PEEP and cardiac output

Abstract

Cyclic opening and closing of atelectatic alveoli with tidal breathing is known to be a basic mechanism leading to ventilator-induced lung injury [1]. To prevent alveo-lar cycling and derecruitment in acute lung injury, high levels of PEEP have been found necessary to counterbalance the increased lung mass resulting from oedema, inflammation and infiltrations and to maintain normal functional residual capacity (FRC) [2]. Therefore, the application of high levels of PEEP is recommended [3], although 'aggressive' mechanical ventilation using high levels of PEEP to maintain or restore oxygenation during acute lung injury can markedly affect cardiac function in a complex and often unpredictable fashion. Except for that from the failing ventricle, PEEP usually decreases cardiac output, a well-known fact since the classic studies published by Cournand et al. [4], in which the effects of positive-pressure ventilation were measured. The conclusion was that positive-pressure ventilation restricted the filling of the right ventricle because the elevated intrathoracic pressures restricted venous flow into the thorax, thereby reducing cardiac output. This formulation of intrathoracic responses to positive-pressure ventilation is still the basis of our present-day understanding of the cardiopulmonary interactions induced by PEEP; although precise responses to PEEP have not been simple to prove and the intrathoracic responses appear multiple and complex. As heart rate usually does not change with PEEP [5], the entire fall in cardiac output is a consequence of a reduction in left ventricular stroke volume (SV). Therefore, the discussion on PEEP-induced changes in cardiac output can be confined to analysis of changes in SV and its determinants, i.e. preload, afterload, contractility and ventricular compliance. Before considering how PEEP affects the determinants of SV, however, we must emphasise that ventilation with PEEP, like any other active or passive ventilatory manoeuvre, primarily affects cardiac function by changing lung volume and in-trathoracic pressure (ITP) [6]. To understand the direct cardiocirculatory consequences of respiratory failure, it is therefore necessary to understand the effects of changes in lung volume, factors controlling venous return, diastolic interactions between the ventricles and the effects of intrathoracic pressures on cardiac, specifically left ventricular, function. This review will attempt to integrate basic mechanisms into the global mechanisms of PEEP and relate these concepts to patient care. Analysis will focus on (1) the relationships between lung volume and intrathoracic pressure and (2) using Chapter 27