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The Journal of Thoracic and Cardiovascular Surgery, Vol 82, 203-210, Copyright © 1981 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Effects of dopamine, ethanol, and mannitol on cardiopulmonary function in patients with adult respiratory distress syndrome

GR Rhodes, M Taylor, JC Newell, DM Shah, WA Scovill and SR Powers

Dopamine, ethanol, and mannitol were investigated to determine if they could increase pulmonary blood flow and oxygen delivery without significantly increasing intrapulmonary shunt. These drugs were studied in adult patients with respiratory distress following trauma, operation, or sepsis. Intravascular pressure, cardiac output, oxygen consumption and delivery, and limb blood flow and peripheral oxygen delivery were measured in all patients. Hypotensive patients received dopamine in incremental doses of 2 mu g/kg/min until either mean arterial pressure increased 15 mm Hg or heart rate increased by more than 15 beats/min. Ethanol was given as 10% ethanol in 5% dextrose at 2 ml/kg/hr. Mannitol was given as 25 gm of a 25% solution in a single bolus followed by infusion of 8 to 25 gm of 20% solution (mean 10 +/- 2 gm) as a continuous intravenous drip over 1 hour. No drug produced a significant change in intrapulmonary shunt. Ethanol produced significant (p less than 0.05) increases in cardiac index, heart rate, oxygen consumption, and oxygen delivery. Dopamine significantly decreased pulmonary vascular resistance while increasing systemic blood pressure. Visceral blood flow apparently increased while the peripheral vascular response to ischemia remained intact. Mannitol increased oxygen delivery and consumption in both the total body and limb. Thus in patients with adult respiratory distress syndrome (ARDS), increases in pulmonary blood flow can be achieved with several distinct pharmacologic agents without significant increases in intrapulmonary shunt. These increases in flow are generally accompanied by increases in oxygen delivery without increased pulmonary vascular resistance.