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

Abnormal lung perfusion scans using radioactive particles were found in five out of six cases of hepatic cirrhosis with arterial hypoxaemia. None had clinical evidence of cardiopulmonary disease or signs of pulmonary embolism on arteriography. The scan defects are probably caused by a disorder of the pulmonary microvasculature, which may show regional variation in severity.
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PMID:Lung perfusion scanning in hepatic cirrhosis. 464 96

The association of pericarditis and pulmonary embolism may be the source of diagnostic error and delay in the administration of anticoagulant therapy. Two cases are reported. Pericarditis occurred late in patients with severe, chronic pulmonary embolism with electrocardiographic changes of acute cor pulmonale. Two physiopathological mechanisms for this association have been proposed. The first, haemodynamic, suggests friction between the pericardium and distended right ventricle and pulmonary artery. The second, an immunological hypothesis, compares the association of pericarditis and pulmonary embolism to that of the Dressler syndrome after myocardial infarction. This assimilation would imply the constitution of an anatomical pulmonary infarction. It is not justifiable to accept this pathogenesis on the evidence of transient pulmonary opacities resulting from intra-alveolar haemorrhage or of linear opacities of pulmonary atelectasis secondary to hypocapnic pneumoconstriction which are radiological signs of anatomo-physiological stages of pre-infarction.
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PMID:[Pericarditis and pulmonary embolism. A difficult differential diagnosis and a confusing association]. 643 34

A vital factor conditioning the usage of the pulmonary perfusion (Q) scan in the evaluation of patients suspected of pulmonary embolism is the prevalence of abnormal Q scans in subjects free of cardiopulmonary disease. Because this prevalence has not been well defined, we performed Q scans in 80 nonsmoking subjects 18 to 29 yr of age having no known active cardiopulmonary disease. Each subject underwent a history, physical examination, electrocardiogram, spirometry, and PA chest roentgenogram, followed by a 6-view Q scan. Two subjects in whom a Q defect was suspected underwent a 133Xe equilibrium-washout ventilation (V) scan. All Q scans were interpreted blindly and independently by 2 experienced readers. Seventy-nine of the 80 Q scans were read as normal. No subject demonstrated a lobar or segmental defect. One of the 80 subjects, who had a mild pectus excavatum, had a left upper lobe subsegmental defect, which was not seen on the V scan. Based on the statistical analysis of these data, no more than 3.68% of normal nonsmoking persons in this age group may have a lobar or segmental Q scan defect and no more than 6.77% may have a subsegmental defect (with 95% confidence). Therefore, our study indicated that Q scan defects, particularly lobar or segmental, are rarely present among normal nonsmokers in this age group.
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PMID:Patterns of pulmonary perfusion scans in normal subjects. 645 45

Pulmonary embolism is poorly diagnosed and therefore not treated in patients with chronic diseases, whereas it is overdiagnosed in formerly healthy patients. The diagnostic level is not satisfactory even in departments of cardiology. Insufficient use of auxiliary laboratory tests constitutes one of the main reasons for the unsatisfactory state of pulmonary embolism diagnostics. The clinical picture of pulmonary embolism depends on a) the size of pulmonary embolism, b) the previous state of the cardiopulmonary system. A massive pulmonary embolism can lead to a) sudden death, b) shock, c) acute cor pulmonale. The most typical diagnostic sign is suddenly developed or deteriorated dyspnea (present in 94% of patients). The presence of venous thrombosis and the appearance of sudden dyspnea always support the diagnosis very strongly. Dyspnea or tachypnea occur in more than 90% of patients. Dyspnea, tachypnea or deep venous thrombosis occur in 99% of patients with acute pulmonary embolism. Electrocardiographic signs of acute pulmonary embolism were present in 67% of our patients with hemodynamically significant pulmonary embolism. Electrocardiographic signs are most marked in cases in which pulmonary embolism originates suddenly, in patients with a normal cardiopulmonary system, if the pulmonary embolism is extensive and the electrocardiogram is carried out early and repeatedly. The electrocardiographic signs of pulmonary embolism in cardiac patients, however, are not specific and only rarely present. The principal advantages of the chest X-ray are simplicity, safety and low costs. A negative chest X-ray was found only in 16.6% of our patients with pulmonary embolism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The diagnosis of pulmonary embolism. 653 69

The dynamic features of the interventricular septum were studied with two-dimensional echocardiography with special reference to the influence of right ventricular (RV) pressure overload. The subjects were 52 patients, including 30 with atrial septal defect (ASD), 14 with rheumatic mitral valvular disease and 8 with pulmonary hypertension (PH) due to cor pulmonale, pulmonary embolism, or primary PH. To assess septal motion, the configuration of the left ventricle (LV) in the short-axis view was quantified as the deformity index, and characterized as the distortion from right circle. As an accurate short axis was required to assess the deformity of the cavity, the transducer was attached to the guide arm, providing comparable positions and directions. The deformity index was highest at the chordal level among other levels in the same cardiac phase. In ASD without PH, the deformity was minimal in end systole and maximal in early diastole. The index curve showed two peaks in early diastole and these times coincided with those of the minute backward notches on the ventricular septal echogram. In ASD with PH, the deformity was minimal in early systole and became greater during systole. The maximum deformity was shown in early diastole, corresponding to the momentary retracting motion of the septum by M-mode echocardiography. At that moment, the septum became convex to the LV. In patients with RV pressure overload, the systolic peak of the RV pressure was delayed and the decrease in pressure became sluggish, resulting in the RV pressure exceeding that of the LV transiently in early diastole. This was the reason for the septum becoming convex to the LV in this phase. Among the patients, the bi-ventricular systolic pressure ratio correlated not only with the index in end systole but also with that in early diastole. Good correlation between systolic pressure ratio and early diastolic deformity index seemed to be attributable to the fact that the higher the RV systolic pressure, the larger the reversed pressure gradient between both ventricles in early diastole.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Ventricular interdependence reflected in interventricular septal motion: with special reference to right ventricular pressure overload]. 653 99

The acute pulmonary and systemic haemodynamic response to low (0.15 mg/kg) and high (0.30 mg/kg) doses of intravenous hydralazine was evaluated in 26 consecutive patients with severe pulmonary hypertension due to cor pulmonale (nine patients), primary pulmonary hypertension (11 patients), or pulmonary embolism (six patients). Hydralazine did not cause a significant change in pulmonary arterial resistance or pressure in any group but produced a significant reduction in systemic resistance, which correlated with plasma concentration, and a significant increase in pulmonary blood flow index in all groups. Ten patients who experienced a reduction in pulmonary arterial resistance of at least 5 U X m2 after administration of hydralazine had higher initial values for pulmonary arterial resistance and systemic resistance and a lower pulmonary blood flow index than those who did not respond. Maintenance oral hydralazine treatment during nine to 36 months of follow up did not seem to affect symptoms or mortality. These results indicate that hydralazine has limited value in acutely reducing pulmonary arterial pressure or affecting clinical outcome in patients with pulmonary hypertension.
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PMID:Haemodynamic response to intravenous hydralazine in patients with pulmonary hypertension. 665

We describe a patient with massive pulmonary embolism and resultant acute cor pulmonale and severe tricuspid incompetence. Fine systolic tricuspid valve flutter was detected by echocardiography during the acute phase, but the flutter disappeared as the patient improved clinically and the signs of tricuspid incompetence were no longer observed. Systolic flutter of tricuspid valve may serve as a useful clue in treating patients with severe tricuspid incompetence due to acute cor pulmonale.
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PMID:Systolic flutter of the tricuspid valve associated with massive pulmonary embolism. 682 83

Five cases with recurrent pulmonary embolism (RPE), all having severe chronic cor pulmonale due to marked pulmonary hypertension, were reported. None of them had a history of thrombophlebitis of the legs. Dyspnea was the common symptom and signs of pulmonary hypertension were usual. Focal oligemia, cardiomegaly and plump pulmonary arteries on chest X-ray films, right axis deviation, clockwise rotation, ST-segment depression and T-wave inversion on electrocardiograms, and dilatations of the pulmonary arterial trunk, the right ventricle and the right atrium, and the posterior displacement of a small, compressed left ventricle on echocardiograms were the common findings. Gas exchange abnormalities were severe and they were considered the characteristic findings of this disease. Multiple perfusion defects were observed by a lung scan in all cases. Marked pulmonary hypertension with low cardiac output was the usual feature of RPE. Actual cutoffs or filling defects were demonstrated on a pulmonary angiogram. Deep vein of the legs were all intact and no thrombi were found. Pulmonary embolectomy was performed on one case. The importance of early diagnosis and early treatment of acute pulmonary embolism was emphasized for preventing the progress of this debilitating disease.
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PMID:Recurrent pulmonary embolism. 685 11

Seventy-six patients with various forms of pulmonary thromboembolic disease were followed-up for 1 to 15 years. All were free of other cardiopulmonary disease at the time of the first examination which was performed at least two months after the last pulmonary embolism. Catheterization was repeated in all survivors on average 4.8 years later. Severe chronic pulmonary hypertension (mean pulmonary artery pressure (PPA greater than 30 mm Hg) did not occur after a single episode of acute embolism, was infrequent after single subacute or recurrent emboli (8 of 9 patients), and was common after occult emboli (12 of 13 patients). Mortality in all clinical groups correlated with PPA and with the presence of right heart failure. In survivors, no correlation was found between the longterm changes of PPA and age, duration of disease, interval between catheterizations, PaO2, or cardiac output. Pulmonary hypertension progressed further in patients with initial PPA greater than 30 mm Hg. In contrast, none of the patients with normal or borderline PPA at the initial examination developed severe pulmonary hypertension during the follow-up. Since the future course of patients could be predicted from the first examination, repeated hemodynamic investigation proved to be of minor prognostic value.
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PMID:Longterm follow-up of patients with pulmonary thromboembolism. Late prognosis and evolution of hemodynamic and respiratory data. 705 79

The prevalence of abnormal pulmonary perfusion (Q) scans in persons without cardiopulmonary disease could condition the usefulness of the Q scan in the evaluation of patients in whom pulmonary embolism is suspected. In a recent study, we found that Q scan defects, particularly lobar or segmental defects, are rarely present in normal young nonsmokers. To determine if normal smokers of the same age group have a higher prevalence of Q defects, we performed 6 view Q scans in 40 subjects 18 to 29 yr of age who had no known active cardiopulmonary disease. Each subject had undergone a history, physical examination, electrocardiogram, spirometry, and posteroanterior chest roentgenogram prior to scanning. All Q scans were interpreted blindly and independently by 2 experienced readers. None of the 40 subjects was found to have an abnormal Q scan defined as the presence of a lobar, segmental, or subsegmental defect on 2 views. When these data were compared with our previous study, statistical analysis found no difference in the prevalence of abnormal Q scans in the 2 groups. We conclude that among young normal persons, abnormal Q scans are extremely uncommon and the prevalence of significant Q defects is not influenced by smoking.
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PMID:Patterns of pulmonary perfusion scans in normal subjects. 707 16


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