Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The importance of recognizing symptomatic heart failure with preserved left ventricular (LV) systolic function has only recently been appreciated. To determine its frequency and identify clinical features that make the bedside diagnosis likely, 82 patients admitted for decompensated heart failure were classified into 2 groups based on their LV systolic performance, as defined by fractional shortening (FS): group I (n = 59), with impaired systolic function (fractional shortening less than 24%), and group II (n = 23) with preserved systolic function (fractional shortening greater than or equal to 24%). Mean fractional shortening was 15 +/- 5% and 39 +/- 1% for groups I and II, respectively. Female gender (p less than 0.05), obesity (p less than 0.01) and diastolic blood pressure greater than or equal to 105 mm Hg (p less than 0.05) predominated in group II. Jugular venous distention was identified more frequently in group I (p less than 0.05). No statistically significant difference between the 2 groups was noted among various demographic variables (age, duration of symptoms, history of hypertension, ischemic heart disease and heavy alcohol drinking) or physical findings (S3 gallop, edema, cardiomegaly, pulmonary congestion and pulmonary edema). Echocardiographic mean left ventricular dimension measured 6.6 +/- 1 versus 5.0 +/- 1 cm (p less than 0.01) and mean posterior wall thickness 1.1 +/- 0.3 versus 1.4 +/- 0.4 cm (p less than 0.01) in group I and II, respectively. The combination of diastolic blood pressure greater than or equal to 105 mm Hg and an absence of jugular venous distention had a high specificity and positive predictive value (100%) for identifying group II patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bedside diagnosis of preserved versus impaired left ventricular systolic function in heart failure. 173 66

A 57-year-old woman presented in severe respiratory distress 30 minutes after ingesting hydrochlorothiazide. Pulmonary edema was evident clinically and radiographically. A noncardiogenic etiology was suggested by the lack of jugular venous distention, S3 gallop, or pedal edema, and the presence of a normal cardiac silhouette on chest radiograph. The patient's pulmonary edema remitted with supportive therapy.
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PMID:Noncardiogenic pulmonary edema following hydrochlorothiazide ingestion. 361 70

Twenty five patients of aluminium phosphide poisoning along with clinical evidence of peripheral circulatory failure were studied. Chief symptoms noted were vomiting and epigastric pain though subsequently three patients developed respiratory distress. Sensorium was normal in most of the patients. Three patients developed pulmonary edema. Raised JVP, feeble heart sounds and S3 gallop beside tachy and bradycardia were other cardiovascular manifestations observed in these patients. In 80% of the patients, various types of ECG changes were observed. ST-T changes were observed in 40% of the patients. Echo-cardiography on day 1 revealed marked LV systolic dysfunction (mean ejection fraction-43.52 +/- 10.18% and mean fractional shortening 17.35 +/- 4.97%) in them whereas repeat echocardiography on day 5 indicated normalisation of these values (mean ejection fraction 71.64 +/- 8.61% and mean fractional shortening 34.35 +/- 8.23%). This might be because of direct toxic action of phosphine on myocardium and later when phosphine gets excreted either through lungs or kidney leads to improvement in LV systolic function.
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PMID:Cardiovascular manifestations in aluminium phosphide poisoning with special reference to echocardiographic changes. 877 39

Acute cardiogenic pulmonary edema (ACPE) is a common cardiogenic emergency with a quite high in-hospital mortality rate. ACPE is defined as pulmonary edema with increased secondary hydrostatic capillary pressure due to elevated pulmonary venous pressure. Increased hydrostatic pressure may result from various causes including excessive administration of intravascular volume, obstruction of pulmonary venous outflow or secondary left ventricular failure due to left ventricular systolic or diastolic dysfunction. ACPE must be distinguished from pulmonary edema associated with injury of alveolar capillary membrane caused by various etiologies, i.e. direct pulmonary injury such as pneumonia and indirect pulmonary injury such as sepsis. Numerous clinical manifestations may differentiate ACPE and Non-ACPE. ACPE usually presents with a history of acute cardiac catastrophe. Physical examination reveals a low-flow state, S3 gallop, jugular venous distention and fine crepitant rales with auscultation. The diagnosis of pulmonary edema is made based on symptoms and clinical signs are found through history taking, physical examination, ECG, chest X-ray, echocardiography and laboratory tests including blood gas analysis and specific biomarkers. Medical treatment of ACPE has 3 main objectives, i.e.: (1) reduced venous return (preload reduction); (2) reduced resistance of systemic vascular (afterload reduction); and (3) inotropic support in some cases. Treatment that can be administered includes: vasodilator when there is normal or high BP, diuretics when there is volume overload or fluid retention, and inotropic drugs when there is hypotension or signs of organ hypoperfusion. Intubation and mechanical ventilation may be necessary to achieve adequate oxygenation.
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PMID:Diagnosis and management of cardiogenic pulmonary edema. 2097 97