LAUSR

Clinicians have known the circulatory consequences of mechanical ventilation since patients were ventilated. By raising pressure in the chest, positive airway pressure reduces venous return and cardiac preload while it alters the afterload of both ventricles. These responses depend on the interaction of thoracic and pulmonary mechanics, cardiac dysfunction, patient’s volume status, and vascular tone. The net result is usually harmful to the patient, but there are exceptions such as left heart failure. Superimposed on the continuous effects of positive end-expiratory pressure, tidal inflation generates swings in biventricular ejection and in pulmonary blood content. If brisk, these oscillations can break the pulmonary capillary barrier and contribute to pulmonary edema when tidal volume is too high. In comparison to its effects on cardiac loading, the interactions of mechanical ventilation and myocardial contractility are underexplored. In this issue of Anesthesiology, Cherpanath et al. bring novel information to this field. The authors studied 42 patients among those who were recruited in a large multicenter trial (Protective Ventilation in Patients without ARDS trial [PReVENT]) testing the clinical outcomes (ventilator-free days, survival, length of stay, pulmonary complications) of low tidal volume ventilation in patients who did not meet the criteria of acute respiratory distress syndrome (ARDS). Patients were randomized to receive low (6 ml/kg predicted body weight) versus moderate (8 to 10 ml/kg) tidal volume within 1 h from initiation of ventilator support. After 24 h with these settings, the subjects studied by Cherpanath et al. received a transthoracic echocardiogram. In addition to standard metrics of right and left ventricular function, the authors calculated the myocardial performance index from tissue Doppler measurements of isovolumetric contraction and relaxation of the ventricles. This measurement is considered less dependent on cardiac loading conditions than more familiar echocardiographic variables such as the ejection fraction. The authors found that most indexes of systolic function, including the performance index, were lower in the moderate tidal volume group as compared with low tidal volume ventilation. They hypothesize that these findings may reflect reduced cardiac contractility due to systemic inflammation. Indeed, excessive lung stretch is associated with loss of inflammatory compartmentalization and release of mediators (biotrauma), which may generate nonpulmonary organ damage. The results of the study by Cherpanath et al. are very interesting, but a few considerations need to be addressed by further research, before we opt for lower tidal volume ventilation for the purpose of minimizing impact on cardiac function. First, the mechanistic link among tidal volume, systemic inflammation, and extrapulmonary organ dysfunction is plausible but, as the authors recognize, it is mostly supported by animal studies, where tidal volumes were generally larger than what is typically used in clinical practice. Second, Cherpanath et al. recruited a small enough sample size that it is possible that heterogeneity between clinical intervention groups potentially could have influenced study findings. For example, there was a 4-mmHg difference in mean central venous pressures between study groups. While this was not a statistically significant difference, it could represent a clinically significant difference in volume status that potentially could favor the outcome of the low tidal volume study group, since the myocardial performance index is not always preload independent. Third, more vigorous inspiratory effort in the low tidal volume “...the idea that tidal volume selection might modulate cardiac function is intriguing.”