BACKGROUND: Arrhythmias play an important role in reducing the performance of racing horse. There are no studies that maintained the same condition for all horses, and in previous studies, the conditions for all horses were not the same. OBJECTIVES: The purpose of this study was to evaluate the prevalence of arrhythmias during exercise include warm-up and trotting. METHODS: This study was carried out on 30 sport horses. Modified base-apex has been used for electrocardiogram recording. Electrocardiogram was taken by telemetry device in all conditions, all horses were examined in the electric lounge. Warm-up period was 10 minutes and consequently 10 minutes trotting was done, and ECG was recorded during exercise. RESULTS: 18 horses had SVPCs during warm-up and 9 showed SVPCs during trotting; also, 4 horses showed VPCs during trotting. AVB II happened in one horse during warm-up. CONCLUSIONS: The occurrence of SVPCs and VPCs during rest is abnormal, but it is common during physical activity. To better understand the importance of these arrhythmias more studies are needed.

Introduction: The prevalence of arrhythmias in dogs and the influence of sex, breed, age, and body weight were analysed over a seven-year span.

Introduction: The prevalence of arrhythmias in dogs and the influence of sex, breed, age, and body weight were analysed over a seven-year span. Material and Methods: In total, 1189 referrals for cardiological examination by electrocardiography were received at one academic centre in Poland between 2008 and 2014. The largest proportion of the examined dogs were cross-breeds with body weight below 25 kg (n = 153, 12.87%), followed by German Shepherds (n = 122, 10.26%), Labrador Retrievers (n = 68, 5.72%), Yorkshire Terriers (n = 63, 5.3%), and Boxers (n = 60, 5.05%). Retrospective analysis was made of 1201 standing or right recumbent electrocardiograms without pharmacological sedation. The prevalence of arrhythmias was examined in terms of sex, age, body weight, and breed of the dogs. Results: A total of 630 (52.46%) electrocardiograms showed no signs of arrhythmia, but 96 (7.99%) and 475 (39.55%) pointed to physiological and pathological arrhythmias respectively. The most commonly diagnosed type was atrial fibrillation with 33.68% incidence, followed by ventricular arrhythmias (28%), sinus pauses (27.58%), supraventricular arrhythmias (24%), and atrioventricular blocks (22.95%). Pathological arrhythmias were most commonly found in male dogs and in German Shepherds. Conclusions: Atrial fibrillation predominated, followed by premature ventricular complexes. Male dogs were generally more prone to heart rhythm disturbances.

Although it is known that the QT interval is dependent on the preceding RR interval, QT interval does not vary during respiratory sinus arrhythmia, despite a wide variation in heart rate. To assess the rate of change of the QT interval following an abrupt increase or decrease in heart rate, QT intervals were measured from ECG of healthy, anesthetized, thoracotomized dogs in which a junctional rhythm had been induced by destroying the sinoatrial node. Atria were paced at 800- or 600-millisecond cycle durations until a steady state was reached, and then the cycle duration was changed suddenly to a new cycle duration (600 or 800 milliseconds, respectively). The time and number of heart beats required until the QT interval achieved a value of 63% (1 time constant) of the new steady state were calculated. Time constants for change in QT interval vs the number of beats following the change were 2.8 (SD = 1.3 s) seconds when heart rate was accelerated and 4.7 (SD = 2.1 s) seconds when heart rate was slowed. Differences were not statistically significant. The time constants for change in QT interval duration vs duration after the sudden change in heart rate were 1.7 (SD = 0.8 s) seconds when heart rate was accelerated and 3.7 (SD = 1.7 s) seconds when heart rate was slowed. These time constants differed significantly (P < 0.01). Response of QT interval, therefore, depended on the number of heart beats following sudden change in heart rate, but not time, except as time determined the number of heart beats. The QT interval did not change until 3 to 5 beats after the heart rate was suddenly changed. This number of beats would be more than that which would occur in 1 respiratory cycle in dogs; therefore, QT interval memory would prohibit changes in QT intervals that occur during respiratory sinus arrhythmia.

We investigated the influence of parasympathetic tone on the arrhythmogenic dose of dobutamine in horses premedicated with xylazine, anesthetized with guaifenesin and thiamylal, and maintained on halothane in oxygen. Six horses were used in 12 randomized trials. In each trial, after end-tidal halothane concentration was stabilized at 1.1% (1.25 times minimum alveolar concentration [MAC]) in oxygen, either saline solution (0.02 ml/kg of body weight) or atropine (0.04 mg/kg) was administered IV. Five minutes later, dobutamine infusion was started at dosage of 2.5 micrograms/kg/min, IV. The dobutamine infusion was continued for 10 minutes, or until 4 or more premature ventricular complexes occurred within 15 seconds, or sustained narrow-complex tachyarrhythmia clearly not sinus in nature occurred. If the criteria for termination were not met, dobutamine infusion was increased by 2.5 micrograms/kg/min, after the hemodynamic variables had returned to baseline. The horses were allowed to recover, and were rested for at least 1 week before the second trial. The arrhythmogenic dose of dobutamine was calculated by multiplying the infusion rate by the elapsed time into infusion when arrhythmia occurred. There was significant difference between the arrhythmogenic dose of dobutamine (ADD) in saline-treated horses (mean +/- SEM, ADD 105.6 +/- 16.3 micrograms/kg) and atropinized horses (ADD 36.2 +/- 8.7 micrograms/kg). There were no differences in the prearrhythmia or immediate postarrhythmia ventricular heart rate (HR) or systolic (SAP), diastolic (DAP), or mean (MAP) arterial pressures between treated and control groups. The change in hemodynamic variables from prearrhythmia to immediate postarrhythmia formation was not different between the 2 groups. Ventricular beats were clearly evident in 8 of the 12 arrhythmias meeting the criteria for establishing the ADD. These results indicate that atropine may lower the arrhythmogenic threshold for dobutamine in halothane-anesthetized horses.

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 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 [Pa(CO2)] = 35 to 45 mm of Hg), at hypercapnia (Pa(CO2) = 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 (Pa(O2)) 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.

We investigated the influence of parasympathetic tone on the arrhythmogenicity of graded dobutamine infusions in horses anesthetized under clinical conditions. Six horses were used in 9 trials. Two consecutive series of graded dobutamine infusions were given IV; each continuous graded dobutamine infusion was administered for 20 minutes. The dobutamine infusion dosage (5, 10, 15, and 20 microgram/kg of body weight/min) was increased at 5-minute intervals. Isovolumetric saline solution vehicle (v) or atropine (A; 0.04 mg(kg) was administered IV, or bilateral vagotomy (VG) was performed as a treatment before the second series of dobutamine infusions. Treatment was not administered prior to the first dobutamine infusion. Significant interaction between treatment and dosage of dobutamine infusion existed for differences from baseline for mean arterial pressure, systolic arterial pressure, diastolic arterial pressure, heart rate, and cardiac index at dosages of 5 and 10 micrograms of dobutamine/kg/min, given IV and for heart rate at dosage of 15 micrograms of dobutamine/kg/min, given IV. Results for group-V horses were different from those for group-A and group-VG horses, but were not different between group-A and group-VG horses in all aforementioned cases, except for heart rate and cardiac index at dosage of 5 micrograms of dobutamine/kg/min, given IV. Normal sinus rhythm, second-degree atrioventricular block, and bradyarrhythmias predominated during low dobutamine infusion rates during the first infusion series (nontreated horses) and in group-V horses during the second infusion series. Only tachyarrhythmias were observed during the second infusion series in the horses of the A and VG groups. The modulating influence of parasympathetic nervous system activity on hemodynamics and development of arrhythmia was conspicuous during low dobutamine infusion rates. Significant differences were not observed in hemodynamic responses to dobutamine, with respect to parasympathetic influence at high dobutamine infusion rates.

The ventricular arrhythmogenic dose of epinephrine (ADE) was determined in 6 dogs anesthetized with halothane alone or with halothane after injection of tiletamine/zolazepam (TZ). Respiratory rate and tidal volume were controlled and sodium bicarbonate was administered to maintain arterial pH and blood gas values within reference range. Heart rate and arterial blood pressure were recorded during determination of the ADE. The ADE (mean +/- SD) was no different during anesthesia with use of halothane alone (8.9 +/- 4.3) than it was when injections of TZ preceded administration of halothane (6.7 +/- 2.8). Tiletamine/zolazepam was also administered IV immediately after determination of the ADE during halothane-induced anesthesia. The TZ administered in this manner did not alter the ADE. Blood pressure and heart rate were significantly greater during infusion of epinephrine than immediately prior to infusion. The administration of TZ did not alter blood pressure response. The ADE was also determined in 6 cats anesthetized with halothane preceded by administration of TZ. The ADE (mean +/- SD) was 0.7 +/- 0.23 microgram/kg, a value similar to that reported for cats during anesthesia with halothane alone.

Eight dogs (body weight, 12.5 to 21.5 kg) were assigned at random to each of 3 treatment groups (IS, IX, IM) that were not given glycopyrrolate and to each of 3 groups that were given glycopyrrolate (IGS, IGX, IGM). Dogs, were anesthetized with isoflurane (1.95% end-tidal concentration), and ventilation was controlled (PCO2, 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered IV and IM at a dosage of 11 micrograms/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, IM), or medetomidine (15 micrograms/kg, IM) was administered 10 minutes after baseline ADE determination. Redetermination of the ADE at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0, 2.5, and 5.0 micrograms/kg/min. The ADE was defined as the total dose of epinephrine that induced at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion, or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline and treatment ADE values was performed by use of one-way ANOVA. Mean +/- SEM baseline ADE values for groups IS, IX, and IM were 1.55 +/- 0.23, 1.61 +/- 0.28, and 1.95 +/- 0.65 micrograms/kg, respectively. Differences for groups IS, IX, and IM were -0.12 +/- 0.05, -0.31 +/- 0.40, and -0.17 +/- 0.26, respectively. Differences for groups IGS, IGX, and IGM could not be calculated because arrhythmias satisfying the ADE criteria were not observed at the maximum infusion rate of 5.0 micrograms/kg/min. Differences among groups IS, IX, and IM were not significant. We conclude that in isoflurane-anesthetized dogs: preanesthetic dosages of xylazine (1.1 mg/kg, IM) or medetomidine (15 micrograms/kg, IM) do not enhance arrhythmogenicity, and at these dosages, there is no difference in the arrhythmogenic potential of either alpha 2-adrenergic receptor agonist.

Spontaneous variations in ECG and continuous Holter monitor recordings of a colony of 31 male and 31 female cynomoigus monkeys were characterized. Electrocardiograms recorded for approximately 1 minute on 2 occasions in nonsedated monkeys were analyzed, and intervals (PR, QRS, and QT), amplitudes (P, Q, F, and T), and heart rate were determined from lead II of these tracings. In addition, Holter monitor recorders were placed on monkeys by use of carrying jackets for 16 to 24 hours of continuous recording twice during the study, and tapes were analyzed. Mean heart rate and intervals and amplitudes were similar for males and females on the first and the second recordings, Mean heart rate for males and females was 232 and 226 beats/min (bpm), respectively. The PR, QRS, and QT interval measurements, 77, 29, and 165 milliseconds, respectively, were recorded for males and 81, 30, and 162 milliseconds, respectively, were recorded for females. The P, Q, R, and T wave amplitudes were 0.16, 0.11, 0.64, and 0.28, mV respectively, for males and were 0.17, 0.10, 0.79 and 0.24 mV, respectively, for females. In addition, ventricular ectopic beats were observed in ECG from 5 females, but not in ECG from the males. Single ventricular ectopic beats were observed in 3 females for either the first or second tracing. One monkey had ectopic beats in both tracings, but in both instances, the number of ectopic beats was low (3 singles in the first and 1 in the second tracing). One monkey had runs of pairs and bigeminal beats in only the first tracing. One monkey had sporadic beats indicative of right bundle branch block morphology in both tracings. In Holter recordings, ventricular ectopic beats were identified in 47 monkeys. Ventricular ectopic beats were observed in only 1 of the 2 Holter monitor tapes for 53% of these monkeys. Most ventricular ectopic beats occurred as single beats, but pairs, ventricular tachycardia, and bigeminy also were observed. Ectopic beats were of a single morphology in 60% of the monkeys, but as many as 4 different morphologies were observed in a single tracing. Sinus arrhythmia or arrest was observed in 66% of the monkeys. Ventricular ectopic beats and sinus arrhythmia can occur without apparent cause in clinically normal monkeys. Higher prevalences of these abnormalities are identified by Holter monitoring relative to routine ECG procedures. These variables should be cautiously evaluated, because the lack of proper characterization of monkeys on test may mislead investigators as to the real importance of these findings.