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

The role of active and passive factors involved in the genesis of Pulmonary Arterial Hypertension (PAH) is analyzed in a group of eighty patients with several cardiopathies and pneumopathies. The group include: 20 patients with Chronic Obstructive Lung Disease (NODC), 20 with Diffuse intersticial pneumopathy (NI), 12 with Cardiorespiratory Syndrome of the grossly obese (OB), 6 with Pulmonary Embolism (TEP), 6 with Mitral Stenosis (CRI), 5 with Hypertensive Ventricular Septal Defect (CIV + HAP) and 11 patients with Pulmonary Arterial Hypertension of Unknown etiology (HAP-ED). For the analysis, the Harvey and Enson's formulas were used. The conclusions of the study are: 1) The compliance of the elastic arteries of the lung in the groups of NOC, NI and OB is normal but in the other groups seems to be modified. 2) In the groups of NI and OB the interrelationship of factors such as alveolar hypoxia and pulmonary wedge pressure (PWP) play the major role in the genesis of PAH, although the role of the PaCO2 in the OB group remains to be established. 3) In the groups of NOC, CRI and TEP the PWP is not determinant. The absence of a significant correlation between arterial oxygen unsaturation and pulmonary diastolic pressure in the NOC group suggests other factors. 4) The vascular structural damage seems to be the most important factor in the genesis of PAH in the HAP-ED and CIV + HAP groups.
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PMID:[Active and passive factors in the genesis of pulmonary arterial hypertension in various cardiopathies and pneumopathies]. 678 61

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

Pulmonary hypertension is the hemodynamic consequence of vascular changes within the precapillary (arterial) or postcapillary (venous) pulmonary circulation. These changes may be idiopathic, as in primary pulmonary hypertension or pulmonary veno-occlusive disease, but more commonly they represent a secondary response to alterations in pulmonary blood flow. The pulmonary and systemic bronchial circulations form broad anastomoses that largely prevent infarction except in settings of markedly elevated pulmonary venous pressure, underlying malignancy, or excessive embolic burden. Causes of precapillary pulmonary hypertension include long-standing cardiac left-to-right shunt, chronic thromboembolic disease, and widespread pulmonary embolism arising from intravascular malignant cells, parasites, or foreign materials. The classic radiologic features of precapillary pulmonary hypertension are central arterial enlargement, sharply pruned peripheral vascularity, and right-sided heart hypertrophy and chamber dilatation. Postcapillary pulmonary hypertension may develop secondary to focal venous constriction or to compromised pulmonary venous drainage due to left atrial neoplasia, mitral stenosis, or left ventricular failure. Radiologic manifestations of postcapillary pulmonary hypertension include prominent septal lines, small pleural effusions, and occasionally air-space opacities. In addition, radiologic evaluation of postcapillary pulmonary hypertension may demonstrate evidence of pulmonary arterial hypertension, secondary to the retrograde transmission of elevated pulmonary venous pressure across the capillary bed.
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PMID:From the archives of the AFIP: pulmonary vasculature: hypertension and infarction. 1071 47

Transesophageal echocardiogram is the procedure of choice in the evaluation of masses located in the cardiac chambers. In this paper three cases of atrial thrombosis are presented: a) a free floating ball thrombus in the left atrium in a patient with moderate mitral stenosis; b) three thrombotic masses adherent to a central venous catheter; c) three thrombotic masses attached to Chiari s network in a patient operated for an ostium secundum atrial septal defect one year before. In all cases transesophageal echocardiogram has played a key role in the diagnosis. Medical therapy has been inadequate and so surgical removal has been performed. Unsuccessful medical therapy, a new episode of thrombosis, intracardiac permanent catheter infections and high risk of systemic and pulmonary embolism are indications for thrombectomy.
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PMID:[Surgical treatment of atrial thrombosis. A transesophageal echocardiogram study]. 1142 99

The antiphospholipid antibody syndrome (APS) may present with serious cardiovascular complications which should be recognised by the cardiologist. The authors report a series of 6 cases of APS diagnosed after thrombotic events and the finding of antiphospholipid antibodies. The APS was primary in 5 cases and associated with tuberculous lymphadenitis in 1 case. There was cardiac involvement in 5 patients with pericardial effusion in 3 cases, complicated by tamponade as the presenting sign of primary APS in the other 2, valvular disease in one case (moderate mitral stenosis with aortic valve disease) and pulmonary embolism in one case. Five patients developed recurrent deep vein thrombosis of the legs. One patient had a transient ischaemic cerebral attack.
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PMID:[Cardiovascular abnormalities of the antiphospholipid antibody syndrome]. 1274 9

Ventricular assist devices (VADs) are systems for mechanical circulatory support of the patient with severe heart failure. Perioperative transesophageal echocardiography is a major component of patient management, and important for surgical and anesthetic decision making. In this review we present the rationale and available data for a comprehensive echocardiographic assessment of patients receiving a VAD. In addition to the standard examination, device-specific pre-, intra-, and postoperative considerations are essential to the echocardiographic evaluation. These include: (a) the pre-VAD insertion examination of the heart and large vessels to exclude significant aortic regurgitation, tricuspid regurgitation, mitral stenosis, patent foramen ovale, or other cardiac abnormality that could lead to right-to-left shunt after left VAD placement, intracardiac thrombi, ventricular scars, pulmonic regurgitation, pulmonary hypertension, pulmonary embolism, and atherosclerotic disease in the ascending aorta; and to assess right ventricular function; and (b) the post-VAD insertion examination of the device and reassessment of the heart and large vessels. The examination of the device aims to confirm completeness of device and heart deairing, cannulas alignment and patency, and competency of device valves using two-dimensional, and color, continuous and pulsed wave Doppler modalities. The goal for the heart examination after implantation should be to exclude aortic regurgitation, or an uncovered right-to-left shunt; and to assess right ventricular function, left ventricular unloading, and the effect of device settings on global heart function. The variety of VAD models with different basic and operation principles requires specific echocardiographic assessment targeted to the characteristics of the implanted device.
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PMID:Perioperative echocardiographic examination for ventricular assist device implantation. 1822 40

Reactive airway disease is often triggered by an upper respiratory viral infection and readily responds to anti-inflammatory and bronchodilator therapy. The differential diagnosis for unresponsive disease includes poorly controlled asthma, noncompliance with medical regimen, vocal cord dysfunction, rhinosinusitis, gastroesophageal reflux disease or recurrent aspiration, foreign body aspiration, allergic bronchopulmonary aspergillosis, Churg-Strauss vasculitis, cardiac disorders such as congestive heart failure or mitral stenosis, or other pulmonary disorders such as chronic obstructive pulmonary disease, alpha-1 antitrypsin deficiency, interstitial lung disease, bronchiectasis, sarcoidosis, hypersensitivity pneumonitis, pulmonary embolism, cystic fibrosis, airway neoplasms, or laryngotracheomalacia. As is often the case, a meticulous history can expeditiously direct the clinician to the diagnosis, especially in a patient without a smoking, asthmatic, or atopic history.
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PMID:A 41-year-old male with cough, wheeze, and dyspnea poorly responsive to asthma therapy. 2081 28

Pheochromocytoma during pregnancy is extremely rare. Its clinical manifestation includes hypertension with various clinical presentations, possibly resembling those of pregnancy-induced hypertension. The real challenge for clinicians is differentiating pheochromocytoma from other causes of hypertension (preeclampsia, gestational hypertension, and pre-existing or essential hypertension), from other cause of pulmonary edema (preeclampsia, peripartum cardiomyopathy, stress or Takotsubo cardiomyopathy, pre-existing cardiac disease [mitral stenosis], and high doses betamimetics), and from other causes of cardiovascular collapse (pulmonary embolism, and amniotic fluid embolism). Although, several cases of pheochromocytoma during pregnancy have been published, fetal and maternal mortalities due to undiagnosed cases are still reported. We report a case of a patient whose delivery by cesarean section was complicated by severe hemodynamic instability resulting in a cardiac arrest. Later on, pheochromocytoma was suspected based on computed tomography (CT) scan findings. Diagnosis was confirmed with special biochemical investigations that showed markedly elevated catecholamines in urine and metanephrines in serum, and later by histopathology of the excised left adrenal mass. This case illustrates the difficulty of diagnosing pheochromocytoma in pregnancy and raises the awareness to when this rare disease should be suspected.
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PMID:Cardiorespiratory crisis at the end of pregnancy: a case of pheochromocytoma. 2418 Jan 71

Acute dyspnea with pulmonary oedema in postpartum is uncommon but life-threatening event. Contributing factors for pulmonary oedema include, administration of tocolytics, underlying cardiac disease, iatrogenic fluid overload and preeclampsia acounting 0.08% of pregnancies. Pulmonary embolism, amniotic fluid embolism, pneumonia, aspiration and pulmonary oedema are some of the potentially devastating conditions that should be considered by the attending physician. Here, we report a case of postpartum acute pulmonary oedema referred to causality after an emergency caesarean section in a private hospital. No matter what the underlying pathology, prompt administration and appropriate resuscitation is always the first priority. Only after the patient has been stabilized attention must be turned to diagnosis and specific treatment. A diagnosis of severe Mitral Stenosis, probably of rheumatic origin was made after stabilizing the patient.
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PMID:Postpartum Acute Pulmonary Oedema with Sub clinical Rheumatic Heart Disease. 2585 1

The left atrium is the most common location of myxomas, which are benign tumors. Only a few cases of myxomas in pregnancies have been reported. Our thorough medical literature search showed only 17 reported cases in the course of pregnancy. Myxomas during pregnancy and in the preterm period constitute a serious phenomenon that can mimic an early sign of a life-threatening pathology like severe mitral stenosis. We describe a 33-year-old woman, who presented with acute dyspnea to a gynecology center and was referred to our hospital for further evaluation of pulmonary embolism. Transthoracic echocardiography showed a huge left atrial myxoma, and computed tomography scan illustrated paradoxical pulmonary embolism in the left upper lung lobe via a large patent foramen ovale. The tumor required urgent cardiac surgery. In this article, we review causes of dyspnea in pregnancy and the cardiovascular effects of myxomas in pregnancy. We also describe the pathophysiological effects of cardiopulmonary bypass on the mother, fetus, and the feto-placental system during open-heart surgery. We performed a successful surgical resection of a myxoma in a pregnant woman. Given the rarity of such cases, individual multidisciplinary assessment and management strategies are essential.
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PMID:Preoperative Emboli in a Pregnant Woman with Myxoma. 2736 58


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