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

Abstract

Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure. V.M. Ranieri, M. Dambrosio, N. Brienza. ERS Journals Ltd 1996. 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. Eur Respir J., 1996Respir J., , 9, 1283Respir J., -1292

CPAP Decreases Lung Hyperinflation in Patients With Stable COPD

“…The increase in lung volume may reduce venous return, directly through compression of the vena cava and right heart, and indirectly through an increase in right atrial pressure, decreasing the pressure gradient for venous return. 10,14 The effects of nasal CPAP on the lung parenchyma of stable COPD patients has been assessed via high-resolution computed tomography. In a recently published study, Holanda et al 28 obtained high-resolution computed tomog- Measurement of R aw may help distinguish airway obstruction due to intrinsic narrowing of the airway by mucus hypersecretion and bronchial wall inflammation (eg, chronic bronchitis) or to the loss of lung elastic recoil (eg, emphysema).…”

“…11,12 Applied PEEP above 10 cm H 2 O increases hyperinflation and worsens respiratory mechanics, muscle activity, and hemodynamics. 13,14 Given the few and contradictory results of studies on the influence of CPAP in patients with stable severe airway obstruction, we investigated the impact and duration of impact of CPAP on hyperinflation and R aw in patients with stable COPD.…”

Ventilatory Inefficiency as a Limiting Factor for Exercise in Patients With COPD

“…1,2 Theoretically, patients with greater bronchial obstruction should exhibit greater limitations in exercise; however, this does not occur in clinical practice, where patients with a lesser degree of obstruction may exhibit greater limitations. This indicates the presence of multiple mechanisms involved in the development of these limitations.…”

Pulmonary hyperinflation and ventilator-dependent patients

“…Pulmonary hyperinflation also has important cardiovascular consequences, which have recently been reviewed [29]. Briefly, large changes in intrathoracic pressures during the respiratory cycle profoundly affect venous return, right cardiac function, and cardiac output in general.…”

“…However, high levels of PEEPi impair cardiac filling and reduce cardiac output, systemic blood pressure and oxygen transport [18,29]. Furthermore, the dynamic hyperinflation associated with large VT may unduly raise the end-inflation pressure, enhancing the risk of alveolar distension and disruption (barotrauma), particularly in patients with acute exacerbation of COPD [53] or asthma [54,55].…”