The Patient with Adult Respiratory Distress Syndrome

Fluid management of the patient with adult respiratory distress syndrome (ARDS) (see Chapter 75 ) involves maintaining colloid osmotic pressure and requires a CVP and PAOP value as low as possible that is consistent with good ventricular function. Oxygen delivery should be sustained, ideally above 600 mL/min/m² , by increasing cardiac index and hemoglobin concentration. Compensation for hemodynamic effects of increased airway pressure is achieved by maintaining adequate right and left ventricular filling volumes. When airway pressure increases, the lung expands in proportion to its compliance. The intrapleural pressure increases in direct proportion to lung expansion and inversely with chest-diaphragm compliance. The increased intrapleural pressure increases CVP, which reduces the gradient between the periphery and the CVP. This reduces venous return unless peripheral venous tone increases or fluids are administered. The increased venous pressure increases fluid filtration out of the capillary bed, tending to produce hypovolemia. The increased pleural pressure is transmitted through the pericardium to reduce the filling pressure gradient for all cardiac chambers. The consequent reduction in end-diastolic volume diminishes preload to all chambers. The elevation of intrapulmonary pressure increases pulmonary artery pressure, which leads to augmented right ventricular afterload. The reduced venous return, decreased right ventricular preload, and increased afterload may severely compromise right ventricular stroke volume, cause stiffening of the interventricular septum, and reduce preload for the left ventricle.

All these consequences can be improved by intravascular volume expansion, except for the increased afterload on the right ventricle. CVP and right ventricular end-diastolic volume are monitored to aid in the decision to institute inotropic therapy. An increase in CVP also compromises lymphatic return from the lung and periphery. Sepsis, the most common coexisting condition with ARDS, causes increased vascular capacity and vasodilation, decreases COP, and results in tissue edema. The net clinical outcome of these factors is that fluid intake usually exceeds output until the ARDS and sepsis begin to subside. Studies comparing crystalloid and colloid management over the entire time course of ARDS are being evaluated. However, after 48 hours, pulmonary function may be somewhat better in patients managed in part with colloid than with crystalloids alone.