Effect of chronic rapid ventricular pacing on total vascular capacitance.
BACKGROUND
Rapid right ventricular pacing (RRVP) at 250 bpm for 3-6 weeks produces chronic heart failure manifested by a reduction in cardiac output and increases in right atrial, pulmonary artery, and capillary wedge pressures.


RESULTS
One week after splenectomy and pacemaker placement, vascular capacitance, unstressed volume, and compliance were determined in 19 anesthetized dogs from pressure-volume curves using transient circulatory arrests induced by acetylcholine. Nine dogs were restudied 31 +/- 1 days later without RRVP, and 10 dogs underwent RRVP at 250 bpm and were restudied at 23 +/- 8 and 38 +/- 8 days in cardiac failure and after 1 and 2 weeks of postpacing recovery. Control animals had no changes in vascular capacitance or compliance. Dogs undergoing RRVP exhibited a marked increase in mean circulatory filling pressure (5.4 +/- 0.4 to 10.5 +/- 1.5 mm Hg) during the development of cardiac failure with a reduction in unstressed volume (81.9 +/- 5.7 to 43.9 +/- 8.1 ml.kg-1) without changing total vascular compliance. Total blood volume decreased (95.4 +/- 6.2 to 66.7 +/- 6.5 ml.kg-1) primarily due to a reduction in packed cell volume. The pressure gradient for venous return and overall venous resistance was unaltered. Central blood volume as a proportion of total blood volume increased (9.3 +/- 1.7% to 16.0 +/- 2.7%). Arterial compliance and capacity and pulmonary vascular compliance were reduced. In the 2-week postpacing period, except for a reduced cardiac response to a volume load, all of these parameters returned to baseline values.


CONCLUSIONS
Chronic RRVP induced cardiac failure with a marked reduction in total vascular capacitance due to a reduction in unstressed volume without altering compliance. The rise in mean circulatory filling pressure was limited by a reduction in total blood volume.
Ogilvie
R I
RI
Clinical Pharmacology Service, Toronto Hospital, Ontario, Canada.
Zborowska-Sluis
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D000818:Animals; D001810:Blood Volume / Q000502:physiology; D002303:Cardiac Output, Low / Q000209:etiology* / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects*; D004285:Dogs; D006439:Hemodynamics / Q000502:physiology*; D010138:Pacemaker, Artificial; D014655:Vascular Resistance / Q000502:physiology*