4.1 Atrial Fibrillation, Atrial Flutter & Supraventricular Tachycardias

Pathophysiology & Hemodynamic Impact of Atrial Fibrillation

Atrial Fibrillation (AF) is the most common cardiac arrhythmia encountered in acute and critical care cardiac units. It is characterized by chaotic, uncoordinated atrial electrical activation occurring at rates between 350 and 600 impulses per minute, leading to mechanical standstill of the atria.

Electrophysiological Mechanisms

1. Pulmonary Vein Sleeve Ectopy: The vast majority of paroxysmal AF episodes are triggered by rapidly firing ectopic foci localized within the muscular sleeves of the pulmonary veins as they enter the left atrium.
2. Multiple Micro-Reentrant Wavelets: Structural remodeling, atrial fibrosis, and cellular hypertrophy promote spatial heterogeneity in conduction velocity and refractoriness. This allows multiple micro-reentrant wavelets to wander continuously throughout both atria, perpetuating the arrhythmia.
3. AV Nodal Filtering & Variable Ventricular Response: The AV node acts as an electrical gatekeeper. Due to its decremental conduction properties and long refractory period, it limits the number of atrial impulses transmitted to the ventricles. However, conduction remains irregular, resulting in the classic 'irregularly irregular' ventricular response on ECG.

Hemodynamic Consequences

• Loss of Atrial Kick: In sinus rhythm, active atrial contraction contributes 20% to 30% of total left ventricular end-diastolic volume (LVEDV), known as the 'atrial kick.' In patients with non-compliant ventricles (e.g., severe aortic stenosis, hypertrophic cardiomyopathy, or heart failure with preserved ejection fraction / HFpEF), loss of the atrial kick precipitously reduces stroke volume and cardiac output, triggering acute pulmonary venous congestion and cardiogenic shock.
• Rate-Induced Diastolic Shortening: Rapid ventricular response (RVR > 110-120 bpm) severely curtails diastolic filling time. Because coronary perfusion occurs predominantly during diastole, tachycardia increases myocardial oxygen demand while simultaneously decreasing myocardial oxygen supply.
• Tachycardia-Induced Cardiomyopathy (TIC): Sustained ventricular rates > 100-110 bpm over weeks to months induce progressive left ventricular dilation, cellular energetic depletion, and systolic dysfunction, which is often reversible upon rate or rhythm restoration.

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Stroke Risk Stratification & Anticoagulation Protocols

Because the atria lack effective mechanical contraction during AF, blood stasis occurs, predominantly within the Left Atrial Appendage (LAA). Fibrin and platelet aggregates form thrombi that can embolize into the systemic circulation, causing ischemic stroke or visceral infarction.

Stroke Risk Assessment: CHA2DS2-VASc Score

All patients with non-valvular AF must be risk-stratified using the CHA2DS2-VASc scoring system to determine the clinical indication for long-term oral anticoagulation.

Clinical Management Rules Based on Score

• Score = 0 in males / 1 in females: Low risk; no antithrombotic therapy recommended.
• Score = 1 in males / 2 in females: Moderate risk; oral anticoagulation may be considered based on individual clinical judgment and patient preferences.
• Score ≥ 2 in males / ≥ 3 in females: High risk; oral anticoagulation is strongly recommended unless absolute contraindications exist.

Anticoagulation Selection

• Direct Oral Anticoagulants (DOACs): DOACs are preferred over Warfarin for non-valvular AF due to lower risks of intracranial hemorrhage, fixed dosing without routine monitoring, and rapid onset. Options include Apixaban (5 mg BID, reduced to 2.5 mg BID if meeting 2 of: age ≥80, weight ≤60 kg, serum creatinine ≥1.5 mg/dL), Rivaroxaban (20 mg daily with evening meal), and Dabigatran (150 mg BID).
• Warfarin (Vitamin K Antagonist): Mandatory in patients with valvular AF (defined as AF in the presence of moderate-to-severe rheumatic mitral stenosis or a mechanical heart valve). Target International Normalized Ratio (INR) is 2.0 to 3.0 (or 2.5 to 3.5 for mechanical mitral valves).
• Bleeding Risk Evaluation: The HAS-BLED score (Hypertension, Abnormal renal/liver function, Stroke history, Bleeding history, Labile INR, Elderly >65, Drugs/alcohol) evaluates bleeding risk. A high HAS-BLED score (≥3) alerts the clinician to correct modifiable bleeding risk factors (e.g., uncontrolled hypertension, concurrent NSAID/aspirin use) but rarely justifies withholding anticoagulation in high stroke-risk patients.

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Rate vs. Rhythm Control & Cardioversion Guidelines

Rate Control Strategy

Rate control accepts AF as the underlying rhythm and focuses on controlling the ventricular response rate. Target resting heart rate is < 110 bpm (lenient control per the RACE II trial) in asymptomatic patients, or < 80 bpm (strict control) if symptoms or LV dysfunction persist.

Rhythm Control & Cardioversion Guidelines

Rhythm control attempts to restore and maintain sinus rhythm using antiarrhythmics or direct current cardioversion (DCCV). Rhythm control is favored in hemodynamically unstable patients, newly diagnosed AF, young patients, or those remaining symptomatic despite adequate rate control.

• Pharmacological Cardioversion Agents: Ibutilide (1 mg IV over 10 min; monitor QTc for 4 hours due to Torsades risk), Flecainide / Propafenone (Class IC 'pill-in-the-pocket' for patients without structural heart disease), Amiodarone, or Dofetilide (requires 3-day inpatient telemetry setup for QTc monitoring and renal dose adjustment).
• Direct Current Cardioversion (DCCV): Synchronized delivery of 120 to 200 Joules biphasic energy on the R wave to prevent delivery during the vulnerable repolarization phase (T wave), which could precipitate VF.

Thromboembolic Risk & Cardioversion Timing Rules

1. AF Duration < 48 Hours: Cardioversion can be performed immediately without prior prolonged anticoagulation if the patient is unstable. Anticoagulation should be initiated as soon as possible before or during the procedure.
2. AF Duration ≥ 48 Hours or Unknown Duration: Cardioversion carries a high risk of dislodging an established LAA thrombus. Two clinical pathways exist:
   • Strategy A (Conventional): Therapeutic anticoagulation for at least 3 consecutive weeks prior to cardioversion, followed by at least 4 weeks of post-cardioversion anticoagulation.
   • Strategy B (TEE-Guided): Perform a Transesophageal Echocardiogram (TEE) to inspect the left atrium and LAA. If no thrombus is visualized, immediate cardioversion is safe, provided therapeutic anticoagulation (e.g., heparin drip or DOAC) is active. Post-cardioversion anticoagulation must still be continued for at least 4 weeks regardless of baseline CHA2DS2-VASc score due to post-cardioversion 'atrial stunning.'

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Atrial Flutter Mechanics & Electrophysiology

Atrial Flutter is a macro-reentrant atrial tachycardia characterized by rapid, highly regular atrial waves ('sawtooth' or 'F' waves) at an atrial rate typically between 250 and 350 bpm (classic rate ~300 bpm).

Electrophysiological Circuit

• Typical (Type I) Atrial Flutter: Dependent on a macro-reentrant pathway circulating around the Cavotricuspid Isthmus (CTI)—the zone of slow conduction bounded by the inferior vena cava orifice, the tricuspid valve annulus, and the Eustachian ridge in the right atrium. Counterclockwise circulation produces inverted sawtooth F waves in inferior leads (II, III, aVF).
• AV Conduction Ratios: The AV node cannot conduct 300 impulses per minute. It typically establishes a fixed conduction block ratio:
  • 2:1 Conduction: Atrial rate 300 bpm → Ventricular response 150 bpm (the classic narrow-complex tachycardia presenting at exactly 150 bpm).
  • 4:1 Conduction: Atrial rate 300 bpm → Ventricular response 75 bpm.
  • Variable conduction can mimic the irregular ventricular response of AF.
• Definitive Treatment: Radiofrequency Catheter Ablation of the cavotricuspid isthmus creating a line of bidirectional conduction block. CTI ablation has a high success rate (>95%) and is the definitive treatment of choice for recurrent typical atrial flutter.

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Supraventricular Tachycardias (AVNRT, AVRT & WPW Syndrome)

Supraventricular Tachycardia (SVT) encompasses tachycardias originating above the bundle branches, characterized by narrow QRS complexes (< 120 ms) and rapid regular rates (150-250 bpm).

AV Nodal Reentrant Tachycardia (AVNRT)

• Mechanism: Dual pathways within the AV node: a fast pathway (rapid conduction, long refractory period) and a slow pathway (slow conduction, short refractory period). A premature atrial contraction (PAC) finds the fast pathway refractory, conducts down the slow pathway, and returns retrogradely up the fast pathway, establishing a reentrant loop.
• ECG Features: P waves are buried within the QRS complex or appear immediately after as a 'pseudo-R'' wave in lead V1 or a 'pseudo-S' wave in inferior leads.

AV Reentrant Tachycardia (AVRT) & Wolff-Parkinson-White (WPW) Syndrome

• Mechanism: Presence of an extranodal muscular accessory pathway (e.g., Bundle of Kent) connecting atrial and ventricular myocardium.
• WPW Triad on Baseline Sinus Rhythm ECG:
  1. Short PR Interval: < 120 ms (0.12 seconds).
  2. Delta Wave: Slurred upstroke of the QRS complex reflecting early ventricular pre-excitation via the accessory pathway.
  3. Wide QRS Complex: > 120 ms due to fused ventricular activation.

Pre-Excited Atrial Fibrillation: A Critical Clinical Emergency

If a patient with WPW develops Atrial Fibrillation, atrial impulses bypass the AV node and conduct 1:1 down the accessory pathway into the ventricles at rates exceeding 250-300 bpm.

• ECG Presentation: Irregularly irregular, extremely rapid (rate 200-300+ bpm), wide-complex tachycardia with marked variation in QRS morphology and axis.
• ABSOLUTE CONTRAINDICATION: Standard AV nodal blocking agents (Adenosine, Beta-blockers, Calcium channel blockers, Digoxin - 'ABCD') are strictly contraindicated. Blocking the AV node removes competitive nodal conduction, forcing ALL 300-500 atrial impulses down the non-decremental accessory pathway directly into the ventricles, precipitating Ventricular Fibrillation and cardiac arrest.
• Emergency Treatment: Immediate synchronized direct current cardioversion if unstable, or IV Procainamide (17 mg/kg IV over 30 minutes) which slows conduction velocity in the accessory pathway.

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Vagal Maneuvers & Adenosine Guidelines

Stepwise Management of Stable Narrow-Complex SVT

1. Vagal Maneuvers: First-line non-pharmacologic intervention to enhance vagal tone and delay AV nodal conduction.
   • Modified Valsalva Maneuver: Patient sits upright and strains against a pressure of 40 mmHg (blowing into a 10 mL syringe) for 15 seconds, followed immediately by supine positioning with passive leg elevation to 45 degrees for 15 seconds. This maneuver significantly increases conversion success compared to standard straining.
   • Carotid Sinus Massage: Auscultate for carotid bruits first. Apply firm pressure over the carotid baroreceptor at the angle of the jaw for 5-10 seconds. Never massage both carotids simultaneously.
2. Pharmacologic Conversion: Adenosine Administration Guidelines
   • Mechanism: Binds A1 adenosine receptors in the AV node, causing transient hyperpolarization and complete AV block to break reentrant circuits.
   • Dosing Protocol: Initial dose is 6 mg IV rapid push through a large-bore proximal IV site (antecubital or central line), immediately followed by an abrupt 20 mL 0.9% normal saline flush and arm elevation.
   • Second Dose: If conversion does not occur within 1 to 2 minutes, administer a second dose of 12 mg IV rapid push.
   • Central Line Adjustment: Reduce initial dose to 3 mg IV if administered via a central venous catheter (e.g., subclavian or internal jugular line) due to high peak concentrations reaching the heart.
   • Drug Interactions: Dipyridamole blocks adenosine uptake, potentiating its effects (reduce dose to 1.5-3 mg). Theophylline, Aminophylline, and Caffeine competitively block adenosine receptors, requiring higher doses.
   • Patient Education: Warn the patient of impending transient symptoms: intense chest fullness, severe flushing, dyspnea, and a sense of impending doom. Provide continuous ECG telemetry monitoring to capture the brief period of asystole during conversion.