Acid-base and electrolyte abnormalities in patients with congestive heart failure

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Acid-base and electrolyte abnormalities in patients with congestive heart failure. Electrolyte abnormalities in 62 study patients with congestive heart failure. Elsaf M and Siamopoulos K, Exp Clin Cardiology Clinic, 1997. Υπονατριαιμία. Υπερτονική (υπεργλυκαιμία). Ισοτονική - PowerPoint PPT Presentation

Transcript of Acid-base and electrolyte abnormalities in patients with congestive heart failure

Acid-base and electrolyte abnormalitiesin patients with congestive heart failure

Elsaf M and Siamopoulos K, Exp Clin Cardiology Clinic, 1997

Electrolyte abnormalities in 62 study patients with congestive heart failure

Υπονατριαιμία

ΥποτονικήΥπερτονική(υπεργλυκαιμία)

Ισοτονική(υπερλιπιδαιμία)

Υποογκαιμική(έλλειψη H20-Na+)

Υπερογκαιμική( H20 >Na+)

KA – κίρρωση

Νορμοογκαιμική(SIADH)

Bettari L et al, Heart Fail Rev (2012) 17:17–26

Mechanisms leading to hypotonic hypervolemic hyponatremia in heart failure

The Challenge of Hyponatremia

Adrogué H and Madias N, J Am Soc Nephrol, 2012

Pathogenesis of hypotonic hyponatremia

as derived from the Edelman equation

The electrolyte-free water clearance:

CeH2O = V (1 - urine K+ + urine Na+

serum Na+

)

The Challenge of Hyponatremia

Adrogué H and Madias N, J Am Soc Nephrol, 2012

Effect of urine electrolyte concentration on serum sodium level in hypotonic hyponatremia

Ανταγωνιστές των υποδοχέων της AVP (……..vaptanes)

Tolvaptan (Samsca, tbl 15 mg)

Pack 10 tablets = 1243 € (ΕΟΠΥ)

Otsuka Pharmaceutical Europe Ltd.

Θεραπεία Υπονατριαιμίας

Successful treatment of hyponatremia with ACEi in patients with congestive heart failure

Cardiology 1995

Clinical and laboratory parameter before and after treatment with captopril

Successful treatment of hyponatremia with ACEis in patients with congestive heart failure

Cardiology 1995

Correlation between the increase in serum sodium and the increased in CeH2O

Amlal H and Soleimani M, Cell Physiol Biochem 2011;28:521-526

Schematic diagram showing a cell model of the thick ascending limb with its different transport pathways involved in the transcellular reabsorption of NaCl as well as the paracellular transfer of Na+ activated by the luminal positive voltage

Amlal H and Soleimani M, Cell Physiol Biochem 2011;28:521-526

Schematic diagram showing a cell model of the distal convoluted tubule (DCT) with its different transport pathways involved in the transcellular reabsorption of NaCl. Early DCTexpresses only NCC whereas late DCT expresses both NCC and ENaC in the apical membrane

Amlal H and Soleimani M, Cell Physiol Biochem 2011;28:521-526

Schematic diagram showing cell types in both cortical collecting duct (CCD) and connecting tubules (CNT) with different transport pathways involved in transcellular reabsorption of NaCl. ENaC is expressed on the apical membrane of principal cells and pendrin (PDS) is expressed on the apical membrane of B-intercalated cells

Amlal H and Soleimani M, Cell Physiol Biochem 2011;28:521-526

Schematic diagram of various nephron segments, including TAL and DCT along with transport proteins targeted by furosemide (NKCC2) or thiazides (NCC). G, glomerulus; PCT, proximal convoluted tubule; PST, proximal straight tubule; TAL, thick ascending limb; DCT, distal convoluted tubule; CCD, cortical collecting tubule; OMCD, outer medullary collecting duct; IMCD, inner medullary collecting duct

Pendrin as a Novel Target for Diuretic Therapy

Amlal H and Soleimani M, Cell Physiol Biochem 2011;28:521-526

Schematic diagram of the nephron showing the action sites for thiazides, inhibitors of NCC, and a new diuretic which can inhibit pendrin