water and sodium

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 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

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