Effect of Atropine on Bradycardia and Hypotension in Acute Myocardial Infarction

Thomas, Michael; Woodgate, Derek; Hoff, Hebbel E.

doi:10.1097/00132586-196808000-00025

Cited by 5 publications

(5 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our observations confirm previous reports of the beneficial effects of atropine in the prehospital phase,27 as well as in the hospital management of patients with this syndrome.3 The prompt reversal of both hypotension and impaired blood flow suggests that atropine blocks an increase in vagal tone that may be initiated from primary cardiac receptors.28-30 Although the increased heart rate produced by atropine may result in increased myocardial oxygen need and extension of myocardial ischemia (and/or further electrical instability),18' 31 the rise in systemic blood pressure would be expected to counteract these effects by increasing coronary perfusion. 32,3 Adverse Effects of Atropine Administration Although our studies confirm the beneficial effects of atropine in patients with acute myocardial infarction and sinus bradyeardia complicated by either PVCs and/or hypotension, the effects of atropine are not totally benign (table 2). Transient sinus tachycardia and/or minor side effects characteristic of parasympatholysis developed in approximately 20% of our patients treated with atropine.…”

Section: Bradycardia-hypotension Syndromementioning

confidence: 59%

Use of atropine in patients with acute myocardial infarction and sinus bradycardia.

Scheinman¹,

Thorburn²,

Abbott³

1975

Circulation

View full text Add to dashboard Cite

Fifty-six patients with acute myocardial infarction complicated by sinus bradycardia (SB) were treated with intravenous atropine and monitored in a coronary care unit. Atropine decreased or completely abolished premature ventricular contractions (PVCs) and/or bouts of accelerated idioventricular rhythm in 27 of 31 patients (87%) and brought systemic blood pressure up to normal in 15 of 17 patients (88%) with hypotension. In addition, atropine administration was associated with improved atrioventricular conduction in 11 of 13 patients (85%) with acute inferior myocardial infarction associated with 2 degrees or 3 degrees atrioventricular block. Seven patients developed ten significant adverse effects: ventricular tachycardia or fibrillation in three, sustainedsinus tachycardia in three, increased PVCs in three, and toxic psychosis in one. These major adverse effects correlated with either a higher initial dose of atropine (i.e., 1.0 mg aa compared with the usual 0.5 or 0.6 mg) or a total cumulative dose exceeding 2.5 mg over 21/2 hours. Atropine is the drug of choice for management of patients with SB and hypotension and is effective in the treatment of ventricular arrhythmias as well as conduction disturbances in patients with inferior myocardial infarction. Serious adverse effects, however, preclude use of atropine without careful medical supervision.

show abstract

Section: Bradycardia-hypotension Syndromementioning

confidence: 59%

Use of atropine in patients with acute myocardial infarction and sinus bradycardia.

Scheinman¹,

Thorburn²,

Abbott³

1975

Circulation

View full text Add to dashboard Cite

show abstract

“…This is repeated if necessary according to the response to the initial dose. The effects of this have been reported by Thomas & Woodgate (1966).…”

Section: Position In Bedmentioning

confidence: 77%

The Westminster Hospital coronary unit—experience with 260 patients admitted consecutively with a diagnosis of acute myocardial infarction

Thurston

1969

Postgraduate Medical Journal

View full text Add to dashboard Cite

Summary In successive years since the opening of a Coronary Care Unit at Westminster Hospital the mortality has been 26 and 20% and for the first 4 months of 1968, 5·3%. Overall mortality for 260 patients was 20%. Resuscitation has been successful in 59% of cardiac arrests within the unit and in 27% of those outside the unit caused by myocardial infarction. Seventeen patients left hospital alive and well who presumably would not have survived had they been treated at home. Given efficient nursing staff and a resuscitation team, there can no longer be any justification for the treatment of patients with myocardial infarction anywhere other than in a coronary care unit, where such facilities are made available, providing admission is arranged within 3 days of the infarcting episode. The disadvantage of an ambulance journey to a patient with a recent infarct after this period of time may outweigh the advantage incurred by the coronary care unit. The Peel Coronary Prognostic Index remains a very useful guide to prognosis in spite of this author’s attempts to demonstrate any inaccuracies in its predictions. A high (20%) ‘misdiagnosis’ rate must be accepted if some patients with bona fide myocardial infarction are not to be excluded from the unit. The occurrence of 435 deaths reported to Her Majesty’s Coroner for Westminster in the relevant period due to myocardial infarction suggests that the time may be ripe for a ‘flying squad’ resuscitation service in London.

show abstract

“…Patients with the bradycardia-hypotension syndrome secondary to acute inferior myocardial infarction also present signs of peripheral vasodilatation (Thomas and Woodgate, 1966;Kuhn, 1967), which, in the presence of prolonged hypotension, indicates failure of the baroreceptor reflex (Costantin, 1963;Kezdi et al, 1974;Thoren, 1973b).…”

Section: Discussionmentioning

confidence: 99%

Origin of ventricular reflexes caused by coronary arteriography.

Pérez-Gómez¹,

García-Aguado²

1977

Heart

View full text Add to dashboard Cite

Left ventricular reflexes have in the past been investigated in anaesthetised animals, generally using an open chest technique. We have studied the degree of bradycardia occurring during coronary arteriography in 200 patients with a view to localising the origin of the ventricular reflexes. We have correlated the decrease of sinus rate with the anatomical distribution and integrity of the coronary tree. The degree of bradycardia was not influenced by the origin of the sinus node or the AV node arteries, while there was a good correlation with the injection of contrast medium into the artery which supplied the inferior wall of the left ventricle. The occurrence of transient sinus arrest was also correlated with the injection into the same artery. The results suggest that the parasympathetic receptors are located mainly in the inferior wall of the left ventricle. This may well be the explanation for the clinical picture of bradycardia, hypotension, and peripheral vasodilatation often seen in acute inferior myocardial infarction.

show abstract

Effect of Atropine on Bradycardia and Hypotension in Acute Myocardial Infarction

Cited by 5 publications

References 4 publications

Use of atropine in patients with acute myocardial infarction and sinus bradycardia.

Use of atropine in patients with acute myocardial infarction and sinus bradycardia.

The Westminster Hospital coronary unit—experience with 260 patients admitted consecutively with a diagnosis of acute myocardial infarction

Origin of ventricular reflexes caused by coronary arteriography.

Contact Info

Product

Resources

About