The Science Journal of the American Association for Respiratory Care

1997 OPEN FORUM Abstracts

Neurological and Cellular Causes of Dyspnea: A Neurologist's Viewpoint

John J. Wald MD, Monday, December 8, 1997.

Dyspnea may be produced by many causes; most often, primary pulmonary (e.g., airway disease) and cardiac (e.g., heart failure) etiologies are responsible. Neurologic causes are considered when there is known pre-existing neurologic disease present, signs/symptoms of neurologic disease, or no clear cardio/pulmonary explanation of the symptoms.

Neurologic and metabolic disorders frequently determined to cause dyspnea include myopathy affecting the muscles of ventilation, myopathy with metabolic derangement leading to altered oxygen utilization/energy production, neuromuscular junction disease (myasthenia gravis), and peripheral neuropathy affecting the phrenic nerves. The relative inaccessibility of the phrenic nerve and diaphragm often limit their testing, so disorders involving only the diaphragm and not limb nerves or muscles may be easily missed. Of the above disorders, myopathy, particularly metabolic myopathy, with only intermittent involvement of limb muscles, may be the most under-diagnosed neurologic condition causing dyspnea.

Common methods of neurologic testing include phrenic nerve conduction and needle electromyography of the diaphragm, though their sensitivity to metabolic muscle disorders is limited. Pulmonary function and exercise testing, routinely used in evaluation of ventilatory and cardiac function, complements neurologic testing. Decreased inspiratory and expiratory pressures (PI_{max}, Pe_{max}), decreased transdiaphragmatic pressures, and restrictive patterns on PFTs all suggest underlying ventilatory muscle weakness. When considering metabolic or mitochondrial myopathies, pulmonary exercise testing can provide measurements of muscle metabolic function and oxygen utilization that may aid in reaching the appropriate diagnosis (even when the diaphragm is unaffected). The underlying biochemical pathways involved in specific metabolic myopathies will be reviewed, and the utility of pulmonary exercise testing (changes in venous lactic acid, expired O_{2}/CO_{2}, comparison of heart rate/cardiac output, lactic acid, and ventilation to oxygen consumption/work produced, and anaerobic threshold) as part of the evaluation for metabolic and mitochondrial myopathies will be discussed.

While therapies for metabolic myopathies are limited, several have been suggested. Serial testing can provide objective evidence of beneficial effects from therapies as well as measure disease progression.

AARC 50th Anniversary, December 6 - 9, 1997, New Orleans, Louisiana.

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