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WATER AND ELECTROLYTE BALANCE

WATER AND ELECTROLYTE BALANCE. DRANITZKI ELHALEL MICHAL, MD NEPHROLOGY AND HYPERTENSION SERVICES. Total Body Water (TBW). Intracellular space Interstitium } extracellular Vascular Space }. TBW. = 60% of Body Weight

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WATER AND ELECTROLYTE BALANCE

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  1. WATER AND ELECTROLYTE BALANCE DRANITZKI ELHALEL MICHAL, MD NEPHROLOGY AND HYPERTENSION SERVICES

  2. Total Body Water (TBW) • Intracellular space • Interstitium } extracellular • Vascular Space }

  3. TBW = 60% of Body Weight 60% of TBW (36% of weight) - intracellular 40% of TBW (24% of weight) - extracellular

  4. Exchange of water between cellular and extracellular fluids 1. OSMOTIC PRESSURE - generated by number of particles per unit volume 2. HYDROSTATIC PRESSURE

  5. Main intracellular osmole  K+Main extracellular osmole  Na+Extracellular osmolarity ~2xNa+Extracellular osmolarity = Intracellular osmolarityNormal osmolarity ~280 mOsmol/Kg ~140 mEq/L of Na+

  6. 70 kg, male TBW - 42 liter Total Body Solute - 42 liter x 280 mOsmol/l = 11.760 mOsmol Intracellular volume - 25 liter Intracellular osmoles - 25 liter x 280 mOsmol/l = 7000 mOsmol Extracellular volume - 17 liter Extracellular osmoles - 17 liter x 280 mOsmol/l = 4760 mOsmol

  7. Substance Plasma Plasma Extracellular Intracellularadded osmolarity sodium volume volumeNaCl    Water    Isotonic NaCl 0 0  0

  8. Plasma Na+ concentration is a measure of concentrationand notof volume, or of total body sodium

  9. Plasma osmolarity  2 x plasma [Na+]+Glucose + Urea----------------------------------------Normal values: PNa - 137 - 145 mEq/L Glucose - 3.5-6.5 mmol/L Urea - 3.5-6.5 mmol/L Posm - 275-290 mOsmol/kg Effective Posm - 270-285 mOsm/kg

  10. Exchange of Water between Plasma and Interstitial Fluid Oncotic pressure Hydrostatic pressure

  11. EFFECTIVE BLOOD VOLUME (EBV) • Volume in arterial system • Pressure perfusing the arterial baroreceptors (carotid, glomerular) REGULATION OF EFFECTIVE BLOOD VOLUME AFFECTS SODIUM STORES BY AFFECTING URINARY SODIUM EXCRETION

  12. REGULATION OF EBV 1. SENSORS - volume/pressure receptors: - afferent arteriole - cardiopulmonary - atria - carotid

  13. REGULATION OF EBV 2. EFFECTORS a. Sympathetic nervous system: - sympathetic nervous tone - secretion of catecholamines from adrenal medulla  Venous constriction Myocardial contractibility and heart rate Arteriolar constriction Renin secretion Renal tubular Na+ reabsorption

  14. REGULATION OF EBV b. Renin - Angiotensin - Aldosterone system: arteriolar vasoconstriction renal Na+ retention (Angiotensin II, aldosterone) c. Atrial Natriuretic Peptide (ANP) d. Regulation of renal Na+ excretion: varies directly with effective blood volume controlled by - GFR - Tubular reabsorption of Na+

  15. VOLUME REGULATION Reduced EBVElevated EBV Sympathetic tone   Renin, Angiotensin, Aldosterone   ANP   Renal sodium excretion  

  16. 60-70% 4% 5% 20-30%

  17. OSMOREGULATION SENSING - Osmoreceptors in hypothalamus EFFECTORS - Thirst  Drinking - Antidiuretic Hormone (ADH)  water excretion

  18. Water Balance Obligatory water output: Urine - 500 ml Skin - 500 ml Respiratory tract - 400 ml Stool - 200 ml

  19. Obligatory Water Intake • Drinking 400 ml • Water content of food 850 ml • Water pruduced by oxidation 350 ml

  20. Excersice on a Hot DayA. Water loss  Osmolarity B. Water + Sodium loss Volume  Osmolarity  Thirst} water retentionADH Volume Urinary sodium excretion  ADH water retention Urine - Osmolarity  Na+, Cl-

  21. Half Isotonic Saline InfusionA. Osmolarity  ADH  B. Volume   Sodium excretion ADH  Urine - Osmolarity  Na+, Cl- 

  22. Isotonic Saline InfusionA. Osmolarity - no changeB. Volume  Sodium excretion  ADH  Urine - Isosmotic urine

  23. Congestive Heart Failure A. EBV  Urinary Sodium excretion  ADH Total Body Sodium  (Edema)Total Body water Plasma Osmolarity Plasma Sodium Urine Osmolarity Urine Na+,Cl-

  24. Primary Renal Sodium RetentionTotal Body Sodium Total Body Water 

  25. Secretory Diarrheas = Isoosmotic Fluid containing Na+ and K+ as in the Plasma EBV - decreased POsm - no change PNa - no change ADH - increased Renin + Aldosterone - increased ANP - decreased  Urinary Sodium Excretion - decreased Urine Osmolarity - increased

  26. Hyponatremia and hypoosmolality = Impaired renal water excretion Hypernatremia and hyperosmolarity = Impaired thirst mechanism or no access to water

  27. Hypoosmolarity and Hyponatremia - SYMPTOMSNauseaMalaiseHeadacheLethargySeizuresComaCause - Brain Edema

  28. Hyponatremia – EtiologyDisorders of impaired water excretionA. Effective blood volume depletionGI lossesRenal losses: diuretics, hypoaldostronism, Na+-wasting nephropathySkin losses: exercise, burnsEdematous states: heart failure, hepatic cirrhosis, nephrotic syndrome, protein loosing enteropathy B. Diuretics: Thiazides, loop diureticsC. Renal failure

  29. Hyponatremia – EtiologyD. Non-hypovolemic states ofADH excess Syndrom of inappropriate ADH secretion Cortisol deficiency HypothiroidismE. Decreased solute intakeF. Cerebral salt wastingDisordders with normal water excretionA. Primary polydipsiaB. Reset osmostat: pregnancy, psychosis, quadriplegia, malnutrition

  30. Diuretics1. Volume depletion2. Inhibition of urinary dilution3. K+ depletionMost common - THIAZIDES

  31. 60-70% 4% 5% 20-30%

  32. Syndrome of Inappropriate ADH Secretion = Impaired water excretion1. Hypoosmolarity and Hyponatremia2. Increased urine osmolarityNO DECREASED EBVNa+ EXCRETION IS NORMAL

  33. SIADH - ETIOLOGY1. Neuropsychiatric disorders2. Drugs3. Pulmonary disease4. Post-operative5. Severe nausea6. Ectopic production7. Exogenous administration of ADH

  34. PSEUDOHYPONATREMIALow plasma Na+ with normal PosmA. Severe hyperlipidemiaB. Severe hyperproteinemiaLow plasma Na+ with elevated PosmA. HyperglicemiaB. Administration of hypertonic Manitol

  35. Hyponatremia - DIAGNOSIS1. Patient history2. Estimate Volume status3. Plasma Osmolarity4. Urine Osmolarity5. Urine Na+ concentration

  36. Hyponatremia – Treatment1. Estimate neurological symptoms2. Estimate volume status3. Decide – water restriction or sodium load or both4. Correct slowly!!!! ~ ½ meq/l/h TREAMENT COMPLICATION: CENTRAL PONTINE MYELINOLYSIS

  37. Estimation of Sodium deficitNa+ deficit = 0.5 x weight (125-plasma Na+)Example: 70kg female, plasma Na+ 113meq/l Na+ deficit = 35(125-113)=420 meq Time of correction: 12meq/l =24h 0.5meq/l/h Fluids: Hypertonic (3%) saline = 513meq/l 420 meq = 818 ml of hypertonic saline

  38. If hypovolemia coexist:Treat with normal (0.9%) saline.First, Sodium will rise slowly in plasma.When hypovolemia will be corrected ADH levels will drop, and water excretion will correct plasma Na+.

  39. Treatment of SIADH1.Water restriction2. Hypertonic saline or NaCl tablets3. Loop diuretics4. Demeclocycline

  40. Hyperosmolarity and Hypernatremia - SYMPTOMSLethergyWeaknessIrritabilityTwitchingSeizuresComaCause - Brain Dehydration

  41. Hypernatremia – Etiologywater lossA. Insensible loss – Increased sweating, evaporation Burns Respiratory infectionB. Renal loss – Central Diabetes Insipidus Nephrogenic Diabetes Insipidus Osmotic diuresisC. Gastrointestinal loss – Osmotic diarrheaD. Hypothalamic disoredersE. Water loss into cells – Seizures Rabdomyolysis

  42. Hypernatremia – Etiology cont.Sodium retentionA. Administration of hypertonic NaCl or NaHCO3B. Ingestion of sodium

  43. Hypernatremia – DIAGNOSIS1. Patient history2. Estimate volume status3. Plasma osmolarity4. Urine volume 5. Urine osmolarity 6. Urine Na+ concentration

  44. DIABETES INSIPIDUS- CENTRAL-ETIOLOGY1.Idiopathic – familial2. Post surgery to hyopthalamus3. Head trauma4. Hypoxic or ischemic encephalopathy (shock, arrest, Sheehan’s syndrom) 5. Neoplastic6. Histiocytosis X7. Sarcoidosis8. Anorexia nervosa9. Cerebral aneurysm10. Encephalitis or meningitis

  45. DIABETES INSIPIDUS – NEPHROGENIC- ETIOLOGY 1.Decreased water permeability of the collecting tubule a. Congenital b. Hypercalcemia c. Hypokalemia d. Drugs (Lithium, Demeclocycline, Streptozocin) e. Sjogren’s syndrom f. Amyloidosis

  46. Diabetes Insipidus – Nephrogenic Etiology – con.2. Interference with countercurrent mechanism a. Osmotic diuresis b. Loop diuretics c. Renal failure d. Hypercalcemia e. Hypokalemia f. Sickle cell anemia3. Increased periferal degradation of ADH a. Pregnancy4. Unknown mechanism a. Isofamid b. Methoxyflurane

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