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SUMMARY

The effect of hypercapnia on the arrhythmo-genic dose of epinephrine (ADE) was investigated in 14 horses. Anesthesia was induced with guaifenesin and thiamylal sodium and was maintained at an end-tidal 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 μg/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 μg/kg/min, at which 4 premature ventricular complexes occurred in a 15-second period. The ADE (mean ± SD) during hypercapnia (1.04 ± 0.23 μg/kg/min) was significantly (P < 0.05) less than the ADE at normocapnia (1.35 ± 0.38 μg/kg/min), whereas the ADE after return to normocapnia (1.17 ± 0.22 μg/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.

Free access
in American Journal of Veterinary Research

SUMMARY

We investigated small-volume (5 ml/kg) 7% NaCl in 6% dextran 70 (HS/D70) as an alternative to large-volume (60 ml/kg) 0.9% NaCl for treatment of experimentally induced canine gastric dilatation-volvulus (gdv) shock. The stomach was surgically displaced and then distended with an intragastric balloon in 11 dogs anesthetized with pentobarbital. All dogs were subjected to gdv for 180 minutes before partial decompression and resuscitation. Hemodynamic values, blood gas values, and plasma volume were measured during control, shock, and resuscitation periods. Resuscitation started with 1 group (n = 6) receiving 5 ml of HS/D70/kg, iv, over 5 minutes, and the other group (n = 5) receiving 60 ml of 0.9% NaCl/kg, iv, over 60 minutes. Both groups received a surgical maintenance dosage (20 ml/kg/h) of 0.9% NaCl after initial resuscitation. Resuscitative effects of small-volume HS/D70 were similar to large-volume 0.9% NaCl during the first hour of treatment; however, cardiac output was significantly higher in the HS/D70 group for the last 2 hours of resuscitation. Changes in heart rate, left ventricular pressure change, and systemic vascular resistance appeared to be responsible for improved perfusion. Mixed venous oxygen partial pressure data supported improved perfusion in the HS/D70 group. Packed cell volume remained higher in the HS/D70 group, indicating less hemodilution and improved oxygen delivery. Resuscitation of this gdv-induced shock model was better sustained with small-volume HS/D70, compared with conventional large-volume 0.9% NaCl.

Free access
in American Journal of Veterinary Research

SUMMARY

The hemodynamic effects of high arterial carbon dioxide pressure (PaCO2 ) during anesthesia in horses were studied. Eight horses were anesthetized with xylazine, guaifenesin, and thiamylal, and were maintained with halothane in oxygen (end-tidal halothane concentration = 1.15%). Baseline data were collected while the horses were breathing spontaneously; then the horses were subjected to intermittent positive-pressure ventilation, and data were collected during normocapnia (PaCO2 , 35 to 45 mm of Hg), moderate hypercapnia (PaCO2 , 60 to 70 mm of Hg), and severe hypercapnia (PaCO2 , 75 to 85 mm of Hg). Hypercapnia was induced by adding carbon dioxide to the inspired gas mixture. Moderate and severe hypercapnia were associated with significant (P < 0.05) increases in aortic blood pressure, left ventricular systolic pressure, cardiac output, stroke volume, maximal rate of increase and decrease in left ventricular pressure (positive and negative dP/dtmax, respectively), and median arterial blood flow, and decreased time constant for ventricular relaxation. These hemodynamic changes were accompanied by increased plasma epinephrine and norepinephrine concentrations. Administration of the β-blocking drug, propranolol hydrochloride, markedly depressed the response to hypercapnia. This study confirmed that in horses, hypercapnia is associated with augmentation of cardiovascular function.

Free access
in American Journal of Veterinary Research

Summary

Intravenous administration of quinidine gluconate converted atrial fibrillation (af) to sinus rhythm in 9 of 12 horses. Twelve horses that were diagnosed by ecg to have af were administered up to 11 mg of quinidine gluconate/kg of body weight in 1.0 -to 1.5-mg/kg bolus injections every 10 to 15 minutes. The total dose of quinidine administered iv ranged from 1.8 to 5.8 g. Increased ventricular rate, apprehension, and mild depression were observed during treatment. Other signs of toxicosis were not observed. One horse was successfully treated with iv administered quinidine gluconate on 3 occasions. Intravenous administration of quinidine is a safe and effective alternative for treatment of af in some horses.

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

The cardiopulmonary effects of 4 positions (standing, right lateral, left lateral, and dorsal recumbency) were evaluated in conscious cattle in which no sedatives or anesthetic drugs were given. Each position was maintained for 30 minutes, during which time there were no significant changes in heart rate, respiratory rate, mean arterial blood pressure, arterial pH, PaCO2 , arterial base excess, or venous blood gas values. Significant decreases in PaO2 developed when cattle were in lateral positions and dorsal recumbency. Cardiac index was unchanged in all positions, except in dorsal recumbency at 30 minutes, when it was significantly decreased.

Free access
in American Journal of Veterinary Research

SUMMARY

Programmed electrical stimulation techniques were used to evaluate the effects of halothane and isoflurane on induction of atrial fibrillation in anesthetized dogs. Experiments were performed in 16 dogs anesthetized with α-chloralose. Critically timed premature stimuli were applied to the right atrial appendage and Bachmann bundle to determine the atrial fibrillation threshold, defined as the minimal current required to induce rapid, irregular atrial electrical activity of at least 8 seconds' duration, Atrial fibrillation thresholds were determined at baseline (0.0% inhalational anesthetic), 0.5 minimal alveolar concentration (mac), and 1.0 mac of halothane (n = 8) and isoflurane (n = 8).

In the absence of inhalation anesthetic, it was significantly (P < 0.01) easier to induce atrial fibrillation at the Bachmann bundle vs the right atrial appendage. Atrial fibrillation threshold at the Bachmann bundle was not affected by increasing concentrations of halothane, but was increased by 1.0 mac of isoflurane (P < 0.05). It was concluded that at 1.0 mac isoflurane, but not halothane, has antifibrillatory effects in atrial tissue.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To determine the effects of perzinfotel, butorphanol, and their combination on the minimal alveolar concentration (MAC) of isoflurane in cats.

Animals—7 healthy sexually intact cats (4 males and 3 females), aged 12 to 17 months and weighing 2.8 to 4.6 kg.

Procedures—In a crossover design, saline (0.9% NaCl) solution, perzinfotel (2.5 to 15 mg/kg; IV, IM, and SC), butorphanol tartrate (0.2 mg/kg, IM), or a combination of 5 mg of perzinfotel/kg and 2 mg of butorphanol tartrate/kg (both IM) was administered to 6 cats before 7 separate episodes of anesthesia with isoflurane in oxygen. Heart rate, arterial blood pressure, bispectral index (BIS), and inspiration and expiration concentrations of isoflurane were continuously monitored. The isoflurane MAC was determined twice during anesthesia.

Results—IV, IM, and SC administration of perzinfotel at 2.5 to 15 mg/kg resulted in a significant decrease in mean isoflurane MAC by 43.3% to 68.0%. The BIS significantly increased after perzinfotel administration via the same routes at 2.5 to 15 mg/kg and after perzinfotelbutorphanol administration IM. Blood pressure was significantly higher after perzinfotel was administered at 5 mg/kg, IM; 10 mg/kg, IV; and 10 mg/kg, SC than after saline solution administration.

Conclusions and Clinical Relevance—Perzinfotel administration decreased the isoflurane MAC and increased several BIS and blood pressure values in anesthetized cats. Administration of perzinfotel prior to isoflurane anesthesia may improve anesthetic safety by reducing inhalant anesthetic requirements and improving cardiovascular function during anesthesia. (Am J Vet Res 2010;71:1270–1276)

Full access
in American Journal of Veterinary Research

Objective

To test the hypothesis that small volumes of hypertonic saline-dextran (HSD) solution can be used to effectively resuscitate dogs in shock induced by gastric dilatation-volvulus (GDV). and, compared with administration of large volumes of lactated Ringer's solution (LRS), can be used to limit the overall volume of fluid needed for resuscitation.

Design

Prospective, clinical study.

Animals

15 dogs with GDV-induced shock.

Procedure

Initially, HSD solution (5 ml/kg of body weight) or LRS (60 to 90 ml/kg) was administered. All dogs then received a maintenance administration (20 ml/kg/h) of LRS. Cardiorespiratory, blood gas, and serum biochemical analyses were performed over a 4-hour period after initiation of treatment.

Results

Systolic arterial and central venous pressures and plasma volume increased more rapidly in dogs in the HSD + LRS group. The cumulative dose of fluids administered to dogs in the HSD + LRS group was significantly less than that administered to dogs in the LRS group. Serum sodium and chloride concentrations and osmolality increased significantly in dogs in the HSD + LRS group, but not in dogs in the LRS group. Ventricular arrhythmias were detected in both groups of dogs, but did not appear to be induced by either form of fluid therapy.

Clinical Implications

Administration of HSD rapidly restored cardiorespiratory function and induced resuscitation equivalent to administration of large volumes of LRS. Use of HSD solutions to treat dogs in GDV-induced shock may be more efficient than use of isotonic fluids. Administration of HSD solution was not associated with noticeable complications.

Free access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine the effects of IV administration of enalaprilat on cardiorespiratory and hematologic variables as well as inhibition of angiotensin converting enzyme (ACE) activity in exercising horses.

Animals—6 adult horses.

Procedure—Horses were trained by running on a treadmill for 5 weeks. Training was continued throughout the study period, and each horse also ran 2 simulated races at 120% of maximum oxygen consumption. Three horses were randomly selected to receive treatment 1 (saline [0.9% NaCl] solution), and the remaining 3 horses received treatment 2 (enalaprilat; 0.5 mg/kg of body weight, IV) before each simulated race. Treatment groups were reversed for the second simulated race. Cardiorespiratory and hematologic data were obtained before, during, and throughout the 1-hour period after each simulated race. Inhibition of ACE activity was determined during and after each race in each horse.

Results—Exercise resulted in significant increases in all hemodynamic variables and respiratory rate. The pH and PO2 of arterial blood decreased during simulated races, whereas PCO2 remained unchanged. Systemic and pulmonary blood pressure measurements and arterial pH, PO2, and PCO2 returned to baseline values by 60 minutes after simulated races. Enalaprilat inhibited ACE activity to < 25% of baseline activity without changing cardiorespiratory or blood gas values, compared with horses administered saline solution.

Conclusions and Clinical Relevance—Enalaprilat administration almost completely inhibited ACE activity in horses without changing the hemodynamic responses to intense exercise and is unlikely to be of value in preventing exercise-induced pulmonary hemorrhage. (Am J Vet Res 2001;62:1008–1013)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To measure QT interval duration and QT dispersion in Boxers and to determine whether QT variables correlate with indices of disease severity in Boxers with familial ventricular arrhythmias, including the number of ventricular premature complexes per day, arrhythmia grade, and fractional shortening.

Animals—25 Boxers were evaluated by ECG and echocardiography.

Procedure—The QT interval duration was measured from 12-lead ECG and corrected for heart rate (QTc), using Fridericia's formula. The QT and QTc were calculated for each lead, from which QT and QTc dispersion were determined. Echocardiography and 24-hour ambulatory ECG were performed to evaluate for familial ventricular arrhythmias. Total number of ventricular premature complexes, arrhythmia grade, and fractional shortening were determined and used as indices of disease severity.

Results—There was no correlation between any QT variable and total number of ventricular premature complexes, arrhythmia grade, or fractional shortening. No difference between QT dispersion and QTc dispersion was identified, and correction for heart rate did not affect the results.

Conclusions and Clinical Relevance—QT interval duration and dispersion did not correlate with indices of disease severity for familial ventricular arrhythmias. Heart rate correction of the QT interval did not appear to be necessary for QT dispersion calculation in this group of dogs. QT dispersion does not appear to be a useful noninvasive diagnostic tool in the evaluation of familial ventricular arrhythmias of Boxers. Identification of affected individuals at risk for sudden death remains a challenge in the management of this disease. (Am J Vet Res 2001;62:1481–1485)

Full access
in American Journal of Veterinary Research