water and sodium
DESCRIPTION
Dr Chow Yok WaiTRANSCRIPT
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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
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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
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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
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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
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Take home message
Content of Na+ determines ECF volume
Concentration of Na+ in the ECF reflects ICF volume
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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
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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
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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)
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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
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0.45 Saline
500mls 0.9% 500mls H20
-2/3 ICF, 1/3 ECF
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Hyponatremia
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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
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Figure 7.1
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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
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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
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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
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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
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Table 7.3
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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
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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
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Chronic hyponatremia
• ‘effective’ ECF volume is decreased (maldistribution)– Edema states– Congestive cardiac failure
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Hypernatremia
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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
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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
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Outline of major principles
• Hypernatremia
– Na+ gain uncommon
– EFW loss
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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)
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Approach to pt with hypernatremia
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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
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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
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Nephrogenic DI
• ADH fails to act– Failure to increase water permeability of
collecting duct
• Loss of medullary hypertonicity– Medullary interstitial defect or infirtrate
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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
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Calculation of Water Deficit- ICF
• ICF assess current vs expected ICF and ECF volumes
• 70kg pt, sodium increase 140160mmol/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
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Short form of Calculation of ICF Water deficit
ICF volume (normal) X effective osmoles (normal)
=
ICF volume (abnormal) X effective osmoles (abnormal)
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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
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