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)

The starting point of cardiogenic shock is an extensive myocardial infarction. Through a backward and forward failure of the left ventricle a shock-specific disturbance of the microcirculation occurs with a reduction of the circulation in the periphery of the body and development of a tissue acidosis (metabolic acidosis). Fall in blood pressure and cardiac volume, congestion of blood in the region of the pulmonary vessels and signs of reduced circulation in the body periphery (severe physical weakness, apathy, cold and clammy skin, oliguria) determine the clinical picture of cardiogenic shock. Therapeutically, intra-aortal balloon counter-pulsation, possibly combined with a cardiosurgical intervention, has reduced the mortality of cardiogenic shock after acute myocardial infarction from 90--100% to 60--70%.
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PMID:[Cardiogenic shock following acute myocardial infarction. Pathophysiology and clinical aspects (author's transl)]. 10 80

Shock continues to be associated with a high mortality rate primarily because of delays in diagnosis and therapy. To diagnose shock early, and thereby increase the chances of reversal before there is extensive deterioration of vital organs, one should look for any decrease in pulse pressure, urine output, urine sodium concentration, alertness or any increase in urine osmolarity, tachypnea or tachycardia. Systolic hypotension, oliguria, metabolic acidosis and a cold clammy skin are late signs of shock. The pathophysiology of early hypovolemic shock includes hyperventilation, vasoconstriction, cardiac stimulation, fluid shifts into the vascular system and platelet aggregation. Late shock is characterized by lysosomal breakdown, subsequent release of kinins (especially bradykinin), impaired cell metabolism and organ function, fluid shifts out of the vascular system because of capillary endothelial damage and intravascular coagulation. The primary cause of shock should not be neglected in favor of treating signs, symptoms, and laboratory data. The resuscitation from the shock process itself involves correction of pathophysiologic changes, based on objective trends and responses rather than isolated measurements. A suggested outline of therapies in order of their use includes: 1) correction of the primary problem; 2) ventilation and oxygen; 3) fluid-loading: 4) inotropic agents; 5) correction of acid-based and electrolyte abnormalities; 6) steroids ("physiologic" or "pharmacologic" doses); 7) vasopressors (especially in elderly, severely hypotensive patients); 8) vasodilators (if excess vasoconstriction); 9) diuretics (if oliguric in spite of the above), and 10) heparin (if DIC). The most common errors are 1) late diagnosis; 2) inadequate control of the primary problems; 3) inadequate fluid loading; 4) delayed ventilator assistance, and 5) excessive reliance on and use if vasopressors and diuretics.
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PMID:Shock in the emergency department. 79 60