Effects of xylazine and acetylpromazine upon induced ventricular fibrillation in dogs anesthetized with thiamylal and halothane.

Ventricular arryhythmias including ventricular fibrillation were produced with epinephrine in dogs induced to an anesthetic state with thiamylal and maintained with halothane. In dogs given (premedicated) xylazine 20 minutes prior to anesthesia, ventricular arrhythmias, including ventricular fibrillation, were induced with much smaller doses of epinephrine than in nonpremedicated dogs. Dogs premedicated with acetylpromazine 20 minutes prior to anesthesia with thiamylal and halothane displayed protection from epinephrine-induced arrhythmias. Caution is advised from using xylazine in the presence of halothane if epinephrine is to be administered.     

Fatal interaction between thiamylal sodium and a proprietary antidiarrheal preparation in the dog

A drug interaction involving thiamylal sodium and a proprietary antidiarrheal preparation caused fatal ventricular fibrillation in a dog. Trials involving 4 dogs were conducted to recreate the interaction, and 1 of the 4 dogs died after ventricular fibrillation developed. The nature of the interaction was hypothesized to be mediated through the anticholinergic drug diphemanil methylsulfate, producing an autonomic imbalance.     

Cardiac dysrhythmias associated with gastric dilatation-volvulus in the dog

Of 16 dogs treated medically and surgically for gastric dilatation-volvulus, 11 developed electrocardiographic evidence of ventricular dysrhythmias. Seven of these dogs had ventricular dysrhythmias for the first time during their hospitalization after surgery. The ventricular dysrhythmias included ventricular premature depolarizations, slow ventricular rhythms, paroxysmal ventricular tachycardia, ventricular tachycardia, and multifocal ventricular tachycardia. Two of these dogs had electrocardiographic evidence of atrial premature depolarizations at the time of hospitalization. Treatment with lidocaine hydrochloride or procainamide hydrochloride was successful in reestablishing sinus rhythm in 9 of the 11 dogs with ventricular dysrhythmias.     

Ventricular Arrhythmias in Dogs Undergoing Splenectomy: A Prospective Study

Fifty dogs undergoing splenectomy for splenic masses (n = 40), torsion of the splenic pedicle (n = 5), and immune-mediated disease (n = 5) were evaluated preoperatively and postoperatively for ventricular arrhythmias and the relationship between ventricular arrythmia and splenic disease. The ability of 1 -minute electrocardiograms recorded every 6 hours (ECGs/q6hr) to detect ventricular arrythmia was compared with continuous 48-hour Holter monitoring. Based on continuous Holter monitoring, splenectomized dogs had a high incidence (22 of 50) of rapid ventricular tachycardia. The incidence of rapid ventricular tachycardia was significantly higher in dogs with ruptured splenic masses (16 of 23) than without rupture (1 of 17) ( P < .001). When the results of ECG/q6hr were compared with the results of continuous Holter monitoring, ECG/q6hr was normal in 29% (4 of 14) of dogs with rapid ventricular tachycardia at > 3,000 ventricular extrasystoles (VE)/hr; 50% (4 of 8) of dogs with rapid ventricular tachycardia at 1,000 to 3,000 VE/hr and 100% (6 of 6) of dogs with 10 to 300 VE/hr without rapid ventricular tachycardia. Although dogs undergoing splenectomy had a high incidence of ventricular arrythmias, one-minute ECGs/q6h were unreliable for detection of ventricular arrythmias even when high-frequency extrasystoles occurred.     

Effect of midazolam preanesthetic administration on thiamylal induction requirement in dogs.

The thiamylal sparing effect of midazolam was studied in 30 healthy Beagle and mixed-breed dogs. Using a replicated Latin square design, all dogs were given placebo (saline solution) and 0.025, 0.05, 0.1, and 0.2 mg of midazolam/kg of body weight prior to IV administration of thiamylal sodium. The 0.1 and 0.2 mg/kg dosages significantly decreased the amount of thiamylal required to obtund swallowing reflex and easily achieve endotracheal intubation. Midazolam at 0.1 and 0.2 mg/kg reduced thiamylal requirement by 16.4% and 18.9%, respectively, whereas the 0.05 mg/kg dosage decreased thiamylal requirement by only 6.8%. The 0.2 mg/kg dosage did not further decrease thiamylal requirement beyond that achieved with the 0.1 mg/kg dosage of midazolam. This study demonstrates that the preanesthetic IV administration of midazolam reduces the thiamylal dose necessary to accomplish intubation. The optimal preanesthetic dosage (lowest dosage with significant effect) was 0.1 mg/kg.     

Thiamylal-Sparing Effect of Midazolam for Canine Endotracheal Intubation A Clinical Study of 118 Dogs

One hundred eighteen dogs were studied at three veterinary teaching hospitals after the administration of midazolam (0.1 mg/kg, intravenously [IV]) or a placebo. Midazolam and placebo treatments were randomized and blinded to the investigators. The dose of thiamylal required for tracheal intubation 3 to 5 minutes after midazolam or placebo was calculated. The dose of thiamylal at the three hospitals was 10.6,9.8, and 10.1 mg/kg IV after midazolam, and 12.1,11.2, and 11.6 mg/kg IV after placebo. Pooled data from the three hospitals yielded a significant (p < .001) decrease in mean IV thiamylal dose after midazolam (10.2 mg/kg) compared with placebo (11.6 mg/kg). Overall, there was a 12% decrease in the dose of thiamylal required for tracheal intubation after midazolam compared to that after the placebo. The thiamylal dose was significantly (p < .001) decreased after midazolam compared with placebo for dogs weighing more than 15 kg but not for dogs weighing less than 15 kg.     

Possible Late Potentials in 4 Dogs with Sustained Ventricular Tachycardia

Signal-averaged electrocardiograms (SAEKGs) were performed on 4 dogs with sustained ventricular tachycardia. Quantitative and qualitative analyses of SAEKGs were consistent with the presence of late potentials. Two of the 4 dogs subsequently died suddenly, and ventricular tachycardia and ventricular fibrillation were observed in 1 dog. High-frequency QRS durations (75–90 milliseconds), duration of low amplitude (less than 40 μV) signals during the terminal QRS complex (LAS₄₀) (28–40 milliseconds), root mean square voltages of the terminal 40 milliseconds of the QRS complex (RMS₄₀) (124–6.5 μV), and root mean square voltages of the terminal 30 milliseconds of the QRS complex (RMS₃₀) (13–2.1 μV) differed from results obtained in 68 of 70 control dogs. Echocardiographic data suggested dilated cardiomyopathy in 2 dogs and the cause of the arrhythmia in 2 dogs was not determined. The SAEKG may be a useful adjunct in identifying a subset of dogs with ventricular tachyarrhythmias that are at high risk for sustained ventricular tachycardia and sudden death. The sensitivity, specificity, and predictive accuracies of the technique remain to be determined.     

Comparison of the cardiopulmonary effects of etomidate and thiamylal in dogs.

The cardiopulmonary effects of etomidate, a nonbarbiturate, short-acting, IV anesthetic, were compared and contrasted with those of thiamylal sodium in chronically instrumented conscious dogs. Etomidate, when administered IV at dosages of 1.5 and 3.0 mg/kg of body weight, produced anesthesia lasting from 8 +/- 5 and 21 +/- 9 minutes, respectively. Heart rate, aortic blood pressure, left ventricular peak pressure, left ventricular end diastolic pressure, left ventricular contractile force, and myocardial oxygen consumption were unchanged after administration of either dose of etomidate; however, the dosage of 1.5 mg/kg produced significant (P less than 0.05) increases in respiratory rate and decreases in tidal volume. The minute volume remained unchanged from base-line values. Significant (P less than 0.05) decreases in tidal volume, arterial pH, and partial pressure of oxygen were produced, and minute volume remained unchanged when 3.0 mg of etomidate/kg of body weight was administered. Thiamylal sodium (8.0 mg/kg of body weight; given IV) produced anesthesia lasting for 14 +/- 5 minutes. Significant increases (P less than 0.05) in heart rate, arterial blood pressure, left ventricular peak pressure, and myocardial oxygen consumption were observed after IV administration. Left ventricular contractility was significantly (P less than 0.05) decreased. Respiratory rate was not significantly (P less than 0.05) affected by thiamylal although tidal volume and minute volume were decreased. These respiratory alterations resulted in significant (P less than 0.05) increases in the arterial partial pressure of carbon dioxide and decreases in pH and the partial pressure of oxygen. On the basis of cardiopulmonary function, etomidate offered rapid, safe, short duration anesthesia superior to that of thiamylal sodium.     

Hemodynamic effects of high-frequency oscillatory ventilation in halothane-anesthetized dogs

Hemodynamic effects of spontaneous ventilation, intermittent positive-pressure ventilation (IPPV), and high-frequency oscillatory ventilation (HFOV) were compared in 6 dogs during halothane anesthesia. Anesthesia was induced with IV thiamylal Na and was maintained with halothane (end-tidal concentration, 1.09%). During placement of catheters, dogs breathed spontaneously through a conventional semiclosed anesthesia circuit. Data were collected, and dogs were mechanically ventilated, using IPPV or HFOV in random order. Ventilation was adjusted to maintain PaCO2 between 38 and 43 mm of Hg during IPPV and HFOV. Cardiac index, aortic blood pressure, and maximum rate of increase of left ventricular pressure were significantly (P less than 0.05) less during HFOV than during spontaneous ventilation, whereas right atrial and pulmonary artery pressure were significantly greater during HFOV than during spontaneous ventilation. During IPPV, only the maximum rate of increase of left ventricular pressure was significantly less than that during spontaneous ventilation.     

Ventricular tachycardia in English bulldogs with localised right ventricular outflow tract enlargement

Objectives : To describe the electrocardiographic characteristics of ventricular tachycardia arising from the right ventricular outflow tract and the particular association between this arrhythmia and the presence of localised right ventricular outflow tract enlargement in English bulldogs. Methods : Five English bulldogs were referred with a history of syncope or cardiogenic shock. In all dogs, 12‐lead surface ECG, thoracic radiograph and echocardiography were collected. In all but one dog 24‐hours Holter monitoring and signal‐averaged ECGs was examined and in one dog electrophysiological study and radiofrequency catheter ablation of the VT substrate was performed. Results : Documented arrhythmias included a single sustained monomorphic wide QRS tachycardia in four dogs, and an alternans of two different monomorphic forms in one dog. Mean QRS duration during tachy‐cardia was 91·6 ±9·83 milliseconds. QRS complexes manifested a left bundle branch block morphology and an inferior axis (81 ±13·73°). R wave notching was present in the caudal (inferior) leads in three tachy‐cardias. Lead I was negative in 3 of 6, positive in 1 of 6 and isodiphasic in 2 of 6. Lead aVL was negative in 5 of 6 and positive in 1 of 6. Signal‐averaged electrocardiograms revealed late potentials in three dogs. Echocardiography showed a localised right ventricular outflow tract enlargement in all dogs. Cardiac map‐ping established two sites of origin of ventricular tachycardia within the right ventricular outflow tract in one dog: caudal free‐wall and cranial‐septal. Clinical Significance : The presence of a localised right ventricular outflow tract enlargement and ventricular tachycardia with left bundle branch block morphology could suggest segmental arrhythmogenic right ven‐tricular cardiomyopathy in the English bulldog.     

Electrocardiographic interpretation of thiobarbiturate-induced dysrhthymias in dogs.

The cardiac dysrhythmia occuring most commonly during intravenous administration of thiamylal sodium is ventricular bigeminy (ventricular premature depolarization coupled to the preceding sinus beat). Electrocardiographic tracings obtained during thiamylal-induced dyshythmias must be interpreted accurately if an accurate prognosis is to be give. Ventricular bigeminy seemed to originate in the ventricle, distal to the bundle of His. When ventricular premature depolarization was late in diastole, occuring simultaneiously with the next sinus-conducted impulse, a fusion beat resulted. The resultant ventricular bigeminy appeared as: (1) alternating ventricular premature dipolarizations, (2) an electrical alternans, and (3) alternating preexcitation syndrome. This dysrhythmia was associated with palpable alternating strong and weak frmoral arterial pulse. The likelihood that ventricular dysrhythmias will be caused by thiamylal is closely related to dose, concentration, and rate of administration. In a 23-month period, clinical occurrence of ventricular bigeminy during induction of anesthesia with thiamylal was approximately 4%.     

Thiamylal-and halothane-sparing effect of diazepam in dogs

The thiamylal- and halothane-sparing effect of diazepam was studied in two experiments using 32 conditioned dogs. Twenty-four dogs received 0.05, 0.1 or 0.2 ml/kg diazepam or 0.9% saline (placebo) prior to the administration of thiamylal sodium i.v. Eight dogs received 0.1 or 0.2 mg/kg diazepam i.v. or placebo prior to or during halothane anesthesia. All three doses of diazepam significantly decreased the amount of thiamylal required to allow orotracheal intubation. The 0.2 mg/kg i.v. dose of diazepam produced the most significant effects. Premedication of dogs with diazepam did not reduce the concentration of halothane required to maintain anesthesia. The administration of 0.1 and 0.2 mg/kg diazepam i.v. during halothane anesthesia decreased the concentration of halothane required to maintain anesthesia. These studies demonstrate that diazepam reduces the amount of thiamylal required for orotracheal intubation, and when given intra-operatively reduces the concentration of halothane required to maintain anesthesia.     

Results of ambulatory electrocardiography in overtly healthy Doberman Pinschers with equivocal echocardiographic evidence of dilated cardiomyopathy

OBJECTIVE: To determine results of ambulatory electrocardiography in and outcome of overtly healthy Doberman Pinschers with equivocal echocardiographic evidence of dilated cardiomyopathy. DESIGN: Case series. ANIMALS: 44 overtly healthy (25 male, 19 female) Doberman Pinschers. PROCEDURE: 24-hour ambulatory electrocardiographic (Holter) recordings with > 90% scan quality obtained the same day that echocardiography was performed were reviewed. RESULTS: Holter recordings from 42 of 44 (95%) dogs contained ventricular premature complexes (VPC). Fifteen of 44 (34%) dogs had > 100 VPC, 9 (20%) had > 500 VPC, and 5 (11%) had > 1,000 VPC. Nonsustained (< 30 seconds) ventricular tachycardia was detected in 4 dogs. Eighteen of 27 (67%) dogs with > 100 VPC, any couplets or triplets of VPC, or ventricular tachycardia developed dilated cardiomyopathy within 1 year, compared with 8 of 17 (47%) dogs with < 100 VPC, no couplets or triplets of VPC, and no ventricular tachycardia. Of the 18 dogs that did not develop dilated cardiomyopathy within 1 year, 11 (61%) did so within 3 years. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that a high percentage of Doberman Pinschers with equivocal echocardiographic evidence of dilated cardiomyopathy will be found to have VPC during 24-hour ambulatory electrocardiography and that most will develop echocardiographic abnormalities indicative of cardiomyopathy.     

Metaproterenol intoxication in a dog

Intoxication with metaproterenol, a mainly beta-2 selective agonist, was diagnosed in a dog with tachycardia, tachypnea, weakness, vomiting, and a history of exposure to the drug. Electrocardiography and echocardiography disclosed sinus tachycardia with episodes of ventricular tachycardia and exuberant systolic ventricular function, respectively. Administration of the beta blocking drugs propranolol and atenolol led to resolution of the clinical signs. Excessive sympathetic stimulation caused by metaproterenol is an unusual intoxication in dogs.     

Radiofrequency catheter ablation of atypical atrial flutter in dogs

Five dogs were presented to our institution for fatigue caused by an incessant supraventricular tachycardia. In all dogs, an ECG on admission showed a narrow QRS complex tachycardia with a median ventricular cycle length of 220 ms (range 180–360 ms), and a positive atrial depolarization identifiable in the ST segment following the previous QRS complex. There was a 1:1 atrioventricular conduction ratio in all but one dog, which presented with 2:1 atrioventricular block. Electrophysiologic studies identified the underlying arrhythmogenic mechanism as a right atrial macro-reentrant tachycardia with two distinct isthmic areas: right septal (RS) in three dogs and right atrial free wall (RAFW) in two dogs. Linear radiofrequency catheter ablation was performed during tachycardia in all dogs at the identified isthmic area, which acutely blocked the macroreentrant circuit. At 18-month follow-up, 3 dogs (1 with RAFW isthmus and 2 with RS isthmus) showed no recurrence of the arrhythmia on Holter monitoring. One dog with RS isthmus showed recurrence of the supraventricular tachycardia 15 days post-ablation, and 1 dog with RAFW isthmus presented with persistent atrial fibrillation 2 months post-ablation.     

Cardiac arrhythmias associated with multiple trauma in dogs

Premature ventricular contractions and ventricular tachycardia were detected in 10 dogs 1 to 48 hours after trauma. All dogs were treated aggressively if the arrhythmias became severe. One dog died, 8 were discharged with stable cardiac rhythm, and 1 was euthanatized. Necropsy revealed gross and microscopic lesions of acute myocardial necrosis, probably of ischemic origin. Cardiac arrhythmias were associated with thoracic trauma, neurologic injury, severe shock, and/or extensive tissue trauma.     

Influence of antiarrhythmia therapy on survival times of 19 clinically healthy Doberman pinschers with dilated cardiomyopathy that experienced syncope, ventricular tachycardia, and sudden death (1985-1998)

Overtly healthy Doberman pinschers, having moderate to severe myocardial failure secondary to dilated cardiomyopathy, which experienced ventricular tachycardia, syncope or collapse, and sudden death were studied to determine the effect of antiarrhythmic medication on their clinical outcome. Antiarrhythmia drug therapy may have retarded sudden death in 13 treated dogs compared to the six dogs not administered antiarrhythmia drugs.     

Comparative pharmacokinetics and anesthetic effects of methohexital, pentobarbital, thiamylal, and thiopental in Greyhound dogs and non-Greyhound, mixed-breed dogs

Pharmacokinetics and duration of anesthesia of methohexital, pentobarbital, thiamylal, and thiopental in Greyhound and non-Greyhound, mixed-breed dogs were compared. In all dogs evaluated, pentobarbital induced the longest duration of anesthesia and methohexital induced the shortest duration. Pharmacokinetics of pentobarbital and methohexital were similar in both groups of dogs. Thiobarbiturates induced longer anesthetic effects in Greyhound dogs than in mixed-breed dogs. Plasma thiobarbiturate concentrations remained above normal longer in Greyhound dogs than in mixed-breed dogs. Disposition of thiobarbiturates in Greyhound dogs was characterized by nonlinearity from 45 minutes to 8 hours after dosing.     

Electrocardiographic and echocardiographic features of trypanosomiasis in dogs inoculated with North American Trypanosoma cruzi isolates.

Purebred Beagles were inoculated with Trypanosoma cruzi isolates from a North American opossum or armadillo (Tc-W), and dog (Tc-D). Although Tc-D established infection in dogs, the dogs did not develop cardiac abnormalities. Dogs inoculated with Tc-W developed acute myocarditis associated with increases in P-R interval, atrioventricular block, depression of R wave amplitude and shifts in mean electrical axis. Echocardiograms were normal during this stage. Three Tc-W-inoculated dogs died during the acute stage. Following the acute stage, 5 of 8 Tc-W-inoculated dogs entered an indeterminate stage in which ECG changes were minor and echocardiograms were normal. Progression to the chronic stage in 5 of the 8 Tc-W-inoculated dogs was indicated by development of ventricular-based arrhythmias, mainly ventricular premature contractions, between postinoculation days 60 and 170. In some dogs, ventricular premature contractions were multifocal. Electrocardiographic abnormalities progressively degenerated to various forms of ventricular tachycardia. Worsening ECG coincided with loss of left ventricular function as measured by echocardiography. Mean percent ejection fraction and percentage of fractional shortening decreased to 63% and 52% of control values, respectively. The left ventricular free wall (LVFW) thickness decreased and % septal: % LVFW thickening ratio increased, indicating a relative preservation of septal wall motion and LVFW hypokinesis.     

Streptococcal toxic shock in a horse

A 14-year-old horse was admitted to the veterinary hospital for treatment of tachycardia and lethargy. Initial diagnoses were ventricular tachycardia and renal dysfunction. During hospitalization other findings included fever, renal failure, hepatic failure, hypotension, and intermittent ventricular arrhythmias. Bacteriologic culture of 2 blood samples collected during febrile crises 7 days apart yielded Streptococcus mitis. These culture results along with other clinical and physical examination findings fulfill the criteria for a diagnosis of streptococcal toxic shock syndrome, previously described for humans and dogs. To our knowledge this is the first reported instance of this disease in a horse.