Study of Haemodynamic Status after Anticholinergic Premedication During Electroconvulsive Therapy — A Comparative Study Between Atropine and Glycopyrolate

Electroconvulsive therapy (ECT) is a highly successful treatment for severe depression and some other psychiatric disorder. 70%-80% patients respond to pharmacological therapy and at least 50% who do not respond to antidepressants do respond favourably to ECT. ECT is quicker, safer and more effective and has fewer side effects than drug therapy. ECT needs general anaesthesia; therefore interactions between psychotropic drugs, ECT and anaesthetic agents can occur. ECT is often associated with acute hyperdynamic response. CNS stimulants on the other hand may prolong seizure, also dysrrhythmias and elevate haemodynamic responses. Initial vagal responses immediately after application of current may lead to bradycardia and salivation, which may cause laryngospasm, bronchospasm and airway obstruction. There may be even asystole and hypoxic episodes. To prevent possible asystole, bradycardia and airway obstruction during ECT, atropine as premedication can be considered. Atropine premedications produces anticholinergic mediated tachycardia, which is in addition to intense sympathetic response after ECT stimulus that contributes to greater myocardial workload. On the other hand, glycopyrolate is a long acting muscarinic antagonist five to six times as potent as atropine. It does not cross blood brain barrier, placenta and eye. It controls secretions with doses that don't cause marked changes in heart rate. Its effect on blood pressure is less than atropine. Atropine crosses blood brain barrier and thus affecting CNS. Our present study was performed to compare haemodynamic status after anticholinergic premedication with atropine and glycopyrolate during ECT. This study was randomized, prospective study. 90 patients for ECT, age 15-50 years, ASA grading II Atropine premedication; glycopyrolate Journal of BSA, Vol. 18, No. 1 & 2, 2005 p.31-37

[1]  W. Tang,et al.  Asystole During Electroconvulsive Therapy: A Case Report , 2001, The Australian and New Zealand journal of psychiatry.

[2]  D. Subbakrishna,et al.  Atropine premedication and the cardiovascular response to electroconvulsive therapy. , 1998, British journal of anaesthesia.

[3]  H. Sackeim,et al.  Acute effects of ECT on cardiovascular functioning: Relations to patient and treatment variables , 1987, Acta psychiatrica Scandinavica.

[4]  R. E. Allen,et al.  Atropine and glycopyrrolate as ECT preanesthesia. , 1986, The Journal of clinical psychiatry.

[5]  J. Brock‐Utne,et al.  The Effect of Hyoscine and Atropine on the Lower Oesophageal Sphincter , 1977, Anaesthesia and intensive care.

[6]  J. Gomez Death after E.C.T. , 1974, British medical journal.

[7]  F. Pitts,et al.  Fatal Heart Block and Cardiac Arrest Following ECT , 1972, British Journal of Psychiatry.

[8]  M. Pachter,et al.  Myocardial infarction and fatal coronary insufficiency during electroconvulsive therapy. , 1968, JAMA.

[9]  M. Weinstein,et al.  Electroconvulsive treatment of a patient with artificial mitral and aortic valves. , 1967, The American journal of psychiatry.

[10]  W. Karliner Accidental convulsion induced by atropine. , 1965, The American journal of psychiatry.

[11]  A. A. Baker,et al.  Deaths associated with electroplexy. , 1959, The Journal of mental science.

[12]  P. J. Crowley CARDIAC ARREST FOLLOWING ELECTROPLEXY , 1958 .

[13]  W. Lewis,et al.  Deaths following electrotherapy; report of five deaths, with autopsy findings in four cases. , 1956, Journal of the American Medical Association.

[14]  W. K. McKNIGHT,et al.  ELECTROCONVULSIVE THERAPY IN THE PRESENCE OF PHYSICAL DEFECTS , 1954, The Journal of nervous and mental disease.

[15]  Maclay Ws Death due to treatment. , 1953 .

[16]  M. Altschule,et al.  Mechanisms underlying pulmonary and cardiac complications of electrically induced convulsions. , 1948, The New England journal of medicine.