Does stroke volume increase after a premature ventricular beat (PVB)?

Stroke Volume After a Premature Ventricular Beat

Yes, stroke volume typically increases after a premature ventricular beat (PVB) due to the post-extrasystolic potentiation phenomenon, though this increase is not proportional to the decrease in stroke volume during the PVB itself.

Hemodynamic Effects of Premature Ventricular Beats

During the PVB

• A premature ventricular beat significantly reduces stroke volume compared to normal sinus beats
• Research shows PVBs decrease stroke volume by approximately 71% compared to normal sinus beats 1
• This reduction occurs primarily due to:
  • Shortened diastolic filling time
  • Altered ventricular activation sequence
  • Reduced ventricular preload

After the PVB (Post-extrasystolic Beat)

• The post-extrasystolic beat has an increased stroke volume compared to normal sinus beats
• This increase is due to:
  • Compensatory pause following the PVB
  • Increased end-diastolic volume (preload)
  • Post-extrasystolic potentiation (increased contractility)
• However, the increase in stroke volume after the PVB (approximately 18% over normal sinus beats) does not fully compensate for the significant decrease during the PVB 1

Clinical Significance

Impact on Cardiac Output

• Frequent PVBs can significantly reduce overall cardiac output
• Ventricular bigeminy, trigeminy, and quadrigeminy can lower cardiac output by 1.3,0.9, and 0.7 L/min respectively 1
• This reduction in cardiac output may contribute to symptoms such as:
  • Palpitations
  • Dyspnea
  • Presyncope
  • Fatigue 2

Relationship to Symptoms

• Interestingly, PVC-related symptoms may not correlate directly with the magnitude of post-PVC stroke volume
• A study found that symptomatic patients actually had lower post-ectopic stroke volumes than asymptomatic patients 3
• The sum of stroke volumes during the PVC and post-PVC beat was significantly lower in symptomatic patients 3

Long-term Implications

• High PVC burden (>10%) may be associated with:
  • Reduced left ventricular function
  • PVC-induced cardiomyopathy in some patients 4, 2
  • Potential stroke-like symptoms even without prior stroke or TIA 5

Determinants of Post-PVC Stroke Volume

• Coupling interval (time between normal beat and PVC)
• End-diastolic volume achieved during the compensatory pause
• Baseline ventricular function
• The post-extrasystolic beat's stroke volume correlates closely with end-diastolic volume 1

Clinical Management Considerations

• For patients with frequent symptomatic PVCs:
  • Beta-blockers or non-dihydropyridine calcium channel blockers are reasonable first-line medications in patients with normal ventricular function 2
  • Catheter ablation should be considered for patients with PVC-induced cardiomyopathy or highly symptomatic patients 4, 2
  • Successful PVC ablation can normalize ventricular function in cases of PVC-induced cardiomyopathy 4

In summary, while stroke volume does increase after a premature ventricular beat, this increase (approximately 18%) does not fully compensate for the significant decrease (approximately 71%) during the PVB itself, resulting in a net reduction in cardiac output with frequent PVCs.