Background-Patientswith severe chronic obstructive pulmonary disease (COPD) have a poor quality of life and limited life expectancy. This study examined whether these patients were relatively disadvantaged in terms of medical and social care compared with a group with inoperable lung cancer.Methods-An open two group comparison was made of 50 patients with severe COPD (forced expiratory volume in one second (FEV 1 ) <0.75 l and at least one admission for hypercapnic respiratory failure) and 50 patients with unresectable non-small cell lung cancer (NSCLC). A multi-method design was used involving standardised quality of life tools, semistructured interviews, and review of documentation. Results-The patients with COPD had significantly worse activities of daily living and physical, social, and emotional functioning than the patients with NSCLC (p<0.05). The Hospital Anxiety and Depression Scale (HADS) scores suggested that 90% of patients with COPD suVered clinically relevant anxiety or depression compared with 52% of patients with NSCLC. Patients were generally satisfied with the medical care received, but only 4% in each group were formally assessed or treated for mental health problems. With regard to social support, the main diVerence between the groups was that, while 30% of patients with NSCLC received help from specialist palliative care services, none of the patients with COPD had access to a similar system of specialist care. Finally, patients in both groups reported a lack of information from professionals regarding diagnosis, prognosis and social support, although patients' information needs were disparate and often conflicting. Conclusion-This study suggests that patients with end stage COPD have significantly impaired quality of life and emotional well being which may not be as well met as those of patients with lung cancer, nor do they receive holistic care appropriate to their needs.
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.
Phrenic nerve stimulation is often considered to be difficult and unreliable. The time taken for the phrenic nerves to be located and adequately stimulated was measured in 110 subjects, aged 21-89 years, 26 of whom had diaphragmatic weakness; and phrenic nerve conduction time was recorded in 76 of these individuals. Each phrenic nerve was stimulated transcutaneously in the neck with square wave impulses 0 I ms in duration at 1 Hz and 80-160 volts while diaphragmatic muscle action potentials were recorded with surface electrodes. The time taken to locate either phrenic nerve ranged from two seconds to 22 minutes (median 10 s). Both nerves were located in 83 of the 84 control subjects (99%) and in 21 of the 26 patients with diaphragmatic weakness (81%). Mean (SD) phrenic nerve conduction time in the control subjects was 6-94 (0-77) ms on the right and 6-61 (0 77) ms on the left. A weak relationship was found between conduction time and the subjects' age and height. Four out of 24 patients with diaphragmatic weakness had a prolonged phrenic nerve conduction time. Transcutaneous stimulation of the phrenic nerves was not a time consuming procedure, and it was well tolerated, reproducible, and successful in 95% of subjects.Assessment of phrenic nerve function is necessary in candidates for permanent diaphragm pacing' and may be required in the investigation of patients with diaphragmatic weakness. Phrenic nerve conduction time provides a sensitive indicator of phrenic nerve function when the nerves are affected either by local lesions or by generalised ieuropathies. Prolonged conduction time has been fo'upd in phrenic neuritis,2 in mediastinal tumour, after surgical trauma,3 and in peripheral neuropathies.4Although percutaneous phrenic nerve stimulation was described in 19515 as a means of providing ventilatory support and again in 19674 as a method of investigation, phrenic nerve studies have not gained wide acceptance. Failure to locate the nerves,6 7 and discomfort have been considered to be important problems. The purpose of this study was to establish how often, how quickly, and how reproducibly each phrenic nerve could be located by means of twitch stimulations, to see whether this investigation could be applied routinely. Studies were performed in control subjects to determine the normal range of phrenic nerve conduction time and in patients with
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)
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