CLINICAL USE OF DIURETICS. PATHOGENESIS AND TREATMENT OF REFRACTORY EDEMA Determinants of diuretic response - site of action, antinatriuretic forces,

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Presentation transcript:

CLINICAL USE OF DIURETICS

PATHOGENESIS AND TREATMENT OF REFRACTORY EDEMA Determinants of diuretic response - site of action, antinatriuretic forces, fall in BP, rate of drug excretion Determinants of diuretic response - site of action, antinatriuretic forces, fall in BP, rate of drug excretion excess sodium intake excess sodium intake decreased or delayed intestinal absorption decreased or delayed intestinal absorption decreased drug entry into lumen decreased drug entry into lumen increased distal reabsorption increased distal reabsorption decreased loop sodium delivery (low GFR and/or enhanced proximal reabsorption decreased loop sodium delivery (low GFR and/or enhanced proximal reabsorption

Match the clinical setting with the preferred diuretic Recurrent nehprolithiasis (Ca+2) Recurrent nehprolithiasis (Ca+2) hepatic cirrhosis with ascites hepatic cirrhosis with ascites metabolic alkalosis in CHF metabolic alkalosis in CHF hypercalcemia hypercalcemia Hyponatremia due to SIADH Hyponatremia due to SIADH

Question The appropriate use of diuretics may induce or exacerbate effective circulating volume depletion in which of the following edematous states? The appropriate use of diuretics may induce or exacerbate effective circulating volume depletion in which of the following edematous states? –CHF –nephrotic syndrome –renal failure –hepatic cirrhosis and ascites

Question What is the simplest way to detect this change? What is the simplest way to detect this change? –Measurement of urine Na concentration –measurement of BUN –estimation of JVP –measurement of systemic BP

CASE Previously well 45 YO male, acute onset of crushing CP and dyspnea. Medical eval confirms AMI and Pulm edema. Treated with O2 and diuretics he becomes edema free. Weight has fallen by 3 KG within 24 hours and his estimated JVP is less than 5 cm H2O. Now he is oliguric, urine Na < 10. BUN increased from 10 to 28mg/dl. Previously well 45 YO male, acute onset of crushing CP and dyspnea. Medical eval confirms AMI and Pulm edema. Treated with O2 and diuretics he becomes edema free. Weight has fallen by 3 KG within 24 hours and his estimated JVP is less than 5 cm H2O. Now he is oliguric, urine Na < 10. BUN increased from 10 to 28mg/dl. –What are 2 most likely causes of oliguria and increase in BUN? –Would a normal EF distinguish between these possibilities? –Does low JVP exclude cardiac dysfunction? –Is total ECF >, =, or, =, or < normal? –What modes of therapy might return BUN and urine output to normal?