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Ventriculoarterial coupling with intra-aortic balloon pump in acute ischemic heart failure

1999; Elsevier BV; Volume: 117; Issue: 1 Linguagem: Inglês

10.1016/s0022-5223(99)70482-4

1097-685X

Osamu Kawaguchi, Walter E. Pae, Bill B. Daily, William S. Pierce,

Cardiac Arrhythmias and Treatments

We analyzed the mechanism of effects of intra-aortic balloon pumping using the pressure-volume relationship and ventriculoarterial coupling in the normal and failing hearts.In 12 anesthetized Holstein calves (weight, 94 +/- 8 kg), the ventricular end-systolic and arterial elastances, pressure-volume area, and external work were analyzed during steady-state contractions with traditional hemodynamic parameters with intra-aortic balloon pumping-off and -on (1:1 synchronous ratio). An acute ischemic heart failure was induced by injecting 10 microm microspheres (4.2 +/- 1.8 x 10(7). 100g left ventricular weight-1) into the left main coronary artery; all measurements were repeated.Intra-aortic balloon pumping did not change hemodynamic parameters in the control. However, during heart failure, intra-aortic balloon pumping decreased the arterial elastance from 3.6 +/- 1.3 mm Hg to 2.9 +/- 1.2 mm Hg. mL-1 while not affecting the ventricular end-systolic elastance, this resulted in an improvement of the ventriculoarterial coupling ratio from 3.1 +/- 0.8 to 2.3 +/- 0.8. Intra-aortic balloon pumping decreased not only end-systolic pressure (from 69 +/- 16 mm Hg to 64 +/- 19 mm Hg) but end-diastolic volume and pressure (from 139 +/- 38 mL to 137 +/- 37 mL and from 13. 9 mm Hg to 12.8 mm Hg, respectively) with the leftward shift of the pressure-volume loop. Pressure-volume area decreased (from 914 +/- 284 mm Hg to 849 +/- 278 mm Hg. mL) although stroke volume increased (from 21 +/- 6 mL to 24 +/- 6 mL).Reduction of the arterial elastance with intra-aortic balloon pumping improved the ventriculoarterial coupling ratio and increased stroke volume. Leftward shift of the pressure-volume loop resulted in the reduction of pressure-volume area, which suggests the conservation of the myocardial oxygen consumption.