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

When shock complicates an acute increase in RV afterload, initial therapy should be directed toward restoration of an adequate BP (RV coronary perfusion pressure) and CO. Current results indicate that norepinephrine, a drug with direct inotropic and pressor effects, may be an excellent agent for acute resuscitation and short-term maintenance of hemodynamic stability when frank circulatory instability complicates pulmonary embolism. Following hemodynamic stabilization, thrombolytic therapy should be initiated. Recent evidence suggests that the lytic agent can be given by bolus technique, but more work is required to determine the optimum dosing regimen. In the absence of shock, when a moderate decrease in CO complicates pulmonary embolism, isoproterenol or hydralazine may be used to improve flow. However, both of these agents may decrease systemic vascular resistance and BP. Accordingly, the latter parameter should be carefully monitored to ensure that excessive falls in BP and RV coronary perfusion pressure do not occur. Whereas in certain conditions volume expansion is appropriate therapy to increase CO, in acute pulmonary hypertension with excessive RV afterload, volume expansion may worsen RV function. Recent canine studies indicate that an increase in vascular closing pressure is the predominant mechanism explaining the increase in PAP and apparent increase in PVR complicating pulmonary embolism. Accordingly, in addition to decreasing vascular resistance, therapy to decrease RV afterload could be directed toward decreasing the vascular response producing excessive closing pressures.
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PMID:Pathophysiology and therapy of right ventricular dysfunction due to pulmonary embolism. 353 3

The effect of the new positive inotropic and vasodilatator bipyridine-derivate Amrinon on catecholamine-refractive heart insufficiency in septic shock is described. A bolus dose of 1 mg/kg b.w., followed by continuous infusion of Amrinon 10 micrograms/kg b.w./min improved the haemodynamic parameters of all seven patients. The severe tachycardia before therapy was diminished more than 30%, the blood-pressure increased about 25-30%. RAP, PAP and PCWP showed a diminution of 35-45%. The cardiac output increased nearly 100% under therapy. All patients had IPPV with high inspiratory oxygen concentration, with inversed-ratio-ventilation and high positive end-expiratory pressure. Under Amrinon-therapy the initial pulmonary insufficiency diminished. The oliguria/anuria existing before Amrinon-therapy was improved also. Amrinon was given over 24-36 hours, the total dose was between 800 and 1440 mg. Six of the seven patients survived their severe illness; one patient died of pulmonary embolism, confirmed by autopsy, four weeks after Amrinon-therapy.
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PMID:[Amrinone in catecholamine refractory heart failure in septic shock]. 409 58

Vasodilators including isoproterenol, nitroprusside, nitroglycerin, and oxygen were administered to 5 patients with chronic pulmonary hypertension secondary to pulmonary embolism. The patients' mean pulmonary artery pressure was 54 +/- 8 mmHg, and their average total pulmonary resistance (TRP) was 17 +/- 11 mmHg/L/min. Each patient experienced a decrease in TRP in response to at least 1 of the vasodilators, and the mean maximal decrease was to 57 +/- 10% of the baseline value. Although these decrements in TRP were accompanied by an increase in cardiac output in all but 1 patient, changes in PAP were variable. Treatment with nitroglycerin was continued in 3 of the 5 patients and all 3 have reported improvement in their exercise tolerance. We conclude that the elevated TPR seen in patients with chronic embolic pulmonary hypertension is due to increased vascular tone in addition to fixed vascular obstruction.
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PMID:Partial reversibility of chronic pulmonary hypertension caused by pulmonary thromboembolic disease. 678 32

The authors describe a rare case of pulmonary thromboembolism with unusual clinical findings and emphasized the large difficulty encountered in formuling a correct diagnosis in a reasonable time. A man, 60 years old, was admitted to a Medical Division of our hospital for the appearance of chest pain and epigastric pain during effort in the last year. He smoked 20 cigarettes a day and drank wine (1 or 2 litres a day). He was affected by hypercholesterolemia and in the past reported relapsed thrombophlebitis in the left leg. Four years before admission to our hospital he underwent large and small left saphenectomy. He had no cardiac events in the past. After a non significant exercise stress test the patient was treated with nitrates and asa and was discharged from the hospital. At home the symptoms increased and after 8 months the patient was admitted again to the Cardiologic Division of the hospital. At admission he reported dyspnea and chest pain at rest, not only during effort and the ECG showed negative T waves in anterior and inferior leads. Intravenous heparine, nitrates and calcium antagonists stabilized the clinical picture. The following examinations revealed: reduction of the T wave negativity at the ECG registered during chest pain; mild enlargement of the heart at the chest roentgenogram; normal value of the left ventricle and apical and midseptal by ipokinesia at the transthoracic echocardiogram; normal coronary artery at the coronary arteriography. "Vasospastic angina" was diagnosed and the patient was discharged after 20 days, asymptomatic. After 15 days he returned to the hospital again for chest pain, dyspnea, hypotension and syncope despite therapy. At physical examination he showed a painful left tibio-tarsal tumefaction, an increased and splitting second heart sound in the pulmonary area and a systolic murmur in the third and fourth left interspace. The ECG showed a severe anterior ischemia, while a new transthoracic echocardiogram revealed a considerable dilatation of the right atrium, right ventricle and the main pulmonary artery with severe tricuspid regurgitation and pulmonary hypertension (mean PAP about 50 mmHg). The following pulmonary perfusion scintigraphy confirmed the diagnosis of pulmonary embolism and the selective right and left pulmonary arteriography exhibited multiple thrombi and large intravascular filling defects. The right heart catheterization confirmed a chronic precapillary pulmonary hypertension (mean PAP = 55 mmHg). About 24 hours after these examinations the patient died because of a cardiac arrest with electromechanical dissociation. Pulmonary thromboembolism is a potentially fatal disease characterized by a largely variable clinical presentation. Frequently pulmonary embolism diagnosis is difficult especially when clinical findings are unusual. In the case observed the "typical" chest and epigastric pains associated with the electrocardiographic findings directed diagnosis towards myocardial ischemia. Also after the coronary arteriography that showed normal coronary artery, the erroneous diagnosis persisted. Pulmonary embolism was correctly diagnosed too late to begin an effective therapy. These unusual clinical findings and diagnostic mistakes are stressed and critically reviewed in the article.
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PMID:[Pulmonary thromboembolism. A clinical case with unusual presentation]. 871 Jan 39

The PAP/PEA (Prevalence of Early Atherosclerosis) study aims to define the prevalence of subclinical atherosclerosis in a typical population of central Italy. A concomitant study evaluates the prevalence of venous diseases. The first group of 850 patients evaluated, indicated the prevalence of superficial ve-nous disease, the prevalence of deep venous thrombosis and pulmonary embolism and the prevalence of the most common venous malformations. Also the costs of venous problems was considered. In conclusion some 12% of the evaluated population sample (male population 46%) had or had been affected in the past by a venous problem and 50% of them had been under some form of treatment.
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PMID:[Prevalence of venous diseases. The San Valentino screening and prevalence study]. 927 70

A 48-years old man complained of dyspnea and was admitted to the hospital. Chest enhanced CT confirmed the presence of the thrombus in the pulmonary artery. Cardiac catheterization showed severe pulmonary hypertension (mean PAP 75 mmHg). ATIII level, protein C and S antigen were within normal range. Anticardiolipin antibody and lupus anti-coagulant determination were negative. He was diagnosed as chronic pulmonary thromboembolism, and underwent pulmonary thromboendarterectomy via median sternotomy under deep hypothermic intermittent circulatory arrest. At the same time IVC filter was inserted. The origin of the thrombus was not detected before operation, but after surgery, MR angiography of total body showed a cavernous hemangioma at left lower limb. We speculated this lesion was the origin of pulmonary embolism.
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PMID:[Surgical treatment of chronic pulmonary thromboembolism caused by a cavernous hemangioma at the lower limb]. 1159 38

MODALITIES FOR THE DIAGNOSIS OF VENOUS THROMBOEMBOLISM: Currently rely on the confrontation of the initial clinical data and the results of D-dimer measurements, a venous Doppler, although reliable, is not a first-line exploration. REGARDING TREATMENT: Indications for thrombolysis are currently limited to massive pulmonary oedema with shock. Alteplase added to heparin improves the progression of severe embolism; it spares the patients from heavy interventions of resuscitation but the mortality remains the same. Concerning anticoagulant treatments, prolonged antivitamin K at classical doses is more effective than low doses and for limited duration if phlebitis is an idiopathic one. FOR HEART FAILURE WITH PRESERVED EJECTION FRACTION: Treatment of these heart failures, formerly know as 'diastolic' is similar to that of the acute phase of systolic heart failure. However, care should be taken with vasodilatators. CONCERNING HEART FAILURE IN GENERAL: The brain natriuretic peptide (BNP) represents a remarkable progress for the aetiological diagnosis of dyspnoea (inferior to 80 pg/ml in the case of pulmonary origin, superior to 300 pg/ml in the case of cardiac origin or severe pulmonary embolism). Regarding treatment, for acute heart failure, it is still the association of nitrates and diuretics, with oxygen therapy and eventually inotropics. Beta-blockers, which have revolutionized the treatment of chronic heart failure, must be maintained whenever possible in the case of the onset of acute pulmonary oedema. Multisite pacing is increasingly used in refractory chronic heart failure. Implantable defibrillation has become common practice. Non-invasive ventilation (Bi or C-PAP) is interesting in acute cardiogenic pulmonary oedema. THE PREVENTIVE ROLE OF N ACETYL-CYSTEINE: N acetyl cysteine reduces the incidence of nephropathies induced by the radio contrast products in patients with chronic kidney failure. Combined with hydratation, it must be proposed the day before and on the day of the procedure in any patient with diabetes or kidney failure.
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PMID:[Diagnostic and therapeutic progress. Venous thromboembolism, cardiac insufficiency and radio contrast agents]. 1522 98

Alteplase is standard therapy for patients with acute, massive pulmonary embolism. The novel plasminogen activator desmoteplase displays high fibrin specificity and selectivity for fibrinbound plasminogen. In a preclinical model desmoteplase was twice as potent with a shorter lysis time and lower reocclusion rate. We conducted a phase II study comparing 125, 180, and 250 microg/kg bodyweight desmoteplase with 100 mg alteplase. Efficacy criteria were total pulmonary resistance (TPR), mean pulmonary artery pressure (mPAP), and Miller Index. Intention to treat analysis of 34 patients. The reduction of TPR after 24 hours was comparable between desmoteplase 180 microg/kg and alteplase (-48.0 +/- 22.4 vs. -50.4 +/- 16.3%; p = n.s. vs. alteplase; p = 0.0002 and p<0.0001 vs. baseline). The greatest effect was achieved with desmoteplase 250 microg/kg (-56.0 +/- 29.4%; p = n.s. vs. alteplase, p = 0.0055 vs. baseline). Two hours after treatment PAP was reduced by 27.9 (p = 0.0004 vs. baseline) and 30.4% (p = 0.015 vs. baseline) with the higher doses of desmoteplase and 29.6% with alteplase (p = 0.0006 vs. baseline). Further PAP reduction after 6 hours was most pronounced in the desmoteplase 250 microg/kg group (-40.1 +/- 18.0%; p = 0.0028 vs. baseline). The reduction of the Miller Index was greatest using desmoteplase 250 microg/kg (-35.0 +/- 21.7%; p = 0.011 vs. baseline), and alteplase (-41.6 +/- 27.2%; p = 0.0003 vs. baseline). Safety did not differ among the 4 groups. The study results suggest that desmoteplase at doses of 180 and 250 microg/kg had similar or greater efficacy compared to alteplase 100 mg. Onset of action was faster, safety was comparable.
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PMID:Desmoteplase in acute massive pulmonary thromboembolism. 1927 20