Hemodynamic Management in the Adult Respiratory Distress Syndrome

Abstract

SUMMARY The guiding principles of cardiovascular management of patients with ARDS should be to maintain adequate cardiac output and tissue oxygenation without worsening the degree of pulmonary edema. Because the pulmonary edema is caused by an increase in lung vascular permeability, therapy should be directed toward maintaining a low left ventricular filling pressure, or pulmonary capillary wedge pressure. A low pulmonary capillary wedge pressure will, based on experimental data, tend to decrease the rate of edema formation and to increase the forces for reabsorption of edema fluid once vascular permeability returns to normal. If cardiac output is low or falls as a function of therapy (PEEP), flow may be increased with inotropic or vasoactive agents, or both. These agents increase cardiac output and stroke volume by reducing ventricular end systolic volume so that flow increases despite constant or reduced left ventricular filling pressure. In the setting of low pressure pulmonary edema, with the exception of hydralazine, interventions that increase cardiac output will most likely increase right-to-left shunt and reduce arterial oxygen tension. If desaturation of arterial blood occurs with increased cardiac output, then this may be corrected with higher levels of PEEP. Because of potential deleterious effects of PEEP on left ventricular diastolic mechanics, right ventricular afterload, and barotrauma, hypoxemia should be treated with the lowest level of PEEP that provides 95 per cent saturation of the circulating hemoglobin during ventilation with nontoxic, inspired oxygen concentrations of 50 to 60 per cent. In the setting of ARDS and pulmonary hypertension, volume expansion may result in right ventricular dysfunction and/or a significant increase in the pulmonary capillary wedge pressure. Alternatively, inotropic agents may be preferable to maintain or increase cardiac output when right ventricular afterload is elevated. Also, while vasodilator therapy is designed to reduce an elevated systemic vascular resistance and may be appropriate when pulmonary vascular resistance is normal, such treatment may result in right ventricular dysfunction secondary to a fall in blood pressure and right ventricular perfusion pressure, when right ventricular afterload is increased. This approach attempts to incoporate principles deduced from clinical and experimental studies to provide a framework for approaching the cardiovascular management of patients with acute respiratory failure or ARDS.