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

The subject of this report is a 57-year-old obese, hypertensive woman who had been well until the onset of severe chest pain and hypotension. She had to be defibrillated four times on her way to the hospital. The diagnosis of acute inferior-posterior infarction was made by electrocardiogram (ECG) and there was a markedly elevated serum creatine kinase (CK) (including the MB fraction). The patient had a very low cardiac output and ejection fraction. A lung scan revealed possible pulmonary embolism for which she was anticoagulated. She remained hypotensive and hypoxemic and, on Day 17 of her hospital stay, she had a bout of severe dyspnea. A new systolic murmur was heard and the clinical diagnosis of ruptured papillary muscle was made and confirmed by echocardiography, and later at autopsy. All three coronary arteries were severely atherosclerotic and, in addition, the right coronary artery was completely closed by a thrombus. This case clearly illustrates the major pathological changes in the heart that correlate with the clinical findings in patients with a myocardial infarct that is complicated by left ventricular papillary muscle rupture. The pathophysiological effects of this condition, as illustrated in this case report, include the following:1. The posterior papillary muscle wa s almost completely separated from its base, with only a thin strip of muscle intact. The mistral valve thus was insufficient (a "flail valve''); this markedly reduced the ejection fraction of the left ventricle, increased its end-diastolic volume and pressure, produced a damming of blood in the pulmonary circulation, and this resulted in the pulmonary edema seen on the chest x-ray.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute myocardial infarction with papillary muscle rupture. 841 63

Although serotonin has been reported to play a substantial role in cardiopulmonary dysfunction, the quantitative effects of serotonin, released from activated platelets, on the development of alveolar flooding and on impaired gas exchange in pulmonary embolism have not been systematically investigated. To elucidate the effects of serotonin on pulmonary hemodynamics, accumulation of edema fluid in alveolar space, and impairment of gas exchange in acute pulmonary embolism, 20 mongrel dogs were given 0.4-0.6 g/kg of glass beads with a diameter of 100 microns, via the internal jugular vein. Before and after embolization, pulmonary hemodynamics, systemic hemodynamics, blood gases, and the distribution of ventilation-perfusion ratios (VA/Q) in the lung were measured, with and without a newly developed selective antagonist of the serotonin S2 receptor, DV-7028. VA/Q distribution was determined by applying the multiple inert gas elimination technique. After glass-bead embolization, the animals that did not receive DV-7028 showed significant increases in pulmonary arterial pressure and in extravascular lung water, widened alveolar-arterial O2 tension differences, and appreciable development of low VA/Q areas (0 < VA/Q < or = 0.1). These changes were prevented in the animals that received DV-7028. However, DV-7028 did not affect the formation of high VA/Q areas (VA/Q > 10). In conclusion, in acute canine pulmonary embolism serotonin not only induces pulmonary hypertension and pulmonary edema, but also worsens gas exchange through the formation of low VA/Q areas.
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PMID:[Role of serotonin in impaired gas exchange during pulmonary embolism]. 853 90

Over an almost 5 year period, 8,017 caesarean sections were done, and there were 51 maternal deaths following caesarean section (of which 5 were done outside). Caesarean section deaths accounted for 1 in 8 overall maternal deaths in the hospital, and institutional mortality for caesarean section was 5.7/1,000 operations. The causes of death included haemorragic shock in 19 (37.3%), general anaesthesia (11.6%), hypertensive disorders 5 (9.8%), general anaesthesia in hypertensive pregnancies 4 (7.8%), septicaemia 7 (13.7%), hepatic failure 3 (5.9%), pulmonary edema 2 (3.9%) and unknown including pulmonary embolism 6 (11.6%). Five deaths followed elective operations. Caesarean section done in cases of antepartum haemorrhage, hypertensive disorders, post caesarean pregnancies with adherent placentae and obstructed labour caused the majority of caesarean mortalities.
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PMID:How safe is caesarean section. 859 Nov 6

Imaging procedures are important for diagnosis and surveillance of patients in intensive care units. Radiologic examination, ultrasound and echocardiography are of paramount importance because they can be done bedside. Portable chest x-ray examination is the procedure of choice for documentation of tubes, lines and devices, estimation of cardiopulmonary function, demonstration of pulmonary edema, ARDS pneumonia, atelectasis and pneumothorax Plainfilm radiologic imaging of the abdomen is indicated when perforation ileus or acute intestinal pseudoobstruction is suspected Echocardiography can give information about ventricular function, pericardial effusion, cardiac valves, functional importance and complications of myocardial infarction, and hemodynamic changes of pulmonary embolism. Transesophageal echocardiography (TEE) is the method of choice when endocarditis, aortic dissection or cardiac thromboembolism is considered. Ultrasound can show many pathologic changes important for the management of intensive care patients concerning liver, gallbladder, bile duct, pancreas, kidney, spleen, pleural space and vessels. Other imaging procedures such as CT, methods of nuclear medicine, MRT, angiography etc. are done outside the intensive care unit and therefore need a more restricted indication.
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PMID:[Imaging methods in intensive care]. 865 7

Pulmonary hypertension may occur in the antiphospholipid syndrome as a result of recurrent pulmonary embolism or microthrombosis of pulmonary vessels. We describe 3 cases of primary antiphospholipid syndrome (APS) and cor pulmonale that fulfilled the criteria for chronic major vessel thromboembolic pulmonary hypertension. Pulmonary thromboendarterectomy was performed in all 3 patients and it was successful in 2. One patient died in the immediate postoperative period from hemorrhagic pulmonary edema. Chronic thromboembolic pulmonary hypertension should be added to the list of pulmonary vascular complications of primary APS. Despite its risk, pulmonary thromboendarterectomy represents a treatment option for this otherwise lethal condition.
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PMID:Primary antiphospholipid syndrome presenting as chronic thromboembolic pulmonary hypertension. Treatment with thromboendarterectomy. 873 Jan 45

We report the case of a young man hospitalized because of an acute pulmonary embolism presenting as a focal pulmonary edema, without evidence of left ventricular failure. This pulmonary embolism was caused by a testicular choriocarcinoma that entailed both a neoplastic venous involvement with pulmonary neoplastic embolism, and a compression of inferior vena cava with thrombosis and subsequent pulmonary thromboembolism. This case combines two unusual associations: (i) Pulmonary embolism causing a localized pulmonary edema, (ii) Neoplastic pulmonary embolism of a testicular choriocarcinoma.
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PMID:Testicular choriocarcinoma revealed by a localized pulmonary edema: a case report. 875 Jan 31

A study was conducted in 14 patients with pericardial syndrome after pulmonary embolism. The role of right ventricular myocardial injury and noncardiogenic pulmonary edema in this syndrome is considered and its existence is established.
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PMID:The Dressler syndrome after pulmonary embolism. 875 17

If lungs could be retrieved from cadavers after circulatory arrest, the critical shortage of donors for lung transplantation might be alleviated. To assess gas exchange after transplantation of lungs from cadaveric donors, we performed double-lung transplantation through sequential thoracotomies in 12 dogs. Donors were sacrificed by intravenous pentobarbital injection and then ventilated with 100% oxygen. Lungs were harvested 2 hours (n = 6) or 4 hours (n = 6) after death and flushed with 2 L modified Euro-Collins solution. Recipients underwent sequential right and left lung transplantation; they were then monitored while under anesthesia for 8 hours, with adjustments of the fraction of inspired oxygen. Nine of 12 recipients survived the 8-hour study period. Four of six dogs with cadaveric lungs retrieved 2 hours after death survived; deaths were from pulmonary embolism at 6 hours and pulmonary edema at 2 hours. Five of six dogs with cadaveric lungs retrieved 4 hours after death survived; one died of hypoxia during implantation of the left lung, while dependent on the right lung graft. Postoperative hemodynamic and gas exchange parameters were similar in both groups. Alveolar-arterial oxygen gradient rose significantly compared with baseline 1 hour after transplantation in both groups (462 +/- 60 vs 38 +/- 31 mmHg for 2-hour group, p < 0.0001, and 484 +/- 63 vs 38 +/- 14 mmHg for 4-hour group, p < 0.0002). By 8 hours after operation, the gradients had significantly decreased in both groups (105 +/- 37 mm Hg for 2-hour group and 146 +/- 53 mm Hg for 4-hour group) and were similar to baseline values. Extravascular lung water also rose significantly 1 hour after transplantation (15.7 +/- 2.8 vs 7.9 +/- 0.5 ml/kg for 2-hour group, p < 0.02, and 16.9 +/- 1.2 vs 6.6 +/- 0.4 ml/kg for 4-hour group, p < 0.0001) and decreased gradually during the 8-hour study period. Donor lungs retrieved at 2 and 4 hours postmortem afford similar recipient outcomes. Improvement in alveolar-arterial oxygen gradient and reduction in extravascular lung water during the study period imply that the ischemia-reperfusion injury induced by this model is reversible. If this approach could be safely introduced to clinical practice, substantially more transplant procedures could be performed.
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PMID:Canine double-lung transplantation with cadaveric donors. 880 Jan 42

A review summarizing recent findings on the causes of the development, pathogenesis, diagnosis and treatment of acute cardiac failure. It is a condition when the heart is unable to pump blood in amounts needed for the metabolic activity of tissues. It may be the first manifestation of disease or acute deterioration of chronic heart failure. The most frequent causes of acute left-sided failure include acute myocardial infarction, arterial hypertension, valvular defects, myocarditis, toxic damage or metabolic myocardial disorders. In right-sided failure pulmonary embolism, extensive affections of the lungs and pleura, right ventricular infarction and affection of the pericardium predominate. The clinical picture of cardiac failure is due to a combination fo the basic disease, evoking causes, signs of an inadequate minute volume, transudation of fluids into the interstitium and the presence of compensating mechanisms. The diagnosis of cardiac failure is based on an analysis of subjective and objective clinical symptoms and other auxiliary examinations such as X-ray examination of the chest, electrocardiogram, echocardiography, examination of blood gases and other laboratory examinations. In right-sided insufficiency the examination is supplemented by pulmonary scintigraphy, possibly by catheterization of the right heart and pulmonary angiography. As to the differential diagnosis, we must differentiate from acute cardiac failure, asthma bronchiale, spontaneous pneumothorax, dyspnoea in neuroasthenic patients, non-cardiac pulmonary oedema. Treatment of cardiac failure involves lifestyle and dietary provisions, medicamentous treatment which has undergone great changes in recent years. Cardiac failure is controlled by reduction of the cardiac filling pressure and support of the efficiency of the cardiac pump (Inotropy) and control of excessive fluid and salt retention. Decisive for the subsequent development of the disease is diagnosis of the basic cardiac or non-cardiac disease and its aimed treatment. In uncontrolled cardiac failure mechanical support of cardiac activity and transplantation of the heart are options.
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PMID:[Clinical aspects of acute heart failure]. 892 24

The authors reviewed all chest radiographs obtained for pregnant women at a university hospital over a 15-year period to determine the intrathoracic complications of pregnancy and diseases occurring during pregnancy. The characteristic physiologic changes seen on chest radiographs during normal pregnancy are reviewed. Examples of intrathoracic diseases that may occur in pregnant patients include pulmonary embolism, amniotic fluid embolism, beriberi, aspiration pneumonia, community-acquired pneumonia, viral pneumonia, asthma, systemic disease, trophoblastic disease and peripartum pulmonary edema. The authors discuss the radiation biology implications of performing chest radiography during pregnancy and conclude that the benefit that the fetus receives from diagnosis and treatment of the mother's disease may be greater than the risk of radiation exposure.
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PMID:Radiographic appearance of intrathoracic complications of pregnancy. 894 17


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