Abstract
Simple SummaryHorses commonly develop low blood oxygen levels during anesthesia, especially when they are placed on their backs. This study investigated whether a 15° head-up tilt, in a homogenous group of anesthetized horses positioned on their backs, would result in better blood oxygen levels as compared to no tilt. The results showed significantly greater blood oxygen levels with tilt compared to no tilt in five out of six horses tested. In one horse the effect was the opposite. The concurrent effect on cardiovascular function remains to be tested in detail. Further studies are needed to confirm these findings in a larger group of horses and to determine the effects on blood pressure and treatment options.Lower than expected arterial oxygen tension (PaO2) continues to be an unresolved problem in equine anesthesia. The aim of this randomized, crossover, and prospective study using six adult horses is to determine if a 15° reverse Trendelenburg position (RTP) increases PaO2 during inhalation anesthesia. Under constant-dose isoflurane anesthesia, dorsally recumbent horses were positioned either horizontally (HP) or in a 15° RTP for 2 h. Lungs were mechanically ventilated (15 mL/kg, 6 breaths/min). Arterial carbon dioxide tension (PaCO2), PaO2, inspired oxygen fraction (FiO2), and end-tidal carbon dioxide tension (EtCO2) were determined every 30 min during anesthesia. Indices of dead-space ventilation (Vd/Vt), oxygenation (P–F ratio), and perfusion (F–shunt) were calculated. Dobutamine and phenylephrine were used to support mean arterial pressure (MAP). Data are presented as median and range. In one horse, which was deemed an outlier due to its thoracic dimensions and body conformation, indices of oxygenation worsened in RTP compared to HP (median PaO2 438 vs. 568 mmHg; P–F ratio 454 vs. 586 mmHg, and F–shunt 13.0 vs. 5.7 mmHg). This horse was excluded from calculations. In the remaining five horses they were significantly better with RTP compared to HP. Results in remaining five horses showed that PaO2 (502, 467–575 vs. 437, 395–445 mmHg), P-F ratio (518, 484–598 vs. 455, 407–458 mmHg), and F-shunt (10.1, 4.2–11.7 vs. 14.2, 13.8–16.0 mmHg) were significantly different between RTP and HP (p = 0.03). Other variables were not significantly different. In conclusion, the 15° RTP resulted in better oxygenation than HP in dorsally recumbent, isoflurane-anesthetized horses, although worsening of oxygenation may occur in individual horses. A study detailing the cardiovascular consequences of RTP is necessary before it can be recommended for clinical practice.
Highlights
Respiratory function impairment, or less than expected arterial partial pressure of oxygen (PaO2), has long been recognized and continues to be very common in equine anesthesia [1,2,3,4,5,6,7,8]
Physical methods appear to improve PaO2 more consistently than pharmacological methods, which seems logical given the prominent contribution of compression atelectasis to impaired oxygenation [5,10]
The results of the current study suggest that a 15° reverse Trendelenburg position (RTP) can significantly improve arterial oxygen tension compared to the horizontal position (HP) in dorsally recumbent, mechanically ventilated, isoflurane-anesthetized horses
Summary
Respiratory function impairment, or less than expected arterial partial pressure of oxygen (PaO2), has long been recognized and continues to be very common in equine anesthesia [1,2,3,4,5,6,7,8]. Several physical and pharmacological interventions aimed at mitigating impaired oxygenation have been studied in anesthetized horses. These include reverse Trendelenburg position (RTP) [13,14], positive end-expired pressure (PEEP) combined with repeated alveolar recruitment maneuvers (RM) [15,16], continuous positive airway pressure [17], intravenous and inhaled β-adrenergic receptor agonists [18,19], inhaled nitric oxide [10,20,21], acepromazine [7], and reducing FiO2 [22,23,24,25]. Physical methods appear to improve PaO2 more consistently than pharmacological methods, which seems logical given the prominent contribution of compression atelectasis to impaired oxygenation [5,10]
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