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

Ruptured papillary muscle due to myocardial infarction was encountered in 14 patients during the period 1975-1983. Five of the 14 patients had a history of angina pectoris and two had a history of prior myocardial infarction. Eleven patients with myocardial infarction developed additional pain due to myocardial ischemia and/or a murmur of mitral regurgitation and pulmonary edema within a week, 3 others had a prolonged course with intermittent pain due to myocardial ischemia and breathlessness for longer periods and then deteriorated. Thirteen of our 14 patients developed a murmur and all but one had pulmonary edema on the chest x-ray. Five patients had infarction patterns on the electrocardiogram, the remainder of the patients had only ST- and T-wave changes. Echocardiograms showed fine flutter and notching of the anterior mitral leaflets and vigorous contractions of the left ventricle. Only one patient was demonstrated to have a papillary muscle tip prolapsing into the left atrium on two-dimensional echocardiography. Twelve patients underwent surgery and 8 survived. Seven patients had single-vessel coronary disease, 4 involving the circumflex system and 3 involving the right coronary system. Four of the 7 patients with single-vessel coronary disease survived surgery. Five patients went to surgery with the intra-aortic balloon pump in place and only 3 survived. Three others had the pump inserted intraoperatively and 2 of these survived. Six of 9 patients who had mitral valve replacement and coronary bypass survived. Ejection fraction ranged from 40 to 79%. Surgical survival did seem to be related to the extent of papillary muscle rupture, with the best results occurring in the group with a small portion of the tip ruptured. Seven patients had a stormy clinical course and required surgery within 10 days of rupture. Four of these 7 survived. It seems reasonable to believe that these patients who often have small infarction and limited coronary disease have good potential for survival. Our approach has been to move toward surgery once the diagnosis is made to avoid the sudden deterioration that frequently occurs. The surgical mortality in this group remains in the 30 to 40% range.
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PMID:Ruptured papillary muscle, a complication of myocardial infarction: clinical presentation, diagnosis, and treatment. 397 8

Sixteen Holstein cattle allotted into 4 groups (4 cattle/group) were each given a single oral dosage of 0.2 g of 3-methylindole (3MI)/kg of body weight. The groups were killed at 12, 24, 48, and 72 hours, respectively, after 3MI administration. Comparison of clinical signs, pathologic pulmonary lesions, and in vitro pulmonary artery responses to pharmacologic stimuli was made between the 4 treated groups and 8 control Holstein cattle of similar age. Clinical signs of pulmonary distress first appeared 8 to 12 hours after 3MI administration. After 20 hours, clinical signs included dyspnea, moderate depression, and a marked expiratory grunt. A partial remission of these clinical signs was seen between 30 and 45 hours after 3MI administration. After remission, the cattle had clinical signs of severe dyspnea and depression and expiratory grunts were more pronounced. Pathologic pulmonary lesions, including heavy rubbery lungs, dilated interlobular septae, and subplural air bullae characteristic of pulmonary edema and interstitial emphysema were observed. The lungs of treated cattle did not collapse when the thorax was incised at necropsy. In vitro pulmonary artery strips contracted dose dependently to norepinephrine (NE). Group I tissues (12 hours after 3MI administration) responded similarly to control samples. Group II tissues (24 hours after 3MI administration) had a significant inhibition (P less than 0.05) in response to NE stimulation as compared with controls.
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PMID:Impairment of sympathetic pulmonary vasoconstriction by 3-methylindole in cattle. 401 39

We describe seven years' experience with the University of Cape Town lenticular mitral valve prosthesis in 122 patients. All the patients had severe mitral valve disease. In 98 severe mitral stenosis was present with or without incompetence and in 24 the dominant or sole lesion was mitral incompetence. Other valves, particularly the tricuspid, were also frequently affected. The disability was severe or total in almost every patient. One hundred and five patients were discharged from hospital, and in 90 per cent of these the clinical improvement was most gratifying, with the disappearance of pulmonary oedema, paroxysmal dyspnoea, angina pectoris, and congestive cardiac failure. Return to full normal activity including physical work was the rule. The hospital mortality was 14 per cent and a further 38 per cent died during the follow-up period. The major post-operative complication was systemic embolism which could occur at any time after operation. The most important factor influencing the frequency of this complication was the nature of the valve seat. A bare steel seat was associated with a 100 per cent embolism, and a significant reduction occurred when a cloth-covered seat of Dacron-velour was introduced. Anticoagulant therapy appeared to prevent large or fresh clots but had no effect on the deposition of fibrin or platelet thrombi. The only other factor of importance was the age of the patient: after the age of 50 life expectancy and trouble-free long-term survival was reduced.
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PMID:Immediate and long-term results of mitral valve replacement with University of Cape Town mitral valve prosthesis. 544 May 20

Water intoxication from intravascular absorption of non-electrolyte irrigating fluid is a well-known and often serious complication of transurethral resection of the prostate. The amount of absorbed fluid depends on the duration of the operative procedure, the number of transected open venous sinuses and the hydrostatic pressure of the irrigating fluid. Arterial hypertension, bradycardia, mental agitation, confusion, headache, nausea, dyspnoea, convulsions and pulmonary edema are the typical syndromes. In this case, severe Angina Pectoris was the first alarming symptom.
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PMID:[Angina pectoris -- an early sign of water intoxication during transurethral prostatectomy (author's transl)]. 617 35

Excessive numbers of moderator bands bridging the left ventricular septum and free wall and entangling papillary muscles were associated with heart failure and death in 21 cats. Clinical findings included dyspnea, anorexia, hypothermia, cardiomegaly, pleural effusion, plumonary edema, heart murmurs, gallop rhythm, electrocardiographic abnormalities (especially conduction disturbances), increased left ventricular end-diastolic pressure, angiocardiographic evidence of left ventricular restriction, and aortic thromboembolism. Pathologic changes included a morphologically distinct network of abnormal numbers of moderator bands in the left ventricle, left ventricular hypertrophy (younger cats--mean age, 4 years) or dilatation (older cats--mean age, 8.7 years), left atrial enlargement and hypertrophy, and pulmonary edema with heart failure cells in the alveoli. Heart weights of affected cats were significantly less than those of cats with congestive, hypertrophic, and restrictive cardiomyopathy (endocardial fibrosis), but were not significantly less than heart weights of clinically normal cats. Pathologic changes were characteristic of the syndrome grossly and histologically, but clinical findings were not clearly definable.
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PMID:Excessive moderator bands in the left ventricle of 21 cats. 621 23

The adult respiratory distress syndrome (ARDS) is an extreme form of noncardiogenic pulmonary edema associated with alveolar-capillary damage. Clinical features include acute respiratory distress, dyspnea and tachypnea, severe hypoxemia refractory to oxygen therapy, and diffuse bilateral pulmonary infiltrates. Any number of serious disorders can cause ARDS, but the processes leading to the alveolar permeability defect are not understood. Therefore, therapy remains nonspecific and supportive. Treatment includes positive end-expiratory pressure, careful fluid management, steroid therapy, and adequate nutrition. Unfortunately, even with the most sophisticated intensive care, the mortality of ARDS is still greater than 50%.
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PMID:The adult respiratory distress syndrome. 634 98

The mitral apparatus is a complex structure composed of several components, each of which can be affected by a variety of diseases, resulting in mitral regurgitation. The physiologic consequences of mitral regurgitation include reduced forward stroke volume; increased left atrial volume and pressure; and reduced resistance to left ventricular ejection. The latter explains why indices of systolic left ventricular function (ejection fraction) are often increased early in the course of mitral regurgitation. With the insidious development of mitral regurgitation, the left atrium dilates to accommodate the increase in volume, thereby reducing the atrial pressure. However, with the acute development of mitral regurgitation into a nondilated left atrium, pressure rises rapidly, producing pulmonary edema. The predominant clinical symptoms in chronic mitral regurgitation of dyspnea and fatigue result from pulmonary venous hypertension and low cardiac output. The cardinal physical finding is a mitral systolic murmur. Since the murmur can assume various configurations, the most reliable way to establish its correct origin is by bedside physiologic maneuvers. Typically, in the beat following a premature contraction or after a long pause during atrial fibrillation, the murmur of mitral regurgitation is unchanged in intensity, but murmurs due to left ventricular outflow obstruction increase. Also, isometric handgrip exercise increases the intensity of the murmur and a Valsalva maneuver decreases it during the strain phase. Echocardiography is the most useful noninvasive technique for evaluating patients with mitral regurgitation. Visualization of the mitral apparatus may establish the etiology of regurgitation, and measurement of left atrial size and left ventricular size and performance is useful for assessing the functional significance of the lesion. Doppler echocardiography can establish the diagnosis of mitral regurgitation in difficult cases with multi valve disease and can estimate the severity of the regurgitation. Cardiac catheterization and angiography are usually reserved for the patient being considered for valvular surgery. The natural history of chronic mitral regurgitation is characterized by slowly progressive symptoms, and often the onset of disabling symptoms is the result of irreversible left ventricular dysfunction. Medical therapy consists of digitalis, diuretics, and vasodilators for symptomatic patients. When symptoms occur despite this therapy, valvular surgery should be considered before left ventricular function becomes abnormal.
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PMID:Mitral valve regurgitation. 637 82

The Gaboon viper has acquired an impressive reputation which is at least partly unfounded. This handsome animal with such striking features is undoubtedly docile which accounts for the very low incidence of bite amongst humans. There are only six detailed clinical reports on the effect of bite and these are summarized in the review. The viper does indeed produce prodigious amounts of venom, but the toxicity, weight for weight, is rather low compared to other poisonous snakes. Venom extractions have been carried out on four snakes over a 13-year-period and the effects of this venom have been studied in a variety of experimental animals. Systemic envenomation is characterized by immediate abrupt hypotension, subsequent cardiac damage and dyspnoea. The individual venom components responsible for these effects have not been isolated but it seems likely that the two enzymes which have been studied extensively (phospholipase A2 and the thrombin-like enzyme, gabonase) do not contribute significantly to lethality. We propose three principal activities which give rise to the major signs of systemic envenomation. Haemorrhagin; causing widespread damage to microvasculature which leads to the pulmonary oedema and hence dyspnoea, and locally causes blistering. Cardiotoxin; a long-acting material causing cardiac muscle damage, arrhythmia and ultimately cardiac failure. Peripheral vasodilator; a short acting effect, operating either locally via bradykinin formation and/or unknown peptides or centrally on the vasomotor centre.
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PMID:The Gaboon viper (Bitis gabonica): its biology, venom components and toxinology. 639 43

The fat overload syndrome developed in a 7-year-old girl who was on home TPN which included 20% Intralipid (total lipid dose 3.2 g/kg/d). Acute respiratory insufficiency developed with cough, dyspnea, tachypnea, and cyanosis. The chest x-ray revealed mild cardiomegaly and pulmonary edema. Blood gases showed profound hypoxia (PaO2 29 torr on room air). Spontaneous resolution occurred over the next seven days as the lipemia cleared.
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PMID:Fat overload syndrome causing respiratory insufficiency. 644 Sep 70

Fluid movement from the pulmonary capillaries into the interstitial space occurs continuously and is drained by the lymphatics. With increased leakage or decreased clearance, excessive extravascular lung water accumulates, initially as interstitial edema and subsequently as alveolar edema. The most common cause of pulmonary edema is an increase in microvascular hydrostatic pressure. An increased permeability of the capillaries is the other mechanism of production of pulmonary edema. An acute, critical reduction in colloid osmotic pressure may play a contributory role in pulmonary edema even at normal hydrostatic pressures. Dyspnea, diaphoresis, and anxiety characterize the clinical picture. A history of heart disease and congestive heart failure may be present in CPE, whereas evidence of an inciting event or disease process suggests NCPE. Hypoxia, decreased lung compliance, and increased shunt fraction are seen in both types of pulmonary edema, but the duration of pulmonary edema tends to be more severe and prolonged in NCPE. Evidence of increased permeability in NCPE distinguishes it from CPE. Clinically, this is assumed when pulmonary edema is demonstrated at normal PCWP and when edema fluid protein concentration and COP are close to those of plasma. The management of pulmonary edema consists of the improvement of gas exchange by methods that range from supplemental oxygen administration to mechanical ventilatory support with PEEP, depending on the severity of the disturbance in lung function. Improvement in myocardial function and a decrease in pulmonary congestion are accomplished with diuretics and morphine; in those patients who do not respond to this therapy, manipulation of preload, afterload, and myocardial contractility by vasodilators and inotropic agents may be required. In acute pulmonary edema, intravenously administered agents with a short half-life and rapid onset of action are preferred. The role of colloids in the treatment of pulmonary edema is controversial. The indications for the use of corticosteroids in ARDS are controversial, and an optimum dose has not been determined. Many clinicians tend to choose steroids to treat these patients, but the value of these agents in this setting awaits the results of controlled trials now under way.
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PMID:Acute pulmonary edema. 644 44


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