How does pulmonary embolism (PE) cause atrial fibrillation (AFib)?

Mechanisms of Atrial Fibrillation in Pulmonary Embolism

Pulmonary embolism (PE) causes atrial fibrillation (AF) primarily through right ventricular pressure overload, which leads to right atrial dilation, increased atrial wall stress, and subsequent electrical remodeling. 1

Pathophysiological Mechanisms

Primary Hemodynamic Effects

• Right Ventricular Pressure Overload:
  • PE obstructs pulmonary arterial bed, causing acute increase in pulmonary vascular resistance 1
  • This creates sudden right ventricular afterload stress
  • The non-hypertrophied right ventricle cannot overcome this initial increase in afterload 1

Atrial Consequences

• Right Atrial Dilation:

  • Increased right ventricular pressure leads to right atrial enlargement
  • Atrial dilation creates an anatomical substrate for reentry circuits 1
  • Stretching of atrial tissue alters electrophysiological properties

• Neurohormonal Activation:

  • Sympathetic activation occurs as compensatory mechanism 1
  • Catecholamine surge can trigger atrial arrhythmias
  • Autonomic imbalance with sympathetic predominance facilitates AF initiation

Hypoxemia and Tissue Injury

• Hypoxemia:

  • Ventilation/perfusion mismatch occurs in PE 1
  • Reduced mixed venous oxygen saturation due to decreased cardiac output
  • Hypoxic stress can trigger arrhythmias and contribute to myocardial injury

• Inflammatory Response:

  • PE triggers inflammatory cytokine release 2
  • Inflammation can alter atrial electrical properties
  • Inflammatory mediators contribute to electrical remodeling

Timing of AF in Relation to PE

AF can occur at different timepoints in relation to PE:

1. Acute Presentation:

   • AF may be the presenting sign of PE 3
   • Occurs due to acute right heart strain and autonomic dysregulation

2. Early Phase:

   • Develops within days of PE diagnosis 4
   • Associated with worse outcomes including increased mortality
   • Often termed "incident AF" when occurring within 2 days of PE 4

3. Late Phase:

   • Can develop during recovery from PE 2
   • May be related to ongoing remodeling or persistent inflammation

Clinical Significance

• Bidirectional Relationship:

  • PE can cause AF through mechanisms described above
  • Conversely, AF can contribute to PE development through right atrial appendage thrombus formation 2

• Prognostic Implications:

  • Both preexisting AF and new-onset AF in PE patients predict adverse outcomes 4
  • Incident AF (new AF within 2 days of PE) is associated with increased 90-day all-cause mortality and PE-related mortality 4
  • Preexisting AF increases risk of ischemic stroke in PE patients 4

Diagnostic Considerations

• Echocardiography:

  • Key diagnostic tool to assess right ventricular dysfunction
  • Can identify right atrial enlargement and potential sources of emboli 3
  • Right ventricular afterload stress detected by echocardiography is a major determinant of short-term prognosis 1

• Patent Foramen Ovale:

  • In about one-third of PE patients, right-to-left shunting through a patent foramen ovale can be detected 1
  • This occurs due to inverted pressure gradient between right and left atria
  • Presence of patent foramen ovale is a significant predictor of stroke and morbidity in major PE 1

Clinical Implications

• PE should be considered in patients presenting with new-onset AF, particularly when other risk factors for PE are present 3
• Patients with AF who develop acute dyspnea should be evaluated for possible PE 2
• The combination of PE and AF requires careful anticoagulation management, considering both conditions 2

Understanding this relationship is crucial as both conditions can coexist and influence each other's management and prognosis.