Dopamine induced hypoxemia in patients with left heart failure.
Previous studies in our laboratory have demonstrated that dopamine produces a significant decrease in arterial PO2 and a mild increase in arterial PCO2 in patients with left heart failure. The present investigations were designed to find out dopamine-induced effects impairing gas exchange. In patients with left heart failure and pulmonary congestion the true pulmonary shunt has been determined by O2-breathing. A statistically significant increase of true shunting could be evaluated. However, from calculations of the components composing AaDO2-air it can be demonstrated that most of dopamine-dependent increase of AaDO2-air is due to an elevated diffusion-distribution gradient. This dopamine effect on arterial PO2 does not limit dopamine application because oxygen administration will outrange the side effect. As changes of ventilation did not occur dopamine is assumed to open up pulmonary vessels producing blood flow in poorly ventilated parts of the lungs and causing an increased disturbance of ventilation/perfusion ratio. The increased true pulmonary shunt can be regarded as result of perfusion of totally unventilated lung areas when dopamine is infused. Haloperidol can attenuate dopamine-dependent decrease in arterial PO2. How haloperidol abolishes this dopamine effect on arterial oxygen tension remains unknown.
D002245:Carbon Dioxide / Q000097:blood; D004298:Dopamine / Q000009:adverse effects*; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D000860:Hypoxia / Q000139:chemically induced*; D011652:Pulmonary Circulation / Q000187:drug effects; D011653:Pulmonary Diffusing Capacity / Q000187:drug effects; D012119:Respiration / Q000187:drug effects*; D014692:Ventilation-Perfusion Ratio / Q000187:drug effects
D002245:Carbon Dioxide; D004298:Dopamine