Dynamic effects of positive-pressure ventilation on canine left ventricular pressure-volume relations

Positive-pressure ventilation (PPV) may affect left ventricular (LV) performance by altering both LV diastolic compliance and pericardial pressure (Ppc). We measured the effect of PPV on LV intraluminal pressure, Ppc, LV volume, and LV cross-sectional area in 17 acute anesthetized dogs. To account for changes in lung volume independent of changes in Ppc and differences in contractility, measures were made during both open- and closed-chest conditions, during closed chest with and without chest wall binding, and after propranolol-induced acute ventricular failure (AVF). Apneic end-systolic pressure-volume relations (ESPVR) were generated by inferior vena caval occlusions. With the open chest, PPV had no effects. With the chest closed, PPV inspiration decreased LV end-diastolic volume (EDV) along its diastolic compliance curve and decreased end-systolic volume (ESV) such that the end-systolic pressure-volume domain was shifted to a point left of the LV ESPVR, even when referenced to Ppc. The decrease in EDV was greater in control than in AVF conditions, whereas the shift of the ESV to the left of the ESPVR was greater with AVF than in control conditions. We conclude that the hemodynamic effects of PPV inspiration are due primarily to changes in intrathoracic pressure and that the inspiration-induced decreases of LV EDV reflect direct effects of intrathoracic pressure on LV filling. The decreases in LV ESV exceed the amount explained solely by a reduction in LV ejection pressure

Left ventricular performance assessed by echocardiographic automated border detection and arterial pressure.

Automated echocardiographic measures of left ventricular (LV) cavity area are closely correlated with changes in volume and can be coupled with LV pressure (PLV) to construct pressure-area loops in real time. The objective was to rapidly estimate LV contractility from end-systolic relationships of cavity area (as a surrogate for LV volume) and central arterial pressure (Pa) (as a surrogate for PLV) in a canine model using automated algorithms. In eight anesthetized mongrel dogs, we simultaneously measured PLV, LV area, and Pa (fluid-filled catheter). End-systolic pressure-area relationships in terms of pressure-area elastance (E'es)] from pressure-area loops during inferior vena caval occlusions were determined during basal conditions (control), dobutamine infusion (5-10 micrograms.mg-1.min-1), and after bolus propranolol (2 mg/kg) with both PLV and Pa by semiautomated and automated iterative regression methods. E'es increased during dobutamine infusion and decreased after propranolol infusion in all animals and with all iterative methods. Estimates of Ees from Pa were closely correlated with E'es from PLV by both the semiautomated and automated methods (r = 0.93; P < 0.01). The relationship between E'es obtained from Pn for the two methods was also closely correlated. Although the automated methods displayed larger differences from the semiautomated iterative technique by Bland-Altman analysis, the change in E'es with all techniques during dobutamine infusion and after propranolol infusion was of similar magnitude and direction among the three techniques. Greater variability with the dobutamine runs was partially due to abnormally conducted ventricular beats that minimized the number of consecutive beats that could be used for these analyses. We conclude that on-line Pa recordings from fluid-filled catheters can be used with echocardiographic automated border detection to rapidly calculate E'es as a means to estimate LV contractility

Determinants of aortic pressure variation during positive-pressure ventilation in man

Study objectives: To define the relation between systolic arterial pressure (SAP) changes during ventilation and left ventricular (LV) performance in humans. Design: Prospective repeat-measures series. Setting: University of Pittsburgh Medical Center Operating Room. Patients: Fifteen anesthetized cardiac surgery patients before and after cardiopulmonary bypass when the mediastinum was either closed or open. Interventions: Positive- pressure ventilation. Measurements and results: SAP and LV midaxis cross- sectional areas were measured during apnea and then were measured for three consecutive breaths. SAP increased during inspiration, this being the greatest during closed chest conditions (p < 0.05). Changes in SAP could not be correlated with changes in either LV end-diastolic areas (EDAs), end- systolic areas, or stroke areas (SAs). If SAP decreased relative to apnea, the decrease occurred during expiration and was often associated with increasing LV EDAs and SAs. SAP often decreased after a positive-pressure breath, but the decrease was unrelated to SA deficits during the breath. Increases in SAP were in phase with increases in airway pressure, whereas decreases in SAP, if present, followed inspiration. No consistent relation between SAP variation and LV area could be identified. Conclusions: In this patient group, changes in SAP reflect changes in airway pressure and (by inference) intrathoracic pressure (as in a Valsalva maneuver) better than they reflect concomitant changes in LV hemodynamics

Tezosentan and Right Ventricular Failure in Patients with Pulmonary Hypertension Undergoing Cardiac Surgery: The TACTICS Trial.

OBJECTIVE: To evaluate the efficacy of tezosentan in reducing the incidence of right ventricular (RV) failure and associated mortality in patients with pre-existing pulmonary hypertension. The primary endpoint was the proportion of patients with RV failure during weaning from cardiopulmonary bypass (CPB), assessed 30 minutes after the end of CPB. DESIGN: Multicenter, double-blind, randomized, placebo-controlled trial. SETTING: Thirty-one cardiac surgical centers in 14 countries. PARTICIPANTS: Two hundred seventy-four patients with pulmonary hypertension aged≥18 years scheduled to undergo cardiac surgery. INTERVENTION: Intravenous tezosentan (5 mg/h) during surgery and up to 24 hours afterwards (1 mg/h), or matched placebo. MEASUREMENTS AND MAIN RESULTS: One-hundred thirty-three patients received tezosentan and 141 placebo. RV failure occurred in 30 patients (10.9%), 37% of whom died. There was no difference in the incidence of RV failure between the two treatment groups (relative risk reduction: 0.07 [95% CI-0.83, 0.53; P = 0.8278]). CONCLUSION: A reduction in RV failure with tezosentan was not observed in this study.(Current Controlled Trials, identifier NCT00458276)