1999 update: ACC/AHA guidelines for the management of patients with acute myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction)

http://www.mmh.org.tw/taitam/car_int/Documents/amipdf99edits.pdf

ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction

Cardiac function is controlled by the autonomic nervous system (i.e., the sympathetic and the parasympathetic nervous systems), which act via adrenoceptors and muscarinic acetylcholine receptors, respectively. At least nine adrenoceptor subtypes and five muscarinic receptor subtypes exist. In recent

Adrenergic and Muscarinic Receptors in the Human Heart

Guidelines for the early management of patients with acute myocardial infarction. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Subcommittee to Develop Guidelines for the Early Management of Patients with Acute Myocardial Infarction)

Executive Summary andListing of Recommendations 

These guidelines are intended for physicians, nurses, and allied healthcare personnel who care for patients with suspected or established acute myocardial infarction (MI)

These guidelines have been officially endorsed by the American Society of Echocardiography, the American College of Emergency Physicians, and the American Association of Critical-Care Nurses

This executive summary and listing of recommendations appears in the November 1, 1996, issue of Circulation The guidelines in their entirety, including the ACC/AHA Class I, II, and III recommendations, are published in the November 1996 issue of the Journal of the American College of Cardiology Beginning with these guidelines, the full text of ACC/AHA guidelines will be published in one journal and the executive summary and listing of recommendations in the other  Reprints of both the full text and the executive summary with its listing of recommendations are available from both organizations

Each year 900 000 people in the United States experience acute MI Of these, roughly 225 000 die, including 125 000 who die “in the field” before obtaining medical care Most of these deaths are arrhythmic in etiology Because early reperfusion treatment of patients with acute MI improves left ventricular (LV) systolic function and survival, every effort must be made to minimize prehospital delay Indeed, efforts are ongoing to promote rapid identification and treatment of patients with acute MI, including (1) patient education about the symptoms of acute MI and appropriate actions to take and (2) prompt initial care of the patient by the community emergency medical system In treating the patient with chest pain, emergency medical system personnel must act with a sense of urgency

When the patient with suspected acute MI reaches the emergency department (ED), evaluation and initial management should take place promptly, because the benefit of reperfusion therapy is greatest if therapy …

ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction:Executive Summary

Atropine in small doses decelerates heart rate. This parasympathomimetic effect, which has been attributed to a central vagal stimulating action of atropine sulfate, was studied in dogs by measuring heart rate and P-R intervals. The action of atropine sulfate (which has access to the brain) was compared to that of its quaternary derivative, atropine methylbromide, which is believed not to cross the blood-brain barrier. Atropine methylbromide was more potent than atropine sulfate in accelerating heart rate. In unanesthetized dogs, but not in dogs anesthetized with chloralose, atropine sulfate and atropine methylbromide in small doses slowed heart rate. In awake and anesthetized dogs both drugs prolonged P-R intervals. Bilateral cervical vagotomy abolished the drug effect on the P-R interval, but when the distal limb of the vagus was stimulated electrically both atropine sulfate and atropine methylbromide again prolonged the P-R interval. We infer that atropine methylbromide and atropine sulfate exerted peripheral parasympathomimetic effects on the heart. The possibility that atropine sulfate has central vagal stimulating effect was not excluded.

C A Kottmeier

Papers

The parasympathomimetic activity of atropine and atropine methylbromide.