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


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Ishida
Susumu
S
Department of Anesthesia and Intensive Care, Nagoya Daini Red Cross Hospital, Nagoya, Japan.
Takeuchi
Akinori
A
Azami
Takafumi
T
Sobue
Kazuya
K
Sasano
Hiroshi
H
Katsuya
Hirotada
H
Fisher
Joseph A
JA
D000818:Animals; D002248:Carbon Monoxide / Q000378:metabolism*; D002263:Carboxyhemoglobin / Q000378:metabolism*; D002302:Cardiac Output / Q000502:physiology*; D002316:Cardiotonic Agents / Q000494:pharmacology; D004280:Dobutamine / Q000494:pharmacology; D004285:Dogs; D006985:Hyperventilation / Q000503:physiopathology*; D023421:Models, Animal; D012143:Respiratory Physiological Phenomena / Q000187:drug effects
D002316:Cardiotonic Agents; D004280:Dobutamine; D002248:Carbon Monoxide; D002263:Carboxyhemoglobin