incomplete management and may be harmful.

A heart rate of 115 in a patient with palpitations, hemodynamic instability, or a wide-complex rhythm on ECG is a different problem entirely. The mechanism matters.

The most important initial question in tachycardia is whether the rate is primary — a rhythm problem — or secondary — a physiologic response to something else.

Secondary tachycardia (sinus tachycardia) is the most common. The sinus node is responding appropriately to an underlying driver: pain, fever, infection, hypovolemia, anemia, hypoxia, anxiety, stimulants, thyrotoxicosis, or pulmonary embolism. The ECG shows a normal P-wave morphology preceding each QRS. The treatment is the underlying cause.

Primary tachycardia arises from an abnormal rhythm mechanism — reentry, automaticity, or triggered activity — independent of physiologic demand. Examples include SVT, atrial fibrillation with rapid ventricular response, atrial flutter, and ventricular tachycardia. These require rhythm-directed evaluation and management.

The ECG is the essential tool. P-wave morphology, PR interval, QRS width, and the relationship between P waves and QRS complexes are the data points that distinguish mechanism.

QRS width is the first ECG branch point in tachycardia evaluation.

Narrow-complex tachycardia (QRS < 120 ms) indicates that ventricular conduction is proceeding through the normal His-Purkinje system. The rhythm originates above the ventricles — sinus tachycardia, SVT, atrial fibrillation, atrial flutter, or junctional tachycardia.

Wide-complex tachycardia (QRS ≥ 120 ms) has a broader differential. It may represent ventricular tachycardia, SVT with aberrant conduction (bundle branch block), or SVT with pre-excitation. Ventricular tachycardia must be assumed until proven otherwise in a hemodynamically unstable patient with a wide-complex rhythm.

The clinical rule: a wide-complex tachycardia in an unstable patient is VT until proven otherwise. Do not delay treatment to establish the mechanism with certainty.

Bradycardia is not inherently abnormal. Well-conditioned athletes commonly have resting heart rates in the 40s and 50s. Vagal tone during sleep produces bradycardia in healthy individuals. These are physiologic and require no evaluation.

Pathologic bradycardia is distinguished by symptoms, hemodynamic consequences, or associated conduction abnormalities. Syncope, near-syncope, presyncope, dyspnea, chest pain, or hemodynamic instability in the setting of bradycardia is a different clinical problem than an incidental finding of a low heart rate in an asymptomatic patient.

The ECG is again essential. Sinus bradycardia, first-degree AV block, second-degree AV block (Mobitz I and Mobitz II), and complete heart block have different mechanisms, different clinical implications, and different management pathways.

Mobitz II and complete heart block carry a higher risk of progression to hemodynamic compromise and often require pacing evaluation. Mobitz I (Wenckebach) is more commonly benign but requires clinical context.

Before attributing bradycardia to intrinsic conduction disease, review the medication list. A significant proportion of clinically encountered bradycardia has a reversible pharmacologic cause.

Beta-blockers reduce sinus rate and slow AV conduction. Calcium channel blockers (non-dihydropyridines — diltiazem, verapamil) have similar effects. Digoxin increases vagal tone and slows AV conduction. Antiarrhythmics — amiodarone, sotalol, flecainide — can suppress sinus node function and AV conduction.

Electrolyte abnormalities — particularly hyperkalemia — can produce bradycardia and conduction abnormalities. Hypothyroidism slows the sinus rate. Hypothermia produces progressive bradycardia and conduction changes.

The clinical implication: identifying and addressing a reversible cause may resolve the bradycardia without requiring permanent pacing. This evaluation belongs early in the workup.

The first management question is whether the rate abnormality is causing hemodynamic compromise. Hemodynamic instability — hypotension, altered mental status, chest pain, or signs of poor perfusion — requires immediate intervention regardless of the specific rhythm.

For unstable tachycardia: synchronized cardioversion is the intervention for unstable SVT, atrial flutter, atrial fibrillation with rapid ventricular response, and stable VT with a pulse. Unsynchronized defibrillation is used for pulseless VT and VF. Vagal maneuvers (Valsalva, carotid sinus massage) and IV adenosine are first-line for stable narrow-complex SVT.

For stable tachycardia: sinus tachycardia requires treating the underlying cause — not rate control. Attempting to slow a compensatory sinus tachycardia (from sepsis, pain, hypovolemia, or anemia) without addressing the cause is harmful. Rate control for atrial fibrillation with rapid ventricular response uses beta-blockers or non-dihydropyridine calcium channel blockers in hemodynamically stable patients.

For symptomatic bradycardia: atropine 0.5 mg IV is first-line for symptomatic bradycardia with a pulse. Repeat dosing up to 3 mg total is appropriate if the initial dose is ineffective. Transcutaneous pacing is the bridge for atropine-refractory symptomatic bradycardia while transvenous pacing is arranged. Dopamine or epinephrine infusions can support rate and perfusion while pacing is established.

Asymptomatic bradycardia with a rate above 40 and no hemodynamic compromise can be observed while reversible causes are addressed. Asymptomatic tachycardia should be evaluated for secondary causes before any rate-directed treatment is initiated.

Escalation criteria: any hemodynamically unstable rhythm, wide-complex tachycardia of uncertain origin, complete heart block, Mobitz II, symptomatic bradycardia refractory to atropine, or any rhythm requiring pacing should prompt immediate cardiology involvement. New-onset atrial fibrillation with rapid ventricular response in a patient with structural heart disease or hemodynamic compromise warrants urgent cardiology consultation.