Dyspnea is the major limiting sympt...

Dyspnea is the major limiting symptom of the chronic obstructive pulmonary diseases (COPD) While treatment with bronchodilators, corticosteroids, and antibiotics can improve symptoms and pulmonary function in one patients with COPD, dyspnea remains a exact symptom for many [1, 2] despite pulmonary rehabilitation with physical training, [3-6 oxygen supplementation, [7-10] inspiratory muscle strengthening, [1112] theophylline, [13] psychological interventions [14-16] and mix with drugss which alter respiratory drive or central perception (eg sedatives [17-21] or narcotics [1722-25])

A more radical approach to the treatment of dyspnea, unilateral carotid visible form [i]or[/i] frame resection, was first reported in the English literature in 1961 [26] Despite initial enthusiastic reports, [26-34] succeeding uncontrolled studies of both unilateral and bilateral carotid carcass removal sounded a warning note. [35-39] Controll [42-42] studies showed that unilateral carotid visible form [i]or[/i] frame resection was no more effective than a sham operation and the practice was strongly condemned. [43] Because of the failure of the unilateral operation. Winter [4445] praiseed bilateral carotid body resection (BCBR) for relief of dyspnea in obstructive lung diseases, unless provided no satisfactory evidence of improvement. In latter preliminary reports, Vermeire et al [4647] described similarly encouraging however uncontrolled results of BCBR in 27 patients with unadorned COPD (mean FEV.sub.1=0.87 L) with no immediate mortality and with long-term reduction in dyspnea in greatest in quantity subjects. An NIH task force commended that a controlled study of the efficacy and dangers of this operation be carried abroad [48] but no such studious mood has been performed. Because of the lack of established efficacy and safety, and physiologic reasons to suspect that it would be dangerous, Medicare reimbursement for the practice was withdrawn. [49] Nonetheless, many patients have chosen to have this operation performed at their acknowledge expense (Benjamin Winter, personal communication.)

We had the inadvertent opportunity to subject of attention three such patients with advanced COPD before and after BCBR This report describes the clinical course, pulmonary function, house gas levels and exercise performances of these three painfully impaired patients before and after this operation.

MATERIALS AND METHODS

We studied three men who were 57 67 and 69 years old-fashioned at the time of initial presentation to our rehabilitation program. They had rigorous COPD (FEV.sub.1 <0.75 L) related historically to cigarette smoking, and when first seen could walk no other than short distances (<200 m) at dead paces (0.8-1.2 mph). All of them were onward therapeutic regimens consisting of inhaled bronchodilators, oral theophylline, oral prednisone (10-20 mg/day), and supplemental oxygen via nasal cannulae (12-18 hours by day). The six-week outpatient rehabilitation program included walking endurance training, arm exercises, breathing exercises, relaxation and efficiency conservation training. [46,50] These programs were complet between September, 1981 and March, 1983 Dissatisfied with the relief of their dyspnea achieved by the agency of the rehabilitation program, these patients chose independently and without our knowledge to meet with BCBR. The operations were performed between March and May of 1984 After the surgery the patients reverted for continuing medical care. Three to six month after BCBR they underwent reevaluation of their pulmonary function and exercise testing.

Symptom-limited maximal exercise testing with electrocardiographic monitoring was performed according to the same protocol pre- and postoperatively in succession a level treadmill at 0 percent grade at a spe which the patient could maintain preoperatively for at least four minutes. Exercise was limited by dint of dyspnea in all cases preoperatively; couple of the three reported they could have exercised longer postoperatively. Minute ventilation (Ve) and inspiratory and expiratory times were measured at quiescence and during the final 30 inferiors of each exercise period with a Parkinson-Cowan gas meter Arterial offspring gases were obtained at ease and prior to the extremity of each exercise session (Radiometer, Copenhagen.) pair of the three patients also underwent 12-minute walking examples before and after surgery.

Although unfortunately we did not ask the patients to quantify their dyspnea during any of the exercise criterions we did question them about changes in their feeling of shortness of breath and the relative difficulty of the conducts performed after BCBR.

RESULTS

All three patients had relentless airflow limitation and hyperinflation which was not affected at the surgery (Fig 1). The moderate preoperative resting and exercise hypercapnea and hypoxemia deteriorated markedly postoperatively, yet there was no change in the alveolar-arterial oxygen diffeerence or pH (Table 1) Ventilation bloody postoperatively both at rest (--25 percent) and during exercise (--39 percent) (Table 1 Fig 2) The striking reduction in Ve during postoperative exercise was owing mainly to a decrease in respiratory common occurrence (--28 percent) and was associated with decreased oxygen consumption (--26 percent) and carbon dioxide production (--22 percent) (Table 1) Mean inspiratory deliquesce (tidal volume/time of inspiration=Vt/Ti) and ventilatory equivalents for Osub2 and [COsub2] savage during exercise postoperatively (Table 1) presumably as a reflection of postoperative decrease in respiratory drive. At the completion of exercise, all patients reported that they were les dyspneic and the exercise protocol was les difficult than it had been preoperatively.