Fluid balance and thirst mechanism

week 9

osmolarity

• the total concentration of all solute particles in a solution

• exact composition of  ICF (intracellular fluid) vs ECF differs, but at equilibrium the osmolarity of each compartment is the same

• The osmolarity of ICF compared to ECF determines whether water will move from one compartment to the other

  • a sudden change in osmolarity will result in water moving down its osmotic gradient altering the volume of one compartment compared to the other 

  • can have significantly deleterious effects on normal physiological functioning of organ systems

sudden decrease in ECF osmolality

• water would move from the ECF into the ICF

• causes swelling of cells

• In parts of the body where the tissue doesn’t have room to expand (e.g. the skull): sudden increase in pressure within the tissue → compromises blood supply

  • swelling brain becomes ischaemic and also herniates out through gaps in the skull such as the foramen magnum further compromising blood supply to vital areas such the brainstem eventually leading to death

sudden increase in ECF osmolality

• causes water to move from the ICF to the ECF

• the cells will shrink

• decrease in membrane stretch (in osmoreceptors) activates the hypothalamic effector cells resulting in the sensation of thirst

mechanism in charge of maintenance of osmolality

thirst ADH mechanism

osmoreceptors

• (membrane) stretch receptors

• located in the hypothalamus

• cells either swell or shrink depending on changes in the local ECF osmolarity

Hypovolaemia

• loss of intravascular volume causes a decrease in stretch – the baroreceptors feed this back to the vasomotor centre in the brainstem

• e.g. sweating

• detected by stretch receptors/baroreceptors

  • (located in the kidney (granular cells) & great vessels: aorta, carotid arteries, vena cava, atria)

• The response of the vasomotor centre to hypovolaemia includes:

  • increase in sympathetic nervous system activity (maintains blood pressure and flow to vital organs)

  • Activation of the hypothalamic thirst centre

  • Activation of the renin angiotensin aldosterone system (RAAS)

  • ADH secretion from the posterior pituitary

ADH purpose

• regulates water output

• triggered by increase in ECF osmolality or decrease in water volume

• produced in hypothalamus → secreted by posterior pituitary gland

ADH process of action

• insertion of pre-formed water channels (aquaporins) into the luminal membrane of principal cells in the renal collecting ducts

  → makes the luminal membrane permeable to water

  → water moves out of the renal tubular fluid (hypo-osmotic) down its osmotic gradient into the hyperosmotic renal interstitium

hyperosmotic

ICF higher osmolality (solute concentration)

hypoosmotic

ECF higher osmolality (solute concentration)

RAAS

Renin angiotensin aldosterone system

• controls volume status via effects on sodium reabsorption in the kidney

• Hypovolaemia → production of renin by the renal granular cells

• rate limiting step in the production of the hormone angiotensin II (AII)

angiotensin II actions

• target of antihypertensive drugs - inhibited by ace inhibitors

• increases Na reabsorption in the kidney

• stimulates production of aldosterone

  • (also Na reabsorption)

• systemic vasoconstriction via AT1 receptors (increase BP)

• preserves renal function by selective vasoconstriction of some renal arterioles (only at low levels, maintains glomerular function)

natriuretic peptides

• released when hypervolemic

• Atrial and brain natriuretic peptides (ANP, BNP) inhibit secretion of renin and aldosterone

burns fluid loss

• systemic inflammatory response - vasodilation and capillary leakiness

  • damage to skin barrier

  • damage to cells - loss of intracellular volume into ECF

  • loss of intravascular volume (blood volume) into ECF

• Fluid from leaky capillaries internally results in oedema of tissues and organs

• Without intervention, hypovolaemic shock occurs

hypovolaemic shock

• Shock: condition in which blood vessels are inadequately filled, blood cannot circulate normally

  • signs: tachycardia, increased capillary refill time

• Hypovolaemic shock: shock due to loss of intravascular volume (either plasma and red cells or just the plasma)

  • common causes: blood loss,  vomiting, severe diarrhoea, extensive burns

intravenous fluids

• most common type: crystalloid: consists of water and electrolytes, same osmolality as ECF

• most common IVs:

  • sodium compound lactate (CSL)

  • normal saline (0.9% NaCl)

Parkland formula

• used to guide fluid management in patients with major burns

• 3-4mls / kg / %burn

• over the first 24 hrs

• half should be given in the first 8hrs, the other half over the following 16hrs

paediatric fluid replacement (e.g. dehydration)

1. volume resuscitation

   • normal saline of CSL until signs of shock resolve

2. maintenance

   • ideally orally-administered isotonic, 5% glucose (prevent hypoglycemia) fluids

   • 4:2:1 formula (Useful guide, but over-estimates requirements)

3. replacement of ongoing losses

   • measure or estimate ongoing losses

baroreceptor stimulation

• indicates increase in MAP