Apneic oxygenation in anesthetized ponies and horses

Abstract

Apneic oxygenation was studied in six ponies for 30 minutes, and six horses for 10 minutes. Arterial blood was sampled at regular intervals for measurement of oxygen and carbon dioxide tensions (PaO2 and PaCO2) and calculation of alveolar-arterial oxygen tension difference (PAO2-PaO2). In both groups of animals, PaO2 decreased rapidly during the first 3 minutes of apnea, then more slowly. Although the mean value was above 100 mmHg at 10 minutes, there was considerable inter-animal variability. Before apnea, PAO2-PaO2 was slightly, but not significantly, larger in horses than in ponies and increased in both groups during the first 3 minutes of apnea, after which the increase was slower. There was no significant difference between ponies and horses up to 10 minutes, suggesting that PAO2-PaO2 is independent of body size. In ponies, the PAO2-PaO2 did not change significantly between 10 and 30 minutes. Final PaO2 could not be correlated with initial PaO2 or initial PAO2-PaO2. The rate of rise of PAO2-PaO2 could not be predicted from baseline values. The rate of rise of PaCO2 was similar and fairly constant in ponies and horses, and did not contribute to the rapid initial decrease in PaO2. It appears that apneic oxygenation should not be used in the equine species, since it is impossible to predict in which animals the technique is safe for more than a few minutes.

An evaluation of apnea or spontaneous ventilation in early recovery following mechanical ventilation in the anesthetized horse

“…Although AMMO was not thought to be an efficacious technique for oxygenating horses for an extended period of time, it may be helpful for the very short period of time required for movement to recovery. (Blaze & Robinson 1987. )…”

“…Surprisingly, this horse's highest PaCO 2 was 66 mm Hg (8.8 kPa) and the lowest PaO 2 (at the time of SV) was 207 mm Hg (27.6 kPa). Individual variation between blood gas tensions and response to oxygenation is marked in equine patients, but this individual is an interesting example of well‐being despite extended apnea with oxygen insufflation (Blaze & Robinson 1987).…”

Cardiovascular, respiratory and metabolic responses to apnea induced by atlanto‐occipital intrathecal lidocaine injection in anesthetized horses

“…In the current study, there was a substantial initial increase in PaCO 2 [median: 11 mmHg (1.5 kPa)] in the first minute of apnea that essentially reached a plateau after 2 minutes [median increase: 14–16 mmHg (1.9–2.1 kPa)], whereas pH decreased only by 0.06–0.08 units. By contrast, PaCO 2 increased almost linearly at an average of 5.5 mmHg minute −1 (0.7 kPa minute −1 ) and pH decreased by approximately 0.03–0.05 units minute −1 during the initial 10 minutes of apnea in hyperoxemic and hemodynamically stable halothane‐anesthetized horses paralyzed with succinylcholine (Blaze & Robinson ). Although the smaller overall change in PaCO 2 in the present study was likely to be attributable to the deterioration of tissue blood flow and a consequent decrease in peripheral CO 2 removal, this level of hypercapnia depresses cardiovascular function (Khanna et al.…”

“…). Higher PaCO 2 , as would be expected to be achieved in apneic horses with adequate oxygenation and cardiovascular function (Blaze & Robinson ), would cause sympathetic and cardiovascular stimulation (Khanna et al. ).…”

“…Delivery of 100% oxygen in the tracheal lumen at flow rates of >15 L minute −1 may prevent hypoxemia if the horse is breathing (Mason et al. ; McMurphy & Cribb ), but may not do so during apnea (Blaze & Robinson ). The physiologic consequences of apnea‐induced severe hypoxemia in anesthetized horses have not been published.…”