Arrhythmias

Sinus Arrhythmias

Sinus arrhythmias are rhythm disturbances that originate in the sinoatrial (SA) node, the normal pacemaker of the heart. On ECG, a sinus rhythm is defined by upright P waves in leads I, II, and aVF, a consistent P-wave morphology, each P wave followed by a QRS complex, and a normal PR interval of 120–200 ms. The normal adult resting sinus rate is 60–100 beats/min; rates below or above this range are termed sinus bradycardia and sinus tachycardia, respectively.

Basic Mechanism: SA Node Automaticity

The SA node is located near the junction of the superior vena cava and right atrium. It is supplied by the right coronary artery in approximately 60% of individuals and the left circumflex artery in approximately 40%; therefore, inferior myocardial infarction can cause sinus bradycardia or sinus node dysfunction.

Unlike ventricular myocytes, SA nodal cells lack a stable resting membrane potential. Their spontaneous depolarization depends on:

• Phase 4 pacemaker current: mediated mainly by the funny current (I_f) through HCN channels, which allows inward Na⁺ current during hyperpolarization.
• T-type and L-type Ca²⁺ channels: contribute to late phase 4 and phase 0 depolarization, respectively.
• K⁺ efflux: mediates repolarization.

Sympathetic stimulation via β₁-adrenergic receptors increases cAMP, enhancing I_f and Ca²⁺ currents, thereby increasing heart rate. Parasympathetic stimulation via vagal M₂ receptors decreases cAMP and increases K⁺ conductance, slowing phase 4 depolarization and decreasing heart rate.

Major Sinus Arrhythmias

Rhythm	ECG Finding	Common Causes	Step 1 Associations
Respiratory sinus arrhythmia	Cyclic variation in P-P interval, usually with normal P waves	Normal vagal tone, especially in children and young adults	Heart rate increases with inspiration and decreases with expiration
Sinus bradycardia	Sinus rhythm with rate <60/min	Athletic conditioning, sleep, hypothyroidism, hypothermia, inferior MI, β-blockers, non-dihydropyridine Ca2+ channel blockers, digoxin	Often benign if asymptomatic; symptomatic cases may cause syncope or hypotension
Sinus tachycardia	Sinus rhythm with rate >100/min, usually <160–180/min in adults at rest	Fever, pain, anxiety, hypovolemia, anemia, hyperthyroidism, pulmonary embolism, sepsis, stimulant use	Usually a physiologic response; treat the underlying cause
Sinus pause/arrest	Transient absence of P waves; pause is not a multiple of the baseline P-P interval	SA node failure, ischemia, medications, degenerative fibrosis	May cause dizziness, presyncope, or syncope if prolonged
SA exit block	Dropped P-QRS-T complex; pause is often an exact multiple of the P-P interval	Impaired conduction from SA node to atrium	Distinguish from sinus arrest by mathematical regularity of the pause

Respiratory Sinus Arrhythmia

Respiratory sinus arrhythmia is a normal physiologic rhythm variation caused by respiratory modulation of vagal tone. During inspiration, intrathoracic pressure decreases, venous return increases, and vagal tone transiently falls, causing the heart rate to increase. During expiration, vagal tone increases and heart rate slows. ECG shows sinus P waves with an irregular rhythm; the P-P interval variation is commonly >120 ms. This finding is most prominent in healthy young individuals and decreases with aging, diabetes, autonomic neuropathy, and heart failure.

Sinus Bradycardia

Sinus bradycardia is defined as a sinus rhythm with rate <60/min. It may be physiologic, especially during sleep or in endurance athletes due to increased vagal tone and increased stroke volume. Pathologic causes include hypothyroidism, hypothermia, increased intracranial pressure, hyperkalemia, inferior wall myocardial infarction, and drugs that suppress SA nodal automaticity.

High-yield drugs causing sinus bradycardia include β-blockers, verapamil, diltiazem, digoxin, amiodarone, and centrally acting α₂-agonists such as clonidine. In symptomatic unstable bradycardia, standard ACLS pharmacology uses atropine 1 mg IV every 3–5 minutes, maximum total dose 3 mg. Atropine is a competitive muscarinic antagonist that blocks vagal M₂ input to the SA and AV nodes, increasing heart rate. Persistent severe bradycardia may require catecholamine infusion or pacing, but Step 1 emphasis is on mechanism rather than procedural management.

Sinus Tachycardia

Sinus tachycardia is sinus rhythm with rate >100/min. It is usually not a primary arrhythmia but a response to increased metabolic demand or decreased effective circulating volume. Fever typically increases heart rate by approximately 10 beats/min per 1°C rise in body temperature. Other causes include pain, anxiety, pregnancy, anemia, hypovolemia, shock, hyperthyroidism, pheochromocytoma, pulmonary embolism, and stimulants such as cocaine, amphetamines, caffeine, and β-agonists.

ECG shows normal sinus P waves before each QRS complex with a regular rhythm. The key diagnostic principle is that sinus tachycardia has a plausible physiologic trigger and usually begins and ends gradually, unlike paroxysmal supraventricular tachycardia, which often starts and stops abruptly.

Sick Sinus Syndrome

Sick sinus syndrome, also called sinus node dysfunction, refers to impaired SA node impulse generation or conduction. It is most commonly due to age-related degenerative fibrosis of the SA node and surrounding atrial tissue. ECG patterns include sinus bradycardia, sinus pauses, sinus arrest, SA exit block, and alternating bradyarrhythmias and atrial tachyarrhythmias, termed tachy-brady syndrome.

The 2018 ACC/AHA/HRS bradycardia guideline emphasizes that there is no absolute heart-rate cutoff or pause duration that mandates permanent pacing in sinus node dysfunction; symptom correlation is essential. For Step 1, remember the classic presentation: an older patient with episodic dizziness, syncope, or palpitations and ECG evidence of sinus pauses or alternating bradycardia and atrial tachyarrhythmias.

Atrial Fibrillation

Atrial fibrillation is a supraventricular tachyarrhythmia characterized by disorganized atrial electrical activation with loss of coordinated atrial contraction. On ECG, it classically shows no discrete P waves, an irregularly irregular R-R interval, and usually a narrow QRS complex unless there is bundle branch block, ventricular pre-excitation, or rate-related aberrancy. The atrial rate is typically 350–600/min; the ventricular rate is variable because the AV node conducts only a fraction of atrial impulses, often producing a ventricular rate of 100–180/min when untreated.

Mechanism and Pathophysiology

Normal sinus rhythm begins in the sinoatrial node and spreads uniformly through atrial myocardium, producing a P wave and coordinated atrial systole. In atrial fibrillation, rapid ectopic firing and multiple reentrant wavelets create chaotic atrial activation. A high-yield anatomic fact is that many initiating ectopic foci arise near the pulmonary vein ostia in the left atrium. Structural atrial disease—especially dilation, fibrosis, inflammation, and increased atrial pressure—promotes nonuniform conduction and reentry.

The hemodynamic consequence is loss of the atrial kick, the late diastolic contribution of atrial contraction to ventricular filling. In healthy adults, atrial kick contributes roughly 10–20% of ventricular end-diastolic volume; its loss is especially important in patients with diastolic dysfunction, hypertrophic cardiomyopathy, mitral stenosis, or heart failure. Blood stasis, particularly in the left atrial appendage, predisposes to thrombus formation and systemic embolization, most importantly ischemic stroke.

Risk Factors and Associations

• Age: prevalence rises markedly with age; atrial fibrosis and conduction heterogeneity increase over time.
• Hypertension: the most common population-level risk factor; causes left ventricular hypertrophy and left atrial enlargement.
• Valvular disease: especially mitral stenosis or regurgitation causing left atrial dilation.
• Heart failure and coronary artery disease: promote atrial stretch, ischemia, and neurohormonal activation.
• Hyperthyroidism: increases beta-adrenergic tone and automaticity; check TSH in new-onset AF.
• Alcohol: acute binge drinking can cause “holiday heart syndrome.”
• Obstructive sleep apnea, obesity, pulmonary disease, post-cardiac surgery, and acute infection are common precipitants.

Classification

Category	Definition
First diagnosed	First detected episode, regardless of duration or symptoms.
Paroxysmal	Terminates spontaneously or with intervention within 7 days.
Persistent	Continuous AF lasting >7 days.
Long-standing persistent	Continuous AF lasting >12 months.
Permanent	AF accepted by patient and clinician; rhythm-control attempts are not pursued.

The term “valvular AF” is clinically important but narrow: it generally refers to AF with moderate-to-severe rheumatic mitral stenosis or a mechanical heart valve. These patients require warfarin rather than direct oral anticoagulants.

Stroke Risk Scoring and Anticoagulation

The CHA₂DS₂-VASc score estimates annual thromboembolic risk. Components are: congestive heart failure 1, hypertension 1, age ≥75 years 2, diabetes 1, stroke/TIA/systemic embolism 2, vascular disease 1, age 65–74 years 1, and female sex 1. Current ACC/AHA-style thresholds recommend oral anticoagulation for estimated annual stroke risk ≥2%, corresponding approximately to CHA₂DS₂-VASc ≥2 in men or ≥3 in women; it is reasonable to consider anticoagulation at 1 in men or 2 in women. The older Step 1 heuristic is: anticoagulate most patients with score ≥2.

DOACs are preferred over warfarin for most nonvalvular AF. Examples include apixaban 5 mg orally twice daily, rivaroxaban 20 mg orally daily with food, dabigatran 150 mg orally twice daily, and edoxaban 60 mg orally daily, with renal and age/weight adjustments. Warfarin inhibits vitamin K epoxide reductase, reducing factors II, VII, IX, X and proteins C/S; target INR is usually 2.0–3.0. Landmark trials supporting DOACs include RE-LY for dabigatran, ROCKET AF for rivaroxaban, and ARISTOTLE for apixaban; apixaban reduced stroke/systemic embolism and major bleeding compared with warfarin.

Rate Control, Rhythm Control, and Cardioversion

Initial management depends on hemodynamic stability. Unstable AF causing hypotension, ischemic chest pain, pulmonary edema, or altered mental status requires synchronized electrical cardioversion, commonly beginning at 120–200 J biphasic. In stable AF, rate control is often adequate. The AFFIRM trial showed no mortality advantage of rhythm control over rate control in many older high-risk patients, while RACE II showed lenient rate control, resting heart rate <110/min, was noninferior to strict control, resting <80/min, for major outcomes.

Drug/Class	Mechanism	Common Use or Caution
Metoprolol	β1 blockade decreases AV nodal conduction.	Rate control; IV often 5 mg every 5 min up to 15 mg. Avoid severe acute decompensated HF or bradycardia.
Diltiazem	Non-dihydropyridine Ca2+ channel blockade slows AV node.	Rate control; IV bolus often 0.25 mg/kg. Avoid significant systolic HF.
Digoxin	Increases vagal tone at AV node; inhibits Na+/K+-ATPase.	Useful in HF or sedentary patients; narrow therapeutic index, toxicity causes arrhythmias and visual changes.
Amiodarone	Class III K+ channel blockade with beta-blocking, Ca2+, and Na+ effects.	Rhythm or rate adjunct; very long half-life, roughly 40–60 days; toxicities include pulmonary fibrosis, thyroid dysfunction, hepatotoxicity, corneal deposits.

If AF duration is >48 hours or unknown, cardioversion can dislodge atrial thrombus; anticoagulation is generally required for 3 weeks before and 4 weeks after cardioversion, or a transesophageal echocardiogram may be used to exclude left atrial thrombus before earlier cardioversion.

Long QT Syndrome

Core definition and electrophysiologic mechanism

Long QT syndrome (LQTS) is a disorder of delayed ventricular repolarization, producing prolongation of the QT interval on ECG and predisposing to torsades de pointes, a polymorphic ventricular tachycardia that can degenerate into ventricular fibrillation and cause sudden cardiac death. The QT interval represents total ventricular depolarization plus repolarization; because it varies inversely with heart rate, it is interpreted as the corrected QT interval:

QTc = QT / √RR using the Bazett formula, where QT and RR are measured in seconds. Normal QTc is generally <440 ms in adult males and <460 ms in adult females. A QTc ≥480 ms is strongly suggestive of LQTS, and QTc ≥500 ms is associated with substantially increased torsades risk.

At the cellular level, LQTS reflects prolongation of the ventricular myocyte action potential, especially phase 2 and phase 3. This is usually due to either decreased outward potassium current or increased inward sodium/calcium current. Prolonged repolarization permits early afterdepolarizations, abnormal depolarizations occurring during phases 2 or 3, which may trigger premature ventricular beats and torsades de pointes.

Congenital long QT syndrome

Congenital LQTS is usually due to mutations in ion channel genes. It classically presents with syncope, seizures misdiagnosed as epilepsy, palpitations, or sudden death in children or young adults. The inheritance patterns are high-yield:

• Romano-Ward syndrome: autosomal dominant congenital LQTS without deafness.
• Jervell and Lange-Nielsen syndrome: autosomal recessive LQTS with congenital sensorineural deafness; usually more severe.

Subtype	Gene/channel	Mechanism	Classic trigger	ECG tendency
LQT1	KCNQ1, slow delayed rectifier K+ current, IKs	↓ outward K+ current	Exercise, especially swimming	Broad-based T waves
LQT2	KCNH2, hERG channel, rapid delayed rectifier K+ current, IKr	↓ outward K+ current	Sudden auditory/emotional stimuli	Low-amplitude or notched T waves
LQT3	SCN5A, cardiac Na+ channel	Persistent late Na+ influx	Rest or sleep	Long isoelectric ST segment

Acquired long QT syndrome

Acquired LQTS is more common than congenital disease and is usually caused by drugs, electrolyte abnormalities, or bradycardia. Many drugs prolong QT by blocking the hERG I_Kr potassium channel. Risk is increased by female sex, older age, structural heart disease, congenital channel variants, renal/hepatic impairment, drug interactions, and baseline QTc prolongation.

Category	High-yield examples	Mechanistic association
Antiarrhythmics	Class IA: quinidine, procainamide, disopyramide; Class III: sotalol, dofetilide, ibutilide, amiodarone	Delayed repolarization via K+ channel blockade; sotalol half-life about 12 hours
Antibiotics	Macrolides such as erythromycin, clarithromycin; fluoroquinolones such as levofloxacin, moxifloxacin	hERG blockade; risk increased with CYP inhibition
Psychiatric drugs	Haloperidol, ziprasidone, tricyclic antidepressants, citalopram	Delayed repolarization; TCAs also block fast Na+ channels in overdose
Electrolyte abnormalities	Hypokalemia, hypomagnesemia, hypocalcemia	Reduced repolarization reserve and increased early afterdepolarizations

Diagnosis and risk stratification

On ECG, torsades de pointes appears as polymorphic ventricular tachycardia with QRS complexes that seem to “twist” around the baseline. LQTS diagnosis uses ECG, history, and family history. The Schwartz score is a commonly tested framework: points are assigned for QTc duration, torsades, T-wave alternans, notched T waves, low heart rate for age, syncope, congenital deafness, and family history. A score >3.0 indicates high probability of LQTS; 1.5–3.0 intermediate probability; ≤1.0 low probability.

• QTc 450–459 ms in males: borderline.
• QTc ≥460 ms: abnormal in many scoring systems.
• QTc ≥480 ms: supports diagnosis when persistent and unexplained.
• QTc ≥500 ms: high-risk threshold for torsades, especially with symptoms.

Management principles and pharmacology

Step 1 emphasizes mechanism-based management rather than procedural details. In acquired LQTS, remove offending drugs and correct electrolytes, targeting potassium in the high-normal range, commonly 4.5–5.0 mEq/L, and normal magnesium. For acute torsades de pointes, magnesium sulfate 2 g IV is first-line, typically given over 10–15 minutes, even if serum magnesium is normal. Magnesium suppresses early afterdepolarizations without necessarily shortening the QT interval.

For congenital LQTS, beta blockers reduce adrenergically triggered events, especially in LQT1 and LQT2. Common agents include nadolol, often 1–1.5 mg/kg/day orally with a half-life of approximately 20–24 hours, and propranolol, often 2–3 mg/kg/day divided with a half-life of about 3–6 hours. Avoid QT-prolonging drugs and genotype-specific triggers. Implantable cardioverter-defibrillators are reserved for selected high-risk patients, such as survivors of cardiac arrest or recurrent events despite therapy.

USMLE key association: a young person with exertional syncope while swimming suggests LQT1; syncope after a loud alarm suggests LQT2; events during sleep suggest LQT3. Long QT predisposes to torsades de pointes, and torsades can progress to ventricular fibrillation and sudden cardiac death.

SVT

Supraventricular tachycardia (SVT) refers to tachyarrhythmias that originate above the ventricles, typically involving atrial tissue, the atrioventricular (AV) node, or an accessory pathway. On ECG, SVT is classically a regular narrow-complex tachycardia with a ventricular rate of approximately 150–250 beats/min and a QRS duration <120 ms, unless there is preexisting bundle branch block, rate-related aberrancy, or antidromic conduction through an accessory pathway.

The key Step 1 principle is that most paroxysmal SVTs are caused by reentry: a self-sustaining electrical circuit requiring two pathways with different conduction velocities and refractory periods. A premature atrial impulse may find one pathway refractory and travel down the other, then retrogradely reenter the first pathway once it has recovered, producing a rapid loop.

Major Mechanistic Classes

SVT Type	Core Mechanism	ECG / High-Yield Features
AV nodal reentrant tachycardia (AVNRT)	Reentry within or near the AV node using a slow pathway and fast pathway	Most common paroxysmal SVT. Regular narrow-complex tachycardia; P waves often hidden in QRS or seen as pseudo-R′ in V1 or pseudo-S waves in inferior leads. Usually short RP.
AV reentrant tachycardia (AVRT)	Reentry involving the AV node and an accessory pathway	Seen in Wolff-Parkinson-White physiology. Orthodromic AVRT is narrow-complex; antidromic AVRT is wide-complex.
Atrial tachycardia	Enhanced automaticity or microreentry from an ectopic atrial focus	Abnormal P-wave morphology; may have “warm-up” and “cool-down.” Less dependent on the AV node than AVNRT/AVRT.

AVNRT: Classic Reentry Physiology

In typical AVNRT, the AV node has a fast pathway with rapid conduction and a long refractory period, and a slow pathway with slower conduction and a shorter refractory period. A premature atrial contraction may arrive while the fast pathway is refractory, so it travels antegrade down the slow pathway. By the time the impulse reaches the distal common pathway, the fast pathway has recovered and conducts retrogradely back to the atrium. This creates a loop that activates atria and ventricles nearly simultaneously, explaining why P waves may be absent or buried in the QRS complex.

AVRT and Wolff-Parkinson-White Physiology

Accessory pathways are abnormal muscular connections between atria and ventricles that bypass the AV node. In Wolff-Parkinson-White (WPW) pattern, antegrade accessory pathway conduction during sinus rhythm produces a short PR interval <120 ms, delta wave from slurred ventricular upstroke, and a widened QRS. In orthodromic AVRT, impulses travel antegrade through the AV node and retrograde through the accessory pathway, producing a narrow-complex SVT. In antidromic AVRT, impulses travel antegrade through the accessory pathway and retrograde through the AV node, producing a wide-complex tachycardia that can mimic ventricular tachycardia.

ECG Approach

• Rate: usually 150–250/min in paroxysmal SVT.
• Regularity: AVNRT and AVRT are typically very regular.
• QRS duration: narrow if <120 ms; wide if aberrancy, bundle branch block, antidromic AVRT, or ventricular tachycardia.
• P waves: absent, retrograde, or closely related to QRS in AVNRT; abnormal morphology in atrial tachycardia.
• RP interval: short RP favors typical AVNRT or orthodromic AVRT; long RP suggests atrial tachycardia, atypical AVNRT, or permanent junctional reciprocating tachycardia.

Acute Pharmacology and Vagal Physiology

Because AVNRT and orthodromic AVRT require AV nodal conduction to sustain the circuit, therapies that transiently slow AV nodal conduction can terminate the rhythm. Vagal maneuvers increase parasympathetic input to the AV node via M2 muscarinic receptors, decreasing cAMP, reducing calcium current, and increasing potassium conductance. The modified Valsalva maneuver is more effective than standard Valsalva; the REVERT trial showed conversion in approximately 43% versus 17% of patients.

Therapy	Mechanism	High-Yield Dose / Fact
Adenosine	A1 receptor activation; Gi-mediated ↓cAMP, ↑K+ efflux, hyperpolarizes AV nodal tissue and transiently blocks AV nodal conduction	6 mg rapid IV push followed by flush; if ineffective, 12 mg may be repeated. Half-life 10 seconds. Causes flushing, chest pressure, dyspnea, and transient asystole sensation.
Beta blockers	β1 blockade decreases cAMP and slows AV nodal conduction	Useful for prevention or rate control in AV node–dependent SVT; examples include metoprolol and esmolol.
Non-dihydropyridine calcium channel blockers	Block L-type Ca2+ channels in AV nodal tissue	Verapamil and diltiazem slow AV nodal conduction; avoid in significant hypotension or severe systolic dysfunction.

Adenosine is both therapeutic and diagnostic: transient AV block can terminate AVNRT/AVRT or reveal underlying atrial flutter waves or atrial tachycardia. It is potentiated by dipyridamole and carbamazepine, while methylxanthines such as caffeine and theophylline antagonize its effect.

Important Safety Distinction

In a regular narrow-complex SVT, AV nodal blockade is usually appropriate. However, in preexcited atrial fibrillation with WPW, the rhythm is typically irregular and wide-complex; AV nodal blockers can paradoxically increase conduction down the accessory pathway and precipitate ventricular fibrillation. This distinction is high-yield: regular narrow SVT suggests AV node–dependent reentry, whereas irregular wide tachycardia in WPW is dangerous.

Definitive Therapy

Catheter ablation targets the slow pathway in AVNRT or the accessory pathway in AVRT. For AVNRT, success rates are commonly >95%, with recurrence generally <5% and risk of complete AV block approximately <1% in experienced centers. For Step 1, the key concept is that ablation removes the anatomic substrate required for reentry, unlike drugs that only modify conduction or refractoriness.

Sudden Cardiac Death

Sudden cardiac death (SCD) is unexpected death from a cardiac cause occurring within 1 hour of symptom onset if witnessed, or within 24 hours of having been seen alive and well if unwitnessed. For USMLE Step 1, SCD is best understood as the lethal endpoint of an electrical instability—most commonly ventricular tachycardia (VT) degenerating into ventricular fibrillation (VF)—superimposed on a vulnerable myocardial substrate.

Core electrophysiologic mechanism

Normal ventricular activation depends on coordinated depolarization through fast voltage-gated Na⁺ channels, followed by Ca²⁺-mediated contraction and K⁺-mediated repolarization. SCD occurs when this organized sequence is replaced by chaotic or extremely rapid ventricular activation, producing no effective stroke volume. Cerebral perfusion ceases within seconds; irreversible brain injury begins after approximately 4–6 minutes without circulation.

The major arrhythmogenic mechanisms are:

• Re-entry: the most important mechanism in ischemic scar. A wavefront repeatedly circles an anatomic or functional obstacle when conduction is slowed and refractory periods are heterogeneous.
• Triggered activity: afterdepolarizations produce extra beats. Early afterdepolarizations occur in prolonged repolarization, especially long QT syndromes; delayed afterdepolarizations occur with intracellular Ca²⁺ overload, as in digoxin toxicity or catecholaminergic states.
• Abnormal automaticity: ischemic or diseased ventricular cells spontaneously depolarize because the resting membrane potential becomes less negative.

Major causes and risk substrates

Category	High-yield examples	Mechanistic link to SCD
Coronary artery disease	Acute MI, prior MI scar	Ischemia decreases ATP, impairs Na+/K+-ATPase, increases extracellular K+, slows conduction, and promotes re-entry. CAD accounts for approximately 70–80% of adult SCD.
Structural cardiomyopathy	Dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy	Fibrosis, hypertrophy, and chamber dilation create conduction heterogeneity and ventricular ectopic foci.
Inherited channelopathies	Long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT	Ion-channel dysfunction causes repolarization instability or catecholamine-triggered ventricular arrhythmias in structurally normal hearts.
Electrolyte/drug causes	Hypokalemia, hyperkalemia, hypomagnesemia; class IA/III antiarrhythmics, macrolides, fluoroquinolones, antipsychotics	Altered membrane excitability or QT prolongation predisposes to torsades de pointes and VF.
Mechanical/other	Commotio cordis, massive pulmonary embolism, aortic rupture	Either primary VF from a timed chest impact or electromechanical circulatory collapse.

Rhythm classification in cardiac arrest

Cardiac arrest rhythms are classified as shockable or non-shockable. This distinction is high-yield because defibrillation terminates disorganized ventricular electrical activity but does not correct absent electrical activity.

Rhythm	ECG concept	Defibrillation?
Ventricular fibrillation	Chaotic ventricular electrical activity; no organized QRS complexes	Yes
Pulseless ventricular tachycardia	Wide-complex tachycardia without pulse	Yes
Asystole	Absent ventricular electrical activity	No
Pulseless electrical activity	Organized electrical rhythm without mechanical pulse	No

Immediate pharmacology and physics of resuscitation

Defibrillation delivers a synchronized mass depolarization of myocardial cells, forcing Na⁺ channels into refractoriness and allowing the sinoatrial node or other pacemakers to regain control. For adult VF/pulseless VT, biphasic defibrillation is typically 120–200 J initially, escalating if unsuccessful; monophasic defibrillation uses 360 J. Early defibrillation is critical: survival from VF arrest falls by about 7–10% per minute without CPR and defibrillation.

Medication	Typical adult arrest dose	Mechanism/high-yield point
Epinephrine	1 mg IV/IO every 3–5 min	α1-mediated vasoconstriction raises aortic diastolic pressure and coronary perfusion pressure during CPR.
Amiodarone	300 mg IV/IO bolus, then 150 mg if needed	Class III antiarrhythmic with K+ channel blockade; also blocks Na+, Ca2+, and β receptors. Very long terminal half-life, approximately weeks.
Lidocaine	1–1.5 mg/kg IV/IO, then 0.5–0.75 mg/kg; max 3 mg/kg	Class IB Na+ channel blocker, preferentially affects ischemic ventricular tissue; half-life about 1.5–2 hours.
Magnesium sulfate	1–2 g IV	Used for torsades de pointes, especially with prolonged QT or hypomagnesemia; stabilizes repolarization.

Prevention: risk stratification and ICDs

The strongest population-level predictor of SCD risk in structural heart disease is reduced left ventricular ejection fraction (LVEF). Normal LVEF is approximately 55–70%. Current guideline-based primary prevention generally considers an implantable cardioverter-defibrillator (ICD) in patients with ischemic or nonischemic cardiomyopathy, LVEF ≤35%, appropriate heart failure symptoms, and expected survival greater than 1 year after optimized medical therapy. In ischemic disease, ICD placement is generally delayed until at least 40 days after MI and often 90 days after revascularization, because early post-MI ventricular dysfunction may improve.

Landmark ICD trials are frequently referenced conceptually: MADIT-II showed mortality benefit in prior MI with LVEF ≤30%; SCD-HeFT showed benefit of ICD therapy in NYHA class II–III heart failure with LVEF ≤35%. ICDs terminate VT/VF by antitachycardia pacing or shocks, addressing the final electrical pathway of SCD but not the underlying cardiomyopathy.

Step 1 integration

Think of SCD as a convergence of substrate plus trigger. The substrate may be scar, hypertrophy, fibrosis, or an ion-channel mutation; the trigger may be ischemia, sympathetic surge, electrolyte abnormality, or a QT-prolonging drug. The final common pathway is usually VT/VF causing abrupt loss of cardiac output. High-yield associations include post-MI scar causing re-entry, hypertrophic cardiomyopathy causing exertional SCD in young athletes, long QT causing torsades, Brugada syndrome causing nocturnal VF, and commotio cordis causing VF after a chest blow during the vulnerable repolarization period.