Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of acute poisoning with amlodipine with deep hypotension, transient oliguria and clinical signs of acute heart failure was described. A woman of 23 years swallowed intentionally 60 tablets of amlodipine (600 mg). After eleven hours of ingestion she was admitted to Warsaw Poison Control Centre. She was in severe clinical condition; tachycardia and deep hypotension were the prominent signs of poisoning. There was not CNS depression. Intensive treatment with i.v. catecholamines (dopamine, norepinephrine), crystalloids (with continuous control of central venous pressure), and i.v. calcium salts (with control of plasma calcium concentration) was started immediately. The patient did not improve but got worse. Acute heart failure developed, especially of left ventricle, so i.v. crystalloids were stopped and dubutamin, morphine, nitroglycerin and glucagon were introduced. Because of oliguria and insufficient effect of high doses of furosemide four-hours hemodiafiltration was set in. The patient's condition slowly improve after third and forth day of hospitalization. The systolic blood pressure rose, heart work was really better and on sixth day--the stabilization of diastolic blood pressure was definitely achieved. The patient was discharge in good condition with heart ejection fraction of 65% measured echocardiographically.
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PMID:[Deep hypotension with transient oliguria and severe heart failure in course of acute intentional poisoning with amlodipine]. 1186 80

Acute heart failure (AHF) is a major cause of hospitalizations. Severe dyspnea, pulmonary congestion and low cardiac output with peripheral vasoconstriction and renal hypoperfusion is a main form of clinical presentation. Most patients with acute worsening have a pre-existing decompensated chronic heart failure (ADCHF), but AHF may also occur as a first manifestation of a previously unknown heart disease. Myocardial ischemia, cardiac arrhythmias, non-compliance with medication and infections are frequent precipitating factors. Management of AHF depends on the underlying heart disease and cause of decompensation. In patients with ADCHF vasodilators and iv diuretics are first-line drugs for rapid reduction of dyspnea and congestion. In patients with signs of low cardiac output and oliguria, inotropic agents are also often administered to prevent further deterioration. Beta-adrenergic agents and phosphodiesterase inhibitors correct the hemodynamic disturbance, but may also induce arrhythmias and worsen myocardial ischemia. Inotropic therapy therefore remains controversial. A novel class of drugs, the calcium sensitizers, represent a new therapeutic option. Levosimendan was shown to improve myocardial contractility without increasing oxygen requirements and to produce peripheral and coronary vasodilation. Its therapeutic effects and tolerance have been tested in several trials. The present review focuses on the clinical pharmacology and therapeutic utility of levosimendan in patients with ADCHF.
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PMID:Newer treatments for decompensated heart failure: focus on levosimendan. 1992 Sep 23