Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231835 (tachypnea)
 2,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A 48-year-old male who had a past history of alcoholic pancreatitis and diabetes mellitus was admitted to our hospital due to chills and vomiting, on August 13, 1998. His body temperature was 38.0 degrees C, and he had the disturbance of consciousness, tachypnea, tachycardia and hepatomegaly with tenderness. Laboratory findings showed highly inflammatory reactions, DIC and hepatorenal dysfunction. Abdominal CT and US revealed multiple liver abscess with portal vein thrombus. Serratia rubidaea was detected in the blood culture. SBT/CPZ and TOB were administered and he recovered. This is a rare case of Serratia rubidaea sepsis. It is also necessary to pay attention to Serratia infections as well as S. marcescens.
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PMID:[Community acquired sepsis by Serratia rubidaea]. 1190 95