Cardiac Arrhythmias

Structural/substrate causes (reentry)

• Prior myocardial infarction and scar: border-zone fibrosis creates slow conduction and heterogeneous refractoriness — the single most common substrate for monomorphic ventricular tachycardia.
• Cardiomyopathy and valvular/atrial stretch: dilated, hypertrophic, and infiltrative disease (sarcoid, amyloid, hemochromatosis) plus mitral disease and left atrial enlargement favor atrial fibrillation and VT.
• Congenital accessory pathway: a muscular bridge bypassing the AV node (bundle of Kent) creates the anatomic reentry circuit of WPW; associated with Ebstein anomaly.

Automaticity and triggered activity

• Ischemia and hypoxia: partial depolarization of injured myocytes enhances phase 4 slope; sinus tachycardia, PVCs, and VF cluster in the first hours of infarction.
• Electrolyte and metabolic derangement: hypokalemia and hypomagnesemia prolong repolarization (EADs → torsades); hyperkalemia slows conduction and causes bradycardia/asystole; calcium overload in heart failure or digitalis toxicity generates DADs.
• Catecholamines and stimulants: sepsis, thyrotoxicosis, pheochromocytoma, cocaine, methamphetamine, caffeine.
• Drugs: QT-prolonging agents (Class IA/III antiarrhythmics, macrolides, fluoroquinolones, antipsychotics, methadone, ondansetron) and AV-nodal blockers/cholinesterase inhibitors for bradyarrhythmia.

• Abnormal automaticity: Spontaneous depolarization of non-nodal tissue occurs when resting membrane potential becomes less negative (closer to threshold), or threshold potential becomes more positive. This can occur in diseased myocardium, inflammatory states, or from enhanced normal automaticity due to catecholamines, hypoxia, or electrolyte derangements. Ectopic pacemakers compete with the SA node, potentially usurping normal rhythm control.

• Triggered activity: Arrhythmias result from afterdepolarizations occurring during or immediately after repolarization. Early afterdepolarizations (EADs) occur during phases 2-3 of the action potential, prolonged by long QT states, hypocalcemia, or Class IA/III antiarrhythmics. Delayed afterdepolarizations (DADs) occur after complete repolarization (phase 4), triggered by calcium overload seen in digitalis toxicity, heart failure, or catecholamine excess.

• Reentry mechanisms: Requires three conditions: (1) two functionally distinct conduction pathways with different refractory periods, (2) unidirectional block in one pathway, and (3) slow enough conduction in the alternate pathway allowing recovery of the blocked pathway's excitability. The impulse travels anterograde down one pathway and retrograde up the blocked pathway, establishing a circular wavefront. Classic anatomically-defined reentry occurs in Wolff-Parkinson-White (WPW) syndrome and atrioventricular nodal reentrant tachycardia (AVNRT), while functionally-defined reentry occurs in atrial fibrillation and ventricular fibrillation.

• Substrate abnormalities: Scarring from prior myocardial infarction, cardiomyopathies, structural heart disease, and fibrosis create areas of slow conduction and heterogeneous refractoriness, facilitating reentrant circuits. Electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia), acid-base disturbances, and autonomic tone modulation alter automaticity and conduction velocity.

• Palpitations: Patients frequently describe awareness of heartbeat, fluttering sensations, or pounding in the chest, often worse with exertion or emotional stress. Syncope or near-syncope accompanying palpitations suggests hemodynamically significant arrhythmia and carries ominous prognostic implications.

• Dyspnea and chest discomfort: Tachyarrhythmias increase myocardial oxygen demand while decreasing diastolic filling time, potentially causing anginal symptoms even in patients without coronary artery disease. In heart failure patients, rapid ventricular response can precipitate acute decompensation and pulmonary edema.

• Syncope and presyncope: Caused by decreased cerebral perfusion due to rapid heart rates preventing adequate diastolic filling and cardiac output reduction, or complete loss of organized cardiac output in ventricular fibrillation. Syncope without prodrome is more concerning than gradual presyncope.

• Asymptomatic arrhythmias: Many patients are unaware of their rhythm disturbance, discovered incidentally on ECG during routine screening. Asymptomatic atrial fibrillation still carries stroke risk and requires anticoagulation assessment.

• Hemodynamic instability: Hypotension, shock, altered mental status, and signs of hypoperfusion indicate hemodynamically unstable arrhythmia requiring immediate intervention (electrical cardioversion) rather than pharmacologic management.

• Fatigue and reduced exercise tolerance: Chronic arrhythmias, especially atrial fibrillation with rapid ventricular response, cause reduced cardiac output and exercise intolerance mimicking heart failure symptoms.

• Electrocardiogram (ECG): The gold standard for arrhythmia diagnosis, providing information on heart rate, rhythm regularity, PR interval, QRS duration, QT interval, and morphology. Serial or continuous monitoring captures paroxysmal events. The ECG precisely identifies arrhythmia type (specific tachycardia mechanism, bradycardia etiology, conduction abnormalities) and guides therapy selection.

• Holter monitor and event monitoring: 24-48 hour ambulatory recordings capture paroxysmal episodes in symptomatic patients with normal baseline ECGs. Event monitors (wearable or implantable) provide longer monitoring periods (weeks to months) with higher diagnostic yield for infrequent events. Newer extended monitoring devices detect asymptomatic arrhythmias.

• Electrophysiology study (EPS): Invasive testing using intracardiac catheters to precisely localize arrhythmia origin, identify dual AV nodal pathways (AVNRT), accessory pathways (WPW), or ventricular reentry circuits. EPS determines inducibility of arrhythmia and guides ablation therapy. Provides definitive mechanism identification when non-invasive testing is inconclusive.

• Echocardiography: Evaluates structural heart disease (cardiomyopathy, valvular disease, atrial enlargement) that predisposes to arrhythmias and helps risk-stratify sudden cardiac death. Identifies ejection fraction affecting antiarrhythmic drug selection and defibrillator indications.

• Stress testing and ischemia workup: Determines if arrhythmias are exercise-induced (suggesting increased automaticity or catecholamine sensitivity) or triggered by myocardial ischemia. Important in risk assessment and directing therapy.

• Laboratory evaluation: Electrolyte panel (potassium, magnesium, calcium), troponin (myocardial infarction), TSH (hyperthyroidism as precipitant), and digoxin levels when applicable. Blood gas analysis assesses acid-base status affecting automaticity.

• Important diagnostic pearls: The irregular irregularity of atrial fibrillation is pathognomonic; absence of P waves favors junctional or atrial fibrillation origin; wide QRS complexes (>120 ms) suggest ventricular origin or SVT with aberrancy; PR interval prolongation and delta waves indicate WPW syndrome with accessory pathway; concordance in precordial leads suggests ventricular tachycardia rather than SVT with aberrancy.

Supraventricular Tachycardias (SVT)

• Acute management of stable SVT: Vagal maneuvers (Valsalva, ice to face in infants) increase vagal tone and slow AV nodal conduction, terminating approximately 25% of SVT. Adenosine 6 mg IV bolus (12 mg second dose) is first-line pharmacotherapy, causing transient AV nodal blockade. Adenosine works within seconds and has 90% efficacy for AVNRT and AVRT; gives characteristic transient asystole visible on monitor. Verapamil or diltiazem (calcium channel blockers) are alternatives in patients without hypotension or heart failure.

• Chronic SVT management: Beta-blockers (metoprolol, atenolol) or calcium channel blockers reduce AV nodal conduction and suppress automaticity. Class IA antiarrhythmics (procainamide) or Class IC agents (flecainide) provide additional efficacy. Radiofrequency ablation is definitive therapy for AVNRT, AVRT, and focal atrial tachycardias, with >95% success rates and minimal recurrence.

• Atrial fibrillation/flutter rate control: Beta-blockers and non-dihydropyridine calcium channel blockers slow ventricular response by blocking AV nodal conduction. Diltiazem or verapamil preferred in acute settings; digoxin useful in sedentary patients or heart failure. Target resting heart rate <110 bpm (lenient control) is non-

Complications of the arrhythmia

• Cardioembolic stroke: stasis in the fibrillating left atrium and appendage promotes thrombus; signaled by abrupt focal deficit in a patient with irregularly irregular pulse. Emergency. The ACC/AHA/ACCP/HRS atrial fibrillation guideline bases prophylaxis on validated risk scores (CHA₂DS₂-VASc) rather than on AF pattern or symptom burden.
• Sudden cardiac death: degeneration of VT into ventricular fibrillation → no cardiac output. The shockable pair is ventricular fibrillation / pulseless VT; immediate defibrillation. Emergency.
• Tachycardia-mediated cardiomyopathy: sustained rapid rates impair diastolic filling and cause energetic depletion; presents as new low-EF heart failure that improves after rate/rhythm control. If HFrEF persists, treat with the four guideline-directed classes (ARNI or ACEI/ARB, beta blocker, MRA, SGLT2 inhibitor).
• Syncope with trauma, demand ischemia, and pulmonary edema: from loss of atrial contribution and shortened filling time, worst in HFpEF, HCM, and severe aortic stenosis.
• Asystole/complete heart block: escape-dependent rhythm in Mobitz II or third-degree block; wide QRS escape at a slow rate predicts collapse. Emergency — atropine, transcutaneous pacing, and transvenous pacing per ACLS.

Complications of therapy

• Proarrhythmia: Class IA/III agents prolong QT → torsades de pointes (treat with IV magnesium). Class IC agents increased mortality in post-infarction patients (CAST), so flecainide is avoided with structural or ischemic heart disease.
• AV nodal blockade in pre-excited AF: adenosine, diltiazem, or digoxin unmask the accessory pathway → very rapid ventricular response and VF. Emergency — use procainamide or synchronized cardioversion.
• Amiodarone toxicity: pulmonary fibrosis, hepatotoxicity, hypo- or hyperthyroidism, corneal microdeposits, blue-gray skin, optic neuropathy; potentiates warfarin and digoxin. Monitor TSH, LFTs, and pulmonary status.
• Anticoagulant hemorrhage: intracranial bleeding is an emergency; reversal with idarucizumab (dabigatran), andexanet alfa (factor Xa inhibitors), or 4-factor PCC plus vitamin K (warfarin).
• Procedural complications: ablation may cause tamponade, phrenic nerve injury, pulmonary vein stenosis, or rare atrioesophageal fistula (fever plus neurologic events — emergency); device implantation risks pneumothorax, pocket hematoma, lead infection, and inappropriate ICD shocks.

• Unstable = electricity, not drugs: hypotension, altered mental status, ischemic chest pain, or acute heart failure with any tachyarrhythmia → immediate synchronized cardioversion (defibrillation if pulseless VT/VF). The commonest stem trap is choosing adenosine or a rate-control drug in a hypotensive patient.
• WPW buzzwords: short PR interval plus a delta wave (slurred QRS upstroke) — pre-excitation shortens PR because the accessory pathway skips the AV nodal delay. In pre-excited (irregular, wide, very fast) atrial fibrillation, the single best next step is procainamide or cardioversion; AV nodal blockers (adenosine, verapamil, diltiazem, digoxin, beta blockers) are the classic wrong answer because they funnel conduction down the accessory pathway toward VF.
• Regular narrow-complex tachycardia at ~150–250 bpm with no visible P waves = AVNRT: vagal maneuvers, then adenosine 6 mg IV push (12 mg if needed). Definitive cure is catheter ablation.
• Wide-complex tachycardia in an older patient with prior MI is VT until proven otherwise — treat as VT; the distractor is calling it "SVT with aberrancy" and giving a nodal blocker. Favor VT with precordial concordance, extreme axis, very wide QRS, and fusion or capture beats.
• Torsades: polymorphic VT with a long QT → IV magnesium sulfate, stop offending drugs, correct K⁺ and Mg²⁺; overdrive pacing or isoproterenol for bradycardia-dependent (pause-dependent) forms.
• Block localization: Mobitz I (progressive PR lengthening, dropped beat) is AV nodal and usually benign; Mobitz II (fixed PR, sudden dropped beat) and third-degree block are infranodal and need a permanent pacemaker per the ACC/AHA/HRS bradycardia guideline. Atropine can worsen infranodal block.
• Anticoagulate by score, not by rhythm: per the ACC/AHA/ACCP/HRS atrial fibrillation guideline, a DOAC is preferred over warfarin except in mechanical valves and moderate-to-severe rheumatic mitral stenosis. Successful cardioversion or ablation does not by itself justify stopping anticoagulation.
• The one association examiners love: hyperthyroidism as an occult cause of new AF — check TSH; also holiday heart after binge drinking.