DPT2 Exam 6: Arrhythmia

Q: What is Phase 4 in SA node action potential?

Spontaneous depolarization (pacemaker potential) due to If funny current and T-type Ca²⁺ channels, reaching threshold at about –40 to –30 mV.

Q: What happens in Phase 0 of SA node action potential?

Depolarization phase where the action potential is initiated, mainly by Ca²⁺ influx through T-type channels.

Q: What occurs in Phase 3 of SA node action potential?

Repolarization due to K⁺ efflux, returning membrane potential toward –60 mV before the next cycle begins.

Q: What happens in Phase 0 of myocyte action potential?

Rapid depolarization caused by Na⁺ influx through fast sodium channels.

Q: What occurs in Phase 1 of myocyte action potential?

Early partial repolarization due to inactivation of Na⁺ current and K⁺ efflux.

Q: What is Phase 2 in myocyte action potential?

Plateau phase caused by slow Ca²⁺ influx (L-type channels), which triggers contraction.

Q: What happens in Phase 3 of myocyte action potential?

Repolarization as Ca²⁺ channels close and K⁺ efflux dominates.

Q: What is Phase 4 in myocyte action potential?

Resting membrane potential maintained by Na⁺/K⁺ ATPase and background currents.

Q: What is the refractory period in myocytes?

Phases 1–3; includes absolute refractory period (no AP possible) and relative refractory period (AP possible with strong stimulus).

Q: What does a normal ECG show?

P wave (atrial depolarization), PR interval (SA to AV conduction), QRS complex (ventricular depolarization), T wave (ventricular repolarization).

Q: Key ECG feature of atrial fibrillation?

Irregularly irregular rhythm, no distinct P waves, fibrillatory baseline, variable ventricular response.

Q: Key ECG feature of atrial flutter?

Sawtooth pattern of flutter waves, usually regular ventricular response (2:1, 3:1 conduction).

Q: How does PSVT appear on ECG?

Sudden onset and termination of rapid, regular narrow QRS tachycardia; P waves often hidden in QRS.

Q: ECG feature of ventricular tachycardia?

Wide QRS complexes (>120 ms), rate >100 bpm, may be monomorphic (same QRS shape) or polymorphic.

Q: What is characteristic of torsades de pointes on ECG?

Polymorphic VT with QRS complexes twisting around the baseline; associated with prolonged QT interval.

Q: How does ventricular fibrillation look on ECG?

Chaotic, irregular waveform with no identifiable P, QRS, or T waves; no effective cardiac output.

Q: What does sinus bradycardia show on ECG?

Normal P-QRS-T sequence but heart rate <60 bpm.

Q: First-degree AV block ECG feature?

Prolonged PR interval (>200 ms), all impulses conducted.

Q: Mobitz I (Wenckebach) ECG feature?

Progressive PR prolongation until a QRS is dropped.

Q: Mobitz II ECG feature?

Constant PR interval with intermittent dropped QRS complexes.

Q: Third-degree AV block ECG feature?

Complete AV dissociation; atria and ventricles beat independently.

Q: How does hyperkalemia affect ECG?

Tall, peaked T waves; severe cases may cause widened QRS and sine-wave pattern.

Q: How does hypokalemia affect ECG?

Flattened or inverted T waves, ST depression, prominent U waves.

Q: How does hypocalcemia affect ECG?

Prolonged QT interval (due to delayed repolarization).

Q: How does hypercalcemia affect ECG?

Shortened QT interval.

Q: Which other metabolic disturbances can alter ECG?

Acid-base imbalances, hypoxia, infections, CNS disorders, endocrine abnormalities.

Q: How do antiarrhythmic drugs affect ECG?

Can prolong QT interval and alter repolarization (T wave and ST segment changes).

Q: What are channelopathies?

Inherited arrhythmogenic diseases involving ion channel mutations (e.g., K⁺, Na⁺, Ca²⁺ channels).

Q: Examples of genetic arrhythmia syndromes?

Long QT Syndrome (LQTS) – prolonged QT interval, risk of torsades de pointes.

Short QT Syndrome (SQTS) – shortened QT interval.

Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) – triggered by stress/exercise.

Q: What is the mechanism of automatic tachyarrhythmias?

Increased slope of phase 4 depolarization or decreased threshold potential in pacemaker or ectopic cells.

Q: Key characteristics of automatic tachyarrhythmias?

No initiating event (spontaneous onset).

Gradual acceleration and deceleration of rate.

Cannot be induced by programmed stimulation.

Initiating and subsequent beats look similar.

Q: Common causes of automatic tachyarrhythmias?

Digitalis toxicity, hypokalemia, hypoxia, increased sympathetic activity, decreased parasympathetic activity.

Q: Examples of automatic tachyarrhythmias?

Sinus tachycardia, atrial tachycardia, ventricular tachycardia (due to enhanced automaticity).

Q: What is the mechanism of reentrant tachyarrhythmias?

Continuous propagation of an impulse through a reentry circuit, repeatedly activating tissue.

Q: Requirements for reentry (anatomic model)?

Two pathways for impulse conduction.

Unidirectional block in one pathway.

Slow conduction in the other pathway allowing retrograde entry.

Q: Key characteristics of reentrant tachyarrhythmias?

Initiating event present (usually a premature beat).

Abrupt onset and termination.

Can be induced by programmed stimulation.

Subsequent beats differ from initiating beat.

Q: Examples of reentrant tachyarrhythmias?

AV nodal reentrant tachycardia (AVNRT), AV reentrant tachycardia (AVRT), atrial flutter, ventricular tachycardia.

Q: During which phase do EADs occur?

Phases 2 or 3 (plateau or repolarization phase).

Q: What causes EADs?

Prolonged action potential duration → delayed repolarization → reopening of Ca²⁺ or Na⁺ channels.

Q: Conditions associated with EADs?

Long QT syndrome

Hypokalemia

Drugs that prolong QT (Class Ia and III antiarrhythmics)

Congenital ion channel abnormalities.

Q: Clinical risk of EADs?

Can trigger torsades de pointes and polymorphic ventricular tachycardia.

Q: During which phase do DADs occur?

Phase 4 (after repolarization, during resting potential).

Q: What causes DADs?

Intracellular Ca²⁺ overload → activation of Na⁺/Ca²⁺ exchanger → inward Na⁺ current → secondary depolarization.

Q: Conditions associated with DADs?

Digoxin toxicity

Catecholamine excess (stress/exercise)

Rapid heart rates

Genetic mutations affecting calcium handling.

Q: Clinical risk of DADs?

Can trigger atrial or ventricular tachycardia.

Q: What are supraventricular arrhythmias?

Arrhythmias originating above the ventricles (atria or AV node), often presenting with palpitations, dizziness, or syncope.

Q: What are the main types of supraventricular arrhythmias?

Atrial flutter (AFl)

Atrial fibrillation (AF)

Paroxysmal supraventricular tachycardia (PSVT)

Automatic atrial tachycardia

Q: Mechanism of AF and AFl?

Reentry is predominant; AF involves multiple pathways, AFl usually a single circuit.

Q: What is PSVT?

Sudden-onset, regular tachycardia originating above ventricles; often due to AV nodal reentry (AVNRT) or AV reentrant tachycardia (AVRT).

Q: Mechanism of AVNRT?

Dual AV nodal pathways (slow and fast); premature atrial beat triggers reentry circuit.

Q: Mechanism of AVRT?

Uses AV node and an accessory pathway (e.g., Wolff-Parkinson-White syndrome).

Q: What is automatic atrial tachycardia?

Multiple ectopic atrial pacemakers; often associated with severe pulmonary disease.

Q: Major complication of AF?

Embolic stroke due to atrial thrombus formation from blood stasis.

Q: What is the most serious complication of atrial fibrillation?

Embolic stroke due to thrombus formation in the atria from blood stasis.

Q: Why does atrial fibrillation increase stroke risk?

Loss of atrial contraction → stagnant blood in atria → thrombus formation → embolization to systemic circulation.

Q: Other complications of atrial fibrillation?

Heart failure (due to rapid ventricular response and loss of atrial contribution to cardiac output).

Tachycardia-induced cardiomyopathy (persistent high heart rate).

Increased mortality risk in patients with underlying heart disease.

Q: What is the ventricular rate in AF and why is it significant?

120-180 bpm; can worsen cardiac output and precipitate symptoms like syncope or angina.

Q: What is ventricular fibrillation?

A life-threatening arrhythmia characterized by chaotic, disorganized ventricular electrical activity.

Q: What is the effect of VF on cardiac output?

No effective cardiac output, leading to immediate hemodynamic collapse.

Q: What is the underlying mechanism of VF?

Classic reentry mechanisms with multiple foci throughout the ventricles.

Q: Common causes of VF?

Ischemic heart disease (especially MI)

Severe left ventricular dysfunction

Heart failure

Electrolyte disturbances.

Q: Mortality and recurrence risk in VF?

Responsible for ~350,000 deaths/year.

High recurrence risk in resuscitated patients.

Q: ECG appearance of VF?

Chaotic, irregular waveform with no identifiable P, QRS, or T waves.

Q: What is ventricular tachycardia?

A rapid rhythm originating in the ventricles, defined as ≥3 consecutive ventricular premature beats (VPBs) at >100 bpm.

Q: What are the two main types of VT?

Monomorphic VT: QRS complexes have a consistent shape and size (single focus).

Polymorphic VT: QRS complexes vary in shape and size (multiple foci).

Q: What is torsades de pointes?

A polymorphic VT associated with prolonged QT interval, characterized by QRS complexes twisting around the baseline.

Q: Common causes of VT?

Ischemia (especially MI)

Electrolyte abnormalities (hypokalemia, hypoxemia)

Drug toxicity (e.g., digitalis)

Structural heart disease (cardiomyopathy, LV dysfunction).

Q: What mechanisms underlie VT?

Enhanced automaticity

Reentry circuits (microreentry in Purkinje network often responsible for chronic VT).

Q: Why is VT dangerous?

Can progress to ventricular fibrillation, causing sudden cardiac death.

Q: What is sinus bradycardia?

Heart rate < 60 bpm, which may reduce cardiac output (normal in well-trained athletes).

Q: How does sinus bradycardia typically present in patients?

Often asymptomatic in healthy individuals or athletes.

Symptomatic cases: fatigue, dizziness, syncope, or reduced exercise tolerance due to decreased cardiac output.

Q: What are common causes of sinus bradycardia?

Idiopathic SA node degeneration

Drug effects (β-blockers, calcium channel blockers, digoxin)

Medical conditions: hypothyroidism, liver disease, hypoxia, acute hypertension, increased vagal tone.

Q: What is the key ECG finding in sinus bradycardia?

Prolonged R–R interval with normal P-QRS-T sequence.

Q: What related conditions may occur with sinus bradycardia?

Sick sinus syndrome (intrinsic SA node disease)

Tachycardia–bradycardia syndrome (episodes of tachyarrhythmia followed by prolonged sinus pause).

Q: What are bradyarrhythmias?

Arrhythmias characterized by slow heart rate due to impaired impulse formation or conduction (usually <60 bpm).

Q: What are the main types of bradyarrhythmias?

Sinus bradycardia

Atrioventricular (AV) block (first, second, third degree)

Tachycardia–bradycardia syndrome.

Q: What are general clinical features of bradyarrhythmias?

Reduced cardiac output

Symptoms: fatigue, dizziness, syncope

May be asymptomatic in athletes or mild cases.

Q: Common causes of bradyarrhythmias?

Increased vagal tone

Drug effects (β-blockers, calcium channel blockers, digoxin)

Ischemia, myocarditis

SA node or AV node disease

Electrolyte imbalances.

Q: What ECG changes are seen in bradyarrhythmias?

Sinus bradycardia: prolonged R–R interval

AV block: prolonged PR interval (first degree), dropped QRS (second degree), AV dissociation (third degree).

Q: What is an AV block?

Delay or interruption of conduction from atria to ventricles through the AV node or His-Purkinje system.

Q: ECG feature of first-degree AV block?

Prolonged PR interval (>200 ms); all atrial impulses reach ventricles.

Q: Clinical significance of first-degree AV block?

Usually benign and often asymptomatic.

Q: What are the two types of second-degree AV block?

Mobitz I (Wenckebach) and Mobitz II.

Q: ECG feature of Mobitz I?

Progressive PR interval prolongation until a QRS complex is dropped.

Q: ECG feature of Mobitz II?

Constant PR interval with intermittent dropped QRS complexes (no progressive lengthening).

Q: Which type of second-degree AV block is more dangerous?

Mobitz II (high risk of progression to complete block).

Q: ECG feature of third-degree AV block?

No atrial impulses conduct to ventricles; atria and ventricles beat independently (AV dissociation).

Q: Clinical significance of third-degree AV block?

Severe symptoms (syncope, fatigue); requires immediate intervention (pacemaker).

Q: Where do these blocks usually occur?

First-degree: AV node

Mobitz I: AV node

Mobitz II: His-Purkinje system

Third-degree: AV node or below.

Q: What is the mechanism of Class I antiarrhythmics?

Block Na⁺ channels in non-nodal cardiac myocytes → ↓ phase 0 upstroke, ↓ conduction velocity.

Q: Subclasses of Class I and their effects?

Ia: ↑ AP duration (also blocks K⁺ channels) – Quinidine, Procainamide.

Ib: ↓ AP duration – Lidocaine, Mexiletine.

Ic: No effect on AP duration – Flecainide, Propafenone.

Q: Mechanism of Class II antiarrhythmics?

Block β-adrenergic receptors → ↓ SA node automaticity, ↓ AV node conduction, ↑ refractoriness.

Examples: Metoprolol, Esmolol.

Q: Mechanism of Class III antiarrhythmics?

Block K⁺ channels → prolong repolarization and AP duration → ↑ refractory period.

Examples: Amiodarone, Dronedarone, Dofetilide, Sotalol.

Q: Mechanism of Class IV antiarrhythmics?

Block L-type Ca²⁺ channels → slow SA and AV node conduction, ↓ automaticity, ↑ refractoriness.

Examples: Verapamil, Diltiazem.

Q: Examples of unclassified antiarrhythmics and their actions?

Adenosine: Activates K⁺ current, hyperpolarizes SA/AV nodes, ↓ automaticity.

Digoxin: Vagotonic effect, ↑ AV node refractoriness.

Magnesium: Stabilizes membrane, used in torsades de pointes.

Q: How do antiarrhythmic drugs slow automatic rhythms?

Decrease slope of phase 4 depolarization (slows pacemaker activity).

Increase threshold potential (harder to reach AP initiation).

Reduce calcium or sodium influx in nodal tissue (Class II & IV drugs).

Q: How do drugs prevent reentry?

Prolong action potential duration (Class III, some Class Ia) → increases refractory period.

Slow conduction velocity (Class I drugs) → disrupts reentry circuit timing.

Q: How do drugs suppress EADs (Early Afterdepolarizations)?

Shorten QT interval or stabilize repolarization (e.g., magnesium for torsades).

Reduce AP prolongation (avoid excessive Class III effect).

Beta-blockers reduce sympathetic stimulation that can trigger EADs.

Q: How do drugs suppress DADs (Delayed Afterdepolarizations)?

Reduce intracellular calcium overload (Class IV calcium channel blockers, beta-blockers).

Digoxin toxicity management (stop digoxin, use anti-digoxin Fab if severe).

Stabilize membrane potential (Class I agents can help reduce triggered activity).

Q: How do Class I antiarrhythmics work?

Block fast Na⁺ channels in non-nodal tissue → ↓ phase 0 upstroke → slows conduction velocity.

Effect: Reduces automaticity and reentry.

Examples:

Ia: Also block K⁺ channels → ↑ AP duration (Procainamide, Quinidine).

Ib: ↓ AP duration (Lidocaine, Mexiletine).

Ic: No effect on AP duration (Flecainide, Propafenone).