Hypoxic ventilatory response in cats lightly anesthetized with ketamine: effects of halothane and sevoflurane in low concentrations

Abstract

The effect of low concentration sevoflurane and halothane on the ventilatory response to isocapnic hypoxia was studied in sixteen cats. The cats were divided into two groups, sevoflurane group and halothane group, of eight subjects each. As parameters of the hypoxic ventilatory response, A value [the slope of the hyperbolic curve, V(E) = V(0) + A/(Pa(O)(2)-32)] and ratio of V(50) (the minute volume obtained from the hyperbolic equation when Pa(O)(2) = 50 mmHg) to V(0) were studied. These two parameters were examined at three states, sedative state with ketamine as the control, ketamine plus 0.1 MAC inhalation anesthetic, and ketamine plus 0.5 MAC inhalation anesthetic. In the sevoflurane group, the A values were 4789 +/- 1518, 2187 +/- 1214, 1730 +/- 880 (mean +/- SE. ml.min(-1).mmHg) at the control state, 0.1 MAC and 0.5 MAC, respectively. In the halothane group, the A values were 6411 +/- 2368, 2529 +/- 842 and 2372 +/- 545, respectively. The ratios of V(50) to V(0) were 1.32 +/- 0.09, 1.22 +/- 0.09, 1.25 +/- 0.08 in the sevoflurane group, 1.47 +/- 0.18, 1.32 +/- 0.11, 1.54 +/- 0.18 in the halothane group, respectively. The A value at 0.1 MAC of the halothane group was less than the control value significantly. This proved that even low concentration halothane depressed the hypoxic ventilatory responses. The depression of hypoxic ventilatory response could cause postanesthetic hypoventilation. On the other hand, we could not find significant depression on the hypoxic ventilatory response in the sevoflurane group, but we should notice that variances of the hypoxic ventilatory response were large.

Sevoflurane Concentrations in Blood, Brain, and Lung After Sevoflurane‐Induced Death

“…This is a less likely cause than that given next because depression of ventilation by sevoflurane would limit the concentration that would be reached in the lungs (i.e., the depression produces an element of negative feedback). Second, hypoxia might result from obstruction to or depression of breathing (11), including depression of the response to hypoxia (12). That is, the subject probably died because his breathing became obstructed and he asphyxiated or (less likely), his cardiorespiratory system became depressed to the point of apnea, and/or cardiovascular collapse.…”

Η Επίδραση Του Σεβοφλουρανίου Και Δεσφλουρανίου Στην Εγκεφαλική Οξυμετρία

“…Και οι δύο παράγοντες αυξάνουν τη μερική τάση του αρτηριακού διοξειδίου του άνθρακα και ελαττώνουν την αναπνευστική απάντηση σε προκαλούμενες αυξήσεις του διοξειδίου του άνθρακα54,55 . Σε αναισθητοποιημένες με κεταμίνη γάτες, η χορήγηση 0,1 και 0,5 MAC σεβοφλουρανίου προκάλεσε καταστολή στην αναπνευστική απάντηση στην υποξία σε ένα βαθμό δυσανάλογο από αυτόν που προκαλείται από το αλοθάνιο56 . Η αναπνευστική καταστολή που σχετίζεται με το σεβοφλουράνιο μπορεί να προέρχεται από ένα συνδυασμό κεντρικής καταστολής των αναπνευστικών νευρώνων του προμήκους 57 και καταστολής της διαφραγματικής λειτουργίας 58 και συσταλτικότητας59 .…”