Abstract
IntroductionBoth experimental and clinical data give convincing evidence to acute cardiac dysfunction as the origin or a cofactor of weaning failure in patients with chronic obstructive pulmonary disease. Therefore, treatment targeting the cardiovascular system might help the heart to tolerate more effectively the critical period of weaning. This study aims to assess the hemodynamic, respiratory and clinical effects of nitroglycerin infusion in difficult-to-wean patients with severe chronic obstructive pulmonary disease.MethodsTwelve difficult-to-wean (failed ≥ 3 consecutive trials) chronic obstructive pulmonary disease patients, who presented systemic arterial hypertension (systolic blood pressure ≥ 140mmHg) during weaning failure and had systemic and pulmonary artery catheters in place, participated in this prospective, interventional, non-randomized clinical trial. Patients were studied in two consecutive days, i.e., the first day without (Control day) and the second day with (Study day) nitroglycerin continuous intravenous infusion starting at the beginning of the spontaneous breathing trial, and titrated to maintain normal systolic blood pressure. Hemodynamic, oxygenation and respiratory measurements were performed on mechanical ventilation, and during a 2-hour T-piece spontaneous breathing trial. Primary endpoint was hemodynamic and respiratory effects of nitroglycerin infusion. Secondary endpoint was spontaneous breathing trial and extubation outcome.ResultsCompared to mechanical ventilation, mean systemic arterial pressure, rate-pressure product, mean pulmonary arterial pressure, and pulmonary artery occlusion pressure increased [from (mean ± SD) 94 ± 14, 13708 ± 3166, 29.9 ± 4.8, and 14.8 ± 3.8 to 109 ± 20mmHg, 19856 ± 4877mmHg b/min, 41.6 ± 5.8mmHg, and 23.4 ± 7.4 mmHg, respectively], and mixed venous oxygen saturation decreased (from 75.7 ± 3.5 to 69.3 ± 7.5%) during failing trials on Control day, whereas they did not change on Study day. Venous admixture increased throughout the trial on both Control day and Study day, but this increase was lower on Study day. Whereas weaning failed in all patients on Control day, nitroglycerin administration on Study day enabled a successful spontaneous breathing trial and extubation in 92% and 88% of patients, respectively.ConclusionsIn this clinical setting, nitroglycerin infusion can expedite the weaning by restoring weaning-induced cardiovascular compromise.
Highlights
Both experimental and clinical data give convincing evidence to acute cardiac dysfunction as the origin or a cofactor of weaning failure in patients with chronic obstructive pulmonary disease
Patients with chronic obstructive pulmonary disease (COPD) have airway obstruction and commonly exhibit pulmonary dynamic hyperinflation [2,3,4], and recent data [9] show that COPD itself is a powerful independent risk factor for cardiovascular morbidity and mortality, suggesting that occult cardiac dysfunction could be frequent in patients with COPD
In potentiallyable-to-wean COPD patients without obvious cardiac disease, a spontaneous breathing trial induced a significant left ventricular ejection fraction reduction not explained by a myocardial contractility decrease due to ischemia, implying a weaning-induced increase in afterload [11]
Summary
Both experimental and clinical data give convincing evidence to acute cardiac dysfunction as the origin or a cofactor of weaning failure in patients with chronic obstructive pulmonary disease. It has been suggested that the enormous workload that these patients face during weaning may result in cardiovascular distress and acute cardiac dysfunction [6] Both experimental and clinical data give convincing evidence of acute cardiac dysfunction as the origin or a cofactor of weaning failure. Considerable negative intrathoracic pressures developed at inspiration during airway obstruction or pulmonary dynamic hyperinflation or both increase venous return (that is, preload) and effectively increase left ventricular afterload [7,8] Such increases may not be tolerated by spontaneously breathing patients with compromised heart function [7]. In potentiallyable-to-wean COPD patients without obvious cardiac disease, a spontaneous breathing trial induced a significant left ventricular ejection fraction reduction not explained by a myocardial contractility decrease due to ischemia, implying a weaning-induced increase in afterload [11]. Pharmaceutical interventions with such agents in COPD patients who fail weaning attempts have not been tested so far
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