Rebreathing anesthetic systems in small animal practice.
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Anesthesia, Closed-Circuit↗
Biomedical subjects
R M Bednarski
Publications and source records attributed to R M Bednarski.
Nonrebreathing anesthetic systems in small animal practice.
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Anesthesia, Inhalation↗
Pharmacokinetics, pharmacodynamics, and analgesic effects of morphine after rectal, intramuscular, and intravenous administration in dogs.
OBJECTIVE: To compare systemic bioavailability and duration for therapeutic plasma concentrations and cardiovascular, respiratory, and analgesic effects of morphine administered per rectum, compared with IV and IM administration in dogs. ANIMALS: 6 healthy Beagles. PROCEDURE: In a randomized study, each dog received the following: morphine IV (0.5 mg/kg of body weight), morphine per rectum (1, 2, and 5 mg/kg as a suppository and 2 mg/kg as a solution), and a control treatment. Intramuscular administration of morphine (1 mg/kg) was evaluated separately. Heart and respiratory rates, systolic, diastolic, and mean blood pressures, adverse effects, and plasma morphine concentrations were measured. Analgesia was defined as an increase in response threshold, compared with baseline values, to applications of noxious mechanical (pressure) and thermal (heat) stimuli. Data were evaluated, using Friedman repeated-measures ANOVA on ranks and Student-Newman-Keuls post-hoc t-tests. RESULTS: Significant differences were not found in cardiovascular, respiratory, or analgesia values between control and morphine groups. Overall systemic bioavailability of morphine administered per rectum was 19.6%. Plasma morphine concentration after administration of the highest dose (5 mg/kg) as a suppository was significantly higher than concentrations 60 and 360 minutes after IV and IM administration, respectively. A single route of administration did not consistently fulfill our criteria for providing analgesia. CONCLUSIONS AND CLINICAL RELEVANCE: Rectal administration of morphine did not increase bioavailability above that reported for oral administration of morphine in dogs. Low bioavailability and plasma concentrations limit the clinical usefulness of morphine administered per rectum in dogs.
Administration, Rectal↗
Effects of acepromazine and butorphanol on positive-contrast upper gastrointestinal tract examination in dogs.
OBJECTIVE: To determine whether acepromazine (ACE) and butorphanol (BUT) combination can be used for restraint of dogs during positive-contrast upper gastrointestinal tract (UGIT) examination. ANIMALS: 6 healthy dogs. PROCEDURE: In a randomized crossover design study, weekly UGIT examinations were performed on each dog for 5 weeks after administration of normal saline solution (0.5 ml), xylazine (1.0 mg/kg of body weight), or a combination of ACE (0.1 mg/kg) and 1 of 3 doses of BUT (0.05, 0.2, 1.0 mg/kg). Gastrointestinal tract emptying time, GI motility, pulse, respiratory rate, and quality of restraint were assessed. RESULTS: Total gastric emptying time was significantly prolonged by use of an ACE and BUT (0.05 mg/kg) combination. Xylazine and higher dosages of BUT significantly prolonged gastric and intestinal emptying times. All anesthetic protocols significantly decreased motility and facilitated nonmanual restraint. Xylazine and BUT (1.0 mg/kg) significantly decreased pulse and respiratory rate. CONCLUSION: The ACE and BUT combination prolonged GI tract emptying times, decreased GI motility, and facilitated nonmanual restraint for duration of the examination. Although GI motility was decreased and total gastric emptying time was prolonged, administration of ACE (0.1 mg/kg) plus BUT (0.05 mg/kg) allowed morphologic examination of the GI tract within 5 hours. Xylazine prolonged GI tract emptying, decreased GI motility, and provided good to excellent initial restraint. Clinical Relevance-The ACE and BUT combination prohibits functional examination of the GI tract; however, morphologic examination is possible when low dosages of BUT (0.05 mg/kg) are used.
Acepromazine↗
[Sedation and anesthesia in dogs and cats with cardiovascular diseases. III. Ventilation, respiratory monitoring, treatment for postoperative pain].
The purpose of this study was to review ventilation and postoperative analgesic technics in 137 dogs and 13 cats with congenital or acquired heart disease. The animals were referred to the Department of Veterinary Clinical Sciences at The Ohio State University, U.S.A, for the following surgical interventions: correction of patent ductus arteriosus (PDA-ligation, 28%), cardiac catheterization with angiogram and angioplasty (22%), pacemaker implantation (18%), exploratory lateral thoracotomy (8.7%), correction of right aortic arch ring anomaly (3.3%), correction of subvalvular aortic stenosis (2.7%), correction of PDA with coil in patients with mitral regurgitation and congestive heart failure (2%), pericardectomy and removal of heart base tumor (2%), and palliative surgery for ventricular septal defect (VSD, 0.7%). Controlled ventilation was used in all animals during thoracotomy. Anesthesia was maintained over 2.3 +/- 1.3 hours by using either isoflurane, halothane, propofol, or diazepam-ketamine in 64%, 32%, 2%, and 0.7% of animals, respectively. Postoperative analgesia was necessary in 20% of animals and was provided by using different technics over several hours. The technics and respective percentages of animals in which they were used, were: intravenous buprenorphine (3.3%), intercostal nerve blocks (8.7%), epidural morphine (4%), and interpleural regional analgesia (4%).
Analgesia↗
[Sedation and anesthesia in dogs and cats with cardiovascular diseases. I. Anesthesia plan considering risk assessment, hemodynamic effects of drugs and monitoring].
The purpose of this study was to review the effects of sedatives and anesthetics in 137 dogs and 13 cats with congenital or acquired heart disease which were referred for diagnostic, therapeutic, and surgical interventions: correction of patent ductus arteriosus (PDA-ligation, 28%), cardiac catheterization with angiogram and angioplasty (22%), pacemaker implantation (18%), exploratory lateral thoracotomy (8.7%), correction of right aortic arch (ring anomaly, 3.3%), correction of subvalvular aortic stenosis (2.7%), correction of PDA with coil in patients with mitral regurgitation and congestive heart failure (2%), pericardectomy and removal of heart-base tumors (2%), palliative surgery for ventricular septal defect (VSD, 0.7%), and sick patients with deleterious cardiac arrhythmias (0.7%). The anesthetic plan considered the risks of anesthesia based upon preoperative patient assessment, classification scheme for functional phases of heart failure, and anesthetic drug effects of the cardiovascular system. The effects of sedatives and anesthetic drugs on determinants of cardiac output are described. The most commonly used drugs for premedication, induction, and maintenance of anesthesia were midazolam-oxymorphone (20%), thiopental or etomidate (30%), and isoflurane (64%). Prompt therapy was given to control arrhythmias and provide organ perfusion, pain relief, muscle relaxation and renal diuresis, using lidocaine, dopamine, fentanyl, atracurium, and furosemide in 17.3% 14.7%, 12%, 10%, and 8.7% of animals, respectively. Methods of routine and advanced patient monitoring are described.
Anesthesia↗
Cardiorespiratory effects of acepromazine maleate and buprenorphine hydrochloride in clinically normal dogs.
Cardiorespiratory effects of the combination of acepromazine maleate (ACP) and buprenorphine hydrochloride (BPN) were studied in 11 healthy, conscious dogs. Values for systemic and pulmonary artery blood pressure, cardiac output, arterial and venous pH and blood gas tensions, and invasive and noninvasive estimates of ventricular systolic function, preload, and afterload were obtained before sedation and after administration of each drug. Acepromazine maleate (0.1 mg/kg, IV) depressed cardiac function, compared with baseline values for unsedated dogs. Cardiac output decreased from a mean (+/- SD) value of 4.2 (+/- 1.5) L/min to 3.1 (+/- 0.8) L/min (P < 0.001), a change not attributed to heart rate. Pulmonary capillary wedge pressure decreased from 8.3 (+/- 4.2) mm of Hg to 6.5 (+/- 4.3) mm of Hg (P < 0.01), but mean right atrial pressure did not change. Left ventricular measurement of the maximal positive rate of pressure change (dP/dtmax) decreased from 2,668 (+/- 356)/mm of Hg/s to 2,145 (+/- 463) mm of Hg/s (P < 0.001), and ventricular stroke volume decreased from 43.2 (+/- 15.2) ml/beat to 32.3 (+/- 8.6) ml/beat. Noninvasive indices of left ventricular function, ventricular shortening fraction, peak aortic velocity, and aortic average acceleration were decreased after ACP administration, but were not statistically different from baseline values. Mean systemic arterial blood pressure decreased from 121 +/- 12 mm of Hg to 96 +/- 13 mm of Hg 15 minutes after ACP administration (P < 0.001). Total systemic vascular resistance was not significantly different from the baseline value.(ABSTRACT TRUNCATED AT 250 WORDS)
Acepromazine↗
[Sedation and anesthesia in dogs and cats with cardiovascular disease. II. Anesthesia planning with respect to pathophysiology, heart arrhythmia].
The purpose of this study was to review the incidence of cardiac arrhythmias in 137 anesthetized dogs and 13 anesthetized cats with congenital or acquired heart disease that were referred for correction of following procedures: patent ductus arteriosus (PDA-ligation, 28%), cardiac catheterization with angiogram and angioplasty (22%), pacemaker implantation (18%), exploratory lateral thoracotomy (8.7%), correction of right aortic arch (ring anomaly, 3.3%), correction of subvalvular aortic stenosis (2.7%), correction of PDA with coil in patients with mitral regurgitation and congestive heart failure (2%), pericardectomy and removal of heart base tumor (2%), and palliative surgery for ventricular septal defect (VSD, 0.7%). The anesthetic plan considered the risks of anesthesia based upon the pathophysiology of cardiac lesions and the anesthetic drug effects on the cardiovascular system. Recommendations are made for dogs with decreased cardiac contractility, cardiac disease with volume overload, cardiac disease with pressure overload, and pericardial tamponade. The percentages of animals and their associated cardiac arrhythmias after premedication and during and after anesthesia were: sinus bradycardia (15.3%), sinus tachycardia (3.3%), atrial flutter (0.7%), atrial fibrillation (0.7%), premature ventricular contraction (14%), and ventricular tachycardia (1.3%). Prompt therapy was given to a percentage of animals in order to control arrhythmia and support cardiovascular system, by using atropine or glycopyrrolate (14%), lidocaine (17.3%), and dopamine (14.7%).(ABSTRACT TRUNCATED AT 250 WORDS)
Anesthesia↗
Effect of phenylephrine on hemodynamics and splenic dimensions in horses.
Pharmacologically induced splenic contraction might be useful during certain medical or surgical procedures in horses. The effects of phenylephrine, an alpha 1-adrenergic receptor agonist, on hemodynamic function and splenic dimensions were examined in 6 healthy adult horses. Phenylephrine infusion (1, 3, or 6 micrograms/kg of body weight/min for 15 minutes) resulted in a dose-related increase in mean pulmonary artery pressure; right atrial pressure; systolic, mean, and diastolic arterial pressures; and packed cell volume (P = 0.0001). Concurrent decreases in heart rate and specific cardiac output (P = 0.0001) were detected, but stroke volume did not vary significantly. The rate-pressure product was increased only at the highest phenylephrine dosage (P = 0.012). Bradycardia was observed at all dosages during drug infusion, and second-degree atrioventricular block was detected in 88% of horses during infusion. Phenylephrine administration caused dose-dependent splenic contraction, as detected by ultrasonographic measurements of splenic area and thickness (P = 0.0001). At the 3- and 6-micrograms/kg/min infusion rates, splenic area was reduced to 28 and 17% of baseline measurement, respectively. Splenic dimensions had returned to baseline values by 35 minutes after the end of infusion. Infusion of phenylephrine at a dosage of 3 micrograms/kg/min for 15 minutes can be used to induce splenic contraction in horses.
Animals↗
Adverse effects of administration of propofol with various preanesthetic regimens in dogs.
The effects of propofol on anesthetic induction were evaluated in 40 dogs anesthetized with isoflurane. Propofol is a rapidly acting, nonbarbiturate drug that induces anesthesia of ultrashort duration with IV administration. Four preanesthetic regimens were used: anesthesia without preanesthetic drugs; or with preanesthetic administration of acepromazine (0.1 mg/kg of body weight, IM), diazepam (0.2 mg/kg, IV), or acepromazine (0.02 mg/kg) and butorphanol (0.4 mg/kg) IM. Heart rate, systolic arterial blood pressure (SAP), respiration, quality of induction and recovery, and adverse effects were induction and recovery, and adverse effects were recorded. Intravenous propofol administration induced a variable period of apnea in 34 of 40 dogs. Cyanosis (in 2 dogs) and signs of pain on injection (in 3 dogs) were infrequently observed during induction. One dog developed ventricular premature depolarizations after propofol administration. Venous CO2 tension increased and pH decreased immediately after propofol administration, regardless of preanesthetic regimen. The SAP significantly (P < 0.05) decreased after propofol administration in dogs treated with acepromazine (SAP, 178 mm of Hg before vs 128 mm of Hg after propofol) and with acepromazine/butorphanol (SAP, 184 mm of Hg before vs 98 mm of Hg after propofol). When used for induction, propofol induces anesthetic-related adverse effects, some of which can be minimized by preanesthetic medication. Recovery characteristics varied with preanesthetic medication, independent of propofol administration.
Anesthesia, Inhalation↗
Vaporizer in circle for delivery of isoflurane to dogs.
An in-circuit vaporizer for delivery of isoflurane was evaluated. The isoflurane concentration within an isolated circle breathing circuit was determined for 1 hour in 6 in-the-circuit vaporizers with the wicks removed. A mechanical ventilator and artificial lung were connected to the circuit. Isoflurane concentration increased as vaporizer setting increased, and delivered concentration (%) at 60 minutes (mean +/- SEM) ranged from 0.46 +/- 0.10 at tap setting 1 to 3.67 +/- 0.30 at setting 5. Temperature of the isoflurane did not change. Cardiovascular and respiratory function were maintained within a clinically acceptable range in 6 dogs anesthetized with thiamylal and maintained with 1.87% end-tidal isoflurane delivered from the in-circuit vaporizer during spontaneous ventilation, controlled ventilation, and closed-circuit anesthesia. The range of vaporizer tap settings (mean +/- SEM) was lower during closed-system anesthesia (2.5 +/- 0.1 to 3.5 +/- 0.6) and during controlled ventilation (2.6 +/- 0.2 to 3.3 +/- 0.2) than during semi-closed system anesthesia (5.4 +/- 0.3 to 6.8 +/- 0.4). The in-circuit vaporizer was used to deliver isoflurane to 36 dogs anesthetized for a variety of surgical and medical procedures. Ventilation was spontaneous, assisted, and in 1 instance, controlled. Cardiovascular function, respiratory function, and recovery times were within clinically acceptable ranges. The initial vaporizer tap setting (mean +/- SEM) was 8.2 +/- 0.4, and this corresponded to an end-tidal isoflurane concentration of 3.5 +/- 0.6. The range of vaporizer settings during the maintenance phase (mean +/- SEM) was 2.8 +/- 0.5 to 4.6 +/- 1.9.(ABSTRACT TRUNCATED AT 250 WORDS)
Acid-Base Equilibrium↗
Effect of hypercapnia on the arrhythmogenic dose of epinephrine in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.
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.
Anesthesia↗
Anesthetic breathing systems.
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Anesthesia, Inhalation↗
Use of low-flow and closed-system anesthesia.
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Anesthesia, Closed-Circuit↗
Precautions when using opioid agonists for induction of anesthesia.
Opioids produce unpredictable anesthesia that is associated with poor muscle relaxation, prolonged onset, and relatively difficult intubation. They often induce bradycardia, which must be countered with atropine or glycopyrrolate, and hypoventilation, which requires ventilatory support. Return to consciousness is often delayed, making postoperative assessment of the patient's condition difficult. Finally opioid induction is relatively expensive compared with other anesthetic induction regimens.
Anesthesia↗
Advantages and guidelines for using nitrous oxide.
Nitrous oxide is useful as an adjunct to methoxyflurane anesthesia and prolonged halothane anesthesia. Nitrous oxide is also useful in the debilitated patient in which the potent volatile anesthetics induce excessive cardiovascular depression. Finally nitrous oxide is useful for smoothing an inadequate anesthetic plane induced by the potent volatile anesthetics.
Adjuvants, Anesthesia↗
Anesthetic concerns for patients with cardiomyopathy.
Hypertrophic cardiomyopathy usually affects cats. The overall cardiac dysfunction associated with hypertrophic cardiomyopathy relates to a decrease in diastolic function. Anesthetic regimens that minimize increases in heart rate and stress-related catecholamine release are desirable. Patients with dilative cardiomyopathy can present asymptomatic or in congestive heart failure. The overall myocardial defect is a depression of systolic function. An anesthetic regimen that minimizes myocardial depression is essential.
Anesthesia↗
Effect of xylazine on the arrhythmogenic dose of epinephrine in thiamylal/halothane-anesthetized horses.
The effect of xylazine on the arrhythmogenic dose of epinephrine (ADE) was studied in 9 horses. Anesthesia was induced by administration of guaifenesin (50 mg/kg of body weight, IV) followed by thiamylal (4 to 6 mg/kg, IV) and was maintained at 1 minimal alveolar concentration (MAC) of halothane (0.89%). Base apex ECG and facial artery pressure were recorded. Epinephrine was infused in a sequence of arithmetically spaced increasing rates (initial rate 0.25 micrograms/kg/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 at least 4 premature ventricular depolarizations occurred in a 15-second period. Xylazine (1.1 mg/kg, IV) was administered after the control ADE was determined. Xylazine did not significantly alter the ADE (control, 1.12 +/- 0.38 micrograms/kg/min; xylazine, 1.21 +/- 0.46 micrograms/kg/min). Blood pressure increased transiently for 8 minutes after xylazine administration. Baseline systolic and diastolic arterial pressures and heart rate were not significantly different from control baseline pressures and heart rate 15 minutes after xylazine administration. Blood pressure and heart rate increased significantly during control and xylazine ADE determinations. Significant differences in pH, PaO2, PaCO2, or base excess were not observed between baseline and ADE in the control or xylazine groups. One horse developed atrial fibrillation, and 2 horses developed ventricular fibrillation during ADE determinations.
Anesthesia, General↗