Veterinary anaesthesia and analgesia · 2025
The effects of preemptive carbon dioxide reduction in prolonged positive pressure breath holding in anesthetized dogs receiving oxygen.
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Chae Junghwa, Nam Changhoon, Kim Nahyun, Kim Jihyun, Cho Younggwang, Lee Inhyung, Son Won-Gyun
Аннотация
OBJECTIVE: To characterize physiological responses to prolonged positive pressure breath holding (PPBH) in anesthetized dogs with oxygen supplementation, and to determine whether lowering initial end-tidal carbon dioxide (Pe'CO2) extends the safe duration of PPBH.
STUDY DESIGN: Prospective, randomized, crossover study.
ANIMALS: A group of five healthy adult Beagle dogs (12.9 ± 1.2 kg).
METHODS: Each dog underwent two PPBH trials at initial Pe'CO2 levels of 40 mmHg (5.3 kPa, control) and 30 mmHg (4.0 kPa, treatment), with 2 week interval. Anesthesia was induced and then maintained using total intravenous anesthesia with alfaxalone (3 mg kg-1, then 12 mg kg-1 hour-1) and rocuronium (1 mg kg-1, then 0.2 mg kg-1 hour-1). Mechanical ventilation with 100% oxygen was used to achieve target Pe'CO2 levels. PPBH was initiated at an end-expiratory pressure of 15 cmH2O for 10 minutes. Arterial blood gases, heart rate and arterial blood pressure were recorded every minute. Primary end points were the time to reach arterial partial pressure of carbon dioxide (PaCO2) ≥ 60 mmHg (8.0 kPa) or pH ≤ 7.2. Time-dependent changes were analyzed using linear mixed models. The duration of PPBH before reaching end points was evaluated using Kaplan-Meier survival analysis.
RESULTS: No hypoxemia was observed. PPBH resulted in progressive increases in PaCO2 and corresponding pH reductions over time (p < 0.001). The time to reach PaCO2 ≥ 60 mmHg (8.0 kPa) was 2.4 ± 0.8 minutes at 40 mmHg (5.3 kPa) and 5.8 ± 1.6 minutes at 30 mmHg (4.0 kPa) (p = 0.006). Similarly, the time to reach pH ≤ 7.2 was significantly prolonged in the 30 mmHg (4.0 kPa) treatment (p = 0.002). Cardiovascular variables remained within reference ranges.
CONCLUSIONS AND CLINICAL RELEVANCE: The results of this study show that adjusting initial Pe'CO2 effectively delays the progression of hypercapnia and acidemia, thereby extending the clinically tolerable duration of PPBH.
STUDY DESIGN: Prospective, randomized, crossover study.
ANIMALS: A group of five healthy adult Beagle dogs (12.9 ± 1.2 kg).
METHODS: Each dog underwent two PPBH trials at initial Pe'CO2 levels of 40 mmHg (5.3 kPa, control) and 30 mmHg (4.0 kPa, treatment), with 2 week interval. Anesthesia was induced and then maintained using total intravenous anesthesia with alfaxalone (3 mg kg-1, then 12 mg kg-1 hour-1) and rocuronium (1 mg kg-1, then 0.2 mg kg-1 hour-1). Mechanical ventilation with 100% oxygen was used to achieve target Pe'CO2 levels. PPBH was initiated at an end-expiratory pressure of 15 cmH2O for 10 minutes. Arterial blood gases, heart rate and arterial blood pressure were recorded every minute. Primary end points were the time to reach arterial partial pressure of carbon dioxide (PaCO2) ≥ 60 mmHg (8.0 kPa) or pH ≤ 7.2. Time-dependent changes were analyzed using linear mixed models. The duration of PPBH before reaching end points was evaluated using Kaplan-Meier survival analysis.
RESULTS: No hypoxemia was observed. PPBH resulted in progressive increases in PaCO2 and corresponding pH reductions over time (p < 0.001). The time to reach PaCO2 ≥ 60 mmHg (8.0 kPa) was 2.4 ± 0.8 minutes at 40 mmHg (5.3 kPa) and 5.8 ± 1.6 minutes at 30 mmHg (4.0 kPa) (p = 0.006). Similarly, the time to reach pH ≤ 7.2 was significantly prolonged in the 30 mmHg (4.0 kPa) treatment (p = 0.002). Cardiovascular variables remained within reference ranges.
CONCLUSIONS AND CLINICAL RELEVANCE: The results of this study show that adjusting initial Pe'CO2 effectively delays the progression of hypercapnia and acidemia, thereby extending the clinically tolerable duration of PPBH.