Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the original description of the syndrome of hyperbradykininism, dyspnea on exertion was not described. However, in five women with the syndrome, ages 31 to 58, four of whom had at least one elevated value of blood kinin as determined by radioimmunoassay, dyspnea on exertion was a prominent complaint. During treadmill walking at a constant power requirement against gravity, expired air gas collections and equilibrium carbon dioxide rebreathing were performed. Seventeen apparently healthy women, ages 18 to 48, served as control subjects. Although oxygen uptake was the same in both groups by design (oxygen uptake 0.91 liters per minute, 0.11 standard deviation [SD], in the control subjects; oxygen uptake 0.97 liters per minute, 0.12 [SD] in the patients), cardiac output was significantly reduced in the patients (cardiac output 8.4 liters per minute, 1.3 [SD], in the control subjects; cardiac output 6.3 liters per minute, 0.9 [SD], in the patients, p less than 0.01). End-tidal carbon dioxide tension was significantly lower in the patients (end-tidal carbon dioxide tension 41 torr, 3 [SD], for the control subjects; end-tidal carbon dioxide tension 33 torr, 7 [SD], for the patients). In one patient, repeated studies over a 12-month period demonstrated a positive relationship between end-tidal carbon dioxide tension and the respiratory exchange ratio. (Respiratory exchange ratio = 0.01 + 0.027 X end-tidal carbon dioxide tension, 0.073 standard error of the estimate [SEE], 0.71 regular correlation coefficient, n = 20). This relationship was opposite to that expected with voluntary overbreathing; it was interpreted to mean that reduced cardiac output with exercise occurred to a variable degree and was the cause of hyperpnea and hypocapnia. In the same patient, studies at exercise with and without the Jobst (antigravity) garment and studies at exercise in the supine and erect position were consistent with the hypothesis that dyspnea and exercise intolerance were caused by venous pooling when standing. It is concluded that hyperbradykininism is characterized not only by orthostatic hypotension and tachycardia with light-headedness, as originally described, but also by severe dyspnea on exertion with exercise intolerance. The mechanism remains obscure, and the treatment is unsatisfactory, but temporary improvement in the abnormal physiology can be achieved in some patients with the use of an antigravity garment.
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PMID:Dyspnea in patients with hyperbradykininism and excessive venous pooling. 374 83

A woman with mixed connective tissue disease (MCTD) developed pulmonary hypertension after delivery of a child, but had little evidence of parenchymal lung disease. This 29-year-old woman had been given a diagnosis of MCTD when she was 19 years old. She was admitted to our department two days after delivery of a child, because of dyspnea on exertion. Acute thromboembolism was suspected because of: (1) chest roentgenogram showing cardiomegaly and enlargement of the left main pulmonary artery, (2) a lung perfusion scan showing a segmental defect in the left S6 and S8 areas, (3) laboratory studies showing abnormally high WBC, LDH, FDP, and D-D dimer, and (4) arterial blood gas analyses showing mild hypoxemia and hypocapnia. Thrombolytic therapy with heparin and urokinase was begun, and was followed by a loop diurtic and anticoagulation with warfarin. One month after admission, cardiac enlargement and the A-aDO2 were found to have decreased. At that time, cardiac catheterization was done and revealed pulmonary hypertension (mean PA pressure: 45 mmHg) and low cardiac output with no detectable thrombosis in the left pulmonary artery. The patient was subsequently treated with a calcium antagonist and a prostacyclin derivative, and her condition was stable for 5 months. Then her exercise tolerance gradually decreased due to shortness of breath, and cardiomegaly gradually increased over the next 3 months. Eight months after delivery of the child, the patient died of right heart failure. In clinically stable patients with MCTD, delivery of a child may lead to pulmonary thromboembolism and pulmonary hypertension.
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PMID:[Puerperal secondary pulmonary hypertension in a patient with mixed connective tissue disease]. 747 71