The hemodynamic effects of artificial ventilation are complex, interrelated, and dependent on the initial cardiovascular state of the subject. It has been proposed that the aortic pressure variation in response to a positive-pressure breath can be used to define, in a nonambiguous fashion, the primary determinants of the existing hemodynamic state. If correct, this bedside test would be useful for evaluating the hemodynamic condition for all patients requiring mechanical ventilation. In the present study, we sought to define the determinants of aortic pressure variation relative to estimates of left ventricular (LV) area and function in humans. anti allergy
Several investigators have defined ventilation-associated changes in arterial pressure as the variable that would define overall heart-lung interactions, Perel et al observed that, when compared with an apneic baseline, systolic arterial pressure (SAP) decreased more in response to a positive-pressure breath in dogs that were hemorrhaged and presumably more preload-dependent, than in animals that were fluid resuscitated. This suggested to these investigators that in preload-dependent states, positive-pressure breathing decreased SAP by decreasing the LV preload. Massumi et al observed that SAP may also increase after positive-pressure ventilation in patients with LV failure. They called this observation “reversed pulsus paradoxus. Pizov et al demonstrated a similar phenomenon in dogs with acute ventricular failure, but only following fluid resuscitation. These data led them to speculate that once LV preload was adequate (following fluid resuscitation), positive-pressure ventilation-induced changes in intrathoracic pressure (ITP) would augment the LV ejection by reducing the LV afterload. The increase in SAP in their studies was thought to represent the associated increase in LV stroke volume.
Whether or not LV stroke volume increases during positive-pressure inspiration in heart failure and the mechanisms by which LV stroke volume increases are not known. Potentially, LV stroke volume could increase by one of three mechanisms: (1) an increase in LV filling (increased end-diastolic volume), as the alveolar vessels are compressed during inspiration; (2) a decrease in right ventricular residual end-diastolic volume, which increases LV diastolic com-pliance; or (3) a decrease in afterload (decreased end-systolic volume), as the increase in ITP during positive-pressure inspiration decreases the transmural LV ejection pressure.