Week 6 Fluid and Electrolyte Imbalance There are several … · - Hypovolaemia or fluid volume...
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Week 6 Fluid and Electrolyte Imbalance Fluid movement through the capillary membrane is due to pressure placed on the membrane by the blood (hydrostatic pressure) - The hydrostatic pressure pushes the fluid out the capillary, whereas osmotic pressure pulls fluid into the capillary There are several mechanisms that create the balance between fluid intake and output: ð Thirst ð Antidiuretic hormone (ADH) ð RAAS ð Arterial naturetic peptide (ANP) Hypovolemia The thirst mechanism: - Thirst centre is activated when the blood volume drops due to water loss or when serum osmolality increases. This mechanism is highly effective in regulating extracellular sodium levels - Increased sodium levels in the extracellular fluid, increase serum osmolality and therefore stimulates the thirst centre - An increase of 2-3% in plasma osmolality triggers the thirst centre of the hypothalamus - Secondarily, a 10-15% drop in blood volume also triggers thirst - This is a significantly weaker stimulus ADH - Regulator of the water excretion by the kidneys - Osmoreceptors located in the hypothalamus respond to an increase in serum osmolality and the associated decrease in the blood volume; this activates ADH production and release - With increased water absorption thanks to the ADH, the urine output falls, blood volume is restored, and serum osmolality drops as the water dilutes bodily fluid RAAS - Works to maintain the balance of intravascular fluid and blood pressure - When there is a decrease to the blood flow and pressure to the kidneys, special receptors are stimulated in the nephrons to produce the renin enzyme - Renin converts angiotensin to angiotensin I - ANG I then travels through the bloodstream into the lungs, where its converted into ANG II
Transcript of Week 6 Fluid and Electrolyte Imbalance There are several … · - Hypovolaemia or fluid volume...
Week6 FluidandElectrolyteImbalanceFluidmovementthroughthecapillarymembraneisduetopressureplacedonthemembranebytheblood(hydrostaticpressure)
- Thehydrostaticpressurepushesthefluidoutthecapillary,whereasosmoticpressurepullsfluidintothecapillary
Thereareseveralmechanismsthatcreatethebalancebetweenfluidintakeandoutput:ð Thirstð Antidiuretichormone(ADH)ð RAASð Arterialnatureticpeptide(ANP)
HypovolemiaThethirstmechanism:
- Thirstcentreisactivatedwhenthebloodvolumedropsduetowaterlossorwhenserumosmolalityincreases.Thismechanismishighlyeffectiveinregulatingextracellularsodiumlevels
- Increasedsodiumlevelsintheextracellularfluid,increaseserumosmolalityandthereforestimulatesthethirstcentre
- Anincreaseof2-3%inplasmaosmolalitytriggersthethirstcentreofthehypothalamus
- Secondarily,a10-15%dropinbloodvolumealsotriggersthirst- Thisisasignificantlyweakerstimulus
ADH- Regulatorofthewaterexcretionbythekidneys- Osmoreceptorslocatedinthehypothalamusrespondtoanincreaseinserum
osmolalityandtheassociateddecreaseinthebloodvolume;thisactivatesADHproductionandrelease
- WithincreasedwaterabsorptionthankstotheADH,theurineoutputfalls,bloodvolumeisrestored,andserumosmolalitydropsasthewaterdilutesbodilyfluid
RAAS
- Workstomaintainthebalanceofintravascularfluidandbloodpressure- Whenthereisadecreasetothebloodflowandpressuretothekidneys,special
receptorsarestimulatedinthenephronstoproducethereninenzyme- ReninconvertsangiotensintoangiotensinI- ANGIthentravelsthroughthebloodstreamintothelungs,whereitsconvertedinto
ANGII
- ANGIIhelpstoincreasetheBP,asit’sapowerfulvasoconstrictor
- Theadrenalcortexisactivatedandaldosteroneisreleasebecauseofthis- Aldosteronehelpswithsodiumandwaterretentioninthedistalnephrons,which
helpstorestorebloodvolumeinthebodyANP
- ANPisahormonereleasedbyatrialmusclecellsafterthedistentionassociatedwith
fluidoverload- Ithasaneffectonmanybodysystems,butprimarilytheRAAS
- ANPopposesthiscompensatorysystembyinhibitingreninsecretionandblockingcapabilitiesofaldosterone
- Becauseofthisprocess,thesodiumwastinganddiuresispromotionresultsinvasodilationinthebody
- Hypovolaemiaorfluidvolumedeficitisadecreaseinintravascular,interstitialand/orintracellularfluidinthebody
