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

Between 1968 and 1981, 40 patients with active endocarditis of the native aortic valve were treated by aortic valve replacement (A.V.R.). There were 8 postoperative deaths (hospital mortality 20%). This included 5 patients who had developed cardiogenic shock prior to surgery. Antibiotic treatment for less than one week and positive cultures on the excised valve had poor prognostic implications but tended to be associated with irreversible haemodynamic failure. Twenty five patients underwent A.V.R. following the onset of severe pulmonary oedema. The hospital mortality in this group was 28% and the 5 year actuarial survival 56% (+/- 11%). Fifteen patients who had developed premature closure of the mitral valve (P.C.M.V.) on M-mode echocardiography but who had no overt signs of cardiac failure underwent A.V.R. with a single death (7% hospital mortality). The 5 year actuarial survival in this group was 87% (+/- 9%). P.C.M.V. is a useful prognostic sign identifying those patients with endocarditis on the native aortic valve likely to benefit from early surgery.
J Cardiovasc Surg (Torino)
PMID:The results of surgery for active endocarditis of the native aortic valve. 648 Jun 84

The purpose of this study is to examine the hemodynamics of the pulmonary circulation and the potential role of pulmonary blood flow in the pathogenesis of cardiogenic pulmonary edema. To do so, the pulmonary circulation was isolated and controlled such that, within a closed circuit, pulmonary blood flow and left atrial pressure (LAP) could be regulated independently: the first by a constant flow pump, the second by a variable height reservoir. The effect of pulmonary blood flow on pulmonary artery pressure and intravascular blood volume was then determined at different LAPs. Contrary to our expectations, the results indicate that (1) pulmonary vascular resistance does not change appreciably as flow increases, (2) the microcirculation comprises the major capacitance vessels of the lung, and (3) increased pulmonary flow in the normal lung causes little change in intravascular pulmonary blood volume, whereas, by contrast, major changes in pulmonary blood volume occur as LAP rises. Next, the effect of pulmonary blood flow on edema formation in the lungs was examined. Below a critical level of LAP (15 mm Hg in these experiments), pulmonary blood flow up to 5 L/min did not produce pulmonary edema. Above this level, however, such an effect was clear. Thus, at an LAP of 20 mm Hg, edema did not develop if pulmonary flow was low (0.7 L/min) but did if flow was increased to 2 L/min. As well, if the LAP was 17.5 mm Hg and pulmonary flow 3.5 L/min, severe pulmonary edema also resulted.
J Thorac Cardiovasc Surg 1984 Jan
PMID:Pulmonary blood flow. A potential factor in the pathogenesis of pulmonary edema. 669 Aug 50

Misinterpretation of confusing cardiac, constitutional, and embolic symptoms delayed the diagnosis of cardiac myxoma and caused two of 18 patients to undergo acute operations during cardiogenic shock with pulmonary edema. In recent cases echocardiographic screening of unclear cardiac symptoms gave the correct diagnosis early. Despite the simple surgical procedure (excision of tumor and underlying endocardium), the postoperative course was complicated by cardiac failure, arrhythmias, and systemic reactions. Prosthetic valve thrombosis and malignancy caused two early deaths. Two patients died later of cerebrovascular insults. Both belonged to a group of five patients having preoperative emboli from fragile myxomas. Four of these five had coronary or cerebral myxomatous pseudoaneurysms. A 6 year follow-up, including recatheterization, showed no tumor recurrence and generally normalization of the clinical condition, heart size, and catheterization findings. Even pronounced mitral insufficiency accompanying left atrial myxomas had subsided spontaneously. Tricuspid insufficiency in two patients with right atrial myxomas persisted, necessitating reoperation in one. When diagnosed, a cardiac myxoma should be removed promptly to reduce cardiac and embolic complications, including myxomatous pseudoaneurysm formation, which might be more frequent than previously recognized.
J Thorac Cardiovasc Surg 1984 Feb
PMID:Surgical considerations in the treatment of cardiac myxoma. 669 16

Postpneumonectomy pulmonary edema has become a worldwide problem. Study of data available from some of these patients implicates excessive perioperative volumes of intravenous fluid. A study done on dogs supports the clinical conclusion. The risk factors for this complication are right pneumonectomy, large perioperative fluid load, and high intraoperative and postoperative urine outputs. Patients undergoing pneumonectomy are at greater risk from intravenous fluid therapy than other types of patients.
J Thorac Cardiovasc Surg 1984 Mar
PMID:Postpneumonectomy pulmonary edema. 670 Feb 43

Left-sided juxtaposition of the right atrial appendage (LJRAA) was seen in 10 patients in a series of 361 consecutive Mustard procedures for transposition of the great arteries (TGA). Dextrocardia complicated LJRAA in four cases. Right atrial capacity and free atrial wall size were smaller than normal in all patients, and a Mustard intra-atrial baffle repair was performed in all instances. Direct caval cannulation or cannulation of either atrial appendage facilitated intra-atrial repair. Nine patients in whom the pulmonary venous atrium was enlarged with a patch survived. One child who did not have a right atrial patch died 1 hour postoperatively of pulmonary edema. Two late deaths occurred 1 year postoperatively. Seven children survived and are well. In one child, superior vena caval baffle obstruction is controlled by digoxin and diuretic therapy. TGA associated with juxtaposition of the atrial appendages (JAA) and dextrocardia may be successfully repaired by the Mustard procedure, provided that the tricuspid valve and right ventricle are normal, an adequate superior vena caval channel is created, and patch enlargement of the pulmonary venous atrium is undertaken.
J Thorac Cardiovasc Surg 1983 Mar
PMID:The Mustard procedure in transposition of the great arteries associated with juxtaposition of the atrial appendages with and without dextrocardia. 682 53

At New York University Medical Center over the past 18 months, a distinctive and potentially lethal syndrome of fulminating noncardiogenic pulmonary edema has been observed in three patients following cardiopulmonary bypass. The clinical appearance is virtually identical to that produced by acute left ventricular failure, and the condition could have been diagnosed incorrectly in the past as myocardial infarction with left ventricular failure and pulmonary edema. Thus it is uncertain whether this is a new syndrome or whether it has long been present. Fulminating noncardiogenic pulmonary edema can be diagnosed by finding a low left atrial or pulmonary artery wedge pressure combined with a high protein content in the pulmonary edema fluid when compared to simultaneous measurements of the plasma protein level. As no other etiologic agent could be identified in our three patients, the probable cause seems to be an unknown type of allergic reaction to blood or blood products, manifested by acute pulmonary edema--the pulmonary capillary membranes being the first to be exposed to fluids administered intravenously. The significant point is that a nearly fatal degree of pulmonary congestion can be managed safely and effectively with corticosteroids, antihistamines, positive-pressure ventilation, diuretics, and albumin. Presently, two important questions remain: (1) Should fluids be restricted and balloon pump counterpulsation and vasopressors utilized to maintain systemic pressure? (2) How long after administration of steroids is it safe to give intravenous albumin? Meanwhile, both the mechanism and frequency of this syndrome remain unknown.
J Thorac Cardiovasc Surg 1980 Dec
PMID:Fulminating noncardiogenic pulmonary edema. A newly recognized hazard during cardiac operations. 696 58

Serum endothelin levels increase during sepsis, ischemia, reperfusion, pulmonary operations, and systemic hypertension after surgery. Despite extensive study, the site and extent of action of endothelin on the pulmonary microcirculation are not well established. To assess the effect of endothelin on the pulmonary vasculature, especially the veins, the circulation of the lung was cast with methyl methacrylate 10 minutes after endothelin-1 was given intravenously to rats. Endothelin-1, at concentrations of 0.1, 1.0, and 10.0 micrograms/kg of body weight, increased the mean systemic arterial blood pressure 8%, 7%, and 17% (p < 0.01) and mean pulmonary arterial blood pressure 15%, 28%, and 53%, respectively (p < 0.01). The proportional increases in the pulmonary pressures were greater than those of the systemic pressures (p < 0.01). Scanning electron microscopy of cast blood vessels showed more contraction of the veins than the arteries. For doses of 0, 0.1, 1.0, and 10.0 micrograms/kg, the respective focal contraction of small veins was 6.7% (+/- 4.4), 15.4% (+/- 9.1), 23.3% (+/- 10.1), and 14.4% (+/- 9.0) of the vessel diameter (p < 0.01). In addition, the diameter of capillaries increased (p < 0.01) and the capillary interspaces decreased (p < 0.01) after endothelin administration, but not in a linear dose-dependent manner. The dose of endothelin correlated with the change in the mean systemic (r = 0.82, p < 0.01) and the mean pulmonary (r = 0.80, p < 0.01) blood pressures. The mean pulmonary pressure change correlated with the focal venous contraction on the casts (r = 0.35, p < 0.01), capillary diameter (r = 0.64, p < 0.01), and capillary interspace distance (r = -0.34, p < 0.01). The venous contraction was related to the capillary diameter (r = 0.26, p < 0.01). The most notable effect of endothelin-1 in rat pulmonary microcirculation is focal constriction of small veins. Because this effect may lead to pulmonary edema, endothelin antagonists may be of benefit in a variety of clinical situations.
J Thorac Cardiovasc Surg 1995 Jul
PMID:Endothelin-1 focally constricts pulmonary veins in rats. 760 38

Severe left ventricular failure, as evidenced by radiographic pulmonary edema or raised left ventricular filling pressure, accompanying acute myocardial infarction, carries a high mortality risk. In this situation, the intravenous loop-diuretic furosemide induces a rapid reduction in the raised left ventricular filling pressure due to an immediate and substantial increase in systemic venous compliance accompanied by increasing diuresis. This diuretic-induced venodilatation is probably due to the release of prostaglandins. The transient systemic arterial constriction and small increase in systemic blood pressure that follows intravenous furosemide probably results from the release of renin and subsequent activation of angiotensin. These diuretic induced hemodynamic changes are accompanied by restoration of the vasodilator reflex, which enables the heart to accommodate an acute volume load. Orally administered loop diuretics achieve slower, but similar, directional hemodynamic changes. There is no information on hemodynamic or neuroendocrine dose-response effects of loop diuretics, and there is no information pertaining to the use of other diuretic groups in this situation. The hemodynamic changes induced by furosemide summate with the changes induced by other anti-heart-failure drugs. In this subset of patients with acute myocardial infarction and severe heart failure, the influence of the diuretics on morbidity incidence and mortality risk remains to be measured.
Cardiovasc Drugs Ther 1993 Dec
PMID:Diuretics in postinfarction heart failure. 801 64

Although airway, arterial, and venous connections required for lung transplantation appear simple, in practice we have encountered morbid early stenosis and obstructions, which are now avoided by technical modifications gradually made since 1985 in 134 cases (60 single lung and 74 double lung). Our initial eight double lung transplant procedures were done with tracheal anastomoses and omental wraps, but ischemic disruption, with a 75% (6 of 8) rate of complications, resulted in the subsequent use of bi-bronchial connections. A total of 192 bronchial anastomoses were reviewed (60 single lung, 66 double lung). Although all anastomoses were constructed between the donor trimmed to one to two rings above the upper lobe origin and the host divided at its emergence from the mediastinum, the suture technique has evolved. Nine (32%) of 28 cases with early bronchial anastomoses with end-to-end suture and intercostal muscle wrap had ischemic or stenotic complications, but the telescoping technique without wrap in 164 bronchial anastomoses reduced the problem to 12% (19 of 164). Twelve anastomoses required temporary intraluminal stenting. Vascular anastomotic obstructions occurred in five arterial (excessive length 2, short allograft artery 1, restrictive suture or clot 2) and two venous (excessive length 1, restrictive suture or clot 1) connections. Suspicion of arterial obstruction was prompted by persisting pulmonary hypertension and reduced flow to the allograft measured by postoperative nuclear scan and hypoxia. Venous obstructions were suggested by persisting radiographic and clinical pulmonary edema. Modifications of earlier techniques have improved our early success in lung transplantation and might be considered by others entering this demanding field.
J Thorac Cardiovasc Surg 1994 Mar
PMID:Anastomotic pitfalls in lung transplantation. 777 67

A pulmonary injury of varying severity occurs routinely after cardiopulmonary bypass. We studied the pulmonary complications of partial cardiopulmonary bypass in four groups of dogs to better define the injury and to evaluate the efficacy of two interventions (addition of a leukocyte filter or cyclooxygenase inhibition) on preservation of systemic oxygenation. All animals received a standard anesthetic (pentobarbital, morphine, and vecuronium) and, after sternotomy, three groups of animals received 3 hours of partial cardiopulmonary bypass. The animals were randomized to receive partial bypass alone (n = 6), indomethacin and bypass (n = 5), or a leukocyte filter and bypass (n = 5). A fourth group (n = 5) did not receive bypass and served as a time control. We measured blood gases and also obtained histologic samples to assess the degree of lung injury. We found that bypass alone caused a significant reduction (p < 0.05) in arterial oxygen tension 1 hour after the conclusion of bypass (175 +/- 53 mm Hg) compared with prebypass values (357 +/- 41 mm Hg). Pretreatment with indomethacin ameliorated the decrease in arterial oxygen tension from prebypass to postbypass values (477 +/- 50 mm Hg versus 339 +/- 57 mm Hg, respectively). Similarly use of a leukocyte filter reduced the decline in arterial oxygen tension from prebypass to postbypass values (440 +/- 71 mm Hg versus 311 +/- 73 mm Hg, respectively). We believe that indomethacin ameliorates the decline in systemic oxygenation associated with bypass by augmentation of hypoxic pulmonary vasoconstriction and that the leukocyte filter acted to reduce pulmonary edema and thereby minimized intrapulmonary shunt.
J Thorac Cardiovasc Surg 1994 May
PMID:Neutrophil-mediated acute lung injury after extracorporeal perfusion. 817 61


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