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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten patients, who were admitted to the Intensive Coronary Care Unit during a one year period with symptomatic bradycardia while on combination therapy with oral diltiazem and beta-blocker agents, are described. The important features of this adverse reaction to drug combination were that it appeared mainly in a relatively elderly age group and with presenting symptoms of lethargy, dizziness, syncope, chest pain, and (in one patient with poor left ventricular function) pulmonary edema. It was not dose dependent and occurred even in very low doses of each drug. Electrophysiologic abnormalities were localized to the sinus node in all 10 patients and the primary rhythm disorders were junctional escape rhythm, sinus bradycardia, and sinus pause. These rhythm abnormalities resolved within 24 h following withdrawal of the offending drugs. Temporary pacemaker insertion was necessary in four patients. The duration of drug combination used before the acute episode range from within hours to up to 2 years. In conclusion, although combination diltiazem/beta blocker therapy is very effective in ischemic syndrome, caution is advised when this combination is used especially in the elderly or in patients with left ventricular dysfunction or antecedent sinoatrial or atrioventricular conduction abnormality.
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PMID:Symptomatic bradycardia induced by the combination of oral diltiazem and beta blockers. 168 24

A spectrum of presentation of phaeochromocytoma in black South Africans is described. Ten patients were reviewed over a 9-year period. Sweating, headache, and palpitations were prominent symptoms in 9 patients; postural dizziness occurred in 5; gastro-intestinal symptoms in 7; diabetes in 3; and hypertension in all. One patient developed a phaeochromocytoma crisis, characterised by hypotension and pulmonary oedema, before operation. One woman presented in pregnancy. Urinary vanillylmandelic acid was elevated in 9 out of 10 subjects tested; plasma catecholamines were elevated in 6 out of 6 tested. Computed tomography detected 7 adrenal tumours and 3 paragangliomas. All patients were stabilised pre-operatively with alpha- and/or beta-receptor blockers. Intraoperative pressor crises were controlled with sodium nitroprusside, phentolamine, or magnesium sulphate infusions. At operation all tumours appeared benign, each was successfully removed, and the diagnosis confirmed on histological examination. There was no operative mortality. Two patients had residual hypertension. This study highlights the various challenges presented by this catecholamine-producing tumour.
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PMID:Phaeochromocytoma. A report of 10 patients. 199 41

Altitude sickness is a clinical syndrome that occurs with abrupt ascents to altitudes of 3000 metres and above. Symptoms include headache, malaise, fatigue, dizziness, anorexia, nausea and vomiting, and oliguria. At higher altitudes more severe illness resulting from pulmonary oedema or cerebral oedema can occur.
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PMID:Altitude sickness. 232 86

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

A hypertensive urgency should be distinguished from a hypertensive emergency. Although the distinction may not always be obvious, certain guidelines may help the clinician determine which therapeutic approaches are most appropriate for each patient. Hypertensive emergencies include those conditions in which new or progressive severe end-organ damage is present and a delay in appropriate therapy might result in permanent damage, progression of complications, and a poor prognosis. Hypertensive urgencies include those conditions with minimal to no obvious end-organ damage in which blood pressure should be lowered expeditiously. The risk of immediate complications or organ damage is less likely to occur, and thus the immediate prognosis is better, although the ultimate prognosis, if untreated, is poor. There is a marked individual, racial, sexual, and age difference in the ability to tolerate high intraarterial pressure, as evidenced by patients' symptoms and signs of end-organ damage. Patients may have no symptoms of elevated blood pressure until significant intraarterial levels are reached. If symptoms are present, they may include headache, dizziness, blurred vision, shortness of breath (especially with exertion), chest pain, rapid pulse, palpitations, malaise and fatigue, nocturia, or pedal edema. Signs of hypertensive disease vary and depend not only on the level of blood pressure but also include funduscopic changes with arteriolar narrowing, atrioventricular nicking, hemorrhages, exudates or papilledema, central nervous system changes and neurologic abnormalities, cardiac changes with gallop rhythm, cardiomegaly, tachycardia, ectopic ventricular beats, left ventricular hypertrophy or signs of congestive heart failure, pulmonary edema, and signs of renal insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertensive emergencies and urgencies: pathophysiology and clinical aspects. 394 53

A simultaneous approach to revascularization for combined coronary and carotid disease today is well accepted. The discussion about combined procedures of carotid and aortoiliac occlusive disease is still going on. We operated upon 3 patients, aged 63,56 and 65 years, who suffered from carotid, aortoiliac and renal artery disease. Main symptoms were hypertensive crisis with pulmonary edema and intermittent claudication. Dizziness, transient ischemic attacks and slight renal insufficiency were present in two, one and two patients respectively. After recompensation a simultaneous operation was performed: carotid endarterectomy with inlying shunt, reconstruction and patch-plasty of the renal arteries and implantation of a aortofemoral artery bypass graft. Postoperative complications: hypertensive crisis, low output syndrome and oliguria (1 pt.) and deep vein thrombosis (1 pt.) could be treated conservatively. 10 and 12 months later the patients are symptom-free except one, who suffers from angina NYHA II. In conclusion we recommend carotid endarterectomy simultaneously with any major vascular procedure, if a critical stenosis is visualized to improve long-term survival in addition to reducing operative mortality.
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PMID:[Simultaneous intervention on the carotid artery, abdominal aorta and their branches]. 400 9

Six cases of oral intoxication with lindane-solvent mixtures are reviewed. The ingested doses of lindane (mean dosage 120 mg/kg +/- 86 mg/kg) and benzene (mean dosage 366 mg/kg +/- 93 mg/kg) exceeded the toxic level. Symptoms (vomiting, dizziness and hyperreflexia) occurred within 30 min and all patients had epileptiform seizures. Two patients suffered from pulmonary edema and one of them had a severe rhabdomyolysis. Diazepam was sufficient to control convulsions in five cases. Gastric lavage was performed in five patients and activated charcoal, liquid paraffin with saline cathartic, and cholestyramine were used as adsorbents. Recovery was complete in all patients.
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PMID:Acute oral poisoning with lindane-solvent mixtures. 619 84

We reported a case of 50-year-old male who was found to have SSS after induction of general anesthesia though his preoperative cardiac function studies including Holter ECG were normal. He was scheduled to have anterior transposition of ulnar nerve for idiopathic ulnar nerve palsy. He had suffered from lung edema during the same operation about 10 months previously at another hospital and the cause had been unknown. We monitored direct radial artery pressure continuously before induction of general anesthesia. About 5 minutes after the induction, ECG showed bradycardia of less than 40.min-1 and systolic blood pressure decreased to 40 mmHg. Intravenous injection of atropine increased heart rate to 60.min-1 only transiently. We began continuous infusion of isoproterenol. It was effective and no bradycardia and hypotension occurred afterwards throughout the operation. About 2 months later, he showed severe dizziness and Holter ECG revealed sinus arrest for 5 seconds. Therefore, a permanent pacemaker was implanted.
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PMID:[Sick sinus syndrome discovered after induction of general anesthesia in a patient with normal preoperative Holter ECG]. 793 75

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of headache, insomnia, anorexia, nausea, and dizziness, to more serious manifestations, such as vomiting, dyspnea, muscle weakness, oliguria, peripheral edema, and retinal hemorrhage. Although the primary cause of these symptoms is related to the reduced oxygen content and humidity of the ambient air at high altitudes, the physiologic pathway relating hypoxemia to AMS and its sequelae remains unclear. Tips on self-diagnosis and symptom recognition are critical elements to be included in educating patients who are contemplating a trip to high altitudes. Preventive strategies include allowing 2 days of acclimatization before engaging in strenuous exercise at high altitudes, avoiding alcohol, and increasing fluid intake. Conditioning exercise for patients older than 35 years is also recommended before departure. A high-carbohydrate, low-fat, low-salt diet can also aid in preventing the onset of AMS. Acetazolamide (125 mg two or three times daily, or once at bedtime) has also been shown to reduce susceptibility to AMS and the incidence of HAPE and HACE. Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS.
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PMID:A trek to the top: a review of acute mountain sickness. 855 56


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