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

Right heart thrombosis (RHT) was found by 2D-echocardiography in 8 cases. Clinical suspicion of RHT could be documented in only 3 patients, while in the other 5 cases syncope, low output syndrome, essential pulmonary hypertension, cerebral embolism or congestive heart failure was the clinical diagnosis on first presentation. Out of the 4 cases of mobile RHT of extracardiac origin 1 patient had an emergency operation, 2 patients died shortly after the 2D-echo diagnosis before treatment could have been started and 1 patient improved on anticoagulant treatment. RHT of intracardiac origin was due to a central line or a ventriculoatrial shunt in 3 cases and no source could be found in 1 patient. Complete recovery was achieved in 2 cases by medical, in one case by surgical management and in 1 patient medical and surgical treatment resulted in clinical improvement. In conclusion authors 1. consider 2D echocardiography necessary in the clinical setting of acute or chronic pulmonary embolism or "primary" pulmonary hypertension and 2. they recommend emergency operation in case of mobile large RHT detected by 2D-echocardiography.
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PMID:[Diagnosis and treatment of thromboembolic diseases of the right heart]. 221 28

1. The limited therapeutic role of pulmonary vasodilation reflects lack of their selectivity for the pulmonary vasculature, and many drugs have been evaluated for effectiveness; however, none has gained widespread clinical use. 2. Milrinone (MIL) is a newly synthetized phosphodiesterase inhibitor, which has potent positive inotropic and vasodilatory effects. 3. The present study shows the effects of MIL on the pulmonary circulation in dogs with pulmonary hypertension due to autologous muscle-induced pulmonary embolism, and also demonstrates a comparison with those of dopamine and dobutamine. 4. As MIL showed potent vasodilatory effects on the pulmonary vasculature, it had a potential clinical role in the treatment of pulmonary hypertension.
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PMID:Vasodilatory effects of milrinone on pulmonary vasculature in dogs with pulmonary hypertension due to pulmonary embolism: a comparison with those of dopamine and dobutamine. 227 26

The prognosis of pulmonary embolism depends chiefly on three conditions, the amount of pulmonary arterial obstruction, the cardio-pulmonary state and tolerance and haemostatic factors. Whereas a single, even massive pulmonary embolism as a rule does not lead to chronic morbidity, repeated though minor emboli may be followed by pulmonary hypertension with eventual right heart failure so that the long term prognosis rests upon the probability of further thrombotic events.
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PMID:[Life expectancy after lung embolism]. 229 Dec 70

Pulmonary vascular tone was investigated by the construction of pulmonary arterial pressure (PAP)/cardiac output (Q) plots, and gas exchange, by the multiple inert gas elimination technique, in 24 anesthetized dogs before and after pulmonary embolization of autologous clots. Three PAP/Q plots were obtained by a manipulation of venous return at baseline and 60 min and 110 min after embolization. Before the third PAP/Q plot, the dogs were randomly allocated to one of the following iv treatments: 1) placebo (n = 6); 2) prostaglandin E1 (PGE1) 0.4 microgram.kg-1.min-1 (n = 6); 3) hydralazine 2 mg/kg (n = 6); and 4) nitroprusside 10 microgram.kg-1.min-1 (n = 6). These vasodilators decreased systemic arterial pressure by a mean of 44%. Ventilation-perfusion (VA/Q) distributions were determined at the same Q (2.4 +/- 0.1 l.min-1.m-2, mean +/- SE) of each PAP/Q plot. Embolization increased the intercept and the slope of the PAP/Q plots (P less than 0.001). Distributions of VA/Q were only moderately impaired, with an increased dispersion of both VA and Q and a shift of VA distributions to higher VA/Q. PaO2 changed from 208 +/- 5 to 172 +/- 8 mmHg (P less than 0.01) (fraction of inspired O2 was 0.4). None of the treatments had any effect on VA/Q distributions. Placebo and PGE1 had no effect on PAP/Q plots. Hydralazine and nitroprusside reduced the slope of the PAP/Q plots. Thus, in this canine model of acute pulmonary embolism: 1) VA/Q distributions were moderately impaired accounting for only slight hypoxemia, and 2) pulmonary hypertension was partially reversible by hydralazine and by nitroprusside without associated non-flow-dependent change in VA/Q distributions and arterial oxygenation.
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PMID:Effects of vasodilators on gas exchange in acute canine embolic pulmonary hypertension. 229 36

Pulmonary thromboendarterectomy is being performed with increasing frequency for incapacitating pulmonary hypertension caused by chronic large-vessel pulmonary embolism. However, patient-related risk factors and procedural complications associated with morbidity and mortality have not been fully defined. From Oct. 1, 1984, to April 10, 1989, we performed pulmonary thromboendarterectomy using deep hypothermia and circulatory arrest in 127 consecutive patients (62.2% male, mean age 50 +/- 16 [standard deviation], range 20 to 82 years) in whom the exposure and dissection of the pulmonary arteries and methods for myocardial protection have been standardized. End points for univariate and multivariate analyses of risk factors were reperfusion pulmonary edema leading to respiratory insufficiency as defined by ventilator dependency (greater than or equal to 5 days) (31.5%, 39/124) and hospital mortality (12.6%, 16/127). Multivariate analyses showed that ascites and need for 4 units of blood or more predicted ventilator dependency (p less than 0.03). Increased cardiopulmonary bypass times predicted both end points (p less than 0.03 to less than 0.0001), and failure to achieve at least a 50% reduction in pulmonary vascular resistance strongly predicted hospital death (p less than 0.0001). However, other factors that exhibited trends for association with one of the end points may prove important with a larger sample size. A hospital mortality rate of 12.6% for pulmonary thromboendarterectomy is acceptable when compared with approximately 25% for heart-lung transplantation, which is the only therapeutic alternative. Increased ventilator dependency and hospital mortality can be anticipated with longer cardiopulmonary bypass times and inadequate reduction of pulmonary vascular resistance.
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PMID:Risk factors for pulmonary thromboendarterectomy. 231 89

Some patients with chronic pulmonary embolism causing severely symptomatic pulmonary hypertension have been managed by heart-lung transplantation with an associated hospital mortality of 24%. To allow comparison with pulmonary thromboendarterectomy (PTE), we have reviewed the hospital morbidity and mortality in 149 consecutive patients. From 1 October 1984 to 18 September 1989, these patients underwent PTE utilizing a standardized procedure consisting of median sternotomy, cardiopulmonary bypass, deep hypothermia and circulatory arrest for bilateral PTE in 91% (136/149) of the procedures with 7.4% (11/149) and 1.3% (2/149) undergoing right or left PTE, respectively. Ventilator dependency (greater than or equal to 5 days on respirator) occurred in 28.3% (41/146). Hospital mortality (death within 30 days or in hospital) was 11.4% (17/149). The most common causes of death were respiratory and multiorgan failure, 10 (59% of deaths) and acute pulmonary hemorrhage, 3 (17% of deaths). We conclude that PTE with an operative mortality of half that of heart-lung transplantation (11.4% vs. 24%) should be the procedure of choice for significantly symptomatic chronic pulmonary embolism. Furthermore, the hazards of immunosuppression and chronic graft rejection are avoided.
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PMID:Current early results of pulmonary thromboendarterectomy for chronic pulmonary embolism. 185 70

The author analyzes the natural course of acute pulmonary embolism and its progression. Treated acute pulmonary embolism has a favourable long-term prognosis which is negatively influenced only by further diseases. While acute pulmonary embolism is the third most frequent cardiovascular disease--the incidence of chronic thromboembolic pulmonary hypertension is very rare and accounts only for 0.38% in necroptic material.
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PMID:[The relation between acute embolism and thromboembolic pulmonary hypertension]. 237 82

The patient was a 29-year-old woman. She was well until autumn 1983, when she presented with polyarthralgia, fever above 39 degrees C, hepatosplenomegaly, swelling of lymphnode and salmon pink rash. Laboratory tests revealed marked leucocytosis with shift to the left, elevated ESR, strong positivity of CRP and abnormal liver function tests. However, anti-nuclear antibody and RA factor were negative. She was diagnosed as adult onset Still's disease (AOSD) by characteristic clinical course and laboratory data. During her disease course these abnormal findings could be well controlled neither by nonsteroidal anti-inflammatory drugs, immunosuppressive agents nor corticosteroids. Two and half years after the first admission, she began to complain of dry cough, dyspnea on efforts. Auscultation revealed an increased pulmonic sound and systolic murmur of cardiac apex. Chest X-Rays showed enlarged main pulmonary arteries. The lung fields were normal. Pulmonary function tests gave no evidence of a significant obstructive or restrictive defect but showed the low DLco and hypoxemia. Ventilation-perfusion lung scanning failed to reveal pulmonary embolism. Finally, right heart catheterization confirmed the pulmonary precapillary hypertension. Her pulmonary hypertension has progressed rapidly, strongly suggesting poor prognosis. Her pulmonary hypertension associated with no apparent parenchymal involvement was thought to be caused by a pulmonary vascular change probably related to AOSD. This case is a first case of AOSD with pulmonary hypertension.
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PMID:[A case of adult Still's disease with pulmonary hypertension]. 237 40

Pulmonary embolism may cause pulmonary hypertension by mechanical obstruction, which might be amplified by vasoconstriction induced by serotonin released from the emboli. The purpose of the present study was to examine whether 5-HT2-receptors are involved in serotonin-induced pulmonary hypertension. Ketanserin was used as 5-HT2-serotonergic antagonist. In nine anesthetized mongrel dogs, the effect of serotonin infusions (10, 50, 100 micrograms/kg . min) on mean pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), cardiac output (CO), stroke volume (SV), cardiac contractility (dP/dtmax), heart rate (HR), and mean aortic pressure (PAO) was studied with and without treatment by ketanserin (20 and 100 micrograms/kg). Serotonin caused dose-dependent increase in PAP, PVR, CO, SV, and dP/dtmax. A dose of 20 micrograms/kg ketanserin did not affect hemodynamics significantly, whereas 100 micrograms/kg of the compound significantly reduced PAO, TPR, and left ventricular dP/dtmax. The serotonin-induced increases in PAP, PVR, dP/dtmax, CO, and SV were reduced significantly by 100 micrograms/kg ketanserin; the lower dose of ketanserin had only a slight blocking effect. Ketanserin blocks serotonin-induced pulmonary vasoconstriction partly, but it seems also to antagonize the positive inotropic effect of the monoamine.
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PMID:Effects of serotonin on the cardiopulmonary circulatory system with and without 5-HT2-receptor blockade by ketanserin. 241 62

The therapeutic regimen in acute pulmonary embolism of different severity is discussed. Heparin is indicated in patients with only small and submassive embolism without impairment of the circulation. Fibrinolysis is the therapy of choice in submassive pulmonary embolism with circulatory insufficiency and massive embolism. In fulminant embolism with circulatory shock or cardiac arrest embolectomy should be performed. If the course of lung embolism is subacute, fibrinolysis may improve the late prognosis in respect to chronic pulmonary hypertension.
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PMID:[Therapy of pulmonary embolism]. 242 13


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