Chest
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Congestive heart failure (CHF) has been associated with the development of restrictive ventilatory abnormalities and decreased pulmonary diffusing capacity. Whether these physiologic changes reflect permanent alterations of lung anatomy or result solely from potentially reversible alterations of lung water is not known. To examine this issue, we reviewed the pulmonary function tests (PFTs) and cardiac catheterization data from recipients of successful heart transplants prior to and 1 year after transplantation. ⋯ Diffusing capacity for carbon monoxide was decreased before transplantation and showed a small decline after transplantation from 82.3 +/- 3.2 to 76.8 +/- 2.6 percent of predicted (p < 0.05). After correction of severe CHF by cardiac transplantation, normalization of FEV1, FVC, and TLC can be anticipated. Diffusing capacity, however, may actually decline after transplantation.
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To determine if spirometric changes reflect early high-altitude pulmonary edema (HAPE) formation, we measured the FVC, FEV1, and FEF25-75 serially during the short-term period following simulated altitude exposure (4,400 m) in eight male subjects, four with a history of HAPE and four control subjects who had never experienced HAPE. Three of the four HAPE-susceptible subjects developed acute mountain sickness (AMS), based on their positive Environmental Symptom Questionnaire (AMS-C) scores. Clinical signs and symptoms of mild pulmonary edema developed in two of the three subjects with AMS after 4 h of exposure, which prompted their removal from the chamber. ⋯ Further, we measured each subject's ventilatory response to hypoxia (HVR) prior to decompression to determine whether the HVR would predict the development of altitude illness in susceptible subjects. In contrast to anticipated results, high ventilatory responses to acute hypoxia, supported by increased ventilation during exposure to high altitude, occurred in the two subjects in whom symptoms of HAPE developed. The results confirm that HAPE can occur in susceptible individuals despite the presence of a normal or high ventilatory response to hypoxia.
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The ability of chest radiographs to determine the size of a pneumothorax was tested in 16 patients using computed tomographic (CT) scan as a reference method. To determine if CT with a slice thickness of 12 mm could be used, its accuracy was assessed in a lung model experiment. The lung model consisted of a water-filled plastic bag (lung) fitted into a plastic chamber (hemithorax), both of approximately the same size and shape as in man. ⋯ The correlation was poor (r = 0.71) irrespective of method of calculation. The size of the pneumothorax estimated by CT showed a good correlation (r = 0.99) to the initial aspirated air volumes in 12 of the 16 patients treated with drainage. A cautious attitude toward the use of chest radiographs for calculations of the degree of lung collapse in patients with pneumothorax is recommended.
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Incapacitating respiratory distress was the presenting manifestation of a choreiform movement disorder. Because the patient also had asthma, respiratory distress was at first mistakenly attributed to this condition. Despite vigorous asthma management, there was no improvement. However, once the neurologic condition was recognized, use of specific therapy (haloperidol and reserpine) resulted in rapid and sustained remission of respiratory symptoms.
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We used mask continuous positive airway pressure (CPAP) in seven patients with acute hypercapnic respiratory failure in an attempt to avoid endotracheal intubation and mechanical ventilation. Mask CPAP was started at 5 cm H2O and then increased to a maximum of 10 cm H2O depending on the clinical response. ⋯ No barotrauma or adverse hemodynamic effects were associated with CPAP. We conclude that a trial of mask CPAP may be warranted before intubation of an alert, acutely hypercapnic patient with COPD.