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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lethal pulmonary embolism is associated with hypoxemia and hypocapnia in the vast majority of cases. The easily calculated ventilation corrected oxygen tension was a very sensitive test in patients breathing air. It yielded no normals, four percent mild hypoxemia, and 96 percent moderate to extreme hypoxemia. The alveolar-arterial oxygen tension difference and oxygen ratio were equally sensitive during air breathing. During oxygen inhalation, alveolar-arterial oxygen difference was most sensitive; oxygen ratio was second best; and oxygen saturation was the least sensitive test.
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PMID:Ventilation corrected oxygen tension in lethal pulmonary embolism. 70 44

The analysis of both clinical findings and diagnostic procedures results were performed in 26 patients with thromboembolic pulmonary disease in order to determine the incidence of signs indicating pulmonary thromboembolism. Sudden dyspnea, hemoptysis and chest pains are the most common symptoms of the disease. These symptoms associated with radiographically confirmed pulmonary infiltrations with the elevation of hemidiaphragm and pleural effusion, particularly if they are bilateral, are the main clues for the diagnosis of pulmonary embolism. Perfusion defect on the pulmonary scintigraphy makes this diagnosis almost certain. Hypoxemia and hypocapnia and respiratory alkalosis are frequent findings in thromboembolic pulmonary disease, as well. Fever, increases RBC sedimentation rate and leukocytosis are present in a great deal of patients. In addition, the presence of risk factors related to the development of thrombosis of the lower limbs deep veins, and particularly those related to the long term immobilization as well as diagnostically confirmed venous thrombus are basic guidelines for the diagnostic of pulmonary thromboembolism.
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PMID:[Personal experience in the diagnosis and therapy of pulmonary thromboembolism]. 130 9

During the past 7 years, 15 patients with acute pulmonary embolism (APE) were treated at Kagawa Medical School and 10 patients were survived. Nine patients had an embolus in a right or left pulmonary trunk (group A) and 6 patients were peripheral APE (group B). In group A abnormal findings in a chest x-ray film and an electrocardiogram were observed in many patients, but in group B these findings were slight. In group A a shock was observed in 89% and cardiac arrest in 4 patients, although in group B neither shock nor death were observed. Marked hypoxia with hypocapnia was observed in 8 patients in group A and only in 2 in group B. All patients in group B were recovered by medical therapy. In group A, however, only 3 patients were recovered by medical therapy. Two patients in group A were performed pulmonary embolectomy (PER), but one of them, who had been in nonreversible shock, died. We conclude that the patient who had marked hypoxia (PO2 less than or equal to 50 mmHg) with hypocapnia (PCO2 less than or equal to 35 mmHg) early at an attack should be taken a pulmonary angiography, and when a large embolus is found out in the proximal pulmonary artery, the PER should be performed as soon as possible.
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PMID:[Indication of pulmonary embolectomy for acute pulmonary embolism]. 143 53

We conducted a retrospective analysis on 311 patients with clinical diagnosis of pulmonary embolism (PE) in a period of 3 years. 163 patients were excluded based on clinical-laboratorial criteria. The remaining 146 patients had a median age of 69 years (range: 30-91 years). 54% of the patients were male. We found dyspnea (94%), abnormal cardiopulmonary observation (89%), risk factors for venous thromboembolism (74%), tachycardia (53%), cyanosis (49%), and neck vein distension (45%) to be the most frequent findings. 64% of the patients had heart failure, 32% had myocardial ischemia, 13% had cancer, and 11% had myocardial infarction. Lactic dehydrogenase (LDH) was higher than two-fold in 54% of the patients. There was severe hypoxemia in 55% of the cases and hypocapnia in 43% of the cases. Creatinine phosphokinase (CPK) was elevated in 16% of the cases. Electrocardiography was suggestive of PE in 37% of the cases. Echocardiography showed right heart dysfunction in 30% of the cases, 92% of the patients were treated with heparin, 37 patients (25%) died, 54% of which during the first 4 days after admittance. Trying to define an index of mortality in PE we evaluated all patients by discriminant analysis coming up with 14 items with good discriminative power. By approximation of their odds-ratios we determined how many points would correspond to each item in the total sum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pulmonary embolism--mortality risk]. 147 67

In the study reported here, rabbits were used to develop an experimental model for inducing pulmonary fat embolism by forced immobilization. The emboli were quantitated by a computerized system. The activity of lipoprotein lipase in post-heparin plasma (PHP-LPL) and concentrations of free fatty acids (FFA) were measured. Also, blood gases were analyzed and pulmonary morphology and ultrastructure were observed. Forced immobilization for 5 hours was found to induce pulmonary embolism. This was accompanied by elevation of PHP-LPL and FFA levels in the blood, hypocapnia, and a tendency for insufficiency of pulmonary surfactant. The results suggest that the disorder of homeostasis caused by immobilization is strong enough to bring about pulmonary embolism without bone fracture.
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PMID:Pulmonary fat embolism in rabbits induced by forced immobilization. 156 12

The clinical profiles of 15 patients with acute pulmonary embolism (APE) were analysed. The most common symptoms of APE were tachypnea and tachycardia with sudden onset. Both PO2 and PCO2 had decreased in almost all patients (mean PO2: 50 mmHg, PCO2: 30 mmHg). Chest roentgenogram (X-P) revealed hyperlucency of the lung field, prominence of proximal pulmonary artery and cardiac enlargement. ECG showed SI QIII TIII and ST-T changes in half of the cases. These changes, however, disappeared within 4 days in most patients. Lung scan and digital subtraction pulmonary angiography were useful for the diagnosis. Sixty percent of patients recovered only by medical therapy, and embolectomy was performed in only two patients. Fifty-three percent of patients were, however, considered to be candidates for the embolectomy, and half of them died because of ineffective medical therapy. From these results we concluded that the combination of severe hypoxemia and hypocapnia with abnormal chest X-P can be used for a diagnostic or therapeutic decision. If a patient has those findings, pulmonary angiography is recommended together with thrombolytic therapy. If a large embolus is detected, embolectomy is mandatory. The need for surgical therapy for APE is greater than we had imagined.
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PMID:[Clinical profile and treatment of acute pulmonary embolism]. 157 48

The diagnostic value of alveolar-arterial PO2 gradient P(A-a)O2 in pulmonary thromboembolism is tested. The significance of alveolar-arterial PO2 gradient in acute pulmonary thromboembolism was determined in prospective study. The study group consisted of 7 patients with pulmonary thromboembolism documented by digital-subtraction angiography (DSA) and lung scans and ten healthy subjects with normal alveolar-arterial PO2 gradient. Hypoxemia was present in 3 patients, hypocapnia in 4 patients and an increased P(A-a)O2 gradient in all 7 patients. The results suggest that a normal P(A-a)O2 gradient in patients during room air breathing can be used as evidence against the presence of pulmonary emboli. P(A-a)O2 gradient is a very sensitive diagnostic parameter in acute pulmonary embolism but procedure is fast.
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PMID:[Significance of the alveolo-arterial PO2 gradient in the diagnosis of pulmonary thromboembolism]. 176 77

We report our experience with five children with pulmonary embolism and infarction. Two with congenital heart disease, one with rheumatic cardiopathy and two with a previously healthy cardiopulmonary system. The risk factors, clinical behavior and ECG were similar to those in adults. In chest roentgenogram we found pulmonary infarction with cavitations in three patients because of a delayed diagnosis. All patients had hypoxemia and hypocapnia, and diagnosis was made on the basis of segmentary or larger defects in perfusion gammagraphy. In just one case we obtained V/Q gammagraphy and pulmonary angiography. In one case we confirmed the clinical diagnosis by autopsy. We conclude that it is very important to keep this diagnosis in mind in all children with respiratory failure.
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PMID:[Pulmonary thromboembolism in children]. 177 17

The authors examined in 60 patients with acute pulmonary embolism values of blood gases and acid-base equilibrium, incl. 30 from arterialized capillary blood, in another 30 subjects from arterial blood. On analysis of capillary blood hypoxaemia was present in all subjects, on analysis of arterial blood only in 63%. Respiratory alkalosis was found on capillary examination in 37%, on arterial examination in 23% of the patients. Hypoxaemia and hypocapnia thus are not specific phenomena in acute pulmonary embolism, in particular when accurate blood collection for analysis is respected, and normal values of paO2 and paCO2 do not rule out the presence of pulmonary embolism. In the development of hypoxaemia in patients with pulmonary embolism participates above all an incomplete right-to-left pulmonary shunt, as revealed during calculation of the magnitude of the shunt by means of the so-called oxygen method in 30 patients with embolism, as compared with a group of 10 healthy subjects.
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PMID:[The importance of blood gas analysis and acid-base equilibrium in pulmonary embolism]. 190 44

We report the case of an 82-year old male patient without history of chronic obstructive lung disease in whom a sudden respiratory distress syndrome with sibilant rales in both lungs revealed a moderately severe pulmonary embolism, later confirmed by angiography. Bronchospasm occurring in the acute phase of pulmonary embolism may be expressed as acute asthma refractory to bronchodilators. This bronchoconstriction, seldom detectable clinically, seems to be related to regional alveolar hypocapnia in the territories embolized and to platelet-produced mediators, through a vagus nerve-mediated reflex. It must not hide pulmonary embolism, particularly in a suggestive context and when bronchodilators are ineffective.
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PMID:[Bronchospasm disclosing pulmonary embolism]. 207 66


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