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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of low doses of heparin (5000 units of sodium heparin every 12 hours for 5 days) on arterial oxygenation was studied in 24 patients in the postoperative period after upper abdominal surgery. Another 24 patients served as a control group. The arterial oxygen tension was the same in both groups preoperatively and was equally significantly reduced during the 1st postoperative day. During the 2nd day, oxygen tension rose in the heparin-treated group to values which no longer differed significantly from the peroperative level. In the control group the significant reduction persisted until the 4th postoperative day. The arterial carbon-dioxide tension did not differ between the groups, neither did it vary significantly between days. There were no clinical signs of large pulmonary embolism during the postoperative period, chest X-ray was normal in all patients examined and a photoscan was normal in 23 of 24 subjects studied. Low-dose heparin treatment may apparently shorten the period of postoperative hypoxaemia, probably by counteracting both large pulmonary emboli and microthromboembolism.
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PMID:Effect of low-dose heparin prophylaxis on arterial oxygen tension after high laparotomy. 5 79

The authors recall the symptoms of peroperative and early postoperative bronchospasm. They emphasise the etiology and the treatment. In fact, bronchospasm may be induced by several causes:--mechanical or chemical vagal stimulation;--direct or allergic-induced histamine liberation, induced by certain drugs (mainly curare);--taking beta-blockaders before operation, favoured by the use of morphine during operation;--finally, any irritation of the bronchi (inhalation of gastric juice, pulmonary embolism, pulmonary oedemal). The treatment is etiological but also symptomatic:--enrich the inspired air with oxygen;--inject I.V. 1/2 to 1mg of atropine;--in case of failure, one should use Salbutamol I.V. which is very effective during contraction of the bronchial muscles;--massive corticosteroid therapy will be effective in mucosal oedema.
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PMID:[Diagnostic, etiologic and therapeutic problems confronting the anesthesiologist in cases of bronchial spasm. Apropos of 4 cases]. 7 21

Electrocardiograms of 90 patients with arteriographically documented acute submassive or massive pulmonary embolism and no associated cardiac or pulmonary disease were studied. Patients were derived from the Urokinase-Pulmonary Embolism Trial National Cooperative Study. In massive embolism, the electrocardiogram was normal in 6 per cent (3 of 50) of patients. With submassive embolism, 23 per cent of patients (9 of 40) had a normal electrocardiogram. Since one or more of the traditional manifestations of acute cor pulmonale (S1Q3T3, right bundle branch block, P pulmonale, or right axis deviation) occurred in only 26 per cent of patients, one could not rely exclusively upon these electrocardiographic abnormalities for the diagnosis of pulmonary embolism. The most common electrocardiographic abnormalities were nonspecific T wave changes which occurred in 42 per cent of patients and nonspecific abnormalities (elevation or depression) of the RST segment which occurred in 41 per cent of patients. Left axis deviation occurring in 7 per cent of the patients was as frequent as right axis deviation. Low voltage QRS complexes, previously undescribed in pulmonary embolism, occurred in 6 per cent of patients. None of the patients had atrial flutter or atrial fibrillation, which appears to occur more typically in patients with pulmonary embolism who have preexistent cardiac disease. All of the varieties of electrocardiographic abnormalities disappeared in some of the patients by 2 wk. Inversion of the T wave was the most persistent abnormality. Larger defects on the lung scan or pulmonary arteriogram occurred in patients with various abnormalities on the electrocardiogram than in patients with normal electrocardiograms. The pulmonary arterial mean pressure and/or right ventricular end-diastolic pressure was significantly higher in patients with several varieties of abnormal electrocardiograms, although the partial pressure of oxygen in arterial blood, in general, did not differ from that in patients with normal electrocardiograms. These hemodynamic correlations, made for the first time in patients, suggest that acute ventricular dilatation, possibly in combination with hypoxemia, is a causative factor of the electrocardiographic changes in acute massive or submassive pulmonary embolism.
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PMID:The electrocardiogram in acute pulmonary embolism. 12 74

Complications of coronary artery surgery were analyzed in a prospective controlled study of 150 patients, one group receiving methylprednisolone before temporary cardiopulmonary bypass. The patient population was comparable in both the groups. The number of deaths were the same in both the groups, myocardial infarction and cardiac arrhythmias were definitely lower in the Solu-Medrol group. Cerebral vascular accidents were higher in the control group and there were none in the drug treated group. Incidences of pulmonary embolism was reduced by the drug. Oxygen consumption by the tissues was higher in the Solu-Medrol treated group. There were no known complications of the drug, such as stress ulcer and infection. One patient did receive prophylactic antibiotics. Solu-Medrol was deliberately given in patients who were known to have uncomplicated duodenal ulcer. Post-operative bleeding in patients with duodenal ulcer was not noted. This could be explained due to the short acting nature of Solu-Medrol. We feel that Solu-Medrol does minimize serious sequelae of heart-lung machine in coronary artery surgery.
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PMID:The effects of methylprednisolone on the complications of coronary artery surgery. 30 83

Arterial hypoxemia is a common finding in acute pulmonary embolism, and its severity is generally assumed to be proportional to the extent of pulmonary artery obstruction. We studied blood gases (during room air breathing and 100% oxygen breathing) and hemodynamic data is seven patients with massive pulmonary embolism and circulatory failure. All measurements were made before and 30 minutes after medical therapy of shock. We observed that a low cardiac output state can result in a misleading improvement in arterial oxygenation during massive pulmonary embolism, and that an improved circulatory status resulting from medical therapy (including inotropic drug infusion with or without blood volume expansion) can paradoxically increase arterial hypoxemia. We conclude that severity of arterial hypoxemia may not reflect the severity of pulmonary artery obstruction in acute pulmonary embolism if shock is present.
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PMID:Hemodynamic factors influencing arterial hypoxemia in massive pulmonary embolism with circulatory failure. 42 4

Complications are the major causes of illness and death after burning and most of them stem from the burn wound. Their origin and importance are reviewed with emphasis on problems and growing points in knowledge. Fluid leakage from the circulation into the burn is the cause of hypovolemic shock, but the underlying permeability changes in the burn are only partly understood. Other nonbacterial complications include acute cardiac failure, acute anemia, hemolytic jaundice, renal failure, encephalopathy, complex hypermetabolic effects including pseudodiabetes, gastric and duodenal ulceration, deep vein thrombosis and pulmonary embolism, pulmonary and glomerular microthrombosis, hepatic jaundice, and arterial thrombosis. Involvement of the airway in conflagrations carries special hazards like glottic edema and inhalation of irritant fumes. Nowadays, bacterial causes are dominant and these remain the main challenge. Bacterial infection and invasion of the burn are usually responsible for septicemia, bronchopneumonia, and pyelonephritis although other sources also contribute. Indirect manifestations of septicemia include paralytic ileus, acute gastric dilatation, toxic myocarditis, and some cases of renal failure. Therapeutic complications like agranulocytosis, thrombocytopenia, and colitis occur at times. High concentrations of oxygen given therapeutically can produce fatal aseptic hypoxic pneumonitis.
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PMID:A review of the complications of burns, their origin and importance for illness and death. 44 73

The response of pulmonary arterial pressure to minor degrees of pulmonary embolism was examined in 18 patients with embolic occlusion of less than 25% of the pulmonary vascular bed. Patients with pulmonary embolism were compared to normal controls matched for age and sex and to patients with a variety of acute pulmonary disorders without pulmonary embolism. Patients with pulmonary embolism and patients with other acute pulmonary diseases had significantly higher pulmonary arterial pressures and significantly lower values for arterial oxygen tension (PaO2) than did normal subjects. The degree of pulmonary hypertension correlated with the PaO2. Pulmonary hypertension occurring after minor degrees of pulmonary embolism may be a response to mild arterial hypoxemia.
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PMID:Pulmonary hypertension secondary to minor pulmonary embolism. 65 52

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 effects of acute pulmonary hypertension on the fraction of cardiac output shunted through pulmonary arteriovenous communications have been studied in dogs as a possible cause of hypoxia following pulmonary embolization. Pulmonary artery pressure was increased twofold and then fourfold above control values by embolization of the pulmonary vascular bed with polystyrene microspheres. Quantitative measurements of arteriovenous shunt were determined from the fraction of 50 mu radioactively labeled microspheres injected into the inferior vena cava which passed through the pulmonary circulation into systemic vascular beds. There was no increase in the fraction of pulmonary blood flow passing through pulmonary arteriovenous connections, 50 mu in diameter or greater, with pulmonary microembolism when FIo2 was 1. There was a small increase in arteriovenous shunt fraction when pulmonary artery pressure was increased with an FIo2 of 0.21. Physiological shunt measured by the oxygen technique did not increase with pulmonary embolism, but total venous admixture rose significantly. Postmortem gravimetric measurements of lung water indicated pulmonary edema. We conclude that anatomic arteriovenous shunt channels have little physiological significance after pulmonary microembolism in the dog lung. The major cause of hypoxia immediately after pulmonary microembolism is ventilation/perfusion imbalance, probably caused by pulmonary edema.
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PMID:Effect of pulmonary microembolism on arteriovenous shunt flow. 70 53

Platelet survival time (autologous labeling with 51chromium) was measured in 63 patients in order to evaluate the role of platelets in the thromboembolic complications of patients with hypoxemia and pulmonary hypertension. Thirty-eight of these patients had chronic obstructive airways disease; 13, primary pulmonary hypertension; seven, recurrent pulmonary embolism; four, the Eisenmenger syndrome; and one, multiple pulmonary arteriovenous fistula. Forty-three patients were hypeakly associated with arterial oxygen tension ( r = 0.50), but not with the arterial carbon dioxide tension or the level of pulmonary artery pressure. Sulfinpyrazone lengthened platelet survival in 12 of 24 (50%) treated patients but this drug did not alter either arterial oxygen tension arterial carbon dioxide tension, or pulmonary artery pressure. Our results suggest that hypoxemia is associated with shortened platelet survival time and that platelets may, therefore, be involved in the thromboembolic complications that develop in patients with hypoxemia.
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PMID:Platelet survival time in patients with hypoxemia and pulmonary hypertension. 83 12


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