Oxygen cost of increasing tidal volume and diaphragm flattening in obstructive pulmonary disease.

Hypercapnia is associated with a shallow breathing pattern in patients with severe chronic obstructive pulmonary disease (COPD). We sought to determine the oxygen cost of increasing tidal volume and to relate this to hypercapnia [arterial PCO2 (PaCO2) > or = 45 Torr] and diaphragm flattening. We studied 3 normal subjects and 12 patients with stable but comparably severe COPD (forced expired volume in 1 s 1.01 +/- 0.09 liters) who had baseline PaCO2 ranging from 36 to 56 Torr. Oxygen consumption was measured during the subject's native breathing pattern and then while tidal volume was increased by 20%; minute ventilation was held constant by proportionately slowing frequency. There was a significant oxygen cost of increasing tidal volume for hypercapnic patients (235 +/- 23 to 260 +/- 25 ml O2/min; P = 0.002); no significant oxygen cost was observed in normal or eucapnic patients. This oxygen cost was positively correlated to baseline PaCO2 (r2 = 0.88, P < 0.001) and degree of diaphragm flattening assessed from chest radiographs (r2 = 0.74, P < 0.05). Although others have shown that force generation is preserved during chronic hyperinflation (G. A. Farkas and C. Roussos. J. Appl. Physiol. 54: 1635-1640, 1983; T. Similowski et al. N. Engl. J. Med. 325: 917-923, 1991), we conclude that diaphragm flattening produces mechanical inefficiency that may contribute to limiting the effective operating range of the respiratory muscles during tidal breathing.

Amiodarone pulmonary toxicity.

Amiodarone is an effective antiarrhythmic agent whose utility is limited by many side-effects, the most problematic being pneumonitis. The pulmonary toxicity of amiodarone is thought to result from direct injury related to the intracellular accumulation of phospholipid and T cell-mediated hypersensitivity pneumonitis. The clinical and radiographic features of amiodarone-induced pulmonary toxicity are characteristic but nonspecific. The diagnosis depends on exclusion of other entities, such as heart failure, infection, and malignancy. While withdrawal of amiodarone leads to clinical improvement in majority of cases, this is not always possible or advisable. Dose reduction or concomitant steroid therapy may have a role in selected patients.

Hypersensitivity pneumonitis.

The lung is constantly exposed to a wide variety of environmental insults. In its defense against these environmental challenges, however, the lung responds through a limited number of pathophysiologic mechanisms. This is well illustrated by a group of diseases which are collectively referred to as hypersensitivity pneumonitis. This syndrome includes a very large number of different diseases. However, in the United States, only farmer's lung, bird-breeder's lung, and ventilation hypersensitivity pneumonitis occur with any significant frequency. Each of these is characterized by flu-like symptoms, in conjunction with a pneumonitis consisting of lymphocytic granulomatous infiltration of the alveoli and terminal bronchioles. This disease is caused by the inhalation of antigenic material which usually originates from the dusts of organic material. A host of different dusts and antigens have been described in conjunction with hypersensitivity pneumonitis but each leads to the same characteristic clinical syndrome. Thus, each of the diseases shares similar clinical features but differs primarily with respect to the nature of the exposure and causative antigens. The clinical features, pathogenesis, course, prognosis, and treatment of these related diseases are reviewed.

Pulmonary gas exchange during dialysis in patients with obstructive lung disease.

Hypoxemia occurs during routine hemodialysis and may contribute to morbidity, but its cause is not well understood. We reasoned that patients with COPD would be more vulnerable to abnormalities in gas exchange with dialysis. Thus, to investigate the cause of dialysis-related hypoxemia, we measured gas exchange in a group of stable dialysis patients with normal pulmonary function (n = 6) and a group of dialysis patients with COPD (n = 6). Measurements were made predialysis, at 1 h, and postdialysis with both acetate and bicarbonate dialysates. Acetate dialysis decreased PaO2 in normal and COPD patients at 1 h and postdialysis. Acetate-induced hypoxemia was associated with reduced respiratory CO2 excretion and hypoventilation but PaCO2 did not change. This decrease in CO2 excretion resulted from CO2 fixation during acetate metabolism and modest CO2 loss across the dialyzer. Hypoxemia occurred only postdialysis with bicarbonate dialysate in normal and COPD patients. An increased P(A-a)O2 occurred postdialysis with both dialysates, and was most consistently observed in the COPD patients. In summary, at least two mechanisms contribute to dialysis hypoxemia. With acetate dialysate, alveolar hypoventilation from CO2 unloading occurs at 1 h and postdialysis due to acetate metabolism. However, abnormalities in ventilation/perfusion contribute to postdialysis hypoxemia observed with both dialysates. In addition, the decrement in PaO2 associated with dialysis is similar in normal and COPD patients, although preexisting COPD makes postdialysis changes more apparent.

Severe restrictive pulmonary defect in a patient with adult-onset Still's disease.

Adult-onset Still's disease is characterized by seronegative arthritis, fever, and an evanescent skin rash. Earlier reports have described pneumonitis and pleuritis as manifestations of this disease. We report a patient with adult-onset Still's disease with severe restrictive ventilatory impairment and evidence of respiratory muscle weakness who responded to corticosteroid and aspirin therapy.