Coronary occlusion site as a determinant of the cardiac rhythm effects of atropine and vagotomy
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Coronary occlusion
Symptomatic sinus bradycardia is routinely treated in the emergency department with atropine and pacing. Two cases are presented that illustrate the importance of considering hyperkalaemia, particularly in the presence of atropine-resistant symptomatic bradycardia. The administration of calcium in such cases acts to stabilise the myocardium and resolve the bradycardia. Blood gas analysis provides a rapid estimate of serum potassium concentrations, facilitating timely treatment.
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The effects of intravenous and intramuscular atropine on pulse rate have been studied in 40 patients undergoing gynecological surgery. Intramuscular atropine 0.5 mg was administered 30 min before induction of spinal anesthesia in 20 patients (i.m. group). Intravenous atropine 0.5 mg was administered immediately after induction of spinal anesthesia in 20 patients (i.v. group). Decrease in heart rate after spinal block was significantly less in i.v. group than in i.m. group. Although no one in i.v. group was given an additional atropine, 10% of the patients in i.m. group was given an additional atropine for bradycardia. Authors conclude that intravenous atropine has more significant effect on prevention of bradycardia during spinal anesthesia compared with intramuscular atropine.
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Glycopyrrolate
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Eight preterm infants are presented to demonstrate the indications and hazards of using atropine for treatment of bradycardia in the high-risk premature nursery. Three infants developed bradycardia following initiation of nipple feedings, one following gavage feedings, three following surgical manipulation of visceral structures, and one associated with presence of chronic pulmonary disease. It is suggested that the first seven cases represent "reflexic bradycardia," probably vagally mediated and thus amenable to atropine therapy, whereas the eighth is an example of "hypoxic bradycardia" where administration of atropine may be detrimental. Polygraphic monitoring, arterial blood gases, and the clinical status are helpful in distinguishing reflexic from hypoxic bradycardia. These parameters should be evaluated prior to institution of atropine therapy.
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The effect of atropine sulfate on the heart rate of the unanesthetized guinea pig was studied using a wide range of doses injected via a chronic jugular cannula; dose-response data are presented for the range of 5 mg/kg to 50 mg/kg. A long-lasting dose-dependent bradycardia was produced. This finding is in contrast to the clasically reported effect of atropine in man and dog: tachycardia sometimes preceded by a transient bradycardia. Thus, the guinea pig may be an excellent model for the study of parasympathomimetic, bradycardia-producing effects of atropine.
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Heart rate response to intravenous atropine therapy in acute myocardial infarction (MI) was assessed from detailed studies performed on 18 of 492 consecutively admitted coronary care unit patients. Atropine was given for extreme bradycardia ( < 40/min) or bradycardia ( < 60/min) coincident with hypotension or ventricular premature beats. 14 patients had posterior and 4 anterior infarction. Degree of cardioacceleration evoked by atropine depended upon drug dose and route of administration. Atropine, 0.0053–0.0088 mg/kg, given within 15 sec increased heart rate by 20–72/min but never beyond a peak rate of 120. Larger atropine doses, 0.120–0.148 mg/kg, increased heart rate by 51-92/min and, in four to five instances, to a peak rate exceeding 120/min. Intramuscular atropine was associated with paradoxical slowing of heart rate in one case. Multiple neural, hormonal, and circulatory factors can modify heart rate response to fixed amounts of intravenous atropine but 0.008 mg/kg represents a safe and suitable initial drug dose for use in acute MI.
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