Weaning and the heart: from art to science*.

August 2014 • Volume 42 • Number 8 Despite decades of attempts to identify the exact mechanisms underlying weaning failure (1), a comprehensive diagnostic algorithm is not available. We still wonder, like Sinha and Donn (2) 14 years ago, whether weaning from mechanical ventilation is art or science. Prolonged weaning may be due to central or peripheral ventilatory drive abnormalities, unbalance between mechanical load and inspiratory muscle strength and, finally, poor cardiac tolerance of spontaneous ventilation (3). Often, different mechanisms coexist in a complex interplay. Weaning from mechanical ventilation may succeed at the first attempt (simple weaning), within 1 week (difficult weaning) or, finally, after more than 1 week (prolonged weaning) (4). The Ventila group, in a survey including more than 2,200 mechanically ventilated patients, found that the adjusted probability of death was higher (13% vs 7%) in patients requiring prolonged weaning compared with patients simple or difficult to wean (5). Prolonged ventilatory dependency is a medical challenge and represents a tremendous psychosocial burden for patients and their relatives. In this issue of Critical Care Medicine, Dres et al (6) report the performance of different methods to diagnose weaninginduced acute cardiogenic pulmonary edema (ACPE). Their data expand our knowledge and raise two relevant issues. First, the authors report a surprisingly high prevalence of weaning-induced ACPE (47.6%). These percentages are in keeping with other studies, for instance, Anguel et al (7): 52%, Jubran et al (8): 42%, and Lamia et al (9): 43%. All these studies relied on a pulmonary artery (PA) catheter to diagnose weaning-induced ACPE. Dres et al (6) report that it is the practice of their institution to perform right heart catheterization for all difficult-to-wean patients when obvious reasons for weaning failure have been discarded. However, inserting a PA catheter in critically ill patients is a debated issue, and this practice is actually uncommon, unless in reference centers like the one of the authors (10). Indeed, the rationale of the study by Dres et al (6) was essentially to validate less invasive alternatives to the “gold standard” PA catheter. Confirming previous studies (7, 11, 12), the authors report acceptable diagnostic power for either blood volume contraction indices (plasma protein and hemoglobin concentration) or brain natriuretic peptides. Furthermore, they show an even better diagnostic performance of weaning-induced increase in extravascular lung water (EVLW), disclosing a novel application field for transpulmonary thermodilution, a technique relatively less invasive than right heart catheterization (13). Second, the authors report that they started diuretics and nitrates after the diagnosis of weaning-induced ACPE. Any weaning trial, and in particular the T-tube spontaneous breathing trial, increases the metabolic oxygen requirements and creates an acute fluid challenge when the intrathoracic pressure shifts from positive (during mechanical ventilation) to negative (during spontaneous breathing). Administering diuretics is a logical approach: fluid overload may be a cofactor able to precipitate ACPE. Nevertheless, a word of caution is needed. The weaning trial may uncover left systolic or diastolic dysfunction, valvular disease, arrhythmias, and right ventricular failure (14). Patients with chronic obstructive pulmonary disease are particularly prone to right ventricular engorgement due to the relevant negative shift in intrathoracic pressure needed to overcome dynamic hyperinflation at the reinstitution of spontaneous breathing; in those patients, ACPE could arise due to leftward interventricular septal shift and diastolic stiffening of left ventricles (15). Accordingly, any suspect of weaninginduced ACPE should prompt a stepwise diagnostic flowchart. The therapeutical approach should then be tailored to the exact mechanism leading to cardiac failure in terms of drugs (e.g., β-blockers, diuretics, nitrates, vasodilators, and inotropes) and/ or other interventions (e.g., cardiac revascularization) (16). In conclusion, the study by Dres et al (6) is doubly important: it shows that measuring EVLW before and immediately after the weaning trial may disclose weaning-induced ACPE and emphasizes the impact of acute heart failure on ventilator dependency. Thanks to several small but focused studies like this one (7–9, 11, 12, 14, 16), we have a number of methods to suspect heart failure involvement in ventilator dependency. It is time to update our diagnostic algorithm for difficult-towean patients.