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

A 67 year old woman with a permanent pacemaker was admitted with pulmonary oedema and mitral valve incompetence two months after a myocardial infarction. Echocardiograms showed good left ventricular function and a large coil of apparent thrombus in the right atrium prolapsing into the right ventricle. Intermittent loss of pacemaker sensing and capture was noticed on admission and probably caused the supraventricular tachycardia and ventricular fibrillation that occurred before an exploratory bypass operation. At operation rupture of the papillary muscle was found and the mitral valve was replaced. A large piece of thrombus was retrieved from the right pulmonary artery. The right heart contained no clot and the pacemaker wire was not displaced. It is envisaged that the strand of venous thrombus was caught in the permanent pacing wire at the tricuspid valve level resulting in an unusual case of pacemaker malfunction. The eventual poor outcome was almost certainly influenced by the arrhythmias and pulmonary embolism caused by the clot and might have been avoided by early operation.
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PMID:Entanglement of embolised thrombus with an endocardial lead causing pacemaker malfunction and subsequent pulmonary embolism. 356 90

During 1977 to 1985 2008 patients suffering from acute ischemic cerebral infarcts were admitted to the Department of Neurology, Giessen University. 213 (10.6%) died during their stay at hospital of 28 days in average. Time of survival, cause of death, localization and etiology of the infarcts were evaluated retrospectively on base of the medical reports, the angiographic, doppler-sonographic, computerized tomographic, and autopsy findings. The same number of patients died because of direct sequelae of stroke and secondary complications respectively. Those with supratentorial infarcts, who died in consequence of a vegetative dysregulation generally did not survive the first week after ictus, often had infarcts exceeding the supply area of one large cerebral artery and frequently had evidence of cardiac embolism. Pathogenetic factors for extension of the ischemic cerebral damage subsequently causing transtentorial herniation were spreading thrombosis, reinfarction, and fatal secondary hemorrhage. Patients dying in consequence of an infratentorial infarct often had a thrombosis of the basilar artery or a large cerebellar infarction. Secondary fatal complications mostly occurred after the first week after stroke. Pulmonary edema, pulmonary embolism and myocardial infarction predominated with different time pattern.
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PMID:[Fatal outcome of ischemic cerebral infarct]. 369 19

Pulmonary embolism is diagnosed by a mismatched perfusion-ventilation lung scan. The probability is increased further when there is an associated "hot spot" in the perfusion study caused by focal pulmonary edema.
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PMID:Focal pulmonary edema. Correlation with perfusion lung scan. 404 10

1. In the rat, pulmonary embolism induced by intravenous administration of gaseous carbon dioxide increases intrapulmonary water content. When the rat is vagotomized before emboli are produced, an important lung edema is found. 2. Strong respiratory stimulation with lung hyperinflation seems to be the cause of this facilitated alveolar transudation. 3. Mechanical factors operating after pulmonary embolism are those which explain transudation after inhalation of hypercapnic gas mixtures in vagotomized rats.
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PMID:[Acute postembolic pulmonary edema in vagotomized rats]. 622 Jul 95

Drug-addicts frequently suffer from pulmonary diseases, particularly those who practice self-injection of the drugs intravenously. Emphasis is at present laid on the various excipients which are thought to induce acute alveolitis with subsequent acute pulmonary oedema in heroin-addicts. It has also been suggested that the deep ventilatory depression that precedes pulmonary oedema may play a part and this is interesting since the depression can now be prevented with naloxone. Infectious lesions, such as septic pulmonary embolism or endocarditis, are easier to explain. The ever increasing use of tablets crushed for injection is responsible for peri-arteriolar granulomas of the lung with possibly severe sequelae. Finally, the almost generalized consumption of marihuana in the United-States has led to the discovery of new properties of this drug, including ventilatory stimulation and broncho-dilatation. However, this is mostly of theoretical interest. The psychotropic effects of marihuana and its irritant effect on the bronchi when inhaled make it unlikely that it will be ever be used for therapeutic purposes.
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PMID:[Pneumopathies in drug addicts]. 663 69

We report a case of severe pulmonary embolism in a 37 years old man admitted to the intensive care unit for severe acute respiratory failure. The presenting signs and symptoms were typical for severe pulmonary oedema. Chest radiograph shortly after admission showed local alveolar shadows. In the absence of sepsis, haemodynamic evidence of left ventricular failure on catheterization of the right heart and because of the history of the recent illness, a tentative diagnosis of pulmonary embolism was made. The diagnosis was confirmed by selective pulmonary angiography. The latter demonstrated that pulmonary oedema had been localized only in areas with patent pulmonary arteries and, in addition, confirmed that left ventricular function was normal. Such a pattern of local pulmonary oedema is uncommon in patients and is reminiscent of that observed in animal experiments with severe pulmonary arterial obstruction and overperfusion of unblocked territories. Possible mechanisms of overperfusion oedema are discussed and the hypothesis that humoral factors may increase the permeability of pulmonary microvasculature in cases of severe pulmonary embolism is put forward.
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PMID:[Pulmonary edema in pulmonary embolism]. 670 66

A cardiorespiratory monitoring system allows the measurement of FAECO2 and FECO2 in the expired air of the patient at the mouth (endtidal CO2) and in a mixing box. From these parameters, combined with the measured PACO2, the alveolo-expired (DuA = PECO2/PAECO2) and alveolar-arterial (Dua = PAECO2/PACO2) ductances which assimilate the respiratory system to a two-stage exchanger have brought about a lot of valuable information 1. DuA improves by 20% in 20 patients after removal of bronchial obstruction (p < 0.001) and by 9% in 7 intubated patients after tracheotomy (p < 0.02). DuA falls by 15% (p < 0.001) in 10 patients with hypocapnia (PaCO2 = 28 mmHg) after a dead space adjunction with the aim of normalizing PaCO2 (paCO2 = 35 mmHg). 2. Dua falls by 33% in six patients after pulmonary embolism, proved by angiography (p 0.001) by 9% in 34 patients after 30 min of pure oxygen breathing (p 0.001). On the other hand, inthe absence of clinical or radiological pulmonary edema, in increases by 19% in 38 patients with hypervolemia after diuresis (furosemide) (p < 0.001). Thus since DuACO2 varies with anatomical dead space and the air distribution disorder, DuaCO2 evolves according to the disorders of the blood distribution and arterial-alveolar diffusion. The determination of these coefficients, in the absence of significant changes in the arterial blood gases, helps the diagnosis, guides the early treatment and allows for the monitoring of its efficiency.
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PMID:The continuous monitoring of CO2 ductances in pulmonary intensive care. 677 20

Pulmonary microemboli may play a role in the adult respiratory distress syndrome, creating both pulmonary oedema and hypoxaemia. We measured the time course of pulmonary oedema and hypoxaemia after pulmonary microemboli of 63-74 mu starch were infused into dogs. Dogs were divided into two groups: six dogs that did not develop pulmonary oedema, and seven that did. Immediately after emboli there was no difference between groups in the large fall in PaO2 or the rise in Qs/Qt. Therefore the hypoxaemia of pulmonary embolism is not created by pulmonary oedema. As pulmonary oedema increased with time in the oedematous dogs, PaO2 fell further. There was no further reduction in PaO2 in the dogs who did not develop pulmonary oedema. We conclude that hypoxaemia after pulmonary embolism may be worsened if pulmonary oedema occurs, but the immediate large reduction in PaO2 after embolism is not created by pulmonary oedema.
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PMID:Hypoxaemia created by pulmonary oedema after pulmonary microemboli in dogs. 683 Dec 90

Pulmonary edema is rare in patients with pulmonary embolism and to our knowledge has not been described in association with thrombolytic therapy. We describe a patient with massive pulmonary embolism in whom the adult respiratory distress syndrome (ARDS) developed shortly after a course of streptokinase therapy. The possible association between streptokinase therapy or pulmonary embolism and ARDS should be recognized as streptokinase gains wider clinical use.
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PMID:Adult respiratory distress syndrome following thrombolytic therapy for pulmonary embolism. 684 25

Bleeding, thrombocytopenia, and osteopenia are recognized as the side effects of heparin administration. We recently noted occurrence of pulmonary edema in a patient with myelofibrosis with myeloid metaplasia being treated with heparin for pulmonary embolism. The hypertensive episodes preceding left ventricular failure were considered related to serotonin released from the immunologically mediated lowering of platelets.
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PMID:Development of pulmonary edema related to heparin administration. 722 18


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