The effect of mechanical ventilation on heart function

Critically ill patients admitted to the Intensive Care Unit frequently require mechanical ventilation to ensure adequate gas exchange. However, mechanical ventilation itself can instigate ventilator-induced lung injury (VILI). The use of high tidal volume ventilation has shown to be the most important contributing factor of VILI with increased morbidity and mortality.

With increasing tidal volume size, the intrathoracic pressures increase linearly resulting in a decrease in stroke volume, mainly by a decrease in left ventricular (LV) preload through a decrease in right ventricular (RV) preload and increase in RV afterload. Possible deleterious effects of high tidal volumes on LV function are largely unknown, partly because of the difficulty of measuring myocardial function independent of changes in loading conditions. The myocardial performance index assessed by non-invasive trans thoracic echocardiography can determine myocardial function in a relatively load-independent way. Experimental studies have suggested that high tidal volume ventilation may induce various inflammatory mediators that leak into the circulation causing injury to distant organs including the heart, in other words "ventilator-induced myocardial dysfunction" (VIMD). We therefore investigate whether tidal volume size has an effect on left and right ventricular function in mechanically ventilated critically ill patients.

High tidal volume ventilation has shown to cause ventilator-induced lung injury (VILI), possibly contributing to concomitant extrapulmonary organ dysfunction. The present study examines whether ventilator-induced myocardial dysfunction (VIMD) is dependent on tidal volume size

After 24 hours of mechanical ventilation

Trans thoracic echocardiography in patients mechanically ventilated longer than 24 hours