Abstract
Objective: To determine physiologic responses to apnea-induced severe hypoxemia in anesthetized horses. Study design: Prospective experimental study. Animals: Six university-owned horses with a median (range) body weight of 500 (220–510) kg and aged 13.5 (0.8–24.0) years scheduled for euthanasia. Methods: Xylazine–midazolam–ketamine-anesthetized horses breathing room air spontaneously were instrumented with a facial artery catheter for pressure measurement and blood sampling, and were made apneic with atlanto-occipital intrathecal lidocaine (4 mg kg−1). Cardiopulmonary, biochemical and hematologic variables were recorded before (baseline) and every minute for 10 minutes after lidocaine injection. Results: PaO2 values were: baseline, 55 mmHg (7.3 kPa); 1 minute, 28 mmHg (3.8 kPa); 2 minutes, 18 mmHg (2.4 kPa); 3 minutes, 15 mmHg (2.0 kPa), and 4–10 minutes, (8–11 mmHg (1.1–1.5 kPa). PaCO2 values were: baseline, 50 mmHg (6.7 kPa); 1 minute, 61 mmHg (8.1 kPa), and 2–10 minutes, 64–66 mmHg (8.5–8.8 kPa). Base excess values at baseline, 1 minute and 2–10 minutes were 5.3 mmol L−1, 6.5 mmol L−1 and 7.0–8.1 mmol L−1, respectively. Pulse rates at baseline, 1 minute and 2–7 minutes were 36, 53 and 54–85 beats minute−1, respectively. Asystole occurred at 8 minutes. Pulse pressures were 50 mmHg at baseline and 1 minute, and 39 mmHg, 31 mmHg, 22 mmHg, 17 mmHg and 1–9 mmHg at 2, 3, 4, 5 and 6–10 minutes, respectively. Lactate was 0.9 mmol L−1 at baseline, progressively increasing to 1.7–2.4 mmol L−1 at 7–10 minutes. Packed cell volume increased after 7 minutes of apnea. There were no other major changes. Conclusions and clinical relevance: Apnea immediately exacerbated hypoxemia and hypercapnia and rapidly caused hemodynamic instability. Apnea in hypoxemic anesthetized horses is associated with a serious risk for progress to cardiovascular collapse.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 590-598 |
| Number of pages | 9 |
| Journal | Veterinary Anaesthesia and Analgesia |
| Volume | 43 |
| Issue number | 6 |
| DOIs | |
| State | Published - Nov 1 2016 |
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Keywords
- heart rate
- hypercapnia
- hypotension
- hypoxia
- mortality
ASJC Scopus subject areas
- veterinary(all)
Cite this
Cardiovascular, respiratory and metabolic responses to apnea induced by atlanto-occipital intrathecal lidocaine injection in anesthetized horses. / Guedes, Alonso; Aleman, Monica R; Davis, Eric; Tearney, Caitlin.
In: Veterinary Anaesthesia and Analgesia, Vol. 43, No. 6, 01.11.2016, p. 590-598.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cardiovascular, respiratory and metabolic responses to apnea induced by atlanto-occipital intrathecal lidocaine injection in anesthetized horses
AU - Guedes, Alonso
AU - Aleman, Monica R
AU - Davis, Eric
AU - Tearney, Caitlin
PY - 2016/11/1
Y1 - 2016/11/1
N2 - Objective: To determine physiologic responses to apnea-induced severe hypoxemia in anesthetized horses. Study design: Prospective experimental study. Animals: Six university-owned horses with a median (range) body weight of 500 (220–510) kg and aged 13.5 (0.8–24.0) years scheduled for euthanasia. Methods: Xylazine–midazolam–ketamine-anesthetized horses breathing room air spontaneously were instrumented with a facial artery catheter for pressure measurement and blood sampling, and were made apneic with atlanto-occipital intrathecal lidocaine (4 mg kg−1). Cardiopulmonary, biochemical and hematologic variables were recorded before (baseline) and every minute for 10 minutes after lidocaine injection. Results: PaO2 values were: baseline, 55 mmHg (7.3 kPa); 1 minute, 28 mmHg (3.8 kPa); 2 minutes, 18 mmHg (2.4 kPa); 3 minutes, 15 mmHg (2.0 kPa), and 4–10 minutes, (8–11 mmHg (1.1–1.5 kPa). PaCO2 values were: baseline, 50 mmHg (6.7 kPa); 1 minute, 61 mmHg (8.1 kPa), and 2–10 minutes, 64–66 mmHg (8.5–8.8 kPa). Base excess values at baseline, 1 minute and 2–10 minutes were 5.3 mmol L−1, 6.5 mmol L−1 and 7.0–8.1 mmol L−1, respectively. Pulse rates at baseline, 1 minute and 2–7 minutes were 36, 53 and 54–85 beats minute−1, respectively. Asystole occurred at 8 minutes. Pulse pressures were 50 mmHg at baseline and 1 minute, and 39 mmHg, 31 mmHg, 22 mmHg, 17 mmHg and 1–9 mmHg at 2, 3, 4, 5 and 6–10 minutes, respectively. Lactate was 0.9 mmol L−1 at baseline, progressively increasing to 1.7–2.4 mmol L−1 at 7–10 minutes. Packed cell volume increased after 7 minutes of apnea. There were no other major changes. Conclusions and clinical relevance: Apnea immediately exacerbated hypoxemia and hypercapnia and rapidly caused hemodynamic instability. Apnea in hypoxemic anesthetized horses is associated with a serious risk for progress to cardiovascular collapse.
AB - Objective: To determine physiologic responses to apnea-induced severe hypoxemia in anesthetized horses. Study design: Prospective experimental study. Animals: Six university-owned horses with a median (range) body weight of 500 (220–510) kg and aged 13.5 (0.8–24.0) years scheduled for euthanasia. Methods: Xylazine–midazolam–ketamine-anesthetized horses breathing room air spontaneously were instrumented with a facial artery catheter for pressure measurement and blood sampling, and were made apneic with atlanto-occipital intrathecal lidocaine (4 mg kg−1). Cardiopulmonary, biochemical and hematologic variables were recorded before (baseline) and every minute for 10 minutes after lidocaine injection. Results: PaO2 values were: baseline, 55 mmHg (7.3 kPa); 1 minute, 28 mmHg (3.8 kPa); 2 minutes, 18 mmHg (2.4 kPa); 3 minutes, 15 mmHg (2.0 kPa), and 4–10 minutes, (8–11 mmHg (1.1–1.5 kPa). PaCO2 values were: baseline, 50 mmHg (6.7 kPa); 1 minute, 61 mmHg (8.1 kPa), and 2–10 minutes, 64–66 mmHg (8.5–8.8 kPa). Base excess values at baseline, 1 minute and 2–10 minutes were 5.3 mmol L−1, 6.5 mmol L−1 and 7.0–8.1 mmol L−1, respectively. Pulse rates at baseline, 1 minute and 2–7 minutes were 36, 53 and 54–85 beats minute−1, respectively. Asystole occurred at 8 minutes. Pulse pressures were 50 mmHg at baseline and 1 minute, and 39 mmHg, 31 mmHg, 22 mmHg, 17 mmHg and 1–9 mmHg at 2, 3, 4, 5 and 6–10 minutes, respectively. Lactate was 0.9 mmol L−1 at baseline, progressively increasing to 1.7–2.4 mmol L−1 at 7–10 minutes. Packed cell volume increased after 7 minutes of apnea. There were no other major changes. Conclusions and clinical relevance: Apnea immediately exacerbated hypoxemia and hypercapnia and rapidly caused hemodynamic instability. Apnea in hypoxemic anesthetized horses is associated with a serious risk for progress to cardiovascular collapse.
KW - heart rate
KW - hypercapnia
KW - hypotension
KW - hypoxia
KW - mortality
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UR - http://www.scopus.com/inward/citedby.url?scp=84990182206&partnerID=8YFLogxK
U2 - 10.1111/vaa.12344
DO - 10.1111/vaa.12344
M3 - Article
C2 - 26849108
AN - SCOPUS:84990182206
VL - 43
SP - 590
EP - 598
JO - Veterinary Anaesthesia and Analgesia
JF - Veterinary Anaesthesia and Analgesia
SN - 1467-2987
IS - 6
ER -