Effect of hypercapnia on the arrhythmogenic dose of epinephrine in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.
Abstract: The effect of hypercapnia on the arrhythmogenic dose of epinephrine (ADE) was investigated in 14 horses. Anesthesia was induced with guaifenesin and thiamylal sodium and was maintained at an endtidal halothane concentration between 0.86 and 0.92%. Base-apex ECG, cardiac output, and facial artery blood pressure were measured and recorded. The ADE was determined at normocapnia (arterial partial pressure of carbon dioxide [PaCO2] = 35 to 45 mm of Hg), at hypercapnia (PaCO2 = 70 to 80 mm of Hg), and after return to normocapnia. Epinephrine was infused at arithmetically spaced increasing rates (initial rate = 0.25 micrograms/kg of body weight/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate, to the nearest 0.25 micrograms/kg/min, at which 4 premature ventricular complexes occurred in a 15-second period. The ADE (mean +/- SD) during hypercapnia (1.04 +/- 0.23 micrograms/kg/min) was significantly (P < 0.05) less than the ADE at normocapnia (1.35 +/- 0.38 micrograms/kg/min), whereas the ADE after return to normocapnia (1.17 +/- 0.22 micrograms/kg/min) was not significantly different from those during normocapnia or hypercapnia. Baseline systolic and diastolic arterial pressures and cardiac output decreased after return to normocapnia. Significant differences were not found in arterial partial pressure of O2 (PaO2) or in base excess during the experiment. Two horses developed ventricular fibrillation and died during normocapnic determinations of ADE. Hypercapnia was associated with an increased risk of developing ventricular arrhythmias in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.
Publication Date: 1993-02-01 PubMed ID: 8430941
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- Journal Article
Summary
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The research article investigates the impact of an elevated level of carbon dioxide in the blood (hypercapnia) on the susceptibility of horses, anesthetized with a certain combination of drugs, to heart rhythm complications triggered by epinephrine. Results suggest that a high carbon dioxide level in the blood heightens the risk of developing ventricular arrhythmias in horses under these anesthetic conditions.
Research Methodology
- The study involved 14 horses where the arrhythmogenic dose of epinephrine (ADE) – the minimum amount of epinephrine required to induce abnormal heart rhythms – was determined under different conditions of blood gas levels.
- Anesthesia was initiated using guaifenesin and thiamylal sodium, maintained with a constant range of halothane concentration.
- Cardiac parameters such as ECG, cardiac output, and blood pressure were continuously monitored and recorded.
- ADE was determined at a normal level of carbon dioxide (normocapnia), a high level (hypercapnia), and after returning to normocapnia.
- The process involved the infusion of epinephrine at progressively increasing rates, with the ADE being designated as the lowest rate at which four premature ventricular complexes (a type of arrhythmia) happened within a 15-second period.
Findings
- The ADE during hypercapnia was significantly lower than during normocapnia, meaning less epinephrine was required to trigger arrhythmias when carbon dioxide levels were high in the blood of the anesthetized horses.
- The ADE after returning to normocapnia was not significantly different from the ADEs recorded during both high and normal carbon dioxide levels.
- Systolic and diastolic arterial pressures and cardiac output decreased after returning to normocapnia.
- No significant changes were observed in the arterial partial pressure of O2 or the base excess during the experiment.
- The experiment was risky as two horses developed a serious variation of arrhythmia, called ventricular fibrillation, and died during normocapnic determinations of ADE.
Implications
- The study concluded that a state of hypercapnia is associated with a heightened risk of developing ventricular arrhythmias in anesthetized horses, implying caution during veterinary anesthesia procedures in situations where elevated carbon dioxide levels in blood could occur.
Cite This Article
APA
Gaynor JS, Bednarski RM, Muir WW.
(1993).
Effect of hypercapnia on the arrhythmogenic dose of epinephrine in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.
Am J Vet Res, 54(2), 315-321.
Publication
Researcher Affiliations
- Department of Veterinary Clinical Sciences, Ohio State University, Columbus 43210.
MeSH Terms
- Anesthesia / adverse effects
- Anesthesia / veterinary
- Animals
- Arrhythmias, Cardiac / blood
- Arrhythmias, Cardiac / chemically induced
- Arrhythmias, Cardiac / veterinary
- Blood Pressure / drug effects
- Dose-Response Relationship, Drug
- Drug Combinations
- Epinephrine / toxicity
- Female
- Guaifenesin
- Halothane
- Heart Rate / drug effects
- Horse Diseases / blood
- Horse Diseases / chemically induced
- Horse Diseases / physiopathology
- Horses
- Hypercapnia / etiology
- Hypercapnia / physiopathology
- Hypercapnia / veterinary
- Male
- Thiamylal
Citations
This article has been cited 2 times.- Pettifer G, Dyson D, McDonell W. The arrhythmogenic dose of epinephrine in halothane and isoflurane anesthetized dogs: an assessment of repeatability. Can J Vet Res 1997 Jul;61(3):221-6.
- Pettifer GR, Dyson DH, McDonell WN. An evaluation of the influence of medetomidine hydrochloride and atipamezole hydrochloride on the arrhythmogenic dose of epinephrine in dogs during halothane anesthesia. Can J Vet Res 1996 Jan;60(1):1-6.
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