Low-molecular-weight heparin is at least as effective and as safe as classic intravenous heparin therapy under the conditions of this study and more convenient to administer. The simplified therapy provided by low-molecular-weight heparin may allow patients with uncomplicated proximal deep-vein thrombosis to be cared for in an outpatient setting.
The hemodynamic responses to acute vasodilator administration were evaluated in 163 patients who were entered into the National Institutes of Health Registry on Primary Pulmonary Hypertension (PPH) between 1981 and 1985. Of a total of 491 drug administrations in these patients, 135 administrations in 104 patients were performed in a manner acceptable to the Registry. A single vasodilator was tried in 79 patients and more than one vasodilator in 25 patients. Two-thirds of the patients were in New York Heart Association Functional Classes III or IV. When the effects of all vasodilators were grouped together, there were significant decreases from baseline in mean pulmonary artery pressure (60 +/- 2 to 57 +/- 2 mm Hg, p less than 0.05) and total pulmonary resistance index (32.5 +/- 1.7 to 25.1 +/- 1.4 mm Hg/L/min/m2, p less than 0.0001), and increases in cardiac index (2.1 +/- 0.1 to 2.7 +/- 0.1 L/min/m2, p less than 0.0001). Mean systemic blood pressure fell (88 +/- 1 to 79 +/- 1 mm Hg, p less than 0.0001), whereas PaO2 was unchanged (70 +/- 3 to 71 +/- 3 mm Hg, p = NS). A fall in total pulmonary resistance greater than 20% was observed in 55% of the adequate drug trials. Adverse effects occurred in 32 of the total 491 patient-drug trials and were generally minor. Hypotension requiring treatment developed in six patients. There were two deaths attributable to vasodilator administration. Patients who died or had hypotension requiring treatment had higher right atrial pressures than did other treated patients (15 +/- 2 versus 9 +/- 1 mm Hg, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
To test the hypothesis that impairment after the adult respiratory distress syndrome (ARDS) is uncommon, we evaluated 41 ARDS survivors using ATS standards for determination of impairment. A total of 101 trials of pulmonary function tests were obtained between 1 and 388 wk after the onset of ARDS. It was possible to evaluate impairment at 1 yr or more after ARDS in 27 subjects. Eighteen of the 27 were impaired. The percentage of ARDS survivors who were impaired on the basis of FVC, FEV1, FEV1/FVC, and DLCOsb was 50.0, 61.1, 33.3, and 82.4%, respectively. Impairment was mild in 13 (72.2%), moderate in four (22.2%), and severe in one (5.6%). Smoking status had no predictive value in determining impairment. Physiologic indices of ARDS severity (maximal pulmonary artery pressure, lowest static thoracic compliance, and maximal level of PEEP) were found to be significantly different when those impaired 1 yr or more after ARDS were compared with those not impaired. Symptoms were found to have no association with impairment. We conclude that, using ATS criteria, impairment 1 yr or more after ARDS onset is common. Patient characteristics and symptoms after ARDS have no association with impairment 1 yr or more after ARDS onset, whereas physiologic indices of severity during ARDS do.
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