Describe the physiological effects and principles of management of a tricyclic antidepressant overdose.
Good answers to this question were those that gave an accurate account of the physiological effects, e.g. inhibition of the fast sodium channels in the His-Purkinje system as well as the atrial and ventricular myocardium, decreasing conduction velocity (differential conduction inhibition of RBB being more susceptible) and increasing duration of repolarization, and the absolute refractory periods. Once having done that the rest of the answer would have flowed more easily, e.g. ECG changes and conduction disturbances. The effects of tricyclic antidepressants on Na channels and as a consequence the cardiovascular conduction abnormalities were often omitted. Anti cholinergic (e.g. slowing GIT motility) and antihistamine effects (e.g. obtundation) were often overlooked. Also frequently overlooked were basic pharmacology relevant to treatment, e.g. lipophilic, large volume of distribution, systemic acidosis reduces the extent of protein binding and increases unbound (active) drug. Additional points were available to those who not only mentioned sodium bicarbonate, but also mentioned the principles behind its use for this circumstance
Physiological effects:
Cardiovascular features
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Central nervous system features
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Anticholinergic features
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Metabolic features
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Principles of management:
Kerr, G. W., A. C. McGuffie, and S. Wilkie. "Tricyclic antidepressant overdose: a review." Emergency Medicine Journal 18.4 (2001): 236-241.
Brown, T. C., et al. "The use of sodium bicarbonate in the treatment of tricyclic antidepressant-induced arrhythmias." Anaesthesia and intensive care 1.3 (1973): 203-210.
McCabe, James L., et al. "Experimental tricyclic antidepressant toxicity: a randomized, controlled comparison of hypertonic saline solution, sodium bicarbonate, and hyperventilation." Annals of emergency medicine 32.3 (1998): 329-333.
Bou-Abboud, Elias, and Stanley Nattel. "Molecular mechanisms of the reversal of imipramine-induced sodium channel blockade by alkalinization in human cardiac myocytes." Cardiovascular research 38.2 (1998): 395-404.