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

The hospital courses of 882 consecutive patients with acute myocardial infarction admitted to the coronary care unit (CCU) during a 3-year period were evaluated. Their courses after discharge from the CCU were assessed with reference to the following serious complications which had occurred during their stay in the CCU; ventricular tachycardia or fibrillation, second-or third-degree heart block, pulmonary oedema, cardiogenic shock persistent sinus tachycardia, persistent hypotension, atrial flutter or fibrillation, or extension, or extension of infarction. Of the 494 patients (56%) with one or more of these complications, 38 (8%) died of cardiac causes in hospital after transfer from the CCU. Of 388 patients (44%) in the uncomplicated group, only 2(0,5%) died of cardiac causes after transfer from the CCU. The same patients were classified according to the Coronary Prognostic Index (CPI) of Norris. None of the 54% of patients with a CPI of less than 6 units died in hospital after transfer from the CCU. It is proposed that patients with a CPI of less than 6 units and with none of the listed serious complications during their CCU stay could safely be discharged from hospital earlier than is customary.
 ...
PMID:Prognostic factors in acute myocardial infarction. 91 92

This report represents our experience with 522 consecutive patients with acute myocardial infarction admitted directly to the Duke Coronary Care Unit. Fifty items of information were used to characterize the patients, their hospital course and follow-up. Serious complications included death, ventricular tachycardia or fibrillation, second- or third-degree heart block, pulmonary edema, cardiogenic shock, persistent sinus tachycardia or hypotension, atrial flutter or fibrillation, and extension of infarction. Forty-nine percent of the patients (252 of 522) experienced a serious complication. All patients who experienced any serious complications had at least one of the above during the first four days of hospitalization. Patients who survived through day 4 were subgrouped on the basis of the occurrence (complicated) or lack of occurrence (uncomplicated) of the above on day 5. Complicated patients had a subsequent hospital mortality of 14% and an incidence of late serious complications of 51%. Patients who were uncomplicated through day 4 had a subsequent hospital mortality of zero and an incidence of late serious complications of zero. These data suggest that it would be feasible and ethically justified to conduct a prospective clinical trial of early discharge (7th day) in patients who meet the above criteria for uncomplicated. The potential economic savings through earlier discharge in uncomplicated patients are of major significance.
 ...
PMID:The course of acute myocardial infarction. Feasibility of early discharge of the uncomplicated patient. 113 53

Clinical characteristics and therapeutic problems of neurogenic pulmonary edema (NPE) occurring in the acute stage of severe subarachnoid hemorrhage (SAH) were examined. The relationship between SAH and NPE was studied in 208 patients who arrived at the hospital in the acute stage (within 24 hours after the onset) of severe SAH in the past nine years. NPE was observed in four (6%) of 64 Grade III patients, nine (18%) of 49 Grade IV patients and 20 (21%) of 95 Grade V patients. Higher grade patients tended to be complicated by NPE more frequently. CT findings of these 33 patients with NPE belonged to Fisher's Group 3 or 4 (23 of 110 group-3 patients and 10 of 88 group-4 patients). Concerning ECG abnormalities, depression of ST segment, abnormal T waves, sinus tachycardia, and right bundle-branch block were observed more frequently in the NPE group than in the non-NPE group. In comparison of the age, blood pressure, PaO2, serum electrolyte, WBC, and blood sugar level on admission between the two groups, significantly higher values of diastolic pressure and blood sugar levels were shown in the NPE group than non-NPE group. The mean interval between the onset of SAH and the diagnosis of NPE on chest film was 2.5 hours, while the NPE findings disappeared within three days after the onset of SAH (mean 1.2 days). In all cases, the NPE findings disappeared after a variety of respiratory managements had been carried out.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Clinical evaluation of neurogenic pulmonary edema following acute stage of subarachnoid hemorrhage]. 157 64

The present study was conducted in 30 cases of snake bite to understand fully the intricacies of the cardiac profile and to render help in the management of the problem arising out of them. All were subjected to routine and specific investigations (ECG, X-ray Chest, SGOT). The present study concluded that 57 per cent of patients of snake bite were in 2nd and 3rd decades of life. Viperine snake bite occurred in 93 per cent and elapide snake bite in 7 per cent of cases. Cardiotoxicity was seen in only 25 per cent patients with viperine bite. Seventy-six per cent of the patients presented within 24 hours of the bite. Seventy per cent of patients had haemorrhagic manifestations and 30 per cent had cardiotoxicity. The disturbance in heart rate was seen in 47 per cent, rhythm disturbance in 6.7 per cent, tachycardia in 36.7 per cent and bradycardia in 10 per cent cases. Hypertension was found in 6.7 per cent, hypotension in 16.7 per cent. Thirty per cent of patients had gallop rhythm and it persisted in 16.6 per cent patients till discharge. One patient had evidence of pulmonary edema and one had basal congestion. Cardiomegaly on chest X-ray was found in one patient and elevated SGOT titres were found in ten per cent. Common electrocardiographic changes were sinus tachycardia, sinus arrhythmia (6.6%), sinus bradycardia (10%), tall T-wave in V2 (3.3%), pattern suggestive of acute anterior wall infarction with reciprocal changes (3.3%), myocardial ischemia (10%), non-specific ST-T changes (16.7%) and atrioventricular block (3.3%). The mortality rate was 10 per cent and all these patients had bleeding manifestations and abnormal electrocardiograms.
 ...
PMID:Profile of cardiac complications of snake bite. 225 4

Several studies in the prethrombolytic era on the treatment of acute myocardial infarction identified selected variables from the patient's history, physical examination, chest roentgenogram and electrocardiogram that could be used to estimate mortality in patients with evolving infarction. To extend such assessment to patients receiving thrombolytic therapy, this study evaluated the prognostic utility of several risk factors in the 3,339 patients (2,742 men, 597 women, aged 24 to 78 years) enrolled in Phase II of the Thrombolysis in Myocardial Infarction (TIMI) trial. Before intravenous tissue plasminogen activator was given, the presence of each of eight risk factors was noted: age greater than or equal to 70 years, female gender, a history of diabetes mellitus or previous myocardial infarction, electrocardiographic evidence of evolving anterior infarction or atrial fibrillation, evidence on physical examination of mild pulmonary congestion or hypotension (systolic pressure less than 100 mm Hg) and sinus tachycardia (heart rate greater than 100 beats/min). Of the 3,339 patients, the 78 with pulmonary edema or cardiogenic shock were excluded because their risk was known to be high. Of the remaining 3,261, 864 (26%) had no risk factor (low risk); their mortality rate at 6 weeks was only 1.5%. In contrast, 2,397 (74%) had one or more risk factors (not low risk); of these, 5.3% died in 6 weeks (p less than 0.001). Among those with one or more risk factors, mortality at 6 weeks was related to the number of risk factors on admission; those with four or more had a mortality rate at 6 weeks of 17.2%. Thus, these eight risk factors can be easily remembered and assessed in patients with myocardial infarction who are candidates for thrombolytic therapy and can be used to estimate short-term mortality.
 ...
PMID:Risk stratification before thrombolytic therapy in patients with acute myocardial infarction. The Thrombolysis in Myocardial Infarction (TIMI) Phase II Co-Investigators. 237 10

Approximately 50% of patients hospitalized with acute myocardial infarction have an uncomplicated course and an excellent prognosis. To be considered as having an uncomplicated course, patients should not have ventricular tachycardia or fibrillation, second or third degree atrioventricular block, pulmonary edema, cardiogenic shock, infarct extension, persistent hypotension, sinus tachycardia, or sustained supraventricular tachycardia occurring within the first 4 days of hospitalization. Patients with recurrent angina in the postinfarction period may also be at increased risk. Early and rapidly progressive rehabilitation programs permit the safe discharge of patients with an uncomplicated course after 7 days. Functional exercise testing before, or soon after, early discharge may identify high-risk patients and alter their management.
 ...
PMID:Early discharge after acute myocardial infarction. 635 32

A case of maternal pulmonary edema occurring in a patient in the 32nd week of gestation is presented. This was our first case of pulmonary edema seen during a period of five years' usage of isoxsuprine in the treatment of premature labor. The patient presented was 28 years old, gravida 2, para 1, admitted to the maternity ward with premature uterine contractions. Her past history eliminate cardiac or pulmonary disease. Isoxsuprine therapy was begun with initial dose of 0.04 mg/min. and increased to 0.32 mg/min., the total dose administered was 560 mg during 48 hours. During this period she was given in dexamethasone 24 mg. Fluid balance on the first day of the treatment was +1.7 liters and on the second day +5.2 liters. Forty-eight hours from the commencement of the treatment, the patient experienced shortness of breath and chest pain. Physical examination disclosed wet rales over both lungs, sinus tachycardia and tachypnea. Laboratory examination disclosed hypopotassemia of 3 mEq/liter, hypoxemia (PO2 of 80 torr on 0.5 FiO2 face mask) with mild hyperventilation 28 torr PCO2 with normal ph 7.43. Recognition of the early signs of pulmonary edema enable swift clinical diagnosis and steps to be taken to prevent disasterous condition due to progressive hypoxemia. The prompt treatment in this complication includes discontinuation of isoxsuprine and fluid administration, placement of the patient in an erect position, intravenous furosemid 40 mg, oxygen supplement by face mask and 25 mg of meperidine. The patient's condition dramatically improved though the lung fields became completely clear from wet rales only eight hours from the start of dyspneic attack.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Pulmonary edema occurring after isoxsuprine and dexamethasone treatment for preterm labor: Case report. 666 29

Hyperthermia is a totally different modality from existing treatment modalities. Systemic hyperthermia (S-HT) is effective against advanced tumors which make resistance to conventional cancer therapies. In S-HT, it is essential and very important to manage cardio-pulmonary function in good condition. Especially, PEEP (about 7 cm H2O) is very effective to prevent lung edema. Fifty-four patients with a variety of neoplasms were subjected to S-HT, alone or in combination with chemotherapy, radiotherapy, and immunotherapy. S-HT was performed under general anesthesia by using extracorporeal circuit in corporating a heat exchanger. Usually, S-HT was given for 4-8 hours with 41.5-42.0 degrees C at 2 weeks intervals. Out of 25 evaluable cases, response was obtained in 11 cases (44%) including 2 cases of complete response. Cardio-pulmonary performance was evaluated using a flow directed pulmonary artery catheter (Swan-Ganz catheter). At treatment temperature, all patients showed hyperdynamic conditions and developed a two-fold mean increase in cardiac index. Altogether 172 treatment sessions were associated with sinus tachycardia and a reduction in diastolic pressures. Laboratory abnormalities included thrombocytopenia without sign of D.I.C., moderate hyperglycemia, mild degree of hypophosphatemia, hypolcalemia and transient elevations in liver enzymes. Serum creatinine levels were elevated in all treatment sessions without elevation of serum BUN. Serum levels of calcium and magnesium were stable. All of abnormalities and toxicities were decreased within 1 to 2 weeks after treatments. It is suggested that with carefully monitored conditions S-HT be performed safely without heart failure.
 ...
PMID:[Clinical practice of systemic hyperthermia therapy and physiological responses of the host]. 687 Feb 90

Rabbit Coronavirus (RbCV) infection was divided into two phases based upon day of death and pathologic findings. During the acute phase (days 2-5) heart weights (HW) and heart weight-to-body weight (HW/BW) ratios were increased with striking dilation of the right ventricle. These changes as well as increased dilation of the left ventricle were especially pronounced during the subacute phase (days 6-12). Myocytolysis, pulmonary edema, and degeneration and necrosis of myocytes, were seen during both phases. Myocarditis, pleural effusion, calcification of myocytes, and congestion in the liver and lungs were seen in the subacute phase. Electrocardiograms (ECGs) exhibited low voltage, nonspecific ST-T wave changes, sinus tachycardia, occasional ventricular and supraventricular premature complexes and 2(0) AV block consistent with myocarditis and heart failure. Forty-one percent of the survivors exhibited increased HW and HW/BW ratios, biventricular dilation, interstitial and replacement fibrosis, myocyte hypertrophy and myocarditis. ECGs exhibited nonspecific ST-T wave changes, sinus arrhythmia, occasional ventricular and supraventricular premature complexes and 2(0) AV block. These data suggest that RbCV infection may result in viral myocarditis and heart failure with a proportion of survivors progressing into DCM.
 ...
PMID:Electrocardiographic changes following rabbit coronavirus-induced myocarditis and dilated cardiomyopathy. 820 55

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
 ...
PMID:Hydrogen peroxide poisoning. 1529 93


1 2 Next >>