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

This report describes a patient with hypertrophic obstructive cardiomyopathy complicated by acute aortic and probably mitral valvular incompetence caused by endocarditis due to Staphylococcus aureus. Following the onset of valvular insufficiency, this patient developed hypotension and pulmonary edema and eventually underwent cardiac surgery in an attempt to control these complications. We review the unique pathophysiology of hypertrophic obstructive cardiomyopathy and its alterations in the presence of acute valvular incompetence and analyze the limitations of medical management of cardiac decompensation in patients with this combination of cardiac abnormalities. The possible need for early surgery in such patients is examined.
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PMID:Acute valvular insufficiency complicating hypertrophic obstructive cardiomyopathy. 57 Apr 72

During 1975, 38 of 44 infants with a birth weight of less than or equal to 1,500 gm who developed pulmonary edema and congestive heart failure due to a patent ductus arteriosus were managed medically until the ductus closed spontaneously days or weeks later. Overall survival was 71%, and there were no deaths among 11 infants weighing more than 1,250 gm. Pulmonary complications were prevalent and were attributed to the extensive use of mechanical ventilation required to control pulmonary edema. The results of this study document the results to be expected when small preterm infants with a symptomatic patent ductus arteriosus are managed without surgical or pharmacologic intervention and provide a basis for the rational design of clinical trials evaluating other management approaches.
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PMID:Medical management of small preterm infants with symptomatic patent ductus arteriosus. 63 94

The ability of the portable roentgenography of the chest to define the amount of physiologic shunting and the severity of noncardiogenic pulmonary edema was evaluated in 37 observations of 11 patients. Ten of the 11 patients had acute respiratory failure. The roentgenologic assessment of the amount of pulmonary edema and the severity of left ventricular failure was compared with the physiologic shunt fraction, tracer measured lung water and the pulmonary arterial wedge pressure. The roentgenologic scores for edema did not predict the shunt fraction or tracer measured lung water. The roentgenologic score for congestive heart failure correlated with the wedge pressure but not well enough to be clinically useful. Five per cent of the roentgenograms were false-positive and 11 per cent were false-negative. Roentgenologic findings lagged behind physiologic derangements. Thus, the roentgenogram could predict the shunt value of the preceding day. Results indicate that it is hazardous to accept a portable roentgenographic diagnosis of congestive heart failure as a cause of pulmonary edema.
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PMID:Limitations of portable roentgenography of the chest in patients with acute respiratory failure. 64 29

The presentation and management of 21 patients with postinfarction ventricular septal defect (VSD) in whom surgical treatment was considered or performed since 1970 have been analysed and reviewed. An acute group of 11 patients, each of whom developed cardiogenic shock, 9 of whom came to surgery within one week from the onset of their VSD, had a poor outlook, only 27% becoming long-term survivors. Six patients were classified as subacute because their surgery was precipitated by worsening congestive cardiac failure in all, and by pulmonary oedema at the time of surgery in three patients. Four chronic patients were operated upon electively. The results in the subacute and chronic groups were excellent, and all are long-term survivors. Operative closure of the defect is best achieved by the use of a patch. Infarctectomy and aneurysmectomy are necessary in more than half of the cases. Left ventricular assistance by the intra-aortic balloon counterpulsation catheter has been disappointing and did not contribute to long-term survival. The major factor determining survival is the integrity of the closure, and the function of the remaining viable myocardium. Reoperation for reopening of the defect should always be considered.
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PMID:Perforation of the interventricular septum complicating myocardial infarction. 68 72

Previous investigations in our unit indicated that acute cardiogenic pulmonary edema is associated not only with an increase in left ventricular end-diastolic pressure and pulmonary arterial wedge pressure but also with a relative increase in colloid osmotic (oncotic) pressure and peripheral hemoglobin concentration. This combination of changes suggested that acute congestive heart failure with pulmonary edema, unlike chronic congestive heart failure, is associated with a contraction of intravascular blood volume. In this study, plasma volume changes were measured before and during the treatment of acute cardiogenic pulmonary edema in 14 patients with arteriosclerotic heart disease. The plasma volume measurement in all 14 patients before the initiation of treatment was either normal or decreased. After treatment with the alpha adrenergic blocking agent phentolamine, the plasma volume increased rather than decreased when measured 4 and 12 hours after the initiation of treatment. During this time colloid osmotic pressure and peripheral hemoglobin concentration progressively decreased. These findings suggest that acute cardiogenic pulmonary edema is associated with the extravasation of large quantities of plasma water from the intravascular compartment into the interstitial compartment and contraction of the intravascular plasma volume. The treatment of acute cardiogenic pulmonary edema is associated with the return of hypo-oncotic fluid from the interstitial compartment back into the intravascular compartment with expansion of plasma volume and reduction of colloid osmotic pressure and hemoglobin concentration.
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PMID:Effect of afterload reduction on plasma volume during acute heart failure. 70 95

A calf into which a biolized, total artificial heart (TAH) had been implanted survived for 145 days. All measured physiological parameters except central venous pressure (CVP) were back to normal one month after implantation, and thereafter the animal's physiological development was similar to that of a normal calf. The intimal weight, which was 96 kilograms at implantation, reached 190 kilogram at the end of experiment, with a daily gain rate of 0.9 kilogram per day. After the nineteenth postoperative week, signs of congestive heart failure appeared, such as high venous pressure, ascites, and enlarged liver although the calf outwardly appeared well. On postoperative day 146, the animal started foaming at the mouth, and a convulsion occurred; then, the experiment was terminated after 3,494 hours of pumping. At autopsy, there were acute bilateral bronchopneumonia involving mostly both upper lobes, pulmonary edema, slight chronic pneumonitis, and hepatomegaly. There were no serious thrombotic deposits inside the cardiac prosthesis.
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PMID:Survival for 145 days with a total artificial heart. 83 53

A 36-year-old woman with a Bjork-Shiley prosthetic aortic valve developed acute congestive heart failure and pulmonary edema. She was found to have a new diastolic murmur, absence of valve clicks, and an immobile prosthetic disk as shown by echocardiography. At surgery the valve, which was covered with fibrin and thrombus, was replaced, and she did well following operation.
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PMID:Clinical and echocardiographic manifestations of a thrombosed Bjork-Shiley aortic valve. 85 Aug 19

Pulmonary venoocclusive disease has been established as a definite clinical entity characterized by congestive cardiac failure with pulmonary arterial hypertension, chronic interstitial pulmonary edema, and normal wedge pressure on cardiac catheterization. This disease was diagnosed and confirmed in a patient during life. A review of the 32 patients reported earlier has been done in an attempt to fine possible etiological agents. Early recognition and treatment with anticoagulants, methylprednisolone, aspirin, and dipyridamole may improve the prognosis.
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PMID:Pulmonary venoocclusive disease. 96 9

During a six-year period 15 consecutive patients with isolated aortic regurgitation due to infective endocarditis were encountered. None had prior significant aortic valve disease. Elective valve replacement was performed in 13 patients; emergency operation was needed in only 1 patient because of intractable pulmonary edema. One patient died suddenly from acute heart block while undergoing medical treatment. Preoperative cardiac catheterization studies in 10 of the 14 patients revealed gross elevations of left ventricular end-diastolic pressure, pulmonary hypertension, depressed cardiac output, and 3 to 4+ aortic regurgitation. There was 1 early and 1 late postoperative death, both due to systemic embolism, yielding an overall surgical mortality of 14%. After a mean follow-up of 18 months, 10 of the 11 patients are in New York Heart Association Functional Class I. Most patients with acute aortic regurgitation secondary to infective endocarditis have clinically observable congestive heart failure and will eventually require valve replacement. If congestive heart failure can be stabilized by a medical regimen, a course of antibiotic therapy can be administered and elective valve replacement can be performed. The time taken for preoperative antibiotic treatment is not associated with irreversible myocardial damage sufficient to influence the results of operation.
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PMID:Surgical treatment of acute aortic regurgitation in infective endocarditis. 99 71

Continuing evaluation of coronary care is necessary to determine its present effectiveness and to establish direction in the effort to decrease mortality after myocardial infarction. Data have been collected on 157 consecutive patients diagnosed as having myocardial infarction who were admitted to the coronary-care unit at St. Joseph's Hospital and Medical Center, Phoenix, Ariz. The hospital is a teaching hospital with a 560-bed capacity. Data sheets were completed on each patient at the time of transfer from the coronary-care unit. The accumulated data were processed by a computer at the end of a 13-month period. The overall mortality for the group was 16.5 per cent. The factors which were found to have a significant effect on mortality were: (1) location of infarction, (2) presence of heart failure, (3) occurrence of cardiogenic shock, (4) age, and (5) the presence of intraventricular conduction defect. In 19 of the 26 deaths after myocardial infarction, the terminal event was associated with congestive heart failure, pulmonary edema, or cardiogenic shock. Three patients died of resistant arrhythmia, four of ventricular rupture. These figures indicate that arrhythmia is not a primary cause of death after myocardial infarction and that attention must also be directed to the early diagnosis and treatment of left ventricular failure if coronary care survival rates are to improve.
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PMID:Continuing evaluation of coronary care. 103 78


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