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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A previously unreported combination of critical pulmonary valve stenosis and mitral stenosis is described. The initial clinical presentation was one of right ventricular failure that obscured the evidence of pulmonary venous hypertension. Following pulmonary valvulotomy, pulmonary edema ensued because of the increased pulmonary blood flow. The importance of urgent cardiac catheterization postoperatively following an operation that increases pulmonary blood flow is discussed.
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PMID:Pulmonary edema following pulmonary valvulotomy. 119 Aug 90

A 21 month old female had voluntarily ingested 0.5-1.51 of isotonic sports drink daily from 10 months of age. She developed hyponatremia and beriberi heart disease, which resulted in metabolic acidosis and cardiogenic shock (shoshin beriberi). Mechanical ventilation was applied for pulmonary edema. Right heart failure was improved after administering vitamin B1. However, 5 days after the shock, hypoxemia and diffuse radiographic infiltrates progressed, and a diagnosis of adult respiratory distress syndrome (ARDS) was made. After the occurrence of an air leak, the patient died of respiratory failure. The cardiogenic shock and pulmonary edema due to cardiac beriberi may have triggered the ARDS.
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PMID:Cardiac beriberi (shoshin beriberi) caused by excessive intake of isotonic drink. 141 37

Hypoxia constricts the pulmonary vessels. An increase in pulmonary vascular resistance is seen in normal subjects during hypoxic breathing at sea level, in acclimatized lowlanders and in high altitude natives. Hypoxic pulmonary hypertension in all these circumstances is most generally moderate, except in high altitude natives at exercise. However, in the absence of high altitude pulmonary edema (HAPE) or chronic mountain sickness, a right heart failure that would be the human counterpart of brisket disease described in cattle, apparently never occurs. In adult patients with HAPE, reported mean pulmonary artery pressures (Ppa) measured during a right heart catheterization range from 22 to 63 mmHg with an average of 39 mmHg. Recent echo-Doppler estimates of systolic Ppa in patients with a HAPE are at an average of 53 mmHg, only moderately higher than in healthy subjects exposed to comparable normobaric or hypobaric hypoxia. Subjects with a previous HAPE often present with an enhanced pulmonary vascular reactivity to hypoxia compared to controls when tested at sea level, but the overlap is great. Non invasive echo-Doppler pulmonary hemodynamic studies at sea level have not been reported to reliably discriminate subjects susceptible to HAPE.
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PMID:Pulmonary circulation in hypoxia. 148 82

In patients with mitral stenosis the need for therapeutic intervention can be assessed by clinical and non-invasive data. Mitral valve replacement is indicated when marked dyspnoea on mild exertion, dyspnoea at rest or pulmonary oedema, haemoptysis, atrial fibrillation, recurrent systemic emboli or right ventricular failure occur in a patient with a mitral valve area of less than 1.5 cm2, as measured by Doppler echocardiography. This treatment will entail life-long anticoagulation in the majority of patients. Closed commissurotomy is no longer considered a valid therapeutic alternative due to its limited success rate but open commissurotomy and balloon valvotomy may be performed in patients with no significant calcification of valve cusps and no major concomitant mitral regurgitation. Preservation of the subvalvular apparatus and left ventricular geometry can be considered the most important advantages of these techniques. More severe chronic symptoms are generally required as indication for mitral valve replacement because of the additional long-term imponderabilities imposed by an implanted artificial device. Therefore, in patients with mitral stenosis different symptoms and clinical findings will eventually lead to different interventions.
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PMID:Treatment of mitral stenosis. 193 35

This report describes a 28-yr-old patient with pulmonary veno-occlusive disease (PVOD). She presented with pulmonary hypertension, hypoxemia, and interstitial pneumonitis. We report the discordance between the response of her hypoxemia and interstitial pneumonitis, which resolved with corticosteroid therapy, and her progressive pulmonary hypertension, which caused fatal right heart failure. This report emphasizes that the radiographic interstitial shadowing of PVOD may be caused by either (1) an inflammatory interstitial pneumonitis (which may be responsive to anti-inflammatory therapy) or (2) interstitial pulmonary edema, or both.
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PMID:Pulmonary veno-occlusive disease. Fatal progression of pulmonary hypertension despite steroid-induced remission of interstitial pneumonitis. 202 25

Chronic pulmonary thromboembolism may produce severe respiratory insufficiency and progressive pulmonary hypertension resulting in an intractable right ventricular failure. Although the pathogenesis of this syndrome has not been completely understood, medical treatment usually has little effect and only surgery can be a life saving remedy. Since 1986, seven patients with this syndrome have had pulmonary thromboendarterectomy at the First Department of Surgery, Chiba University Medical Center. Surgery is indicated mainly for patients who present with a mean pulmonary arterial pressure greater than 30 mmHg. All procedures were performed through a unilateral thoracotomy with a cardiopulmonary bypass on stand-by use. Two patients (#1 and #6) needed bilateral surgery which was carried out in two stages, in the remainder only a right side being operated on. When a major pulmonary artery was clamped, the systolic pulmonary arterial pressure rose to equalize or even exceeded that of systemic artery, however since no further hemodynamic deterioration was observed, cardiopulmonary bypass was not used in any case. Although the key feature of this procedure is commonly said to establish an exact cleavage plane between thrombus and arterial wall, it can be carried out without difficulty through thoracotomy approach. Grasping the thrombus, blunt dissection is further proceeded until the entire thrombotic material comes free as a cast of the vessels. All patients survived the operation without major complications including severe reperfusion pulmonary edema. Postoperative catheterization, performed one month following surgery, demonstrated a marked reduction of pulmonary arterial pressure with significantly reduced pulmonary arterial resistance (PAR).
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PMID:[Surgical results of pulmonary thromboendarterectomy for chronic pulmonary thromboembolism]. 203 36

A case of right ventricular assistance required after emergency heart transplantation is reported. The patient was a 62 year-old man with terminal congestive heart failure due to ischaemic cardiomyopathy. Preoperatively, this patient had a cardiac index of 1.93 1.min-1.m-2, moderate pulmonary hypertension (mean Ppa: 34 mmHg) and pulmonary arteriolar resistances at 440 dyn.s.cm-5; clinical examination revealed pulmonary oedema, cardiac liver and oliguria with renal failure. Cardio-pulmonary bypass lasted 145 min, including 50 min of assistance after graft reperfusion. Despite postoperative dopamine and dobutamine treatment, oliguria and central venous pressure increased, and higher doses of catecholamines (adrenaline, noradrenaline) and pulmonary intraarterial prostaglandin E1 infusions were required. Despite these agents and haemofiltration, mechanical assistance was needed and a centrifugal pump set up. Diuresis and haemodynamic parameters improved. The patient was weaned from this assistance after 102 h. A satisfactory haemodynamic status was then maintained, but still required 1.4 micrograms.kg-1.min-1 noradrenaline and 0.02 microgram.kg-1.min-1 prostaglandin E1. Six days later, the patient was weaned from the ventilator, but he rapidly developed fatal aspergillus septicaemia. This case demonstrates that temporary mechanical assistance can be useful for treating right ventricular failure occurring after transplantation.
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PMID:[Right ventricular assistance using a centrifugal pump after heart transplantation]. 233 Oct 86

A 67-year-old female presented seven years after insertion of a mitral prosthesis with mild to moderate pulmonary edema and severe right heart failure with pulmonary and tricuspid insufficiency. Clinical examination and noninvasive tests did not demonstrate prosthetic valve dysfunction. Cardiac catheterization revealed a marked V wave but no mitral regurgitation and no significant mitral diastolic gradient. A clinical diagnosis of a stiff left atrium was made and confirmed at autopsy. The pathophysiology of the syndrome is discussed.
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PMID:Stiff left atrial syndrome. 317 89

Three recent cases from one institution using the total artificial heart (TAH) before transplantation are reviewed. The first patient was implanted for 12 hours with the pneumatic Phoenix total artificial heart after failure of a donor heart 1 day after transplant. Following retransplantation the patient died from severe pulmonary edema, pulmonary hypertension, right ventricular failure, and Pseudomonas septicemia. The second patient was implanted with the Jarvik-7 total artificial heart for rapidly deteriorating idiopathic cardiomyopathy. Major complications during the 9 1/2-day implant consisted of severe pulmonary edema for the first 4 days and a multifocal cerebral embolic event on the seventh day after implantation from which he fully recovered. Major problems after transplant included disseminated toxoplasmosis and two mild episodes of rejection. The patient was discharged 68 days after surgery and remains well. The third patient was a 40-year-old woman with rapidly progressing acute influenza A viral myocarditis. Despite immunosuppressive and antiviral therapy, cardiogenic shock with multiple organ failure developed. The 70 ml Jarvik-7 was implanted for 4 1/2 days. Acute humoral rejection from autoantibodies and alloantibodies led to a cardiac arrest on the second day after transplantation. A second 70 ml Jarvik-7 implant was followed by severe multisystem and infectious complications. After prolonged intensive care support, the patient recovered and is now awaiting transplantation. Nearly 100% cytotoxic antibody reactivity caused by multiple antigenic stimuli is preventing ready access to donor hearts for this patient. We view the current role of the total artificial heart as a tool to preserve life until a suitable donor heart can be found, reverse the end-organ effects of progressive heart failure and low output, and restore transplant candidacy in selected patients with temporary reversible contraindications to transplantation.
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PMID:Three recent cases of the total artificial heart before transplantation. 330 69

Acute heart rejection; unresponsive to immunosuppressive therapy, results in cardiogenic shock and death. In the absence of another donor heart, a total artificial heart can be used as a suitable bridging device to re-transplantation. A thirty-three year-old man rejected his allograft forty-eight hours after transplantation. A total artificial heart was used for eleven hours until another donor heart became available and was transplanted. During the bridging period, the hemodynamic performance of the mechanical prosthesis was satisfactory. The patient died forty-eight hours after re-transplantation of donor right heart failure due to pulmonary edema. This edema was felt to be related to the long periods of cardiopulmonary bypass. This unique experience illustrates the need for a prompt decision to proceed with cardiac replacement, avoiding long periods of cardiopulmonary bypass, the need for a suitable mechanical device availability, technical expertise in device implantation and allograft transplantation.
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PMID:Interim heart replacement with a mechanical device: an adjunct to management of allograft rejection. 391 27


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