An intravenous radionuclide method for repeated shunt determinations.

Using a subtraction technique, repeated shunt determinations were successfully performed on 25 patients with a high degree of correlation.

Response of enlarged alveolar vessels to acute hypoxia.

Because the postulated mechanism of high altitude pulmonary edema is inhomogeneous vaconstriction and hyperperfusion of unconstricted vessels, pulmonary blood flow through vessels larger than 10 micron was determined at baseline and during acute hypoxia sufficient to reduce arterial oxygen saturation to 65%. Women demonstrated a uniform response of decreasing such flow, whereas responses in men were highly variable. Hyperperfusion of enlarged vessels during hypoxia is not an acute phenomenon in the majority of subjects and is therefore either unique to some individuals or a sub-acute occurrence.

Anatomical lung shunting in pulmonary fibrosis.

Eleven patients with cryptogenic fibrosing alveolitis were evaluated for the presence of pulmonary shunting by injection of radiolabelled particles of macroaggregated albumin larger than 10 micron in diameter and by body scanning with a gamma camera. The mean shunt of 9% (SD 2%) in the patients was not significantly different from the mean shunt of 7% (2%) measured in 10 normal controls. These findings suggest that shunting is not an important part of the gas exchange abnormalities noted in such patients.

Enlarged pulmonary arteriovenous vessels in COPD. Another possible mechanism of hypoxemia.

Among 27 patients with moderate-to-severe chronic obstructive lung disease, 22 had anatomic intrapulmonary shunting greater than that seen in normal subjects. The shunted blood passed through enlarged pulmonary vessels, as demonstrated with particles 10-90 microns in diameter. The shunt magnitude was correlated with the decrement in lung diffusing capacity. It did not correlate well with pulmonary mechanical abnormalities such as air flows and volumes or resting blood gas data. Nevertheless, shunting through enlarged pulmonary vessels may play a role in the hypoxemia seen in COPD patients, especially at exercise.

Analysis of pleural effusions using automated flow cytometry.

Flow cytometry allows rapid and accurate analysis of the deoxyribonucleic acid (DNA) content of a large number of cells. In solid tumors, the presence of aneuploidy has been shown to correlate wall with the presence of neoplastic cells. Both cytologic examination and DNA analysis by flow cytometry were performed on pleural effusions from 33 patients. Results of the two examinations were in agreement in 10 of 12 malignant pleural effusion (two false-negatives) and in 20 of 21 benign effusions. One patient with cirrhosis, ascites and Nocardia pneumonia had hypodiploid cells (false-positive) in the pleural fluid. All patients who had a malignancy, but whose pleural effusion proved to be due to a benign cause, had cells with normal DNA content in their pleural effusion. DNA analysis using flow cytometry can be rapidly performed and is highly specific and sensitive. The finding of hyperdiploid cells is highly suggestive of malignancy.

Angiotensin-converting enzyme in sarcoid perivasculitis.

A young woman was treated with topical and oral steroids for sarcoidosis manifested by systemic symptoms, involvement of the respiratory and musculoskeletal systems, and anterior uveitis. Her symptoms, ocular findings, pulmonary function, and serum angiotensin-converting enzyme level all improved in response to therapy. After tapering the steroid dosage retinal perivasculitis developed associated with a small but significant elevation of the serum angiotensin-converting enzyme level. Increasing the dosage of oral steroids resulted in prompt resolution of her retinal findings but no change in the level of the serum angiotensin-converting enzyme. This suggests that changes in the serum angiotensin-converting enzyme level may not parallel the course of ocular sarcoidosis limited to the posterior segment.

Pulmonary embolism.

Patients who are bedridden because of debilitating illness and patients who are recovering from major surgery are at particularly high risk of deep venous thrombosis and subsequent pulmonary embolism. "Mini-dose" heparin therapy has proved useful in preventing deep venous thrombosis. Because the clinical signs of pulmonary embolism are nonspecific, the patient's condition may deteriorate before the diagnosis is suspected. Ventilation and perfusion scans or pulmonary angiography confirm the diagnosis. Heparin continues to be the mainstay of therapy for pulmonary embolism.

Thoracic computed tomography in the critically ill patient.

Thoracic computed tomography (CT) was performed on 19 ICU patients to define chest abnormalities not clearly seen on conventional portable chest radiographs. In five (26%) of these cases, the CT demonstrated new findings that substantially altered the patient's course including malpositioned thoracostomy tubes, loculated pleural fluid, unsuspected pneumothorax, and pericardial effusion. In selected cases, thoracic CT can provide precise definition of intrathoracic problems in the critically ill patient.

Effect of methylprednisolone on experimental noncardiogenic pulmonary edema.

Methylprednisolone, 30 mg/kg body weight, was given to dogs 30 min and 4 h after injection of monocrotaline to produce noncardiogenic pulmonary edema. Control animals received monocrotaline but not corticosteroids. After 6 h the steroid-treated animals demonstrated significantly butter gas exchange and significantly less pulmonary edema. A possible mechanism of this beneficial effect of steroids is inhibition of complement-leukocyte interactions which may mediate pulmonary microvascular injury. The results lend some support to the clinical practice of short-term pharmacologic doses of steroids in noncardiogenic pulmonary edema.

Effect of PEEP on lung water content in experimental noncardiogenic pulmonary edema.

After administration of monocrotaline to dogs to produce noncardiogenic pulmonary edema, one-half of the animals (controls) were treated with intermittent positive pressure breathing (IPPV), and one-half with that ventilation plus the addition of 10 cm H2O of positive end-expiratory pressure (PEEP). After 6 h, the animals treated with PEEP demonstrated significantly better arterial oxygenation and reduced AaDO2, but lung water, quantitated either postmortem or in vivo by indicator-dilution techniques, was no less than controls. Although PEEP improves gas exchange, it fails to modify the degree of pulmonary edema represent.

The effect on respiratory drive of a prolonged physical conditioning program.

Nine sedentary men 21 to 35 yr of age took part in a physical conditioning program involving regular aerobic exercise over a period of 6 to 8 wk. There was significant improvement in indexes of cardiorespiratory fitness. Ventilatory and mouth occlusion pressure responses to CO2 at rest and during threadmill exercise was measured before and after training. The slopes of the regression VE/PCO2 increased during exercise (p < 0.05), but not significantly at rest. The slopes of the regression of occlusion pressure at 100 ms versus PCO2, (P100/PCO2) did not change significantly at rest or during exercise. The VE/PCO2 and P100/PCO2 did not change from rest to exercise, and showed no relation to indexes of fitness. It is suggested that the low respiratory drive seen in some athletes is not due to the adaptation that results from short-term training. The possibility that long-term training may result in decreased responsiveness to CO2 cannot be excluded.

Smoke inhalation in firemen.

Thirty firemen were studied with pulmonary function tests immediately after a severe smoke exposure and then one and a half and 18 months later in order to evaluate acute and chronic changes in their spirometry. The results were compared with predicted values and with those from a group of closely matched control subjects. We found no significant differences between the acute post-exposure spirometry values and those recorded at six weeks and 18 months later. A trend toward an increased rate of volume loss in the FVC and FEV1 was noted which is similar to other published observations. However, we did find a significant decrement in FVC compared with predicted value, and in FVC and FEV1 compared with control subjects. This is further evidence that firemen may develop lung disease related to their occupational exposure.

Treatment after blow-up (uncontrolled ascent to the surface).

A 31-year-old commercial diver suffered an uncontrolled ascent from 220 ft. His neurologic examination was grossly normal on arriving at the surface and he was immediately recompressed to 200 ft. After decompression, detailed neurologic evaluation, including encephalography, evoked cortical responses, electronystagmography, and detailed neurophysiologic testing revealed no neurologic deficit. The details of the decompression are discussed.