Water and Sodium Flashcards
How many litres of water in a 70kg male?
Total body water:
60% of body weight, 42L
Intracellular fluid:(in cells)
40% of body weight, 28L
Extracellular fluid:(in the plasma) 20% of body weight, 14L
Intravascular: plasma (circulates as the fluid component of blood) 3L
Intersitial: between cells (surrounds the cells, but does not circulate) 11L
Water movement
Water is freely permeable through ICF and ECF
Determined by osmotic contents
Any change leads to a water shift from high osmolality to low osmolality so eventually:
Always equal = isotonic
ECF
Sodium is the main contributor to ECF osmolality and volume
Anions chloride and bicarbonate.
Glucose and urea- contribute to osmolality
Protein = colloid osmotic pressure (oncotic)
ICF
Predominant cation is potassium
Plasma Osmolality
Largely determined by sodium and associated anions
Estimated plasma osmolality =
2[Na] + 2[K] + urea + glucose mmol/L
Intra- and extracellular osmolality are equal
Change in plasma osmolality pulls or pushes water across cell membranes
Under normal circumstances fluid intake = fluid loss
slide 7 + 8
Water in: food and drink mainly, metabolic production
Water loss: skin, lungs, lots through urine, faeces
Why don’t we give water intravenously?
It is hypo-osmolar/hypotonic vs cells (lower osmotic pressure and lower nutrients etc in blood compared to the cells)
So Water enters blood cells causing them to expand and burst: haemolysis
However, this only occurs in the vicinity of the intravenous cannula
If you could achieve instantaneous mixing it wouldn’t occur
ECF Osmolality
Is very tightly regulated
Changes in ECF osmolality lead to a rapid response
Normal plasma osmolality 275-295 mmol/kg REMEMBER VALUE
Water deprivation or loss will lead to a chain of events
ECF Volume
Changes in ECF volume cause a slower response compared to osmolality
Water deprivation/Dehydration
Increase in the ECF osmolality
Firstly, The water will move from the cells (from ICF to ECF)
Other thing that happens is that the hypothalamus is stimulated and thirst centre is stimulated- increasing water intake
Another thing that happens is increase in ADH from the posterior pituitary. This affects the renal gland and so the kidneys.
ADH causes the walls of the distal convulated tubules and the collecting duct to become more permeable to water so more water leaks out back into the body.
So you end up with a very small volume of concentrated urine
Renin-angiotensin- aldosterone system
Firstly, the kidney detects a fall in ECF volume because there’s a decrease in renal perfusion pressure
This acts on the juxtaglomerular apparatus causing the release of renin into the system
Renin now acts on a protein called angiotensinogen which is the precursor to angiotensin I. Renin cleaves angiotensinogen into angiotensin I
angiotensin I is now converted into angiotensin II by a protein called ACE (angiotensin converting enzyme). This conversion occurs in the lungs as that is where ACE is produced
Adrenal gland detects the angiotensin II and secretes aldosterone
Aldosterone acts on the distal tubes of the kidneys and so it changes the re absorption of potassium and sodium and water retention (increase in water retention). This changes the effect in circulating volume
Aldosterone can also act in another way- ADH secretion again by the pituitary gland so there is more absorption of through the collecting ducts of the kidneys and there will also be a system wide arterial vasoconstriction which will increase the blood pressure as well. This changes circulating volume
Process repeats again
Causes of water depletion
reduced intake
sweating
vomiting
diarrhoea
diuresis/diuretics
Dehydration
Thirst
Dry mouth
Inelastic skin
Sunken eyes
Raised haematocrit- proportion of blood that is made up
of the red blood cells
Weight loss
Confusion – brain cells
Hypotension
Water excess
Decrease in ECF osmolality
Water moves from ECF to ICF, causing cells to swell.
No stimulation of thirst centre in hypothalamus
Inhibition of ADH from posterior pituitary gland so increase in dilute urine volume
Risk of cerebral over hydration if acute excessive intake (water intoxication)
Consequences of water excess
Hyponatraemia
Cerebral overhydration
Headache
Confusion
Convulsions
Hydrostatic pressure
Pressure difference between plasma and interstitial fluid
Water moves from plasma into interstitial fluid
Oncotic pressure
Pressure caused by the difference in protein concentration between the plasma and interstitial fluid
Water moves from interstitial fluid into plasma
Normal
slide 24-25
Loss from plasma= gain to plasma
No net change
Oedema
Excess accumulation of fluid in interstitial space
What causes oedema?
Disruption of the filtration and osmotic forces of circulating fluids
Obstruction of venous blood or lymphatic return
Inflammation;↑capillary permeability
Loss of plasma protein
Serous effusion
Excess water in a body cavity
Pathogenisis of oedema and serous effusion
Increased fluid leakage into interstitial spaces OR
Impaired reabsorption of fluid
Different types of oedema
Inflammatory
Venous
Lymphatic
Hypoalbuminaemic
Pleural effusions
The normal pleural space contains ~10 mL of fluid
Balance between
-hydrostatic and oncotic forces in the visceral and parietal pleural vessels.
-lymphatic drainage.
Pleural effusions result from disruption of this balance
In a pleural effusion, different fluids can enter the pleural cavity
Transudate is fluid pushed through the capillary due to high pressure within the capillary.
Low protein content
Exudate is fluid that leaks around the cells of the capillaries caused by inflammation &↑permeability of pleural capillaries to proteins.
High protein content
Why is pleural fluid protein measured?
Pleural fluid protein is measured to differentiate between exudative (eg malignancy, pneumonia) and transudative (eg LVF, cirrhosis, hypoalbuminaemia, peritoneal dialysis) effusions
Disorders of plasma sodium: general principles
Normal (reference) range 135 -145 mmol/L
Concentration is a ratio, not a measure of total body content
High or low [Na] are more often due to gain or loss of water, rather than Na
Clinical effects are on the brain due to constrained volume (skull)
Rate of change is more important than absolute levels
Hypernatraemia (↑ Na+) e.g. Caused by
Water deficit:
Poor intake
Osmotic diuresis (increased urination)
Diabetes insipidus (not related to diabetes)
Sodium excess:
Mineralocorticoid (aldosterone) excess
Salt poisoning
Effects: Cerebral intracellular dehydration (tremors, irritability, confusion)
Hyponatraemia (↓ Na+) e.g. Causes by
Artefactual
Sodium loss
Diuretics
Addison’s disease
Excess water
IV fluids (iatrogenic)
SIADH
Excess water ++ and sodium +
Oedema
Effects: Cerebral intracellular over-hydration (headache, confusion, convulsions)
