Pulmonary angiography in the diagnosis of pulmonary embolism

In patients in whom there is clinical suspicion of pulmonary thromboembolic disease, because of the risk of inadequate treatment, definitive radiologic evaluation should be carried out. Of the diagnostic procedures available, conventional pulmonary angiography has the greatest sensitivity and specificity in the detection of pulmonary embolism or other pulmonary vascular disease. Pulmonary angiography is indicated for patients with an indeterminate lung scan, for those with a high-probability lung scan in whom confirmation is necessary because of high risk for bleeding complications from anticoagulation, if embolism is massive and embolectomy is contemplated, if thrombolytic therapy or vena cava interruption is considered or if there is significant clinical evidence for an alternative diagnosis as well as for those with low-probability scans with a high degree of clinical suspicion and to complete a workup in patients with pulmonary hypertension. Refinements in the technique have simplified and expanded its application. The hemodynamic evaluation with right-heart catheterization before and after pulmonary angiography plays an important role in the choice of treatment of pulmonary embolism. In patients with multiple bilateral lobar or segmental perfusion defects, performance of right and left pulmonary arteriography in the right and left posterior oblique projections should be carried out. In the presence of additional pulmonary hypertension, the lung in which perfusion is most abnormal is selected first for angiography with a low bolus contrast dose. The angiographic criteria for the diagnosis of pulmonary embolism are intraluminal vascular filling defects or an abrupt cutoff of a large vessel. For selective opacification of lobar pulmonary branches occlusion pulmonary angiography is helpful. The mortality of pulmonary angiography in experienced centers is approximately 0.3%. Complications may include cardiac perforation in up to 1% and subendocardial injury in less than 0.2%. In patients with pulmonary embolism but no pulmonary hypertension, treatment with heparin for ten to 14 days should be followed by coumadin anticoagulation for at least three to six months. For obstruction of greater than or equal to 50% of the pulmonary vascular cross-sectional area and pulmonary hypertension thrombolytic therapy should be given and insertion of an inferior caval filter can be considered. In those with more than 75% pulmonary vascular obstruction and corresponding hemodynamic derangement, pulmonary artery embolectomy or thrombolytic therapy should be carried out.4     

Nitroglycerin-responsive pulmonary hypertension in idiopathic pulmonary hemosiderosis

Idiopathic pulmonary hemosiderosis (IPH) is an uncommon disease found predominantly in pediatric patients. It can produce severe chronic pulmonary injury that results in chronic hypoxemia, pulmonary insufficiency, and progressive pulmonary fibrosis, leading to irreversible pulmonary hypertension and death. We studied the pulmonary hemodynamics in an 9-yr-old boy with IPH to determine if pulmonary hypertension contributed to exacerbations of this disease. Our results showed that this patient demonstrated pulmonary hypertension during acute exacerbations. Initially, the elevated pulmonary artery pressure responded both to oxygen and to a pulmonary vasodilator in the form of nitroglycerin. However, this improvement was not sustained. We conclude that pulmonary hypertension is probably a result of chronic hypoxemia experienced by patients with pulmonary hemosiderosis. Further investigation is warranted to assess whether or not intervention aimed at reducing pulmonary artery pressure in IPH improves outcome.     

Pulmonary "capillary" wedge pressure not the pressure in the pulmonary capillaries

In 1949, Hellems, Haynes, and Dexter proposed that the pressure in a catheter wedged so as to occlude a pulmonary artery was an "estimate" of the pressure in the pulmonary capillaries. Their report led to the designation of this pulmonary artery wedge pressure as the pulmonary "capillary" wedge pressure. In fact, the pulmonary artery wedge pressure is a distorted measure of the pressure in the pulmonary veins. Usually this pressure differs only slightly from the capillary pressure, and the misconception fostered by the inaccurate name is inconsequential; however, sometimes this misconception leads to errors in diagnosis. This report briefly reviews the early history of pulmonary vascular catheterization, offers an explanation of pulmonary artery wedge pressure, and discusses a disease in which pulmonary artery wedge pressure is normal, even though capillary pressure is elevated.     

Pulmonary hypertension in systemic lupus erythematosus

Systemic lupus erythematosus is associated with several forms of pulmonary hypertension. It can cause pulmonary hypertension through pulmonary thromboembolic disease, left heart disease and lung disease as well as causing an isolated pulmonary vasculopathy called pulmonary arterial hypertension. The true prevalence of pulmonary arterial hypertension in patients with lupus is not known but probably is no more than 1%. Currently, treatment for lupus-associated pulmonary arterial hypertension is with pulmonary vasodilators including phosphodiesterase-5 inhibitors, endothelin receptor antagonists and prostacyclin analogues, as it is for other causes of pulmonary arterial hypertension. Case series suggest there may be a special role for immunosuppression in this rare group of patients. We present two brief case histories and summarise our experience over 15 years. Prognosis is better in lupus-associated pulmonary arterial hypertension than in systemic sclerosis-associated pulmonary arterial hypertension, but unfortunately it remains a fatal condition in most patients.     

A primary epithelioid hemangioendothelioma localized in the pulmonary valve

A case of epithelioid haemangioendothelioma sited at pulmonary valve, with an excrescence growing invading pulmonary artery troncus and its principal branches, in a 56-year-old woman is reported. The evolutive behavior simulated some clinical situations which made difficult the diagnosis: a mild-moderate pulmonary stenosis, a general syndrome, and, finally, an acute pulmonary thromboembolism that carried to an aggressive management which conducted to the entity diagnosis.     

High-altitude pulmonary edema is initially caused by an increase in capillary pressure

BACKGROUND: High-altitude pulmonary edema (HAPE) is characterized by severe pulmonary hypertension and bronchoalveolar lavage fluid changes indicative of inflammation. It is not known, however, whether the primary event is an increase in pressure or an increase in permeability of the pulmonary capillaries. METHODS AND RESULTS: We studied pulmonary hemodynamics, including capillary pressure determined by the occlusion method, and capillary permeability evaluated by the pulmonary transvascular escape of 67Ga-labeled transferrin, in 16 subjects with a previous HAPE and in 14 control subjects, first at low altitude (490 m) and then within the first 48 hours of ascent to a high-altitude laboratory (4559 m). The HAPE-susceptible subjects, compared with the control subjects, had an enhanced pulmonary vasoreactivity to inspiratory hypoxia at low altitude and higher mean pulmonary artery pressures (37 +/- 2 versus 26 +/- 1 mmHg, P<0.001) and pulmonary capillary pressures (19 +/- 1 versus 13 +/- 1 mmHg, P < 0.001) at high altitude. Nine of the susceptible subjects developed HAPE. All of them had a pulmonary capillary pressure >19 mm Hg (range 20 to 26 mmHg), whereas all 7 susceptible subjects without HAPE had a pulmonary capillary pressure < 19 mm Hg (range 14 to 18 mm Hg). The pulmonary transcapillary escape of radiolabeled transferrin increased slightly from low to high altitude in the HAPE-susceptible subjects but remained within the limits of normal and did not differ significantly from the control subjects. CONCLUSIONS: HAPE is initially caused by an increase in pulmonary capillary pressure.     

Effect of red cell volume reduction on pulmonary blood flow in polycythemia of cyanotic congenital heart disease

The acute effects of red cell volume reduction (erythropheresis) on pulmonary blood flow and pulmonary vascular resistance were measured in 16 patients with severe shunt-induced polycythemia. In subjects with D-transposition of the great arteries and no significant pulmonary stenosis (Group A) erythropheresis was associated with a decrease in pulmonary vascular resistance and an increase in pulmonary blood flow and in mixing between the systemic and pulmonary circulations. Systemic arterial saturation decreased slightly. By contrast, erythropheresis in patients with severe pulmonary stenosis or atresia and a ventricular septal defect (Group B) was associated with a decrease in pulmonary blood flow and left to right shunt and an increase in right to left shunt. These alterations resulted in a significant reduction in systemic arterial oxygen saturation despite relatively little change in effective pulmonary blood flow. The acute hemodynamic effects of packed red cell transfusion in five patients with D-transposition of the great arteries, no significant pulmonary stenosis and relative anemia were more variable.The observations in patients with shunt-induced polycythemia are probably related to a reduction in blood viscosity produced by a lowering of hematocrit concentration. The reduced viscosity decreases the impedance to flow in the systemic and pulmonary circulations. When pulmonary blood flow is largely derived from the systemic circuit, erythropheresis will diminish pulmonary flow and reduce systemic oxygen saturation. If the pulmonary blood flow is largely independent of the systemic circuit (as in D-transposition of the great arteries without pulmonary stenosis), an increase in total and effective pulmonary flow occurs.     

Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction

Acute massive pulmonary embolism has a high mortality rate. Fatal haemodynamic deterioration is caused by an acute increase in pulmonary vascular resistance. Traditionally, the degree of mechanical obstruction of the pulmonary vasculature by the embolic thrombus is considered to be the major determinant of this increase in right ventricular afterload. However, there is evidence to suggest that another factor plays an important role, since there is a marked discrepancy between the haemodynamic manifestations of acute pulmonary embolism and the degree of mechanical obstruction. Historic studies indicate that this discrepancy is largely explained by pulmonary vasoconstriction caused by vasoactive mediators, released mainly by activated platelets. Thromboxane-A(2) and serotonin are probably the two most important pulmonary vasoconstrictors in this context. Antagonising their effects dramatically increases tolerance to experimental pulmonary embolism in animals. In humans, this concept should eventually find its way into clinical practice. In the future, acute massive pulmonary embolism could be treated with antagonists to pulmonary vasoconstrictors, or with direct pulmonary vasodilators.     

Haemodynamics in patients with chronic post-embolic pulmonary hypertension

Haemodynamic studies were undertaken in 30 patients with chronic post-embolic pulmonary hypertension (CPEPH), and the findings were compared with those found in acute thromboembolism of the pulmonary artery. The study showed that radiocardiographic examination is a useful supplementary method for diagnosing postembolic lesions of pulmonary arteries and for dynamic examination of patients after pulmonary embolism. The appearance of a "single-hump" curve on the radiocardiogram was an unfavourable prognostic sign and attested both to an increase of pulmonary hypertension or to a latent heart failure. The importance of radiocardiographic examination for determining the prognosis of the disease and for choosing the most suitable method of its treatment is analysed.     

Pleural effusion in pulmonary embolism

An estimated 300,000 to 500,000 patients develop a pleural effusion secondary to pulmonary embolism each year in the United States. The pleural effusions due to pulmonary embolism are usually small. They occupy less than one third of the hemithorax in 90% and are frequently manifest only as blunting of the costophrenic angle. The pleural fluid with pulmonary embolism is almost always an exudate. When pulmonary embolism is considered a diagnostic possibility, the clinical probability of pulmonary embolism should be assessed. If the probability is low, measurement of D-dimers is useful. If the D-dimer test is negative, the diagnosis is virtually excluded. If the D-dimer test is positive or if there is a high clinical probability of pulmonary embolism, the best test to assess the possibility of pulmonary embolism is probably the computed tomographic angiogram (CTA). Patients who have a high probability of pulmonary embolism should be anticoagulated while the definitive test is being performed. The presence of a pleural effusion does not alter the standard treatment for pulmonary embolism. The two complications of pleural effusions in patients with pulmonary embolism are hemothorax and pleural infection. If the pleural effusion increases in size while a patient is being treated for pulmonary embolism, a diagnostic thoracentesis should be performed to rule out these complications.     

肺动脉支架应用现状和进展

肺动脉狭窄在复杂性先天性心脏病中较为常见,随着经皮介入治疗技术的发展,肺动脉支架置入成为肺动脉狭窄的有效治疗手段。在肺动脉狭窄、右室流出道狭窄、复杂先天性心脏病矫治术后外管道狭窄、体肺分流管道和侧支血管狭窄等病变中均显示了良好的效果。尽管现有肺动脉支架应用于先心病治疗中尚有一些固有缺陷,但是随着新型支架问世,在未来先天性心脏病治疗领域中肺动脉支架将有更为广阔的前景。     

Hemodynamics and gas exchange in acute lung embolism

The main hemodynamic consequence of pulmonary embolism is the acute mechanical reduction of the pulmonary vascular cross-sectional area. This results in a sudden increase of the pulmonary vascular resistance, and if the cardiac output is to be maintained, in an increase in pulmonary artery pressure and right ventricular work. The extent of hemodynamic changes in pulmonary embolism are determined primarily by the size of the emboli and whether or not the patient has underlying cardiopulmonary disease. Although humoral factors and neural reflexes play a role in determining the severity of hemodynamic responses to pulmonary embolism in experimental animals, their role in patients is uncertain. In patients free of preembolic cardiopulmonary disease, the extent of embolic obstruction can be related directly to the mean pulmonary artery pressure. Accordingly, either the extent of obstruction or the mean pulmonary artery pressure may be used as a measure of right ventricular afterload. Obstruction of 25 to 40% leads to an increase in mean pulmonary artery pressure of 20 to 30 mm Hg, massive obstruction over 75% to a pressure of 40 to 45 mm Hg. Continuous hemodynamic monitoring helps to estimate the speed of the resolution of emboli and to a certain extent the adequacy of treatment. Right arterial pressure is consistently elevated by a mean pulmonary artery pressure over 30 mm Hg and provides also a rough estimate of the degree of pulmonary vascular obstruction. A previously normal right ventricle will dilate at a mean pulmonary artery pressure of 40 to 45 mm Hg. which may result in acute tricuspid insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)     

Development of pulmonary aneurysm in primary pulmonary hypertension: a case report

Selected cases of severe primary pulmonary arterial hypertension and associated pulmonary vascular disease have been related to the oral ingestion of aminorex fumarate, an anorexigen obviously responsible for an epidemic of primary pulmonary hypertension in Western Europe between 1967 and 1970. This report describes a fifteen year follow-up of a female patient with aminorex fumarate related pulmonary hypertension and the uncommon finding of the formation of an excessive fusiform pulmonary trunk aneurysm in the late stage of the disease process. The progressive clinical course was followed by serial chest x-ray films and repeat right heart catheterization. The diagnosis of a main stem pulmonary artery aneurysm was noninvasively established by two-dimensional echocardiography and confirmed by contrast-enhanced computed tomography and radionuclide blood pool imaging. The patient is alive, thus no histologic correlate of this entity is available at present.     

An unexpected pulmonary arterial aneurysm in a COPD patient

We present a case of an idiopathic pulmonary artery aneurysm in an asymptomatic patient who was treated for an irrelevant medical condition. Pulmonary artery aneurysms (PAA) are quite rare and can either be congenital or acquired. Congenital aneurysms are usually associated with cardiac malformations leading to pulmonary hypertension. Acquired aneurysms can be idiopathic or associated with infections (tuberculosis, syphilis), trauma, pulmonary valvular stenosis, or collagen diseases. Pulmonary artery aneurysms are not common and an idiopathic pulmonary artery aneurysm is a rare finding that could be diagnosed incidentally.     

Treatment of saddle pulmonary embolism with streptokinase in an 83 year-old man - a case report

Saddle pulmonary embolism (PE) is an embolus at the level of the bifurcation of the pulmonary trunk that extends into both main pulmonary arteries. Because of the unstable, large clot burden in the pulmonary artery and the risk of sudden haemodynamic collapse and sudden death, identifying a saddle embolus is extremely important. In this report, we describe successful treatment with streptokinase of a saddle PE in an elderly patient.     

Right ventricular growth in a case of pulmonic stenosis with intact ventricular septum and hypoplastic right ventricle.

Adequate growth of the hypoplastic right ventricle in a patient with severe pulmonary stenosis with an intact ventricular septum was documented after pulmonary valvotomy in infancy. It is postulated that the growth of the ventricular chamber is largely the result of pulmonary regurgitation resulting from successful pulmonary valvotomy. Based on this and the observations of others on the growth of the hypoplastic right ventricle in pulmonary atresia (with intact septum) cases, an organized approach to eventual total surgical correction is recommended.     

Paradoxical pulmonary vasoconstriction induced by nitroglycerin in idiopathic pulmonary hypertension

Administration of intravenous nitroglycerin in a patient with idiopathic pulmonary hypertension resulted in an increase in pulmonary artery pressure associated with a decrease in blood flow that is best explained by an increase in pulmonary vascular resistance. This observation highlights the need for hemodynamic monitoring when potent vasodilators are used in this disorder.     

Pulmonary Stenosis as a Predisposing Factor for Infective Endocarditis in a Patient with Noonan Syndrome

Noonan syndrome is an autosomal dominant dysmorphic syndrome. Pulmonary stenosis is the most common cardiac anomaly in Noonan patients, with an incidence of 60%. A 9-year-old girl was referred to our institution with pericardial effusion. Transthoracic echocardiography indeed confirmed massive pericardial effusion and revealed, further, valvular and arterial pulmonary vegetations that accompanied a dysplastic tricuspid pulmonary valve. We decided to perform emergency pericardial tube drainage and to continue the anti-biotic regimen for 2 more weeks before undertaking open-heart surgery. After 2 weeks, the patient underwent an operation wherein the valvular vegetations were excised and a pulmonary valve commissurotomy was performed, yielding a competent pulmonary valve with 3 distinct but moderately dysplastic cusps. In addition to the pulmonary valve, the main, left, and right pulmonary arteries were filled with mobile vegetations, which were removed during the procedure.In this patient, a dysplastic and stenotic pulmonary valve may have contributed to the progression of endocarditis and to the growth of vegetations that occupied the pulmonary arteries. In conclusion, we hypothesize that although pulmonary stenosis is not considered a common predisposing factor for infective endocarditis, it can contribute to the progression of infective endocarditis in Noonan patients.Key words: Endocarditis, heart defects, congenital, pulmonary artery/surgery, pulmonary valve stenosis/complications, Noonan syndrome/therapyThe pulmonary valve is the least commonly involved valve in infective endocarditis, and isolated pulmonary valve endocarditis is extremely rare: predisposing factors are congenitally abnormal pulmonary valve, intravenous drug abuse, and the presence of pulmonary artery catheters. In children, most cases of pulmonary valve endocarditis are secondary to congenitally abnormal pulmonary valves, whereas in adults most cases are due to intravenous drug abuse.¹ Noonan syndrome, the estimated incidence of which is 1 in 1,000 to 2,500 live births, is an autosomal dominant dysmorphic syndrome characterized by hypertelorism, down-slanting palpebral fissures, low-set posterior-rotated ears, and short stature—together with cardiac anomalies, of which pulmonary stenosis is the most frequent feature.^2,3 We herein report a case of pulmonary valve endocarditis with massive pulmonary artery vegetations, in a girl with Noonan syndrome.     

Pulmonary eosinophilia following lung transplantation for sarcoidosis in two patients

Pulmonary eosinophilia is an uncommon problem in lung transplant recipients. We report the unique occurrence of two cases of pulmonary eosinophilia in pulmonary allografts for sarcoidosis. Both patients rapidly acquired bronchiolitis obliterans syndrome (BOS) after resolution of pulmonary eosinophilia. It is known that peripheral eosinophilia is a marker for pulmonary allograft rejection, but its potential in the pathogenesis of BOS is unclear.     

Pulmonary function tests in preoperative pulmonary evaluation.

Pulmonary function testing (PFT) is used extensively by pulmonary specialists to address two common clinical questions: (1) What is the risk of a postoperative pulmonary complication in an individual with lung disease? and (2) Will the patient be able to tolerate lung resection surgery? Today, there are numerous tests available to measure pulmonary function; making judicious use of these tests essential. In this article, the authors describe significant postoperative pulmonary complications, and discuss the surgical and patient factors contributing to the risk of these complications. They provide an evidence-based approach using pulmonary function data to determine an individual patient's risk for pulmonary complications associated with three types of surgical procedures-upper abdominal, cardiac, and lung resection-and discuss recommendations for risk education.