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 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of dobutamine stress echocardiography for the evaluation of coronary artery disease is rapidly expanding. Despite its widespread use, the feasibility and safety of dobutamine stress echocardiography has not been sufficiently documented. Between November 1992 and June 1995, we performed 1000 dobutamine stress echocardiographies. There were 744 men and 256 women with a mean age of 59 +/- 11 years. Anti anginal medication was not routinely withdrawn before the test. The mean maximal dobutamine dose was 41,4 +/- 10 mu g/kg center dot min(-1). Atropine was given additionally in 440 patients, with a mean dose of 0.5 mg. In patients receiving beta-blockers additional atropine was more often necessary as compared to those not receiving beta-blockers (278/457 = 61% versus 162/543 = 30 %, p < 0.0001). Reasons for discontinuing dobutamine infusion were achievement of target heart rate (64 % of cases) and maximal dose (12 % of cases). In 791 (79,1 %) patients no side-effects of dobutamine stress echocardiography were noticed. Termination of the study because of adverse side-effects occurred in 6.6 %. A total of 103 (10,3 %) noncardiac side-effects were observed: dizziness or nausea 6.4 %, headache 1.7 %. In one patient a focal cerebral seizure occurred. 156 cardiac side-effects occurred: blood pressure decrease of more than 20 mm Hg in 25 patients, extreme palpitations in 16 patients and pulmonary edema in one case. Most common cardiac side-effects consisted of arrhythmias (11.4 %): 9.1 % ventricular and 2.3 % supraventricular arrhythmias. Most ventricular arrhythmias were less severe (uniform and multiform premature ventricular beats, ventricular bigeminy or couplets in 71 patients). Nonsustained ventricular tachycardia, with a maximum duration of 20 s, occurred in 18 patients. In one patient sustained ventricular tachycardia developed and progressed towards ventricular fibrillation. This patient could be successfully defibrillated. Supraventricular arrhythmias presented as new atrial fibrillation in 10 patients, supraventricular tachycardia in three patients, junctional rhythm with a short decline in heart rate in nine patients and a second-degree AV block in another case. Dobutamine stress echocardiography has proven to be a safe and feasible method in the diagnosis of coronary heart disease. Minor side-effects are common and sometimes unpleasant for the patient, but do not often require termination of the study. Severe side-effects are seldom (< 1 %), but nevertheless, adequate medical and technical (defibrillator) support should be rapidly available.
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PMID:[Feasibility and safety of dobutamine stress echocardiography: experiences with 1,000 studies]. 871 45

A syndrome of acute pulmonary edema has been previously reported among scuba divers in cold, European waters. Because of the temperatures involved, the name "cold-induced pulmonary edema" was coined in the original 1989 description. We report six individuals who developed the identical syndrome, five while diving in Puget Sound and one in the Gulf of Mexico. The four women and two men ranged in age from 24 to 60 yr. They experienced one to six episodes apiece, each with the development severe dyspnea at depth without excessive exertion. Associated symptoms included cough, weakness, expectoration of froth, chest discomfort, orthopnea, wheezing, hemoptysis, and dizziness. Emergency medical evaluation of four divers revealed rales on examination and pulmonary edema on chest radiograph. In one diver with pulmonary edema on chest radiograph, pulmonary capillary wedge pressure was normal when measured acutely. Symptoms resolved either spontaneously over 1-2 days or with standard medial treatment for pulmonary edema. Prior history of cardiovascular disease was negative except for hypertension and mitral valve prolapse in one diver. Cardiac evaluations following recovery from the acute episodes were normal. Episodes in the cold waters of Puget Sound sometimes occurred despite the use of dry suits. Furthermore, one diver developed recurrent episodes in 27 degrees C water off Cozumel, Mexico. Development of pulmonary edema while scuba diving constitutes a distinct clinical entity which may occur in either "cold" or "warm" water. It is not associated with a decompression mechanism. Personnel caring for divers should be aware of the syndrome in order to provide optimal medical management.
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PMID:Pulmonary edema of scuba divers. 906 53

Hydrochlorothiazide is one of most commonly prescribed antihypertensive diuretics. In this case, an allergic reaction to hydrochlorothiazide resulted in severe pulmonary edema. Hydrochlorothiazide, one of the most commonly prescribed drugs, is a diuretic which is usually well tolerated. Common side effects include dizziness, weakness, fatigue, and cramps. These side effects are usually caused by fluid and electrolyte imbalances. Acute pulmonary edema, first reported by Steinberg in 1968, is a rare but potentially life-threatening allergic reaction to hydrochlorothiazide. This case illustrates many of the typical presenting features of the reaction.
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PMID:Acute pulmonary edema caused by ingestion of hydrochlorothiazide. 908 57

Carbon monoxide (CO) may be the cause of more than one-half of the fatal poisonings reported in many countries; fatal cases also are grossly under-reported or misdiagnosed by medical professionals. Therefore, the precise number of individuals who have suffered from CO intoxication is not known. The health effects associated with exposure to CO range from the more subtle cardiovascular and neurobehavioral effects at low concentrations to unconsciousness and death after acute or chronic exposure to higher concentrations of CO. The morbidity and mortality resulting from the latter exposures are described briefly to complete the picture of CO exposure in present-day society. The symptoms, signs, and prognosis of acute CO poisoning correlate poorly with the level of carboxyhemoglobin (COHb) measured at the time of hospital admission; however, because CO poisoning is a diagnosis frequently overlooked, the importance of measuring COHb in suspicious settings cannot be overstated. The early symptoms (headache, dizziness, weakness, nausea, confusion, disorientation, and visual disturbances) also have to be emphasized, especially if they recur with a regular periodicity or in the same environment. Complications occur frequently in CO poisoning. Immediate death is most likely cardiac in origin because myocardial tissues are most sensitive to the hypoxic effects of CO. Severe poisoning results in marked hypotension, lethal arrhythmias, and electrocardiographic changes. Pulmonary edema may occur. Neurological manifestation of acute CO poisoning includes disorientation, confusion, and coma. Perhaps the most insidious effect of CO poisoning is the development of delayed neuropsychiatric impairment within 2-28 days after poisoning and the slow resolution of neurobehavioral consequences. Carbon monoxide poisoning during pregnancy results in high risk for the mother by increasing the short-term complication rate and for the fetus by causing fetal death, developmental disorders, and chronic cerebral lesions. In conclusion, CO poisoning occurs frequently; has severe consequences, including immediate death; involves complications and late sequelae; and often is overlooked. Efforts in prevention and in public and medical education should be encouraged.
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PMID:Carbon monoxide poisoning--a public health perspective. 1077 Nov 27

The symptoms and severity of anemia depend on various factors, including the degree of anemia, the rapidity of its onset, and the age and physiologic status of the patient. Although the human body tries to counterbalance the effects of anemia by various mechanisms, almost every organ system of the human body is eventually affected. The symptoms experienced by patients vary from cold skin, dizziness, and palpitations to pulmonary edema, heart failure, depression, and severe impairment of cognitive function. Anemia substantially impacts patients' quality of life, a fact that has been shown in several clinical trials in patients with renal disease as well as in patients suffering from various malignancies undergoing chemotherapy. These studies evaluated the administration of recombinant human erythropoietin (r-HuEPO, epoetin alfa) to anemic patients, and it was shown that raising hemoglobin levels with epoetin alfa ameliorated the symptoms of anemia and significantly improved the functional status and overall quality of life in cancer patients. Furthermore, preliminary data indicate that the correction of anemia in cancer patients may in addition improve treatment efficacy and possibly overall survival.
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PMID:Symptomatology of anemia. 1139 46

Carbon monoxide (CO) has the toxic effects of tissue hypoxia and produces various systemic and neurological complications. The main clinical manifestations of acute CO poisoning consist of symptoms caused by alterations of the cardiovascular system such as initial tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, paresis, convulsion and unconsciousness. CO poisoning also produces myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, erythrocytosis, leucocytosis, hyperglycemia, muscle necrosis, acute renal failure, skin lesion, and changes in perception of the visual and auditory systems. Of considerable clinical interest, severe neurological manifestations may occur days or weeks after acute CO poisoning. Delayed sequelae of CO poisoning are not rare, usually occur in middle or older, and are clinically characterized by symptom triad of mental deterioration, urinary incontinence, and gait disturbance. Occasionally, movement disorders, particularly parkinsonism, are observed. In addition, peripheral neuropathy following CO poisoning usually occurs in young adults.
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PMID:Carbon monoxide poisoning: systemic manifestations and complications. 1141 Jun 84

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

Sodium azide, used mainly as a preservative in aqueous laboratory reagents and biologic fluids and as a fuel in automobile airbag gas generants, has caused deaths for decades. Its exposure potential for the general population increases as the use of airbags increase. In order to characterize the known health effects of sodium azide in humans and the circumstances of their exposure, the authors conducted a systematic review of the literature from 1927 to 2002 on human exposure to sodium azide and its health effects. The most commonly reported health effect from azide exposure is hypotension, almost independent of route of exposure. Most industrial exposures are by inhalation. Most laboratory exposures or suicide attempts are by ingestion. Most of the reported cases involved persons working in laboratories. The time between exposure and detection of hypotension can predict outcome. Fatal doses occur with exposures of >or=700 mg (10 mg/kg). Nonlethal doses ranged from 0.3 to 150 mg (0.004 to 2 mg/kg). Onset of hypotension within minutes or in less than an hour is indicative of a pharmacological response and a benign course. Hypotension with late onset (>1 hour) constitutes an ominous sign for death. All individuals with hypotension for more than an hour died. Additional health effects included mild complaints of nausea, vomiting, diarrhea, headache, dizziness, temporary loss of vision, palpitation, dyspnea, or temporary loss of consciousness or mental status decrease. More severe symptoms and signs included marked decreased mental status, seizure, coma, arrhythmia, tachypnea, pulmonary edema, metabolic acidosis, and cardiorespiratory arrest. The signs and symptoms from lower exposures (<700 mg) are physiological responses at the vascular level and those at or above are toxicological responses at the metabolic level. There is no specific antidote for sodium azide intoxication. Recommended preventive measures for sodium azide exposure consist of education of people at high risk, such as laboratory workers, regarding its chemical properties and toxicity, better labeling of products containing sodium azide, and strict enforcement of laboratory regulations and access control.
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PMID:Human health effects of sodium azide exposure: a literature review and analysis. 1285 Nov 50

Clinical reports on unintentional mass exposure to extreme concentrations of carbon dioxide are rare. We describe an industrial incident caused by a container of liquid carbon dioxide that was unintentionally opened in an enclosed working environment. Twenty-five casualties reached our emergency department. Symptoms included dyspnea, cough, dizziness, chest pain, and headache. ECGs (n=15) revealed ST-segment changes in 2 (13.3%) patients, atrial fibrillation in 2 patients, and non-Q wave myocardial infarction in 1 patient. Chest radiographs (n=22) revealed diffuse or patchy alveolar patterns, consistent with pneumonitis, in 6 (27%) patients and pulmonary edema in 2 (9%) patients. Eleven (44%) patients were admitted to the hospital: 8 were discharged 24 hours later and the others within 8 days. No patient died. Exposure to high concentrations of carbon dioxide resulted in significant but transient cardiopulmonary morbidity with no mortality when victims were promptly evacuated and given supportive therapy. Cardiac complications were frequently observed and should be actively sought.
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PMID:Exposure to extremely high concentrations of carbon dioxide: a clinical description of a mass casualty incident. 1474 8

There is growing awareness of sick sinus syndrome (SSS) and related arrhythmias as treatable causes of epilepsy, syncope, dizziness, confusion and some psychoses, as well as non-neurological symptoms such as episodic congestive heart failure, pulmonary edema and palpitations. Six cases are presented which occurred in family practice in a period of 18 months; four required ventricular pacing, one declined and one is asymptomatic.
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PMID:The neurological presentation of sick sinus syndrome. 2129 1


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