Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure.

Abstract

Deviation of end-expiratory lung volume from the elastic equilibrium volume of the respiratory system is recognized as a cardinal feature in mechanically-ventilated patients with severe chronic obstructive pulmonary disease (COPD) and acute ventilatory failure (AVF). The presence of dynamic hyperinflation implies that alveolar pressure remains positive throughout expiration. At the end of the expiration, this positive pressure is named intrinsic positive end-expiratory pressure (PEEPi). Recent studies have suggested that, in COPD patients with expiratory flow limitation, the application of external PEEP during assisted mechanical ventilation, or the use of continuous positive airway pressure (CPAP) in spontaneously breathing patients, can counterbalance and reduce the inspiratory threshold load imposed by PEEPi, without causing further increase in lung volume and alveolar and intrathoracic pressures until a critical value of PEEP (Pcrit) is reached. Above this critical limit further hyperinflation is observed. A specific and characteristic role of PEEPi in compromising the heart function in COPD patients during AVF may be identified based on: 1) an increase in right ventricular impedance due to lung hyperinflation; 2) an increase in the venous return to the right ventricle and, consequently, a leftward shift of the septum caused by the large negative deflections in intrathoracic pressure due to the inspiratory threshold load; 3) a further increase in venous return to the right ventricle, with the eventual collapse of the vena cava caused by the expiratory recruitment of abdominal muscles; and 4) hypoxia and hypercapnia consequent to acute ventilatory failure, which may further increase right ventricular impedance and venous return to the right ventricle. All these phenomenon are directly correlated to the large negative intrathoracic pressure developed by the respiratory muscles to overcome the inspiratory threshold caused by intrinsic positive end-expiratory pressure (preload effect), and to the increase in lung volume (afterload effect). Application of positive end-expiratory pressure/continuous positive airway pressure in chronic obstructive pulmonary disease patients during acute ventilatory failure may, hence, unload the respiratory muscles as well as the heart.