Influence of Atropine and of Vagally Mediated Bradycardia on the Occurrence of Ventricular Arrhythmias following Acute Coronary Occlusion in Closed-Chest Dogs
Robert E. GoldsteinRichard B. KarshEldon R. SmithMichael M. OrlandoDouglas J. NormanGARY FARNHAMDavid R. RedwoodStephen E. Epstein
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Abstract:
In contrast to previous opinions, recent investigations have suggested that increasing heart rate (HR) with atropine when moderate sinus bradycardia accompanies acute myocardial infarction is not necessarily beneficial. To further characterize the influence of vagally mediated changes in HR during ischemia, we evaluated the effects of atropine and of electric stimulation of the vagus nerves on the incidence of ventricular arrhythmias during acute coronary occlusion in closed-chest dogs. Protection from occlusion-induced arrhythmia was not observed when 28 dogs receiving atropine were compared with 27 control dogs. Rather, the total incidence of ventricular arrhythmias was significantly higher ( P < 0.05) and ventricular fibrillation tended to occur more frequently in the atropine-treated group. Moreover, fewer ventricular arrhythmias (and total absence of ventricular fibrillation or close-coupled premature beats) were noted in 12 control animals with spontaneous bradycardia (HR<60 beats/min) compared with 15 nonbradycardic animals. When vagal stimulation produced bradycardia (HR = 40-60 beats/min) during coronary occlusion, occurrence and character of ventricular arrhythmias were the same as in dogs with normal rates (HR = 80-100 beats/min). Although these results may not necessarily apply to man, further studies are needed before it can be assumed that all individuals with moderate bradycardia during acute myocardial infarction should receive vagolytic agents.Keywords:
Coronary occlusion
Sinus bradycardia
In contrast to previous opinions, recent investigations have suggested that increasing heart rate (HR) with atropine when moderate sinus bradycardia accompanies acute myocardial infarction is not necessarily beneficial. To further characterize the influence of vagally mediated changes in HR during ischemia, we evaluated the effects of atropine and of electric stimulation of the vagus nerves on the incidence of ventricular arrhythmias during acute coronary occlusion in closed-chest dogs. Protection from occlusion-induced arrhythmia was not observed when 28 dogs receiving atropine were compared with 27 control dogs. Rather, the total incidence of ventricular arrhythmias was significantly higher ( P < 0.05) and ventricular fibrillation tended to occur more frequently in the atropine-treated group. Moreover, fewer ventricular arrhythmias (and total absence of ventricular fibrillation or close-coupled premature beats) were noted in 12 control animals with spontaneous bradycardia (HR<60 beats/min) compared with 15 nonbradycardic animals. When vagal stimulation produced bradycardia (HR = 40-60 beats/min) during coronary occlusion, occurrence and character of ventricular arrhythmias were the same as in dogs with normal rates (HR = 80-100 beats/min). Although these results may not necessarily apply to man, further studies are needed before it can be assumed that all individuals with moderate bradycardia during acute myocardial infarction should receive vagolytic agents.
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ABSTRACT A patient with acute myocardial infarction and sinus bradycardia has been treated with 0.5 mg atropine intravenously. Shortly after the injection he showed a sinus tachycardia, then developed ventricular ectopic beats, ventricular tachycardia and ventricular fibrillation, which was treated successfully with electrical countershock.
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Summary A 36‐year‐old athlete was anaesthetised for a minor surgical procedure. His heart rate fell to 30 beats/minute during the operation, the electrocardiogram showed A‐V junctional rhythm. Sinus rhythm of 58 beats/minute was restored by atropine 1.2 mg. His resting 12‐lead electrocardiogram showed sinus bradycardia and features consistent with a diagnosis of ‘athlete's heart’. A review is presented of the physiological and electrocardiographical features of this phenomenon. The current popularity of running as a leisure pursuit makes it important that anaesthetists recognise the peculiarities of the trained athletic heart.
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Objective To investigate the changes in the heart rates and the clinical effectiveness of aminophylline injections in acute cervical spinal cord injury (ACSCI) patients with bradycardia. Methods This retrospective study was conducted by studying the clinical data of 100 ACSCI patients also suffering from bradycardia admitted to our hospital from June 2019 to June 2020. The patients were randomly placed into a control group (n=50) that was administered atropine therapy and a test group (n=50) that was administered aminophylline injections. The changes in the patients' heart rates and the clinical effectiveness were analyzed. Results After the treatment, the test group had a significantly higher average heart rate, shorter heart rate recovery times, and a lower bradycardia recurrence rate than the control group (all P 0.05). Conclusion For ACSCI patients also suffering from bradycardia, aminophylline injections ameliorate the clinical heart rate and have a good clinical effectiveness with few adverse reactions, so the treatment merits clinical promotion and application.
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We observed 2 cases of repeated episodes of syncope after alcohol ingestion. Both patients were light drinkers and had carotid sinus hypersensitivity. In both cases, alcohol loading tests repeatedly induced sinus bradycardia and hypotension 1.0-1.5 hours after drinking alcohol. Atropine was effective in improving symptoms. A loading test using a glucose solution of equivalent osmolarity and volume was negative. Acute alcohol ingestion usually increases heart rate with variable effects on blood pressure. However, our 2 cases exhibited unusual alcoholinduced sinus bradycardia and hypotension, suggesting a paradoxical increase in parasympathetic activity and/or decrease in sympathetic activity.
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Oxymorphone was administered intravenously (IV) to 10 dogs (0.4 mg/kg initial dose followed by 0.2 mg/kg three times at 20‐minute intervals). Four hours after the last dose of oxymorphone, heart rates were less than 60 bpm in six dogs. After atropine (0.01 mg/kg IV) was administered, heart rate decreased in five dogs and sinus arrhythmia or second degree heart block occurred in four of them. A second injection of atropine (0.01 mg/kg IV) was administered 5 minutes after the first and the heart rates increased to more than 100 bpm in all six dogs. Ten minutes after the second dose of atropine, heart rate, cardiac output, left ventricular minute work, venous admixture, and oxygen transport were significantly increased, whereas stroke volume, central venous pressure, systemic vascular resistance, and oxygen extraction ratio were significantly decreased from pre‐atropine values. The PaCO 2 increased and the PaO 2 decreased but not significantly. The oxymorphone‐induced bradycardia did not produce any overtly detrimental effects in these healthy dogs. Atropine reversed the bradycardia and improved measured cardiovascular parameters.
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