Hemodynamic Effects of PEEP in Patients With ARDS

Introduction

Acute respiratory distress syndrome (ARDS) is a clinical syndrome defined by the association of an acute onset of hypoxaemia and bilateral pulmonary infiltrates following a trigger insult; it is characterized by inflammation of the pulmonary tissue, with subsequent development of non-cardiogenic edema. The extent of edema may be such that the weight of the lung may increase up to 2-3 times its original weight. As a consequence, the lung tends to collapse on itself, more so in the dependent areas, i.e. the posterior/dorsal areas when the patient in lying supine, with the consequent development of zones of atelectasis.

These areas, when perfused, are the main cause for the development of the severe form of hypoxemia commonly seen in this condition. Hypoxemia, if severe enough, may bring by itself to the death of the patient. It has to be noted that, despite the advances in the management of critically ill patients, mortality attributable to ARDS currently is about 50%, with a range between 30-70%.

The use of positive end-expiratory pressure (PEEP) has been reported ever since the first description of the syndrome, as a tool to manage and correct hypoxemia. PEEP has thus been used for 40 years, and is an essential part of the management of the syndrome. While the effectiveness of PEEP in improving the oxygenation of the wide part of critically ill patients with ARDS it is out of doubt, its efficacy with respect to outcomes such as mortality has not, so far, been demonstrated. The question is then still open with regards to the setting of an optimal level of PEEP in ARDS.

Frequently, ARDS is associated with the development of hemodynamic instability and shock, to the extent that up to 2/3 of patients suffering from the syndrome require the infusion of catecholamines or show signs of hypoperfusion; circulatory failure seems to be the factor more strongly associated to mortality in these patients, and the strength of the association is higher compared to that of the degree of hypoxemia. In ARDS shock is secondary to three main factors: 1) acute cor pulmonale due to pulmonary hypertension secondary to microvascular occlusion by thrombi or arteriolar remodeling and/or hypoxic pulmonary vasoconstriction; 2) the deleterious hemodynamic effects of mechanical ventilation, especially on right cardiac function; and 3) the possible development of septic myocardial depression.