thiamylal and Arrhythmias--Cardiac

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. (ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Anesthesia, General; Animals; Arrhythmias, Cardiac; Atropine; Blood Pressure; Dobutamine; Drug Administration Schedule; Electrocardiography; Female; Halothane; Heart Rate; Horses; Infusions, Intravenous; Male; Orchiectomy; Thiamylal; Xylazine

We report the case of an 8-year-old boy with left ventricular noncompaction cardiomyopathy (LVNC) and QT prolongation who experienced further prolongation of the QTc during general anesthesia for extraction of a maxillary mesiodens. Pronounced prolongation of the QTc was observed after induction of general anesthesia with thiamylal and during emergence. No notable fluctuations in blood pressure, heart rate, and estimated continuous cardiac output were observed. We considered it likely that the QT prolongation was triggered by thiamylal and increased sympathetic nervous system activity. During general anesthesia for children with LVNC and QT prolongation, it is necessary to monitor intraoperative hemodynamic fluctuations and prepare for the possible occurrence of arrhythmias.

Topics: Anesthesia, General; Arrhythmias, Cardiac; Cardiomyopathies; Child; Electrocardiography; Humans; Long QT Syndrome; Male; Thiamylal

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.

Topics: Anesthesia; Animals; Arrhythmias, Cardiac; Blood Pressure; Dose-Response Relationship, Drug; Drug Combinations; Epinephrine; Female; Guaifenesin; Halothane; Heart Rate; Horse Diseases; Horses; Hypercapnia; Male; Thiamylal

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.

Topics: Anesthesia, General; Animals; Arrhythmias, Cardiac; Blood Pressure; Dose-Response Relationship, Drug; Epinephrine; Guaifenesin; Halothane; Heart Rate; Horses; Thiamylal; Xylazine

Topics: Adult; Aged; Aged, 80 and over; Anesthesia, Intravenous; Arrhythmias, Cardiac; Contusions; Emergencies; Female; Fractures, Bone; Heart Injuries; Humans; Hypotension; Intraoperative Complications; Male; Succinylcholine; Thiamylal; Wounds, Nonpenetrating

The arrhythmogenic dose of epinephrine (ADE) was determined in heartworm-infected and noninfected (control) dogs during thiamylal-induced and halothane-maintained anesthesia to assess the myocardial sensitization. The ADE in heartworm-infected dogs (2.42 +/- 0.26 micrograms/kg of body weight) was significantly lower than that for the controls (3.36 +/- 0.29 micrograms/kg). After 2 weeks, ADE was determined again in these dogs after atropine treatment. Atropine treatment lowered the ADE to 1.76 +/- 0.33 micrograms/kg and 1.77 +/- 0.19 micrograms/kg in heartworm-positive and -negative dogs, respectively. After 2 weeks more, the ADE was determined after administration of prazosin, an alpha 1-antagonist. Only 2 of 6 controls and 3 of 6 heartworm-positive dogs had arrhythmias after a threefold increase of ADE. The mean ADE in the dogs that responded to treatment were 7.4 micrograms/kg and 7.2 micrograms/kg for heartworm-positive and -negative dogs, respectively. The finding of this study indicated that ADE in heartworm-infected dogs were lower than those in the control dogs, which makes the heartworm-infected dogs more vulnerable to arrhythmia during anesthesia. Atropine did not protect the dogs of either group. However, prazosin protected the dogs of both groups by significantly increasing the threshold of the ADE. On the basis of our findings, to reduce the risk of arrhythmia, we suggest that routine screening of dogs for heartworm infection be done before anesthetics are used.

Topics: Anesthesia, Inhalation; Animals; Arrhythmias, Cardiac; Atropine; Blood Pressure; Carbon Dioxide; Dirofilariasis; Dog Diseases; Dogs; Epinephrine; Halothane; Heart Rate; Oxygen; Prazosin; Premedication; Thiamylal

Topics: Adult; Anesthesia; Anesthetics; Arrhythmias, Cardiac; Drug Interactions; Humans; Sparteine; Thiamylal

We have used immature commercial swine (13-25 kg) successfully in a variety of experimental cardiopulmonary surgical procedures in our laboratories since 1981. Multiple drug anesthetic protocols using barbiturates, narcotics, paralytic and antiarrhythmic agents have been employed in over 400 procedures per year. Complications, including fatal cardiac arrhythmias, have been greatly reduced by anesthetic protocols and surgical procedures developed through experience.

Topics: Acepromazine; Anesthesia; Animals; Arrhythmias, Cardiac; Bradycardia; Cardiopulmonary Bypass; Cardiovascular Surgical Procedures; Female; Fentanyl; Halothane; Heart Transplantation; Male; Pancuronium; Pentobarbital; Pneumonectomy; Succinylcholine; Swine; Thiamylal; Thiopental; Ventricular Fibrillation

Epinephrine-induced ventricular arrhythmias were studied in 8 dogs anesthetized at weekly intervals with halothane (1.09% end-tidal concentration) preceded by thiamylal or thiopental (20 mg/kg of body weight). Lead II, bundle of His and high right atrial electrograms, and femoral artery and airway pressures were recorded. Epinephrine was infused in logarithmically spaced increasing rates (initial rate = 0.25 micrograms/kg/min) for a maximum of 2.5 minutes. The maximal (greater than or equal to 4 ventricular premature depolarizations within 15 s of each other) and minimal (all other ventricular or junctional rhythms) arrhythmogenic doses were calculated (infusion rate X time to arrhythmia). The mean (+/- SD) minimal arrhythmogenic dosages for the thiamylal-halothane, thiopental-halothane, and halothane-only groups were 1.84 +/- 0.66, 1.83 +/- 0.64, and 3.69 +/- 1.32 micrograms/kg, respectively; the mean (+/- SD) maximal arrhythmogenic dosages were 2.32 +/- 0.77, 3.37 +/- 1.30, and 8.86 +/- 4.40 micrograms/kg, respectively, with no change after 4 hours of anesthesia. During infusion of the maximal arrhythmogenic dosages, the mean infusion of the maximal arrhythmogenic dosages, the mean percentage increase in serum K+ for thiamylal-halothane, thiopental-halothane, and halothane-only groups was 33 +/- 14%, 31 +/- 13%, and 38 +/- 18%, respectively.

Topics: Anesthesia, General; Animals; Arrhythmias, Cardiac; Blood Pressure; Dog Diseases; Dogs; Drug Synergism; Epinephrine; Halothane; Heart Rate; Heart Ventricles; Thiamylal; Thiopental

The cardiac arrhythmogenic infusion rate of epinephrine, dopamine, and dobutamine in vagotomized dogs was determined during thiamylal-halothane and pentobarbital anesthesia. Epinephrine, dopamine, and dobutamine were administered until 4 or more ventricular arrhythmias on duplicated trials were produced or until a predetermined maximum infusion rate was attained. The mean ventricular arrhythmogenic infusion rates (micrograms X kg-1 X min-1) during thiamylal-halothane anesthesia were: epinephrine, 0.57 +/- 0.24; dopamine, 23.7 +/- 8.26; and dobutamine, 10.21 +/- 3.54. Few arrhythmias were produced at the maximum administered infusion rate during pentobarbital anesthesia (2 of 6 with epinephrine, 3 of 6 with dopamine, and 0 of 6 administered dobutamine). Heart rate and blood pressure increased progressively with increasing infusion rates for all 3 catecholamines during thiamylal-halothane anesthesia. Heart rate and blood pressure changes were similar during pentobarbital anesthesia except for blood pressure changes during dobutamine infusion.

Topics: Anesthesia, General; Animals; Arrhythmias, Cardiac; Blood Pressure; Catecholamines; Dobutamine; Dogs; Dopamine; Epinephrine; Halothane; Heart Rate; Pentobarbital; Thiamylal; Vagotomy

The arrhythmogenicity of epinephrine, dopamine, and dobutamine, administered by constant-rate infusion, was determined in vagotomized and nonvagotomized thiamylal-halothane anesthetized dogs. Electrocardiograms and atrioventricular bundle electrograms revealed the development of atrial, junctional, and ventricular arrhythmias. The 3 drugs produced atrial arrhythmias at dosages smaller than those required to produce ventricular arrhythmias. The mean dosages (microgram/kg-1/min-1) required to produce ventricular arrhythmias on duplicate trials in vagotomized dogs were for epinephrine, 0.6 +/- 0.2; dopamine, 22.8 +/- 14.8; and dobutamine, 11.6 +/- 5.2. The corresponding doses for nonvagotomized dogs were for epinephrine, 0.8 +/- 0.3; dopamine, 35.3 +/- 13.5; and dobutamine, 21.9 +/- 13.9. Most ventricular arrhythmias originated from a single focus in the left ventricle. Heart rate and blood pressure were significantly increased immediately before ventricular arrhythmia appeared. We conclude that epinephrine, dopamine, and dobutamine are capable of producing cardiac arrhythmias in vagotomized and nonvagotomized thiamylal-halothane anesthetized dogs and that bilateral vagotomy decreases the dosage of epinephrine, dopamine, and dobutamine required to produce cardiac arrhythmias.

Topics: Anesthesia, Inhalation; Animals; Arrhythmias, Cardiac; Catecholamines; Dobutamine; Dog Diseases; Dogs; Dopamine; Electrocardiography; Epinephrine; Halothane; Heart; Thiamylal; Vagotomy

Topics: Animals; Antidiarrheals; Arrhythmias, Cardiac; Benzoates; Dog Diseases; Dogs; Drug Synergism; Parasympatholytics; Thiamylal; Ventricular Fibrillation

Topics: Anesthesia; Arrhythmias, Cardiac; Enflurane; Fentanyl; Heart Ventricles; Humans; Male; Middle Aged; Nausea; Pyloric Antrum; Thiamylal; Vagotomy; Vomiting

Changes in cardiac rate and rhythm were determined in atropinized dogs prior to, during, and after anesthetic induction with thiamylal sodium and maintenance with 1% halothane in 50% nitrous oxide and 50% oxygen. The incidence of cardiac dysrhythmias and sinus tachycardia was significantly higher prior to and after anesthetic induction in dogs given atropine, compared with dogs not atropinized. Second-degree atrioventricular block was the most frequent dysrhythmia prior to anesthetic induction in atropinized dogs. Most cardiac dysrhythmias were detected during the anesthetic induction and early maintenance periods. The most common dysrhythmias during these periods were unifocal ventricular premature depolarizations and ventricular bigeminy.

Topics: Anesthesia, Inhalation; Anesthesia, Intravenous; Animals; Arrhythmias, Cardiac; Atropine; Dog Diseases; Dogs; Female; Halothane; Heart Block; Heart Rate; Male; Thiamylal

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%.

Topics: Anesthesia, Intravenous; Animals; Arrhythmias, Cardiac; Blood Pressure; Cardiac Complexes, Premature; Dog Diseases; Dogs; Electrocardiography; Female; Heart Ventricles; Male; Thiamylal

Topics: Adolescent; Adult; Anesthesia, Endotracheal; Anesthesia, Local; Arrhythmias, Cardiac; Autonomic Nerve Block; Child, Preschool; Electrocardiography; Female; Ganglia, Autonomic; Humans; Lidocaine; Male; Morphine; Nitrous Oxide; Pancuronium; Stellate Ganglion; Syndrome; Thiamylal; Ventricular Fibrillation

Constantly coupled ventricular bigeminy in dogs can be elicited by intravenous boluses of thiamylal sodium. Properties of the bigeminal rhythm are similar to those produced by halothane or cyclopropane inhalation anesthetic-epinephrine-induced dysrhythmias. The mechanism responsible for the initiation of ventricular bigeminy, and perhaps most dysrhythmias in the dog during thiobarbiturate anesthesia, appears to be an imbalance between parasympathetic and sympathetic efferent activity. Moderate increases in arterial blood pressure and atrial rate augment the tendency for dysrhythmia production. Atropine was effective in abolishing ventricular bigeminy in most cases through overdrive suppression. Propranolol appeared to abolish ventricular bigeminal rhythms by suppression of sympathetic efferent activity without causing noticeable changes in arterial blood pressure.

Topics: Animals; Arrhythmias, Cardiac; Atropine; Autonomic Nervous System; Blood Pressure; Cardiac Pacing, Artificial; Dog Diseases; Dogs; Female; Femoral Artery; Heart Atria; Heart Rate; Heart Ventricles; Male; Propranolol; Thiamylal; Vagus Nerve

Topics: Anesthesia, Intravenous; Animals; Arrhythmias, Cardiac; Cardiac Complexes, Premature; Dog Diseases; Dogs; Female; Heart Ventricles; Male; Thiamylal; Ventricular Fibrillation; Wolff-Parkinson-White Syndrome

Topics: Anesthesia, General; Anesthetics; Arrhythmias, Cardiac; Child; Female; Halothane; Humans; Male; Thiamylal

Topics: Animals; Arrhythmias, Cardiac; Dog Diseases; Dogs; Thiamylal

Topics: Animals; Arrhythmias, Cardiac; Dog Diseases; Dogs; Thiamylal

Sinus tachycardia bigeminy, ventricular rhythm, ventricular tachycardia, and ventricular fibrillation are produced by relatively small intravenous doses of epinephrine in nonanesthetized dogs and in dogs anesthetized with thiamylal sodium. Origin of the abnormal beat in coupled bigeminal rhythms generated from the bundle o of His or above. Increases in arterial blood pressure may predispose to arrhythmia formation during thiamylal anesthesia.

Topics: Anesthesia, Intravenous; Animals; Arrhythmias, Cardiac; Blood Pressure; Bundle of His; Cardiac Complexes, Premature; Dog Diseases; Dogs; Epinephrine; Heart Rate; Nitroglycerin; Phenylephrine; Tachycardia; Thiamylal; Ventricular Fibrillation

Topics: Animals; Arrhythmias, Cardiac; Dog Diseases; Dogs; Female; Male; Thiamylal

Topics: Anesthesia, Intravenous; Animals; Arrhythmias, Cardiac; Barbiturates; Dogs; Female; Heart; Heart Conduction System; Heart Ventricles; Male; Thiamylal; Thiopental

Topics: Animals; Arrhythmias, Cardiac; Blood Pressure; Bradycardia; Dogs; Electric Stimulation; Electrocardiography; Heart Rate; Isoproterenol; Pharmacology; Research; Tachycardia; Thiamylal; Thiopental; Vagus Nerve