1.4 Cardiac Arrhythmias & Conduction Disorders

Cardiac Arrhythmias & Conduction Disorders

PANCE High-Yield Focus: Cardiac arrhythmias and conduction blocks are major testable concepts. Key focus areas include rate vs. rhythm control in atrial fibrillation, stroke risk stratification using the CHA2DS2-VASc score, dangerous pharmacology traps in Wolff-Parkinson-White (WPW) syndrome, and distinguishing between benign and dangerous atrioventricular (AV) blocks on ECG.

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Supraventricular and Atrial Arrhythmias

Atrial Fibrillation and Flutter

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. It arises from multiple chaotic, disorganized re-entrant electrical wavelets within the atria, typically triggered by ectopic beats originating in the pulmonary veins. Atrial flutter, by contrast, is characterized by a single, large macro-reentrant circuit around the tricuspid valve annulus in the right atrium.

• Pathophysiology: In AF, the rapid, chaotic atrial rate (350–600 bpm) leads to variable AV node conduction, resulting in an irregularly irregular ventricular response. The absence of coordinated atrial contraction ("atrial kick") causes stasis of blood in the left atrial appendage, raising the risk of thromboembolic stroke.
• Risk Factors: Advanced age, chronic hypertension, coronary artery disease, valvular heart disease (especially mitral stenosis), obesity, obstructive sleep apnea, and alcohol consumption ("holiday heart syndrome").
• Clinical Presentation: Patients present with palpitations, fatigue, dyspnea, lightheadedness, or syncope. The classic physical exam finding is an "irregularly irregular" pulse. In atrial flutter, a regular or regularly irregular pulse may be present, and the ECG demonstrates a classic "sawtooth" pattern of flutter waves (F-waves), most prominent in inferior leads (II, III, aVF).

Rate vs. Rhythm Control

For stable atrial fibrillation, the initial decision is choosing between rate and rhythm control.

• Rate Control: Typically preferred as the initial strategy. First-line agents include beta-blockers (e.g., Metoprolol, Esmolol) or non-dihydropyridine calcium channel blockers (e.g., Diltiazem, Verapamil). These agents slow conduction through the AV node.
  • Contraindication: Avoid non-dihydropyridine CCBs in patients with heart failure with reduced ejection fraction (HFrEF), as their negative inotropic effects can cause acute decompensation. Use Digoxin or Amiodarone instead in these patients.
• Rhythm Control: Recommended for patients who remain symptomatic despite rate control, younger patients, or those with heart failure exacerbated by AF. Rhythm control is achieved via electrical cardioversion, chemical cardioversion (using class I antiarrhythmics like Flecainide or Propafenone, or class III agents like Amiodarone, Sotalol, or Ibutilide), or radiofrequency catheter ablation.

Stroke Risk Assessment and Anticoagulation

Anticoagulation decisions are guided by the CHA2DS2-VASc scoring system:

• C: Congestive heart failure / LV dysfunction (1 point)
• H: Hypertension (1 point)
• A2: Age >= 75 years (2 points)
• D: Diabetes mellitus (1 point)
• S2: Stroke, TIA, or thromboembolism history (2 points)
• V: Vascular disease (prior MI, PAD, or aortic plaque) (1 point)
• A: Age 65–74 years (1 point)
• Sc: Sex category (Female) (1 point)

Clinical Decision Rules:

1. CHA2DS2-VASc Score >= 2 in men or >= 3 in women: Chronic oral anticoagulation is strongly recommended.
2. CHA2DS2-VASc Score of 1 in men or 2 in women: Anticoagulation can be considered based on shared decision-making.
3. DOACs vs. Warfarin: Direct Oral Anticoagulants (e.g., Apixaban, Rivaroxaban, Dabigatran) are preferred over Warfarin due to lower bleeding risks and no requirement for routine INR monitoring.
   • PANCE Exception: Warfarin is mandatory (and DOACs are contraindicated) for "valvular" atrial fibrillation, defined as AF in patients with a mechanical heart valve or moderate-to-severe mitral stenosis.
4. Cardioversion Timeline: If AF duration is <48 hours, cardioversion can be performed immediately. If AF has been present for >=48 hours or is of unknown duration, the patient must be anticoagulated for at least 3 weeks prior to cardioversion, OR a transesophageal echocardiogram (TEE) must be performed to rule out a thrombus in the left atrial appendage. In all cases, anticoagulation must be continued for at least 4 weeks post-cardioversion.

Wolff-Parkinson-White (WPW) Syndrome

WPW is a congenital pre-excitation syndrome involving an accessory conduction pathway (Bundle of Kent) that bypasses the AV node.

• ECG Triad: Shortened PR interval (<0.12 seconds), a slurred delta wave upstroke on the QRS, and a widened QRS complex (>0.12 seconds).
• PANCE Trap: If a patient with WPW develops atrial fibrillation, AV nodal blocking agents (ABCD: Adenosine, Beta-blockers, CCBs, Digoxin) are strictly contraindicated. Blocking the AV node allows rapid, unhindered conduction down the accessory pathway, which can lead to ventricular fibrillation and sudden death. Procainamide is the drug of choice for stable, pre-excited AF.

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Ventricular Arrhythmias

Ventricular Tachycardia (VT)

VT is defined as three or more consecutive premature ventricular contractions at a rate >100 bpm with a widened QRS complex (>0.12 seconds).

• Monomorphic VT: Regular rhythm with uniform QRS complexes, typically caused by a re-entrant circuit around a myocardial scar (e.g., post-MI).
• Polymorphic VT (Torsades de Pointes): Characterized by QRS complexes that continuously change in amplitude and twist around the baseline. It is caused by early afterdepolarizations in the setting of a prolonged QT interval (triggered by hypokalemia, hypomagnesemia, or QT-prolonging drugs like macrolides, fluoroquinolones, or antipsychotics).
• Management:
  • Stable VT with a pulse: Administer antiarrhythmic infusions, with intravenous Amiodarone or Lidocaine as first-line options. Procainamide is preferred in patients with preserved ejection fraction or WPW.
  • Unstable VT with a pulse: Perform immediate synchronized electrical cardioversion.
  • Pulseless VT or Ventricular Fibrillation (VF): Immediate defibrillation (unsynchronized cardioversion) and cardiopulmonary resuscitation (CPR).
  • Torsades de Pointes: Treat immediately with intravenous Magnesium Sulfate, regardless of the patient's baseline magnesium level. Discontinue all QT-prolonging drugs.

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Bundle Branch Blocks

Bundle branch blocks (BBB) are conduction delays in the His-Purkinje system below the AV node.

• Right Bundle Branch Block (RBBB): QRS > 0.12 seconds with an rSR' pattern in V1 and a wide, deep S wave in lead I and V6. Commonly benign in young, healthy patients; may be seen in atrial septal defect, right ventricular hypertrophy, pulmonary embolism, and coronary disease.
• Left Bundle Branch Block (LBBB): QRS > 0.12 seconds with a broad, notched R wave in V5/V6 and I, and a deep QS in V1. New LBBB is concerning — it can indicate acute myocardial ischemia/infarction and warrants evaluation with serial troponins and comparison to prior ECGs. Sgarbossa criteria identify STEMI equivalents in patients with LBBB.

PANCE Pearl: A wide QRS complex (>0.12 s) without a clear rhythm diagnosis should raise consideration of BBB, ventricular pacing, ventricular tachycardia, hyperkalemia, or WPW with aberrancy.

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Bradyarrhythmias and Conduction Blocks

Sinus Bradycardia

Defined as a sinus rhythm with a heart rate <60 bpm.

• Clinical Management: Treatment is only required if the patient is symptomatic (e.g., hypotension, altered mental status, chest pain, syncope). The first-line pharmacological treatment is intravenous Atropine (an anticholinergic agent that increases SA node discharge). If Atropine is ineffective, initiate transcutaneous pacing or start an epinephrine or dopamine infusion.

Atrioventricular (AV) Blocks

AV blocks result from delayed or blocked conduction of electrical impulses from the atria to the ventricles.