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Lung function and respiratory muscle strength after propranolol in thyrotoxicosis
Australian and New Zealand Journal of Medicine
|August 1, 1986
Summary
Thyrotoxicosis may cause inspiratory muscle weakness, potentially linked to adrenergic excess. Treatment with antithyroid drugs improved respiratory function, including inspiratory and expiratory muscle strength.
Area of Science:
- Endocrinology
- Pulmonology
- Internal Medicine
Background:
- Thyrotoxicosis, a hypermetabolic state, can affect multiple organ systems.
- Respiratory muscle function may be impaired in patients with thyrotoxicosis.
Purpose of the Study:
- To investigate the effects of propranolol and antithyroid drugs on respiratory function in thyrotoxic patients.
- To explore the role of adrenergic excess in thyrotoxic inspiratory muscle weakness.
Main Methods:
- Assessed respiratory parameters including lung volumes, capacities, flow rates, diffusing capacity, and maximal mouth pressures in 35 thyrotoxic patients.
- Patients were evaluated before and after treatment with propranolol and antithyroid drugs.
- Arterial blood gas analysis was performed on a subset of patients.
Main Results:
- Propranolol significantly improved maximal static inspiratory mouth pressure (PImax), suggesting a role for adrenergic excess in inspiratory muscle weakness.
- Antithyroid drug treatment led to significant improvements in PImax, maximal static expiratory mouth pressure (PEmax), forced expiratory volume in the first second (FEV1), and vital capacity (VC).
- No significant changes were observed in other lung function parameters (FRC, RV, TLC, MMFR, DLCO) or blood gases after either treatment.
Conclusions:
- Adrenergic excess may contribute to inspiratory muscle weakness in thyrotoxicosis.
- Antithyroid drug therapy effectively improves respiratory muscle strength and lung function in thyrotoxic patients.