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)

Simple cardiopulmonary functions were studied serially in 26 mountaineers between sea level and an altitude of 25,200 ft. Up to 12,000 ft there was no altitude sickness, though there were complaints of leech bite (26.9%) and blisters (3.8%). One member died of exhaustion, two developed pulmonary oedema, one "flu" (at 15,600 ft) and one pleural rub (at 21,000 ft). Up to 16,000 ft altitude, 4 to 7.7% developed diarrhoea or epistaxis only, but at higher levels 25 to 50% subjects developed several symptoms, besides excessive dyspnea. These included diarrhoea (35-60%), vomiting (30%) abdominal pain (35-60%), rectal bleeding (15%), chest pain (10-40%), dry cough (40-60%), giddiness (30%) and poor memory (7.7%). A small rise in blood pressure was seen (for systolic at lower and diastolic at greater altitudes). After 18,200 ft the steady increase seen in VE slowed and the rise in heart rate and respiratory rate (f) became steeper. After a small rise at 7,800 ft, FVC and FEV1 showed a gradual decline at higher altitudes. After a large initial increase in PEFR up to 12,000 ft, a gradual decline was seen. The mean weight loss during the expedition was 8 +/- 2.7 kg. These changes seem to be due to an incomplete acclimatisation, which future mountaineering teams should take into consideration to avoid health problems and improve performance.
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PMID:Cardiopulmonary functional changes in acute acclimatisation to high altitude in mountaineers. 225 31

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

The clinical features of 304 patients with acute myocardial infarction with and without hypertension were studied retrospectively. This inner city population consisted of 172 (57%) males and 132 (43%) females; 155 (51%) patients were black, 88 (29%) Hispanic, and 61 (20%) white by self-identification. Hypertension (greater than or equal to 160/95 mmHg) was present on admission in 46% (139) of patients. Typical ischaemic chest pain was the most common presenting symptom and occurred with a similar frequency in patients with and without hypertension. However, the group with hypertension consisted of proportionately more females than males, more frequently had previously diagnosed hypertension and congestive heart failure, and more often presented with shortness of breath and pulmonary oedema. The racial distribution, mean ages, prevalence of angina, previous myocardial infarction, diabetes, smoking, family history of cardiovascular disease, type of myocardial infarction, peak creatinine phosphokinase, plasma cholesterol, and mortality rates were similar in both groups. Thus, female sex, history of hypertension, history of congestive heart failure, and pulmonary oedema characterised patients with compared to those without hypertension. These findings suggest that the higher mortality rate observed in hypertensives during follow-up after myocardial infarction may be due, at least in part, to more severe underlying left ventricular dysfunction.
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PMID:Atypical myocardial infarction and hypertension: an inner city experience. 233 76

We developed consensus management guidelines for patients admitted with chest pain, pulmonary edema, and syncope and used these guidelines to examine practice variation and the effects of physician feedback on decision making in 1145 consecutive admissions to three medical intensive care units. Data collection included a 6-month baseline period and two 6-month physician feedback periods. Hospital length of stay fell from 8.34 days to 7.41 and 7.14 days during feedback; intensive care unit length of stay fell from 2.45 days to 2.23 and 2.07 days. Feedback was associated with an increase in the percentage of patients conforming to the management guidelines. Multiple linear regression showed that feedback correlated with reductions of 0.79 days (confidence interval, 0.12 to 1.46) in hospital length of stay and 0.21 days (confidence interval 0.05 to 0.37) in intensive care unit length of stay. This effect was most apparent in patients not requiring any intervention, but with a major complication. During the 6-month follow-up, mortality, readmission, and urgent readmission rates were similar for patients admitted in baseline and feedback periods.
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PMID:Length of stay in the intensive care unit. Effects of practice guidelines and feedback. 237 92

In the 3 Western Washington thrombolytic therapy trials, 54.9% of patients with acute myocardial infarction arrived at the hospital within 2 hours of symptom onset. These early arrivers were younger and more likely to be hypotensive and in cardiogenic shock than were patients arriving later. There were decreases in the time from symptom onset to hospital arrival (p = 0.0002) and in the time from hospital arrival to institution of thrombolytic therapy (p less than 0.0001) in the 8 hospitals that participated in both the Western Washington intravenous streptokinase and tissue plasminogen activator trials from 1983 to 1988. For those patients receiving thrombolysis, early arrival was associated with increased survival (p = 0.031) after adjustment by Cox regression analysis for important clinical predictors of long-term survival. These covariates included pulmonary edema, anterior wall acute myocardial infarction, hypotension and absence of chest pain at hospital arrival. Reductions in barriers to timely administration of thrombolytic therapy can be achieved and can result in improved survival.
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PMID:Early versus late hospital arrival for acute myocardial infarction in the western Washington thrombolytic therapy trials. 249 71

The clinical features of an inner-city population of 304 patients presenting with acute myocardial infarction (MI) with and without typical chest pain, were studied retrospectively. This population consisted of 172 men and 132 women; 155 (51%) were black, 88 (29%) hispanic, and 61 (20%) white, by self-identification. Typical ischemic chest pain was the presenting symptom in 85% (258); 15% (46) presented with nonchest symptoms, most frequently shortness of breath, abdominal pain, and dizziness. But the frequency of such nonchest symptoms was similar in both groups. When patients were grouped by the presence or absence of chest pain, the proportions of those without chest pain were significantly higher for blacks (22.7%) than hispanics (9.1%, P = 0.001) or whites (4.9%, P less than 0.01). Patients without chest pain also had higher admission systolic (P less than 0.01) and diastolic (P less than 0.01) blood pressures and more frequent histories of congestive heart failure (P less than 0.05), and more often presented with pulmonary edema (P = 0.001) than those with chest pain. Both groups were similar in age, sex, history of hypertension, and presence of hypertension on admission, defined as greater than or equal to 160/95 mmHg, prevalence of diabetes, history of smoking, previous MI, type of MI, history of angina, and mortality rates. Patients without chest pain were characterized by black race, history of congestive heart failure, elevated blood pressure and pulmonary edema than those with typical ischemic chest pain. Thus significant delays in the diagnosis and treatment of this important clinical entity may be reduced by alerting clinicians to these features and by educating selected patient groups.
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PMID:Clinical features of patients with acute myocardial infarction presenting with and without typical chest pain: an inner city experience. 252 Aug 50

Nitrofurantoin is a widely prescribed antibiotic used for the treatment of urinary tract infections. In some patients it can produce an acute pulmonary reaction ranging from mild dyspnea to noncardiogenic pulmonary edema. Symptoms include fever, dyspnea, chills, cough, and chest pain. Physical examination generally reveals an acutely ill, extremely apprehensive patient in varying degrees of respiratory distress. Fever is usually present and there is an increase in heart rate and respiratory rate. Cyanosis, rales, and a maculopapular rash are common findings. Laboratory studies typically demonstrate a leukocytosis with eosinophilia, varying degrees of hypoxia and hypocapnia, and a mild to moderate elevation of the erythrocyte sedimentation rate. The chest x-ray study may be normal but more often demonstrates bilateral lower lobe interstitial infiltrates frequently accompanied by pleural effusions. Treatment in the majority of cases requires only stopping the drug, but steroids, bronchodilators, or antihistamines may be used in selected cases. Once the diagnosis is made and the drug withdrawn, prognosis for full recovery is excellent.
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PMID:Acute pulmonary toxicity to nitrofurantoin. 270 84

In a prospective study, 22 patients with prolonged chest pain were monitored by serial serum tumour necrosis factor-alpha (TNF; cachectin) measurements. In five patients serum TNF markedly increased, peaking at greater than 145 ng l-1; all these patients had large infarcts complicated by hypotension, pulmonary oedema and/or arrhythmia. Two of these patients died. In contrast, TNF levels were either normal or only slightly raised in patients with small or uncomplicated infarcts and in patients with prolonged angina without evidence of infarction. The results show that extensive myocardial infarction induces the release of the monocyte/macrophage-derived polypeptide hormone TNF into circulation. This finding may be clinically relevant with respect to systemic metabolic consequences of myocardial infarction.
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PMID:Circulating tumour necrosis factor-alpha (cachectin) in myocardial infarction. 273 71

The chest radiographs of 71 patients who had chest pain or shortness of breath following the smoking of highly potent "crack" cocaine were retrospectively evaluated. Nine patients had abnormal findings on radiographs as follows: atelectasis or localized parenchymal opacification in four, pneumomediastinum in two, pneumothorax in one, hemopneumothorax in one, and pulmonary edema in one. Radiographic detection of these abnormalities was important in the clinical management of these patients. This spectrum of findings is presented with a discussion of the pathophysiologic mechanisms responsible.
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PMID:Chest pain and dyspnea related to "crack" cocaine smoking: value of chest radiography. 274 26

A 27-year-old man was accidentally given 2 mg intravenous epinephrine instead of 2 mg naloxone. He immediately developed chest pain, nausea, and diaphoresis. An ECG taken shortly after the epinephrine administration showed widespread ischemia. Forty-five minutes later the tracing still showed an early repolarization pattern, but ST elevation was less marked and the patient was asymptomatic. Serum potassium was 3.2 mEq/L and serum catecholamines, drawn approximately 20 minutes after the epinephrine administration, were 10 times normal (dopamine, 173 ng/L; epinephrine, 1,628 ng/L; norepinephrine, 1,972 ng/L). There are seven other reports of intravenous epinephrine overdose in the English literature. Two of the previously reported cases had 12-lead ECGs within the first hour. In both there was evidence of transient ischemia similar to that observed in this case. Most of the patients had symptoms consistent with angina, and several developed pulmonary edema. These findings suggest that, in humans, large intravenous doses of epinephrine are likely to produce coronary artery spasm and may decrease coronary artery perfusion.
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PMID:Coronary artery spasm induced by intravenous epinephrine overdose. 275 14


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