Arterial-end tidal P CO 2 equilibration in the cat during acute hypercapnia

Abstract

We have studied the problem of pulmonary capillary-alveolar CO 2 exchange in the cat during acute hypercapnia. Three cats, anesthetized with xylazine and pentobarbital sodium and prepared with acute tracheostomy and femoral arterial catheter, and three awake cats, prepared with a small tracheal catheter and femoral arterial catheter, were subjected to acute hypercapnia (F I CO 2 = 0.00, 0.06, and 0.08). During steady states, end tidal P CO 2 was determined with an infrared analyzer, and arterial P CO 2 was measured with a Radiometer ABL-2 analyzer in simultaneously drawn samples. In vitro studies indicated that our blood sampling techniques resulted in a 6% reduction in P CO 2 . Blood P CO 2 readings were corrected for (1) non-ideal performance of the analyzer as determined by tonometry, (2) 6% reduction due to sampling, and (3) differences between electrode and rectal temperature. Mean arterial-end tidal P CO 2 differences were not significantly from zero in any condition in either group (except for 0.08 CO 2 in the awake group when the difference was 2.0 Torr). These findings in the cat agree with the classical view that P CO 2 in pulmonary capillary blood approaches P CO 2 in alveolar gas. Further, our findings provide evidence that CO 2 loss from blood samples is an important technical factor which can cause systematic underestimation of blood P CO 2 and, hence, contribute to the observation of negative P CO 2 gradients.