DOPAMINE INDUCED HYPOXEMIA IN PATIENTS WITH LEFT HEART-FAILURE

  • 1 January 1976
    • journal article
    • research article
    • Vol. 14  (3) , 217-224
Abstract
Previous studies in this laboratory demonstrated that dopamine produces a significant decrease in arterial PO2 [O2 tension] and a mild increase in arterial PCO2 [CO2 tension] in patients with left heart failure. In patients with left heart failure and pulmonary congestion, the true pulmonary shunt was determined by O2-breathing. A statistically significant increase of true shunting was evaluated. From calculations of the components composing AaDO2 [alveolar arterial difference for O2 tension] air it was demonstrated that most of the 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 O2 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 a 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 O2 tension remains unknown.