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Water And Sodium
 

Water And Sodium

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Dr Chow Yok Wai

Dr Chow Yok Wai

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    Water And Sodium Water And Sodium Presentation Transcript

    • Sodium and Water Physiology
      • Consider water and Na separately as regulation is independent
      • ECF  Na +
        • Na + content  ECF volume
        • Na + concentration  ICF volume
          • Reflects tonicity of body fluids
          • Hyponatremia  swollen cells
          • Hypernatremia  shrunken cells
    • Sodium and Water Physiology
      • Thirst and release of ADH are stimulated by shrunken cells + ECF volume contraction
      • ADH is major hormone controlling water excretion
      • Water  60% of body mass
        • 2/3 of body water  ICF
        • 1/3 of body water  ECF
    • Sodium and Water Physiology
      • Particles restricted to a compartment determine its volume
        • Na + (and Cl, HCO3) determines ECF volume
        • K + (held by macromolecular anions) determines ICF volume
    • Sodium and Water Physiology
      • Water crosses cell membrane rapidly till osmolality is equal on both sides of the membrane
      • But some particles do not
        • Permeability differences
        • Transporters
        • Active pumps
      • Tonicity (effective osmolality) = total osmolality – urea - alcohol
    •  
    • Take home message
      • Content of Na + determines ECF volume
      • Concentration of Na + in the ECF reflects ICF volume
    • Distribution of Ultrafiltrate across capillary membranes
      • Movement of ultrafiltrate of plasma across capillary membranes do not cause water to shift between ECF – ICF
      • Hydrostatic pressure (HP) – Colloidal osmotic pressure (COP)  UF
      • Increase HP  venous HPT  CCF, venous obstruction
      • Support stockings increase HP
    • Water Physiology
      • Defense of tonicity involves thirst and excretion or conservation of electrolyte free water (EFW)
      • Control of tonicity is sensitive, responding to 1-2% changes
      • Change of tonicity is synonymous with [Na + ] in plasma
        • Reduction in tonicity  thirst reduction, increase EFW excretion
    • Mechanism of excretion of EFW
      • Osmolality/tonicity receptors in thirst center and ADH release center  drink more + conserve EFW from kidneys
      • Excretion of a dilute urine requires 3 steps
        • Delivery of saline to thick ascending limb of loop of Henle
        • Separation of salt and water (reabsoprtion of NaCl without water)
        • Maintenance of separation (AND secretion must cease)
    • More to remember….
      • To assess medullary hyperosmolality, measure urine osmolality after ADH acts
      • To assess ADH action, you must know the medullary osmolality
      • To assess if urine will lead to rise/fall in plasma Na, to determine [Na + ] and [K + ] in urine. Compare this sum of [e - ] urine with plasma
    • 0.45 Saline
      • 500mls 0.9% 500mls H20
      • -2/3 ICF, 1/3 ECF
    • Hyponatremia
    • Outline of major principles
      • Plasma [Na + ] reflects ICF volume
      • Na + content reflects ECF volume
      • Acute Hyponatremia- What is the source of EFW?
      • Chronic Hyponatremia- Why is ADH present?
      • Basis for hyponatremia
        • Source of EFW
        • ADH secretion to prevent EFW excretion
    • Figure 7.1
    • Acute Hyponatremia
      • 3 common causes of EFW
        • D5% administration as IV
        • Clear fluid administration
        • Generation of EFW by desalination when isotonic/hypotonic saline is adminstered
          • Kidney must excrete urine that’s hypertonic to infusate
      • Immediate goal is to shrink expanded ICF volume
      • Hypertonic saline
    • Prevention
      • Do not give solutions that are hypotonic to the urine if polyuria is present
      • Do not give solutions that are hypotonic to the body fluids in the oliguric patient
      • Give isotonic fluids only to replace losses and to maintain hemodynamics
      • Suspicious of good U/O as urine might be hypertonic to the infused solutions and generate EFW
    • Acute hyponatremia- therapy
      • Correct Na + with hypertonic saline till Na + is 130mmol/l
      • Prevention of further fall of sodium
        • Input
          • If input=output with respect to Na, K and H20, then  no change in sodium concentration
          • If hypertonic urine is excreted, the same volume and same composition of hypertonic saline must be administered
    • Acute hyponatremia- therapy
      • Output
        • Aim is to lower [Na + + K + ] in urine so that isotonic fluids can be administered
        • Loop/ osmotic diuretic can render urine less hypertonic
        • Once ADH release is no longer present/ diminished, can then stop diuretics and plasma [Na + ] will rise
    • Table 7.3
    • Chronic hyponatremia
      • Most common electrolyte abnormality in hospitalised patients
      • Most pt is asymp as adaptive responses have taken place (brain cells have normalised ICF volume)
      • Danger is too rapid rise in plasma [Na + ]  central pontine myelinosis
      • To develop hyponatremia, source of EFW + excretion/release of ADH must be present
    • Chronic hyponatremia
      • ADH is released when ECF volume is low
      • Deducing whether ECF volume is contracted
        • Loss of Na via renal cause
          • Diuretic
          • Renal salt wasting
          • Osmotic agents (glucose)
          • Rate of K + should be examined
            • Low urine [K + ] + renal Na + loss + ECF contraction  low aldosterone bioactivity
            • High urine [K + ] + renal Na + loss + ECF contraction  abnormal loss occurred in PCT, loop of henle, early DCT
        • Loss of Na via non renal cause
          • GIT
          • Skin
    • Chronic hyponatremia
      • ‘ effective’ ECF volume is decreased (maldistribution)
        • Edema states
        • Congestive cardiac failure
    •  
    • Hypernatremia
    • Outline of major principles
      • Hypernatremia is not a disease
        • Look for its cause and underlying disease
      • Hypernatremia
        •  ICF volume contraction
        • Brain is most susceptible  CNS hemorrhage
      • Thirst
        • Pt will not permit hypernatremia if thirst mechanism is intact
    • Outline of major principles
      • Urine Osmolality
        • Diabetes Insipidus
          • Large urine amount
          • Low osmolar urine
        • Osmotic/pharmacological diuresis
          • Large urine amount
          • Slightly hyperosmolar urine
        • Non renal water loss without water intake
          • Small urine amount
          • Maximally hyperosmolar urine
    • Outline of major principles
      • Hypernatremia
        • Na + gain  uncommon
        • EFW loss
    • Etiology of Hypernatremia
      • True [Na + ] plasma  152 mmol/l
      • 6-7% non aqueous volume (lipids, proteins)
      • Hypernatremia is almost always d/t water loss in the present of a thirst defect
      • 4 questions to ask
        • What’s the ECF volume? (Na + gain)
        • Body weight change? (H2O gain)
        • Normal thirst response?
        • Normal renal response? (ADH response)
    • Approach to pt with hypernatremia
    • Hypernatremia due to water loss
      • Non renal water loss
        • Respiratory tract, skin, fever, hyperventilation, GIT (Hypotonic)
      • Renal water loss
        • Usually a/w thirst defect
        • Usually a/w polyuria
        • Usual causes
          • Diabetes Insipidus
          • Osmotic diuresis
    • Central DI
      • d/t lack of ADH
        • ADH is synthesized from paraventricular and supraoptic nuclei
        • ADH then transported via axonal flow to posterior pituitary
      • CNS disorder
      • Polydypsia, polyuria
      • Large urine amount (3-20L depending on GFR)
      • Hypo-osmolar urine (< 150 mosm/l)
      • ECF normal
      • Hypernatremia
      • Hypernatremia worsens and polyuria occurs with judicious water administration
      • ADH administration raises urine osmolality
    • Nephrogenic DI
      • ADH fails to act
        • Failure to increase water permeability of collecting duct
      • Loss of medullary hypertonicity
        • Medullary interstitial defect or infirtrate
    • Treatment of water deficit
      • Stop ongoing Water Loss
        • Rectify ADH deficiency
        • Stop osmotic agent
      • Replacing Water Deficit
        • D5%- ideal EFW administration
        • ½ NS- not appropriate if polyuria is present and [Na + ] in urine < in IVD
          • 1L 1/2NS
            •  500mls EFW available
            •  1/3 stay in ECF, 2/3 goes into ICF
        • More hypotonic solutions can be used but hemolysis is a risk
    • Calculation of Water Deficit- ICF
      • ICF  assess current vs expected ICF and ECF volumes
          • 70kg pt, sodium increase 140  160mmol/l, ECF normal on physical examination, usual ICF 30L and ECF volume 15L.
            • No of effective osmoles in ICF:
              • ICF volume X 2(plasma [Na + ])
              • 8400 mOsm
              • After water loss, assume no change in effective osmoles in ICF
              • New effective osmolality is 320 (160X2)
              • New ICF volume  8400/320=26.25L
              • Water deficit  3.75L
    • Short form of Calculation of ICF Water deficit
      • ICF volume (normal) X effective osmoles (normal)
      • =
      • ICF volume (abnormal) X effective osmoles (abnormal)
    • Calculation of Water Deficit- ECF
      • Change in ECF volume-
        • Not reflected by plasma [Na + ]
        • Reflected by clinical assessment of vascular and interstitial volume
        • Plasma [Na + ] X estimated ECF volume
        • 140X15L= 2100mmol
        • 160X15L= 2400 mmol
        • 300mmol of Na + is needed to achieve Na + balance
    •