Anesthesia for the Asthmatic Patient

The question of how to best manage the asthmatic patient under anesthesia has lingered for years, and though it has been partially resolved from time to time by the discovery of new agents or techniques, it still remains. The purpose of this article is not to unequivocally answer that question but to give the practitioner additional insight with which to deal with it. In review, a balance is struck between adrenergic and cholinergic activity upon the pulmonary system, which maintains homeostasis within. Beta adrenergic stimulation causes bronchodilatation, while alpha adrenergic stimulation causes bronchoconstriction. Cholinergic stimulation also causes bronchoconstriction. Two types of beta receptors have been discovered: beta' and beta . Beta' receptors cause cardiac stimulation, while beta receptors cause bronchodilatation and also vasomotor depression.' In the early 1960's, Szentivanyi advanced the theory of beta adrenergic blockade as a unifying mechanism in asthma. In the words of Wilson and Galant: "This theory proposes that many of the stimuli which result in the clinical syndrome of asthma do so by causing the release of potent chemical mediators of inflammation such as the kinins, slow reacting substance of anaphylaxis(SRSA), histamine, serotonin and acetylcholine. These mediators, in turn, result in bronchoconstriction and secretion of epinephrine as a homeostatic response. If beta adrenergic receptors are normally responsive, activation of these by epinephrine will balance alpha adrenergic and cholinergic receptor stimulation and airway patency will be maintained. However, if beta receptors are defective, bronchoconstriction is favored." 2 Is asthma, then, a phenomenon of autonomic imbalance caused by defective beta receptors? The published evidence points to this conclusion. At this time the beta adrenergic receptor is thought to incorporate adenyl cyclase, an enzyme catalyst which converts adenosine triphosphate (ATP) to cyclic 3', 5' adenosine monophosphate (CAMP) in its structure. A second enzyme, phosphodiesterase, reduces CAMP to inactive 5' adenosine monophosphate (AMP) .s The presence of increased levels of CAMP influences bronchial smooth muscle in two ways. It inhibits (lung mast cell) the release of mediators of bronchoconstriction following antigen exposure, and also exerts a direct influence on smooth muscle favoring relaxation. An opposite effect, favoring