Thirty patients with breathlessness and diaphragm weakness were studied by measuring transdiaphragmatic pressures during maximal inspirations to total lung capacity, maximal static inspiratory efforts from residual volume, and maximal sniffs from functional residual capacity. Maximal static respiratory mouth pressures were also recorded, and rib cage and abdominal movements were monitored with pairs of magnetometers. Sniff transdiaphragmatic pressure was abnormally low in all patients and was correlated with transdiaphragmatic pressure during other maneuvers, and with maximal static inspiratory mouth pressures. There was no relationship between the severity of dyspnea and transdiaphragmatic pressure in the group as a whole. The weakest patients had orthopnea and paradoxical inward inspiratory motion of the anterior abdominal wall; measurements suggested that at least 30 cm H2O transdiaphragmatic pressure was required to overcome the hydrostatic pressure of the abdominal contents. By contrast, patients with mild diaphragm weakness had neither orthopnea nor abdominal paradox. Thus, patients with breathlessness and diaphragm dysfunction may have varying degrees of diaphragm weakness that may be difficult to detect clinically; the diagnosis and quantification of diaphragm weakness requires the measurement of transdiaphragmatic pressure.
Global respiratory muscle function and diaphragmatic strength were assessed and compared with quadriceps femoris muscle strength in 17 patients with generalized mild-to-moderate myasthenia gravis and breathlessness. Initial measurements, made 10 h after the last dose of oral anticholinesterase therapy, demonstrated reduced maximal static expiratory (52.4 +/- 26.8% predicted) and inspiratory (54.0 +/- 23.5% predicted) mouth pressures in 16 patients, and reduced quadriceps femoris muscle strength in all cases. Vital capacity (VC) (70.9 +/- 19.0% predicted) was abnormal in 12 patients. Transdiaphragmatic pressure recorded during maximal sniffs (sniff Pdl) was reduced in eight patients, whereas pressure recorded during bilateral phrenic nerve stimulation at 1 Hz (twitch Pdi) was reduced in only three. There was no relationship between the grade of myasthenia or the severity of dyspnea and any of the measurements of respiratory muscle strength. After the administration of edrophonium hydrochloride (Tensilon), there was a significant increase in maximal static expiratory and inspiratory mouth pressures in quadriceps muscle strength and in sniff Pdi. The small increase in VC was not significant, and twitch Pdi increased in only one patient. Phrenic nerve conduction time was normal before and after Tensilon. Two patients with severe long-standing myasthenia showed no improvement in any measurement after Tensilon. We conclude that expiratory and inspiratory muscle weakness was not uncommon in patients with myasthenia gravis. Respiratory muscle strength improved after Tensilon. Vital capacity was a less sensitive measure of respiratory muscle strength than were respiratory mouth pressures and sniff Pdi. Diaphragmatic involvement was not detected by twitch Pdi unless the weakness was severe.(ABSTRACT TRUNCATED AT 250 WORDS)
Global respiratory muscle strength was studied in 22 normal healthy volunteers during a 4-month winter period. Twelve subjects developed naturally acquired upper respiratory tract infections. Maximal static expiratory and inspiratory mouth pressures fell significantly during these infections. The greatest falls were documented between the third and seventh days of clinical illness. Full recovery occurred by the fourteenth day. We conclude that significant abnormalities of respiratory muscle function can occur during upper respiratory tract infections in otherwise healthy young adults.
Transdiaphragmatic pressures were measured in 3 patients with cerebellar atrophy. Recordings were made during 3 types of voluntary maneuver--maximal sniffs, full inspirations, and maximal static inspiratory efforts, and during bilateral supramaximal phrenic nerve stimulation at 1 Hz. Although diaphragmatic weakness was demonstrated during the voluntary maneuvers, transdiaphragmatic pressures recorded during phrenic nerve stimulation were normal. These findings indicate that diaphragmatic dysfunction, probably caused by ataxia during voluntary maneuvers, may occur in association with cerebellar atrophy. In the presence of diaphragmatic weakness, normal values of transdiaphragmatic pressure during phrenic nerve stimulation may suggest an upper motor neuron lesion affecting the diaphragm.
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