Effect of jet ventilation on heart failure: decreased afterload but negative response in left ventricular end-systolic pressure-volume function.

OBJECTIVE

To examine the mechanism of cardiac assist with systolic jet ventilation, specifically effects on loading conditions and left ventricular pressure-volume function. Both systolic and diastolic jet ventilation were compared in the absence and presence of heart failure.

DESIGN

Prospective, two-factor, repeated-measures study.

SETTING

Animal laboratory.

SUBJECTS

Ten anesthetized, closed-chest dogs.

INTERVENTIONS

The measurement protocol consisted of two phases: a) apnea, randomized jet ventilation (systole- and diastole-synchronized); b) postjet ventilation apnea, before and after heart failure, induced with a propranolol-imipramine-plasma expansion treatment.

MEASUREMENT AND MAIN RESULTS

Systolic and diastolic jet ventilation was associated with mean airway pressures of approximately 7 mm Hg and intrapleural pressures of approximately 3 mm Hg in both heart conditions. In normal hearts, jet ventilation (either mode) decreased transmural left ventricular end-diastolic pressure by 40% to 60% (p < .05), left ventricular end-diastolic volume 25 +/- 8%, and stroke volume by 28% to 30%. Heart failure was associated with decreases (41 +/- 6%) in end-systolic pressure-volume function (i.e., pressure change/volume change or elastance), transmural left ventricular end-systolic pressure (22 +/- 3%), and stroke volume (16 +/- 4%), and increased transmural left ventricular end-diastolic pressure (139 +/- 6%). Application of jet ventilation (either mode) during heart failure did not affect stroke volume but significantly (p < .05) attenuated transmural left ventricular end-diastolic pressure by 30% to 40%, left ventricular end-diastolic volumes by 33 +/- 9%, and transmural left ventricular end-systolic pressure by 11% to 19% (p < .05). After jet ventilation, left ventricular elastance was decreased 36 +/- 8% in normal hearts and 35 +/- 11% in failing hearts. Stroke volume, however, returned to baseline levels because of increases in transmural left ventricular end-diastolic pressure in both heart conditions, and also in failing hearts, because transmural left ventricular end-systolic pressure remained decreased approximately 30% (p < .05).

CONCLUSIONS

Jet ventilation did not decrease stroke volume in failing hearts because of the afterload-reducing benefit (decreased transmural left ventricular end-systolic pressure) of increased intrapleural pressure in dilated ventricles. Moreover, jet ventilation did not have positive effects on myocardial function and had negative effects on left ventricular elastance in the postjet ventilation period in both normal and failing hearts. Cardiac assist by jet ventilation was not cycle specific, suggesting no selective benefit of jet ventilation over conventional positive-pressure ventilation during heart failure. These studies demonstrate a negative inotropy associated with jet ventilation that, during heart failure, may compromise the general benefit of positive-pressure-mediated increases in intrapleural pressure.