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AV pacing: Hemodynamic effect

Loss of the atrial “kick” (contraction) or AV dyssynchrony can result in a significant increase in mean atrial pressure and pulmonary congestion. AV pacing in these patients, therefore, can augment ventricular filling and cardiac output through the Frank-Starling relationship, improves venous return, and assist AV valve closure. AV sequential pacing results 10±50% improvement in cardiac output compared with ventricular pacing alone in patients with normal and diseased hearts. Higher left ventricular end-diastolic volumes and mean and systolic arterial pressures and lower venous pressures and pulmonary wedge pressures have all been reported in AV sequential pacing compared with VVI pacing. With increased heart rates, diastolic time shortens and the role of atrial contraction becomes even more important.

AV pacing can also be used to augment cardiac output purely by increasing the heart rate (remember, cardiac output is a function of stroke volume multiplied by heart rate). However, on the flip side, AV pacing at a rapid rate (overdriving the heart) can be utilized to purposefully not allow enough filling time and therefore decrease cardiac output and arterial pressure.

References

  1. Buckingham TA1, Janosik DL, Pearson AC. Pacemaker hemodynamics: clinical implications. Prog Cardiovasc Dis. 1992 Mar-Apr;34(5):347-66. PubMed Link
  2. T V Salukhe, D Dob, R Sutton Pacemakers and defibrillators: anaesthetic implications. Br J Anaesth: 2004, 93(1);95-104 PubMed Link