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

Pathophysiological Mechanisms of Atrial Fibrillation in Pulmonary Embolism

Pulmonary embolism (PE) can trigger atrial fibrillation (AF) through right ventricular pressure overload, leading to right atrial stretch, increased sympathetic tone, and inflammatory cytokine release that disrupt normal atrial electrical conduction. 1

Primary Mechanisms Linking PE to AF

1. Right Ventricular and Atrial Pressure Overload

• PE causes abrupt increase in pulmonary vascular resistance (PVR) when >30-50% of pulmonary arterial bed is occluded 1
• This creates acute pressure overload in the right ventricle (RV), leading to:
  • RV dilation
  • Tricuspid valve insufficiency
  • Right atrial enlargement and stretch
  • Increased right atrial pressure

2. Neurohormonal Activation

• PE triggers excessive neurohumoral activation due to 1:
  • Abnormal RV wall tension
  • Circulatory shock
  • Sympathetic nervous system activation
• Elevated catecholamine levels (particularly epinephrine) create a pro-arrhythmic state
• This neurohormonal response can directly affect atrial electrophysiology and promote AF

3. Inflammatory Response

• PE induces significant inflammatory reactions:
  • Massive inflammatory cell infiltrates in the RV myocardium 1
  • Release of inflammatory cytokines
  • PE-induced "myocarditis"-like state 1
• These inflammatory mediators can disrupt normal atrial electrical conduction

4. Interventricular Dependence and Hemodynamic Changes

• PE causes prolongation of RV contraction time into early LV diastole 1
• This leads to:
  • Leftward bowing of the interventricular septum
  • Desynchronization of ventricles
  • Impeded LV filling
  • Reduced cardiac output
  • Potential development of right bundle branch block
• These mechanical and electrical changes create conditions favorable for AF development

5. Myocardial Ischemia

• PE can cause RV ischemia through:
  • Increased RV oxygen demand due to pressure overload
  • Decreased RV oxygen supply due to reduced coronary perfusion
  • Systemic hypotension impairing coronary driving pressure 1
• This ischemic state can extend to atrial tissue and promote arrhythmias

Clinical Implications and Timing

• AF can present as:
  • A presenting sign of PE
  • During the early acute phase of PE
  • Later in the course of recovery from PE 2
• New-onset AF within 2 days of PE diagnosis (incident AF) is associated with:
  • Increased 90-day all-cause mortality
  • Increased PE-related mortality 3

Bidirectional Relationship

• While PE can cause AF, pre-existing AF is also a risk factor for PE development 2, 4
• This creates a potentially cyclical relationship:
  • AF promotes right atrial appendage clot formation
  • These clots can embolize to the pulmonary circulation
  • Resulting PE can worsen or perpetuate AF

Clinical Considerations

• Electrocardiographic changes in PE often include:
  • Sinus tachycardia (most common, in 40% of patients)
  • Right bundle branch block
  • AF (especially in more severe cases) 1
• AF with slow ventricular response following PE has been reported as a rare complication 5
• The presence of AF in PE patients should prompt consideration of:
  • Source of embolic material (echocardiography is valuable)
  • Severity assessment of PE
  • Prognosis evaluation (AF negatively impacts mortality in PE patients) 4

Understanding these pathophysiological mechanisms is crucial for appropriate management of patients with concurrent PE and AF, as both conditions require specific therapeutic approaches and may complicate each other's treatment and prognosis.