Baltimore tuberculosis symposium.
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Biomedical subjects
Publications and source records attributed to W W Addington.
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Of 852 patients admitted to Cook County Hospital with bacteriologically-proved pulmonary tuberculosis, 16 suffered respiratory failure. Of these 16, 5 died and 11 recovered. On follow-up, the survivors demonstrated significant improvement in oxygenation, but continued to show a severe restrictive ventilatory defect. Our patients, unlike those in previous reports, did not show airway obstruction. The principles of management are the same as for other pulmonary patients. Arterial blood gas analyses should be done on patients with advanced tuberculosis so that abnormalities of gas exchange will not be missed.
Sixty-seven episodes of acute asthma were treated in an emergency room. The characteristics of the attacks and subsequent course were then analyzed to determine criteria that could be used for an early decision in regard to the need for hospitalization. Attacks that were not successfully treated in the emergency room were most often characterized by very severe obstruction and a poor response to an initial injection of epinphrine. It is suggested that severely obstructed patients (peak flow less than 16% of predicted) whose peak flow remains less than 60 liters/min, or who exhibit a less than 16% improvement following 0.3 ml epinephrine, be promptly admitted.
6-Chloropicolinic acid is the sole detectable metabolite, other than carbon dioxide, arising from decomposition of 2-chloro-6-(trichloromethyl) pyridine in soil. The pyridine compound is a potent inhibitor of nitrification now in use with ammonium fertilizers. The purpose of this study was to evaluate the relative influence of various soil and climatic factors on rates of degradation of 6-chloropicolinic acid in soil. Experiments with a wide range of soil types (23 soils) demonstrate that the most important factor influencing the decomposition rate of 6-chloropicolinic acid is soil temperature. When temperature is not a variable, the quantity of organic matter (0.9 to 6.9% by weight) and pH (4.8 to 8.1) significantly affect the rate of decomposition, but sand, silt, and clay percentages do not. Moisture content was without apparent effect because the range of values investigated was too narrow. A fractional-order rate law (0.7) describes the disappearance rate best. Application of the Arrhenius equation to the data for the decomposition of 6-chloropicolinic acid in soil indicates an activation energy of 6.57 kcal per mole, suggesting that the chemical is biologically rather than chemically degraded. It was not possible to develop a suitably precise equation for prediction of loss rate as affected by the above soil and climatic factors because undefined biological factors in the soils override the effect of measurable properties of soil and climate.
We observed a patient who developed diffuse bronchiectasis subsequent to heroin-induced pulmonary edema. Unlike the previously reported cases, there was rapid clearing of pulmonary infiltrates and little evidence of severe aspiration. The development of bronchiectasis was attributed to a bronchial infection subsequent to clearing of the pulmonary edema. Physiologic dysfunction was characterized by marked obstruction, pulmonary hypertension, and mild hypoxemia.
A medical librarian joined the pulmonary medicine health care team at Cook County Hospital in order to provide a quick response to information needs regarding patient care, graduate medical education, continuing education, and research. Regular attendance at rounds and conferences enabled the librarian to initiate immediately literature searches in response to both clinical problems and educational requirements. A basic reference supplied to the medical librarian/information specialist by a physician frequently expedited literature research. It was found that patient care and education were enhanced by the rapid access to recent information and that team members used the library more. Close cooperation between the information specialist and physicians significantly facilitated the searches and saved time for health care team members.
Tissue hypoxia as a result of a wide variety of clinical situations had frequently been implicated as a cause of systemic acidosis due to the accumulation of lactic acid. Four patients suffering from smoke inhalation had lactic acidosis in association with carboxyhemoglobinemia. There was no evidence of decreased tissue perfusion, hypotension, arterial hypoxemia, or anemia. The following were tested in all patients: arterial pH (7.25 to 7.40), Pco-2 (19 to 27 mm Hg), Po (63 to 116 mm Hg), HCO-2- (11 to 19 meq/litre), carboxyhemoglobin (13% to 37%), and lactic acid (5.1 to 9.3 meq/litre). After therapy with oxygen and intravenous corticosteroids, there was prompt return of lactic acid levels, carboxyhemoglobin values, and arterial pH to normal. It is concluded that the cause of lactic acidosis in the presence of carboxyhemoglobinemia during smoke inhalation is tissue hypoxia. This tissue hypoxia is due to the reduction of the oxygen-carrying capacity of the blood and the concomitant shift of the oxyhemoglobin dissociation curve to the left, both known to result from carboxyhemoglobinemia.
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Respiratory and metabolic functions were studied at rest and during exercise in 13 Olympic oarsmen at peak of training at sea level and after one month's residence at 2350 m. At sea level each subject completed two severe five minute treadmill runs at 5 mph on a 20% incline inspiring 21% O2 for one run and 16% O2 for the other. Two more runs at the same speed and incline were carried out at altitude with F102's of 21% and 28%. Pulmonary function tests were carried out at sea level and altitude and steady state diffusion capacity was determined during rest and exercise while breathing 21% O2. Heart rates were monitored by direct electrocardiography. At altitude significant increases were found in MVV (10%), FEV1 (6%), MMEF (15%) and PF (9%) but not in VC. A rise of the DLCO during exercise from 64.8 to 75.4 ml/min/mm Hg was largely the result of increased ventilation. The response to acute hypoxia (16% O2) and to chronic hypoxia were as follows: VE from 113 to 135/122 1/min; VE/O2 from 2.55 to 3.14/3.08 1/100ml; and PETCO2 from 40 to 36/34 mm Hg. The effect of chronic hypoxia could be abolished by acute normoxia (28%O2) within five minutes; VE returned to 99 l/min, VE/Vo2 to 2.46 1/100 ml, and PETCO2 to 40 mm Hg. Vo2 for the standard exercise (5 mph - 20% grade) for normoxic and acute hypoxic conditions were similar; 4421 and 4301 ml/min, but this variable decreased significantly upon chronic altitude exposure; 3966 ml/min. This decrement in Vo2 was attributed in part to a lower work of breathing.
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