Physiological perspectives of therapy in bronchial hyperreactivity.
OBJECTIVE
This paper reviews the literature on the aetiology and therapy of bronchial hyperreactivity to describe the underlying pathophysiology, identify patients at risk and update knowledge on new and existing therapies.


METHODS
Information was obtained from monograms on New Drugs for Asthma, Respiratory Medicine: recent advances, Agents and Actions Supplements, Pulmonary Pharmacology, Anesth Analg, the European Journal of Respiration and a Medline literature search.


RESULTS
Reduced airway calibre, increased bronchial contractility, altered permeability of the bronchial mucosa, humoral and cellular mediators, and dysfunctional neural regulation are critical factors for bronchial hyperreactivity, a characteristic feature of hyperreactive airways which results in bronchoconstriction after exposure to varied stimuli. Preoperative anaesthetic considerations in these patients include FEV1 and PEFR testing to assess the severity and for optimal control of the condition. Bronchospasm causing hypoxaemia is the major intraoperative problem anticipated in these patients. Current therapeutic management of bronchoconstriction focuses on the beta 2 agonists, theophylline and steroids. Besides relaxing the airway smooth muscle these agents are all capable of altering bronchial inflammatory responses. Future developments of therapy are directed towards the inflammatory components of the disease.


CONCLUSIONS
This review has presented background information on physiological mechanisms of smooth muscle contractility, pathophysiological alterations of bronchial contractility and the pharmacological basis of therapy in bronchoconstrictive disease. Information is presented to enable the prompt arrest and reversal of airway constriction, and to maintain prophylactic treatment during the perioperative period. Intraoperative bronchospasm is managed by adequate oxygenation and reversal of bronchoconstriction.
Pinto Pereira
L M
LM
Department of Paraclinical Sciences, Faculty of Medical Sciences, University of the West Indies, St. Augustine, Trinidad and Tobago.
Orrett
F A
FA
Balbirsingh
M
M
D001980:Bronchi / Q000098:blood supply; D016535:Bronchial Hyperreactivity / Q000503:physiopathology / Q000628:therapy*; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000502:physiology; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D015221:Potassium Channels / Q000502:physiology; D011976:Receptors, Muscarinic / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology
D015220:Calcium Channels; D005938:Glucocorticoids; D015221:Potassium Channels; D011976:Receptors, Muscarinic; D002118:Calcium