Disorders of electrolytes and water

3rd Year NotesDr Niroj Obeyesekere

The extracellular fluid compartmentIn adults, body water ~ 60%ICF – 2/3ECF – 1/3Capillary endothelial membrane divides ECF into,1.Intravascular - plasma2.Extravascular

Extravascular compartment can be divided into,1.Interstitial water (25% of TBW)2.Transcellular water (4% of TBW)

Transcellular – CSF, gastro-interstitial fluid and fluid in eyes and serous surfaces.

ICF and ECF are in osmotic equilibrium.Na salts being the most abundant salt in the ECF, are the most important determinant of ECF.The most fundamental characteristic of fluid and electrolyte homeostasis is the maintenance of ECF volume and circulatory stability.

Tonicity and osmolality

Osmolality of a solution is the number of osmoles of solute per kilogram of solvent .

Osmolality is a property of a particular solution and is independent of any membrane.

Tonicity is a property of a solution in reference to a particular membrane.

Urea – hyperosmolar but isotonic

High glucose in untreated DM – hyperosmolar and hypertonic

Water balance and renal water excretion

• Individuals maintain a physiologic serum osmolality between 285 – 290 mOsm/kg.

• We can excrete hypertonic or hypotonic urine in relation to plasma.

• This is done by counter- current system present in the kidney.

Nephron and collecting duct

The counter-current system

The counter current system

• Renal cortex osmolality ~ 290mOsm/kg renal medulla ~1200 mOsm/kg.

• Thin descending loop permeable to water, but relatively impermeable to Na.

• Thin ascending limp and TAL are essentially impermeable to H20.

Counter current systemFluid entering thin descending limb is ~290 mOsm/kg.

However, the na re-absorption that occurs in the thick ascending limb increases osmolality in the medulla.

Active Na-H pump (in the TALH) and Na-Cl-K co transporter.(the site of action of loop diuretics)

This hyperosmolar fluid drags water out of thin descending limb and fluid entering ascending limb is hyperosmolar compared to plasma.

But this osmotic gradient can be used to deliver hypotonic urine to the distal tubule. (at any level in the ascending limb the osmalality is less than the surrounding tissue)

Vasopressin• Also known as arginine vasopressin or ADH• Secreted by the hypothalamus.• Secreted in response to osmotic and non-osmotic stimuli.• These osmo-receptors are located in the hypothalamus.• Substances that are restricted to the ECF such as

hypertonic saline or mannitol act as effective osmoles and enhances osmotic water release. This stimulates ADH.

• But, urea and glucose cross cell membranes freely so no change cell volume and therefore does not effect ADH release.

• Non-osmolar - decreased effective circulating volume (HF, cirrhosis), nausea, postoperative pain and pregnancy.

Action of vasopressin – collecting tubules

Thirst and osmolality

Control of serum sodium

• Counter-current mechanism • Hypothalamic receptor and vasopressin• Thirst• Serum osmolality = 2(na) + BUN/2.8 +

glucose/18• Hyperglycemia is a cause of hyponatraemia. A

decrease of 1.6mmol of na per 5.6mmol/l increase in BSL.

Approach to hyponatraemia

Assessing volume state

• General appearance – sunken orbits (rare), moribund appearance of severe dehydration, thirst.

• Face – dry mucus membranes• Neck – JVP patterns. (very important)• Hands, chest – skin turgor• BP – postural drop and/or tachycardia• Oedema

JVP

• Internal jugular – medial to sternomastoid muscle.

• Measure with patient at 45 degrees.• The height is measured from the sternal angle.• Differences between carotid and jugular

pulsation. Jugular 1 – visible but not palpable, 2- complex wave form two flickers, 3- moves with respiration normally decreases with inspiration, 4- when pressed fills from above.

Isotonic and hypetonic hyponatremia

• Non hypotonic hyponatremia is diagnosed by the presence of an osmolar gap.

• Osmolar gap = difference between measured plasma osmolality – and calculated osmolality. Serum osmolality = 2(na) + BUN/2.8 + glucose/18

• If there is a osmolar gap then its due to pseudohyponatremia or the presence of a non sodium effective osmole in the circulation. But it has to be effective osmole

pseudohyponatremia

• Sodium biological activity is determined by the concentration in plasma water. So true hypotonic hypontremia is a decreased concentration of na in the aqeous phase of plasma.

• Plasma is 93% water and 7% proteins and lipids.• So in states of hyperlipidemia or hyperproteinemia

the na is reduced even thouhg the concentration remains the same

• Eg . HIV, Hep C, IVIG• Direct vs indirect ISE

Hypertonic/isotonic hyponatremia

• Effective osmole attracting water from cells to plasma. So cells are shrunken.

• Hyperglycemia, mannitol and IVIG.• Isotonic – TURPs isomotic fluid

Hypotonic hyponatremia adaptive responses

• Cells are swollen.• Ie brain in a confined space. How do we

compensate?• Ancient trait by activating a mechanism called

RVD volume regulatory decrease in which osmotically active solutes are extruded from the cell. Eg K, CL,(10 -20% dcerase) organic osmolytes (upto 90% decrease) and limit brain swelling.

Brain adaptations

• Blood brain barrier. – impedes substances that are not lipid soluble. Capillary endothelium and astrocyte end feet. Not neurons so astrocytes are swollen and not neurons. Through aquaporin 4.

• Acute vs chronic hyponatremia . Less than 24 vs more than 48 hrs.

• Physiology – in hypertonicity organic osmolytes are transported in cells opposite of hyponatremia. Eg taurine.

Brain adaptive responses

• In chronic hypertonicity these transporters are upregulated. Helps explain the stubborn persistence of osmolytes in pts with hypernatremia and resultant cerebral oedema that occurs when corrected too quickly/

• In chronic hypoNa these transporters are downregulated. And are slow to return to cells esp when corrected too quickly. – osmotic demyelination syndrome

• Usually 1 day after so aim for 10 -12 mq/l a day.

Acute hyponatremia

• Some interesting bits.• 1. exercise induced. – ultra long marathon runner 56

km or more. Can get Hypona. Their AVP is up even with a normal Na. this most likely due to volume drop than osmotic issue. Also BNP, cortisone.

• Sweat glands – 90k run 8.6 l of sweat.• Sweat glands have a secretory coil. Which produces

isomotic sweat and a reabsorptive duct which actively reabsorbs Na.

Exercise induced hypona

• Na is via the amiloride sensitive channel and Cl is through the cystic fibrosis transmembrane channel. So when not much sweat – hypotonic sweat. High sweat – na reabsortpion is rate limited.

• Increase loss of na and AVP increase may decrease na.

• Other causes psychosis and post operative, ectasy

Chronic hyponatremia

• Is an abnormality of free water excretion. Most have a increased vasopressin release.

• Decrease effective volume ie. Heart failure, liver failure. Easy dx.

• Difficult between true vs euvolemic hyponatremia. (siad)

siad

• 1. hypoosmolality• 2. urine that is less than maximally dilute >100• 3. absence of diuretics• 4. urine na concentration more than 30• 5. reversal of na wasting with water restriction• Gold standard bt true vs euvolamic- isotonic

saline reduced vasopressin release and urine becomes dilute. Hard to differentiate.

Symptoms

• Fatigue vomiting, consuion, dysarthria, gait disturbances and lethargy,

• Seizures, coma.• Gait – like having a BAL 0.06% gait and

tandem gait tests.

causes

• 1. ##drugs• 2.tumours – small cell lung cancers ectopic

prduction of vasopressin• 3. ##pneumonia• 4.endocrine addisons and hypothyroidism.• 5. meningitis• 6. ABI

Rx

• Fluid• Water restrict• Vasopressin antagonists – in heart failure