Cardiac output increases the rate of carbon monoxide elimination in hyperpneic but not normally ventilated dogs

Abstract

The very high solubility of carbon monoxide (CO) in blood suggests that its elimination depends predominantly on ventilation and not perfusion. Nevertheless, hyperventilation is not used for CO elimination because of the adverse effects of hypocapnia. With isocapnic hyperpnea (IH), ventilation can be increased considerably without hypocapnia. This raises the issue of whether CO elimination is limited by perfusion during IH. We studied the effect of increasing cardiac output on t1/2, the half-time of decline of blood carboxyhemoglobin concentration ([COHb]), during normal ventilation (NV) and during IH. After ethics approval was received, 13 pentobarbital-anesthetized ventilated dogs were exposed to CO to increase their [COHb]. They were then ventilated with NV or IH. At each level of ventilation, dogs were randomly assigned to treatment with dobutamine (to increase cardiac output) or to no dobutamine treatment. After the return of [COHb] to control levels, each dog was re-exposed to CO and treated with the same ventilatory mode, but the alternative inotropic treatment. Gas exchange, [COHb], and hemodynamic measures were recorded during the study. Cardiac index values in the IH group were 4.1 +/- 0.5 and 8.2 +/- 1.2 l.min(-1).m(-2) without and with dobutamine infusion, respectively. Dobutamine infusion was associated with a reduction in t1/2 from 20.3 +/- 3.6 to 16.9 +/- 2.4 min (P = 0.005) in the IH group, but no change in the NV group. These findings suggest that CO elimination during IH treatment is limited at least partly by pulmonary blood flow and may therefore be further augmented by increasing cardiac output.