Tierärztliche Hochschule Hannover Vergleichende Studie zur

Publikation 2
As in this study the RR rate of Group INH increased, but the p a CO 2 remained at a
high level (Fig. 3), we proposed that the central respiratory depressant effect of
isoflurane (Hikasa et al. 1997) may lead to a reduced tidal volume (V T ) or an
increased dead space ventilation, or both. As we did not include pre-anaesthetic
pulmonary function measurements in this study, we had no base value for the
standing unanaesthatised calf for comparison. However, a study on healthy calves of
similar age (Reinhold et al. 2002) determined a V T of 0.64 ± 0.9 L, which is decidedly
above the intra-operative level of Group INH (gradually increasing from 0.27 to
0.33 L), hence we infer that a decrease in V T in Group INH occurred after inducing
anaesthesia and positioning the calves in dorsal recumbancy. It is also known that
the normal stimulation of ventilation caused by increased p a CO 2 is depressed by the
inhalation anaesthetics, presumably due to their direct actions on the medullary and
peripheral chemoreceptors (Hirshman et al. 1977; Knill et al. 1983). The excessive
supply of oxygen may in this case mask an actual ventilation-perfusion mismatch, as
enough oxygen diffuses into the blood, but insufficient CO 2 gets removed from it.
In Group INJ considerable hypoxaemia, reaching mean paO 2 levels of 66.2 mmHg,
was observed. This is well below recommended values of 80 - 110 mmHg
(McDonnell & Kerr 2007). The respiratory depressant effect of xylazine (Rings & Muir
1982) is seen as the cause of the hypoxia, which was further exacerbated by the
respiratory depression following slow IV ketamine redoses. The hypoxaemia and the
significantly increased PVR in Group INJ suggest a definite ventilation-perfusion
mismatch, which is confirmed by the increased pulmonary shunt. It should therefore
be stressed that if no alternative to the combined xylazine and ketamine anaesthesia
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