What is the pathophysiology and management of reentry arrhythmias?

Reentry Pathophysiology and Management

Core Pathophysiology

Reentry is the most common mechanism underlying cardiac arrhythmias, occurring when a propagating electrical impulse fails to die out after normal cardiac activation and persists to re-excite the heart after the refractory period has expired. 1

Essential Requirements for Reentry Initiation

Reentry requires four critical elements to develop:

• Unidirectional conduction block in one limb of a circuit, which may occur from heart rate acceleration or when a premature impulse encounters tissue in its refractory period 1
• Slow conduction through at least one pathway, necessary for both initiation and maintenance of the circus movement 1
• A defined circuit around either a fixed anatomic obstacle (anatomic reentry) or through functional properties of tissue alone (functional reentry/leading circle mechanism) 1, 2
• Recovery of excitability in the initially blocked pathway, allowing retrograde activation to complete the circuit 1

Types of Reentry Circuits

Anatomic reentry involves a predetermined circuit around a fixed obstacle:

• Typical atrial flutter uses the cavotricuspid isthmus as the critical pathway 1
• Atypical flutter (non-cavotricuspid isthmus-dependent macroreentry) includes perimitral flutter around the left atrial roof and circuits around surgical or ablation scars 1
• AVRT (atrioventricular reentrant tachycardia) utilizes a circuit involving the AV node, ventricle, accessory pathway, and atrium 3

Functional reentry occurs without a fixed anatomic obstacle:

• Propagation occurs through relatively refractory tissue with absence of a fully excitable gap 1
• The "leading circle" mechanism represents purely functional reentry where the circuit is determined by tissue properties rather than anatomy 2, 4

Substrate Development

Any disturbance of cardiac architecture increases susceptibility to reentry, with structural changes creating the substrate for arrhythmia perpetuation. 1, 5

Critical substrate factors include:

• Myocardial fibrosis, the most common feature in both experimental and clinical reentrant arrhythmias, creates areas of slow conduction and conduction block 1
• Inflammation, hypertrophy, and cellular necrosis from conditions like hypertension, coronary artery disease, valvular disease, and cardiomyopathies 1
• Heterogeneous conduction properties from ion channel abnormalities, gap junction dysfunction, and cellular heterogeneity in specialized tissues 1, 5
• Increased dispersion of refractoriness, creating regions where some tissue is excitable while adjacent tissue remains refractory 6

Management Approach

Acute Termination Strategies

For hemodynamically unstable reentrant arrhythmias, immediate synchronized cardioversion is the definitive treatment. 3

For stable patients, the management algorithm depends on the specific reentry circuit:

AV nodal-dependent reentry (AVNRT, orthodromic AVRT):

• Vagal maneuvers (Valsalva, carotid massage) should be attempted first, as these slow AV nodal conduction and can terminate the circuit 1, 3
• Adenosine (6-12 mg IV rapid push) transiently blocks AV nodal conduction 3
• IV beta-blockers, diltiazem, or verapamil if adenosine fails 3

Atrial flutter:

• Electrical cardioversion or radiofrequency catheter ablation are often required for termination, as atrial flutter is typically a persistent rhythm 1
• Rate control with AV nodal blocking agents if cardioversion is not immediately pursued 1

Ventricular tachycardia from reentry:

• Amiodarone is effective for acute suppression: 150 mg IV over 10 minutes for breakthrough episodes, followed by continuous infusion 7
• High-dose amiodarone (approximately 1000 mg over 24 hours) significantly reduces VT/VF episodes compared to low-dose regimens (median 0.5 vs 1.7 episodes per day) 7

Definitive Management

Catheter ablation is the definitive therapy for most reentrant arrhythmias and should be offered as first-line treatment when feasible. 3

Typical atrial flutter:

• Cavotricuspid isthmus ablation has high success rates and prevents recurrence while allowing continued antiarrhythmic therapy for coexistent AF 1
• Important caveat: 80% of patients will develop AF within 5 years after flutter ablation, reflecting the close relationship between these arrhythmias 1

Atypical flutter/macroreentrant atrial tachycardia:

• Requires electrophysiological study with detailed atrial mapping to identify the specific circuit, as these are not abolished by cavotricuspid isthmus ablation 1
• Complex circuits with multiple loops may coexist and require individualized ablation strategies 1

AVRT:

• Accessory pathway ablation provides excellent prognosis and cure 3
• Should be strongly recommended to prevent tachycardia-mediated cardiomyopathy from persistent arrhythmia 3

Pharmacologic Suppression

When ablation is declined or not feasible:

For supraventricular reentry:

• Oral beta-blockers, verapamil, or diltiazem for chronic suppression 3
• Avoid sodium channel blockers (flecainide, propafenone) in patients with atrial flutter, as these can paradoxically facilitate 1:1 AV conduction or convert AF to atrial flutter 1

For ventricular reentry:

• Amiodarone for chronic suppression in patients with structural heart disease 7
• Steady-state concentrations of 1-2.5 mg/L are associated with antiarrhythmic effects and acceptable toxicity 7

Critical Pitfalls to Avoid

• Do not mistake AF for atrial flutter when AF activity is prominent on ECG—this leads to inappropriate treatment strategies 1
• Recognize that sodium channel blockers can convert AF to atrial flutter with potentially dangerous 1:1 AV conduction 1
• Do not assume all atrial flutter is typical—atypical circuits require mapping and targeted ablation rather than empiric cavotricuspid isthmus ablation 1
• Monitor for hypotension with IV amiodarone (occurs in 16% of patients) and be prepared to manage hemodynamic compromise 7
• Understand that ablation of typical flutter does not prevent AF—patients require continued surveillance and management of AF risk factors 1