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

Nifedipine is a calcium antagonistic drug which reduces elevated vascular resistances. The hemodynamic effects of 20 mg of sublingual nifedipine were studied in 10 patients with chronic pulmonary hypertension. The etiology of pulmonary hypertension was chronic lung disease in 4, congenital heart disease in 2, mitral stenosis in 1, recurrent pulmonary embolism in 2 and primary pulmonary hypertension in one case. 30' after the drug administration there was a fall both of total pulmonary vascular resistance (from 992 +/- 586 to 648 +/- 428 d s cm-5, p less than 0.02) and of systemic vascular resistance (from 1416 +/- 868 to 896 +/- 440 d s cm-5 p less than 0.02) with an increase of systemic cardiac index from 3.2 +/- 1 to 4.5 +/- 2 l/min/m'2 (p less than 0.02). No significant change in systemic arterial oxygen saturation was noted, while pulmonary arterial oxygen saturation increased from 56 +/- 16 to 62 +/- 13% (p less than 0.01). These hemodynamic changes persisted for 120' when a significant fall of mean pulmonary arterial pressure was also noted (from 59 +/- 11 to 52 +/- 9 mm Hg, p less than 0.02). These data indicate that nifedipine may be useful to reduce pulmonary resistance in pulmonary hypertension. However this effect was less pronounced in patients with chronic lung disease compared to the other cases. It is suggested that the type of pulmonary arterial changes may determine the hemodynamic response. Nifedipine may be particularly indicated when vasoconstriction (as in primary pulmonary hypertension) is the main determinant of pulmonary hypertension.
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PMID:Hemodynamic effects of nifedipine in pulmonary hypertension. 716 46

31 patients suspect for acute pulmonary emboli were studied by measuring arterial PO2 (room air) and right to left shunt (100% oxygen breathing) to determine if measurement of the right to left shunt aided in the diagnosis of pulmonary embolism. Ventilation/perfusion or serial perfusion lung scans were performed on each patient. All patients exhibited arterial hypoxemia (PaO2 less than or equal to 80) and 27 had a shunt greater than 7%. The shunt was 15.1 +/- 3.6% in 9 patients with lung scans highly suggestive of emboli. 20 patients with lung scans of low probability for emboli had significantly less shunting averaging 10.9 +/- 3.7%. 5 patients of the latter group had shunts averaging 15.2 +/- 3.8% attributable to occult pneumonia not initially apparent. An increased right to left shunt fraction is not diagnostic of pulmonary emboli, but a normal one makes the diagnosis unlikely.
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PMID:Right to left shunt measurement in patients suspect for pulmonary embolism. 728 Mar 71

In an investigation on deep venous thrombosis and pulmonary embolism, where neither dextran nor antithrombotic drug prophylaxis were employed, 30 patients undergoing total hip replacement were randomly allotted to one of two groups receiving either epidural or general anaesthesia. The epidural group (n = 15) was given 0.5% bupivacaine with epinephrine (5 micrograms/ml) and this was prolonged into the postoperative period for pain relief. The general anaesthesia group (n = 15) was operated on under artificial ventilation with nitrous oxide/oxygen via an endotracheal tube and intravenously administered fentanyl and pancuronium bromide. In this group of patients narcotic analgesics (ketobemidone) were given intramuscularly on demand for pain relief postoperatively. The frequency of deep venous thrombosis involving the femoral veins, as observed at phlebography, was significantly lower in patients receiving continuous epidural block (3 of 15; 20%), than in those receiving general anaesthesia and parenteral analgesics postoperatively (11 of 15; 73%). Further, the frequency of pulmonary embolism, as determined by pulmonary perfusion lung scanning, was lower in patients receiving continuous epidural block (2 of 15) than in the general anaesthesia group (7 of 15). Possible explanations for these findings are discussed, including a hyperkinetic lower limb blood flow and lower fibrinolysis inhibition activity in patients given epidural block. Lower blood transfusion requirements in patients given epidural block might also play a role, as well as a "stabilizing" effect of local anaesthetics on platelets, leukocytes and endothelial cells.
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PMID:Comparative influences of epidural and general anaesthesia on deep venous thrombosis and pulmonary embolism after total hip replacement. 732 41

The activation of the clotting cascade leading to deep venous thrombosis begins during total hip arthroplasty, but few studies have assessed changes in coagulation during surgery. A better understanding of thrombogenesis during total hip arthroplasty may provide a more rational basis for treatment. In 3 separate studies, the following observations were made. Circulating indices of thrombosis and fibrinolysis: prothrombin F1.2, thrombin-antithrombin complexes, fibrinopeptide A, and D-dimer, did not increase during osteotomy of the neck of the femur or during insertion of the acetabular component, but rose significantly during insertion of the femoral component. Thrombin-antithrombin complexes, fibrinopeptide A, and D-dimer were higher after insertion of a cemented component than insertion of a noncemented femoral component. A significant decline in central venous oxygen tension was observed after relocation of the hip joint and after insertions of cemented and noncemented femoral components, providing evidence of femoral venous occlusion during insertion of the femoral component. In patients receiving a cemented femoral component, mean pulmonary artery pressure increased after relocation of the hip joint, indicating intraoperative pulmonary embolism. No changes in mean pulmonary artery pressure were noted with noncemented total hip arthroplasty. Administration of 1000 units of unfractionated heparin before insertion of a cemented femoral component blunted the rise of fibrinopeptide A. The results of these studies suggest that (1) the greatest risk of activation of the clotting cascade during total hip arthroplasty occurs during insertion of the femoral component; (2) femoral venous occlusion and use of cemented components are factors in thrombogenesis during total hip arthroplasty; and (3) measures to prevent deep venous thrombosis during total hip arthroplasty (such as intraoperative anticoagulation) should begin during surgery rather than during the postoperative period and be applied during insertion of the femoral component.
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PMID:The John Charnley Award. Thrombogenesis during total hip arthroplasty. 755 26

A 54-year-old man was hospitalized for a right renal tumor with intraluminal extension into the vena cava. He underwent radical nephrectomy with thrombectomy and regional lymphadenectomy. On the 8th postoperative day, he suddenly complained of dyspnea with tachypnea and cyanosis. Arterial blood gas analyses under an oxygen flow of 4L/min revealed PaO2 32.1 mmHg. Pulmonary angiography revealed filling defects in the right main pulmonary artery and left descending branch. Under the diagnosis of acute pulmonary embolism, thrombolytic and anti-coagulation therapy was performed and the patient recovered from the disease. We should be aware of pulmonary embolism as a postoperative complication of urological surgery.
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PMID:[Acute pulmonary embolism after radical operation for renal cell carcinoma with vena caval extension: a case cured by thrombolytic therapy]. 759 38

Mechanisms of hypoxemia and hypocapnia in pulmonary embolism (PE) are incompletely understood. We studied 10 patients at diagnosis (D) and five of these again after 10 to 14 d of heparin treatment (T). Patients had right heart catheterization, assessment of ventilation-perfusion ratio (VA/Q) distribution by inert gas, radioisotopic perfusion and ventilation scans, and angiography. At D, two-thirds of the pulmonary circulation was obstructed, patients were hypoxemic (PaO2 = 63.0 +/- 11.7 mm Hg) and hypocapnic (PaCO2 = 30.0 +/- 4.1 mm Hg), mixed venous oxygen pressure (PvO2) was reduced (30.9 +/- 3.9 mm Hg), minute ventilation (VE) markedly increased (14.1 +/- 5.1 L/min), and cardiac output measured by applying the Fick principle to arteriovenous oxygen content difference (QT) slightly low (4.7 +/- 1.7 L/min). Hypoxemia was mainly explained by VA/Q inequality, reduced PvO2 also contributed. Hypocapnia was the result of hyperventilation. VA/Q inequality was characterized by shift of VA and Q distribution mean to regions with higher VA/Q ratio through a fraction of blood flow (19.0 +/- 24.3% of cardiac output) went to lung units with low VA/Q ratio. Log SDQ and log SDvA were increased. Shunt, diffusion limitation, or true alveolar dead space occurred in occasional patients but were generally insignificant. Regional ventilation and perfusion maps indicated that in the unperfused lung segments, ventilation was reduced. Furthermore, they disclosed overperfused lung segments. At T, hypoxemia and hypocapnia improved considerably. However, temporal imbalances in recovery between regional ventilation and perfusion occurred with the former normalizing sooner. However, perfusion recovered sooner than ventilation in some regions.
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PMID:Mechanisms of hypoxemia and hypocapnia in pulmonary embolism. 759 43

12 patients with pulmonary hypertension, primary pulmonary hypertension 3, secondary to recurrent pulmonary embolism 4, chronic obstructive pulmonary disease 2, and complicated with congenital heart disease 3, inhaled nitric oxide (NO). The NO concentration was adjusted in the range between 20-160 ppm to get a maximum hemodynamic effects. On inhaling NO, pulmonary artery pressure decreased in all patients. The maximum hemodynamic effects showed that pulmonary systolic, diastolic and mean artery pressure dropped by 22.9%, 21.0% and 20.3% (P < 0.001) respectively. Total pulmonary resistance decreased by 32.7% (P < 0.01). Cardiac index and oxygen delivery increased by 33.2% and 24.8% (P < 0.01) respectively. The ratio of pulmonary systolic artery pressure and systemic systolic artery pressure changed from the baseline 0.73 to 0.54. It is indicated that NO dilated pulmonary artery selectively in patients with hyperkinetic, obliterative and hypoxic pulmonary hypertension.
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PMID:[Hemodynamic effects of inhaled nitric oxide in patients with pulmonary hypertension]. 765 63

Patients with acute pulmonary embolism are at risk for early death or chronic morbidity. Appropriate therapy can dramatically reduce the incidence of both. Oxygen and heparin therapy should be started as soon as the diagnosis is suspected. The condition of a hypotensive patient with right ventricular overload from acute pulmonary embolism usually is made worse by a fluid challenge; hypotension may be relieved by preload reduction or even by gentle diuresis. Norepinephrine (Levophed), isoproterenol hydrochloride (Isuprel), and epinephrine are the pressor agents of choice. Immediate thrombolysis is the standard of care for any patient with significant hypoxemia or hypotension due to proven pulmonary embolism. Beyond this, the potential benefit of using thrombolytic agents should be considered routinely for every patient with proven pulmonary embolism. Surgical embolectomy is useful for unstable pulmonary embolism when there are absolute contraindications to thrombolysis or when thrombolytic therapy fails. Empirical use of thrombolysis may be considered as a last-ditch effort for a critically ill patient when there is a high clinical suspicion of pulmonary embolism. Standard closed-chest cardiopulmonary resuscitation is ineffective when the pulmonary circulation is obstructed by thrombus. Emergency thoracotomy or femorofemoral cardiopulmonary bypass is appropriately used in patients with full cardiac arrest from pulmonary embolism.
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PMID:Acute pulmonary embolism. Aggressive therapy with anticoagulants and thrombolytics. 781 17

In this review, the second of a two part series, the analytic techniques introduced in the first part are applied to a broad range of pulmonary pathophysiologic conditions. The contributions of hypoxic pulmonary vasoconstriction to both homeostasis and pathophysiology are quantitated for atelectasis, pneumonia, sepsis, pulmonary embolism, chronic obstructive pulmonary disease and adult respiratory distress syndrome. For each disease state the influence of principle variables, including inspired oxygen concentration, cardiac output and severity of pathology are explored and the actions of selected drugs including inhaled nitric oxide and infused vasodilators are illustrated. It is concluded that hypoxic pulmonary vasoconstriction is often a critical determinant of hypoxemia and/or pulmonary hypertension. Furthermore this analysis demonstrates the value of computer simulation to reveal which of the many variables are most responsible for pathophysiologic results.
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PMID:Role of hypoxic pulmonary vasoconstriction in pulmonary gas exchange and blood flow distribution. 2. Pathophysiology. 793 36

Ischemia/reperfusion mechanisms contribute to lung injury after transplantation, pulmonary embolism, and resolution of atelectasis. Alveolar tissue becomes hypoxic and deprived of substrate only when both ventilation and perfusion are interrupted, a situation modeled in vivo by complete, unilateral lung collapse. Because previously hypoxic mitochondria may be an important intracellular source of superoxide and hydrogen peroxide (H2O2) during reperfusion and re-oxygenation, the authors, in this study, investigated whether mitochondrial H2O2 release changed as a result of lung hypoxia/hypoperfusion resulting from collapse. Mitochondria were isolated from hypoxic (previously collapsed) right or contralateral left rabbits' lungs and from control rabbits' lungs. Mitochondrial H2O2 release, a marker of superoxide production, was measured fluorometrically after incubation with or without 1 mmol/L cyanide and 0.1 mmol/L nicotinamide adenine dinucleotide. Mitochondrial recovery was determined by assaying succinate dehydrogenase activity in mitochondrial preparations and lung homogenates. Lung succinate dehydrogenase activity and mitochondrial recovery were comparable among groups. Calculated lung mitochondrial content did not change (control subjects: left 7.9 +/- 0.5, right 13.8 +/- 1.7; hypoxic: left 10.3 +/- 1.3, right 10.5 +/- 2.4, all mg mitochondrial protein/lung). Mitochondria released hydrogen peroxide at approximately 5.6 nmol/h/mg pro in buffer alone and 14.8 nmol/h/mg pro in buffer with cyanide and nicotinamide adenine dinucleotide. However, lung collapse and resulting hypoxia caused no change in mitochondrial number or capacity to release H2O2 in vitro. Based on these findings, it is suggested that other sources of reactive oxygen metabolites, including xanthine oxidase and activated neutrophils, contribute to the oxidant injury observed in this model.
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PMID:Hydrogen peroxide release by mitochondria from normal and hypoxic lungs. 794 83


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