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Prompt and aggressive support of lung and hemodynamic function are required if the incidence of recovery from acute respiratory insufficiency is to be improved. Prophylactic ventilator and inotropic therapy are required to prevent progressive deterioration of blood gas exchange and maintain myocardial function in the face of an acutely elevated right ventricular afterload. Methods for early diagnosis are now readily available; the criteria for therapeutic intervention are discussed.

Acute respiratory failure, particularly if associated with sepsis, results in diffuse changes in pulmonary vascular geometry and the afterload characteristics against which the right ventricle must perform. Therapy in these patients frequently requires replacement of intravascular volume which, if pulmonary vascular resistance is abnormally elevated, may cause a substantial enlargement in right ventricular (RV) end-diastolic volume. The low compliance characteristics of the RV invalidate the use of filling pressure (CVP) as a guide to RV size. We have examined RV volume in critically ill patients by means of the gated 99TAc scan and noted a substantial increase in RV volume despite filling pressure in the upper normal range. This enlargement appears to encroach upon LV function because the ejection fraction of the LV remained high despite elevation of pulmonary capillary wedge pressure (PCWP). Older patients with "silent" right coronary artery disease may become hemodynamically limited during therapy for acute respiratory failure and sepsis due to RV enlargement, increased wall tension and RV ischemia, a condition not readily diagnosed at the bedside with the usual monitoring techniques.