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

A 32-year-old man (weight 132 kg, height 190 cm) suddenly became unconscious and cyanosed with an unrecordable pulse and ventricular flutter on ECG. After resuscitation, the blood pressure was 200/100 mm Hg; the patient moved his arms and legs at times, but he did not regain consciousness. Focal neurological signs and meningism were not demonstrable. Subsequent ECGs showed a raised ST segment, followed later by terminal T wave inversion; marked pulmonary oedema was present clinically and radiologically. The creatine kinase activity was 344 U/l. As lateral myocardial infarction was suspected, the patient received heparin (1000-1700 IU/h) and nitroglycerin intravenously. Because the CK-MB isoenzyme failed to rise significantly and there was no reduction of R wave on the ECG, a CT scan of the brain was performed: this showed brain oedema as well as severe subarachnoid haemorrhage in the basal subarachnoid space, the posterior horn of the lateral ventricles and over the cerebral hemispheres. Despite implantation of an epidural pressure gauge, hyperventilation and administration of dexamethasone, osmotic diuretics and thiopental, the patient died 14 days after collapsing. At autopsy the heart showed no signs of myocardial infarction. The cause of the subarachnoid haemorrhage was a ruptured aneurysm of the anterior communicating artery.
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PMID:[Subarachnoid hemorrhage with pulmonary edema and electrocardiographic changes. The differential diagnosis of myocardial infarct]. 157 49

Exercise-induced pulmonary uptake of thallium-201 in patients with ischemic heart disease is probably due to transient pulmonary edema and left ventricular failure induced by exercise. The significance of increased lung uptake of thallium-201 at rest after acute myocardial infarction (AMI) has not been described. Ninety-six patients admitted with chest pain for suspected AMI or unstable angina underwent thallium-201 imaging at rest. Using conventional diagnostic criteria, 62 had AMI, 12 had unstable angina and 22 had neither. Increased lung uptake of thallium-201 was present in 24 of the total 96 (25%) patients, 20 of the 62 (32%) patients with AMI and 4 of 34 (13%) patients with no evidence of infarction. In the AMI group, those with increased lung thallium-201 uptake had a higher mean +/- standard deviation segmental thallium-201 defect score (22 +/- 7 vs 12 +/- 8, p less than 0.0001), lower ejection fraction (35 +/- 14 vs 49 +/- 14%, p less than 0.002), higher peak creatine kinase levels (2,410 +/- 1,247 vs 1,496 +/- 1,228 IU/liter, p less than 0.01), higher wall motion abnormality score (25 +/- 13 vs 13 +/- 12, p less than 0.0001), increased incidence of clinical in-hospital heart failure (15 of 20 vs 7 of 42, p less than 0.0001) and higher short-term mortality (4 of 20 vs 1 of 42, p less than 0.02) compared to those without increased lung thallium-201 uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and prognostic significance of lung thallium uptake on rest imaging in acute myocardial infarction. 229 83

Sixty-four patients with cardiac contusion documented by electrocardiographic changes and creatine kinase MB fraction assay following blunt chest injury were reviewed to assess the impact of cardiac contusion on subsequent management. Fifty-eight patients had elevated creatine kinase MB levels; 35 patients had electrocardiographic abnormalities, including ST-segment and T-wave changes (25), premature ventricular contraction (ten), right bundle-branch block (nine), atrioventricular block (three), atrial fibrillation (three), and premature atrial contraction (two). Thirty patients underwent general anesthesia. There were only four perioperative complications: ventricular ectopy, ventricular fibrillation, nodal rhythm, and pulmonary edema. There were no deaths attributable to cardiac contusion. In summary, patients with blunt trauma who have sustained a cardiac contusion can undergo elective operation with a low incidence of complication. In the emergency setting, however, hemodynamic monitoring for early detection of arrhythmias is indicated.
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PMID:Cardiac contusion. The effect on operative management of the patient with trauma injuries. 232 24

A 56-year-old woman with no history of cardiac disease developed acute pulmonary edema following a subarachnoid hemorrhage. A constellation of findings, including elevated creatine kinase MB isoenzyme activity in the absence of electrocardiographic or scintigraphic evidence of acute myocardial infarction, elevated pulmonary artery wedge pressure, segmental wall motion abnormalities, and depressed ejection fraction of the left ventricle demonstrated by two-dimensional echocardiography and radionuclear ventriculography, pointed to a direct myocardial injury leading to cardiac failure. The evidence for cardiogenic origin of pulmonary edema provided by this case is in contrast to the belief that "neurogenic" pulmonary edema is of noncardiac origin.
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PMID:Pulmonary edema associated with subarachnoid hemorrhage. Evidence for a cardiogenic origin. 382 38

A report is made of a 44-year-old female who died of malignant hyperthermia during general anesthesia for an operation of left subtrochanteric femoral fracture. Symptoms began with increases in heart rate and blood pressure after the introduction of anesthesia with halothane and were accelerated by the administration of succinylcholine, followed by muscle rigidity and high temperature. The typical wine red urine was observed. The oral temperature of 42 degrees C was recorded within 1 h after succinylcholine. The rectal temperature was 30 degrees C 22 h after death. Severe pulmonary edema and tubular necrosis of the kidney were found by postmortem examination. No latent myopathy was observed. The creatine phosphokinase levels in plasma obtained after the onset of malignant hyperthermia and at the time of autopsy were abnormally high and were 5632 and 34,854 mU/ml, respectively. Plasma myoglobin levels were 130,000 and 2.8 X 10(6) ng/ml, respectively.
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PMID:An autopsy case of malignant hyperthermia. 398 93

The extent of abnormality in early thallium-201 and gated cardiac blood pool scintigrams has been reported to be useful for predicting mortality in patients with acute myocardial infarction (AMI). To compare the two techniques, 91 patients admitted consecutively with evident or strongly suspected AMI underwent both imaging studies within 15 hours of the onset of symptoms. Patients with pulmonary edema or shock were excluded. AMI developed in 84% of patients, and 6-month mortality for the entire group was 16%. A thallium defect score of 7.0 or greater (corresponding to at least a moderate reduction of activity involving 40% of the left ventricular circumference) identified a subgroup of 14 patients with 64% 6-month mortality rate. Similarly, a left ventricular ejection fraction of 35% or less identified a high-risk subgroup of 10 patients with a 6-month mortality of 60%. Mortality in the remaining patients was 8% for thallium score less than 7 and 11% for ejection fraction greater than 35%. The mortality rate was highest among patients who had concordant high-risk scintigrams (five of six, 83%), lowest in those with concordant low-risk studies (five of 64, 8%) and intermediate in those with discordant results (four of 11, 36%). Of a number of clinical variables, only the appearance of Q waves, peak creatine kinase greater than 1000 IU/I, and history of infarction were significantly associated with mortality. High-risk thallium or blood pool scintigraphic results were significantly more predictive and a thallium score of 7 or greater was more sensitive for detecting nonsurvivors than ejection fraction 35% or less at a similar level of specificity. Stepwise multiple logistic analysis showed that the thallium score was the best predictor of mortality, but that appearance of Q waves and ejection fraction were additive. Using these three variables, 11 patients were calculated to have a 50% or greater chance of dying and eight (73%) actually died, compared with six of 70 (9%) with a calculated chance of death of less than 50%. These results in a prospectively identified and consecutive group of patients support the value of early thallium and blood pool scintigraphy for separating high- and low-risk subgroups of hemodynamically stable infarct patients.
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PMID:Comparison of early thallium-201 scintigraphy and gated blood pool imaging for predicting mortality in patients with acute myocardial infarction. 630 24

Monensin was administered orally to 3 sheep at dosages of 12 (the LD50), 16, and 24 mg/kg of body weight, respectively. Clinical signs of monensin toxicosis were observed in the sheep in 24 to 36 hours of administration. Clinical signs included CNS depression, anorexia, diarrhea, and stiffness. Increased serum creatine phosphokinase and aspartate aminotransferase activities identified possible muscle damage. Sheep were euthanatized at 54 hours after dosing; at necropsy, there were skeletal muscle hemorrhages, pale myocardium, and pulmonary edema. Ultrastructural lesions were in the liver, diaphragm, and myocardium; diaphragm and myocardium were most severely affected. Mitochondrial swelling and cristolysis, swollen sarcoplasmic reticulum, and disruption of myofibrillar architecture were prominent. These ultrastructural changes are consistent with the hypothesis that monensin causes muscle cell necrosis due to its ionophorous properties and disruption of cellular Na+:Ca2+ balance. It is proposed that this upset of normal ionic processes allows increased intracellular calcium, which directly leads to the functional and structural mitochondrial changes observed.
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PMID:Acute monensin toxicosis in sheep: light and electron microscopic changes. 674 73

In a controlled randomized study of 328 consecutive patients admitted within 24 hours after the onset of acute myocardial infarction, 163 patients received a sodium nitroprusside infusion during 24 hours, followed by six times a day 5 mg isosorbide dinitrate for seven days and 165 patients received a glucose 5% infusion. Excluded from the study were patients with either pulmonary edema and/or cardiogenic shock, two or more previous myocardial infarctions or a systolic blood pressure of less than 95 mmHg just before entering the study. Sodium nitroprusside was titrated in such a way that systolic blood pressure was kept between 95 and 105 mmHg. Standard medical treatment for both groups was the same. CK-MB was sampled every four hours until peak value was reached. Endpoint of the study was a significant reduction in mortality within a week after starting treatment.
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PMID:Treatment of acute myocardial infarction with sodium nitroprusside during 24 hours, followed by isosorbide dinitrate. 703 72

This prospective evaluation of 55 consecutive patients, aged 60 years or older, admitted in 1977-1978 to a community hospital coronary care unit for treatment of cardiogenic pulmonary edema, examines morality during hospitalization and during the subsequent one-year follow-up. Their treatment was based on clinical criteria, without the "advantage" of Swan-Ganz catheters and before widespread use of vasodilators for severe congestive heart failure. Multiple clinical and laboratory features were reviewed to determine possible prognostic clues. The nine patients who died during the initial hospitalization provided several clues to immediate mortality, including admission systolic blood pressure of less than 150 mm Hg, dyspnea for more than four hours, and peak creatine kinase values greater than 1,000 IU/L. The study identified high-risk patients who may benefit from more aggressive in-hospital therapy. The one-year mortality among the 46 patients discharged from the hospital was high (43%). Most noninvasive methods were not useful in attempting to predict one-year survival. The important question of whether newer therapeutic methods including vasodilators will favorably alter the relatively poor long-term prognosis in the elderly needs further study.
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PMID:Acute cardiogenic pulmonary edema in the elderly: factors predicting in-hospital and one-year mortality. 707 13

A reversible and presumably neurogenic form of myocardial dysfunction may occur following subarachnoid hemorrhage (SAH), but the relationship of this finding to electrocardiographic abnormalities remains unclear. To clarify this issue, serial electrocardiograms (ECGs, mean 6.2 per patient) and echocardiograms (mean 3.4 days after SAH) were obtained in 57 SAH patients without preexisting cardiac disease. The goal was to determine which specific electrocardiographic changes, if any, reflect abnormal left ventricular wall motion in acute SAH. Wall motion abnormalities were identified in five (8%) of 57 patients. Four of these affected patients experienced hypotension (systolic blood pressure < 100 mm Hg) and three exhibited pulmonary edema within 6 hours of SAH, compared to none of the 52 patients with normal wall motion (p < 0.0001). Patients with abnormal wall motion were more likely than patients with normal echocardiograms to have symmetrical T wave inversion (five of five vs. seven of 52, p < 0.001) and severe (> or = 500 msec) QTc segment prolongation (five of five vs. three of 52, p < 0.001) on serial ECGs. These associations maintained their significance with analysis limited to single ECGs performed on or near the day of echocardiography. Abnormal wall motion was also associated with borderline (2% to 5%) creatine kinase MB elevation (five of five vs. three of 52, p < 0.001) and poor neurological grade (p < 0.0001). Although no combination of findings on a single ECG resulted in 100% sensitivity for abnormal wall motion, the presence of either inverted T waves or severe QTc segment prolongation on serial ECGs was associated with 100% sensitivity and 81% specificity. These results demonstrate an association between reduced left ventricular systolic function, mild creatine kinase MB elevation, and electrocardiographic repolarization abnormalities in acute SAH. Symmetrical T wave inversion and severe QTc segment prolongation best identified patients at risk for myocardial dysfunction and may serve as useful criteria for echocardiographic screening following SAH.
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PMID:Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage. 747 60


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