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Chapter 27: Fluid, Electrolyte and Acid-Base Balance

pH range of ECF and ICF
• 7.35-7.45
• Intracellular Fluid
• largest component of fluid
• all fluid outside of ICF
• interstitial fluid (largest source)
• plasma
minor ECF areas
• lymph / CSF / synovial fluid / peri / endolymph / aqueous humor /
serous fluid
IF / plasma fluid exchange
• occurs across capillaries and lymph
• via hydrostatic pressure and osmosis
fluid balance
• daily balance between amount of water gained / lost to environment
digestive system
• primary source of water gains
human body composition
• 50-60% water
urinary system
• primary source of water loss
IF / ICF fluid exchange
• occurs via osmosis
• transport of solutes across plasma membrane (H2O follows)
homeostatic mechanisms
• measure fluid pressure and osmotic concentration
• cannot directly measure fluid or electrolyte amounts
• they monitor ECF only (not ICF)
• ions released through dissociation of inorganic compounds
• can conduct electrical current in solution
electrolyte balance
• gains = losses
• rate of absorption across digestive tract balanced with rate of loss at kidneys / sweat glands
• directly effects H2O balance due to osmosis
acid - base balance
• precicely balances production and loss of hydrogen ions (pH)
• body generates acids during normal metabolism (lowers pH)
fluid gains
• digestive tract
• metabolic activity (sugars + O2 > CO2 + H2O)
fluid losses
• urine
• sweat
• lungs
• feces
electrolyte gains
• digestive tract
electrolyte losses
• urine / sweat / feces
• fluid balance regulatory hormone
• osmoreceptors in hypothalamus detect high solute concentration in ECF & release via posterior pituitary
result of ADH release
• H2O conservation at kidneys
• increased thirst
> more H2O added to ECF
H2O conservation at kidney
• caused by ADH release
• water channels increased in collecting duct
• allows more H2O to follow Na out of duct and into peritubular fluid
• fluid balance regulatory hormone
• activated by low Na or high K concentrations @ adreanal gland or by low blood pressure / volume stimulating renin release
result of Aldosterone release
• increase in # of Na / K pumps at DCT / collecting tubule
• kidneys reabsorb more Na and lose K (3:2)
> H2O follows Na
natriuretic peptides
• stimulated by high BP (detected at baroreceptors in R atrium)
• release hormones to block ADH and aldosterone
• increased secretion of urine
result of natriuretic peptide release
• increased thirst
• diuresis
• too much IF
• caused by excess fluid from capillaries and / or not enough reabsorbed by capillaries / lymph
fluid shift
• rapid movement of H2O between ECF & ICF
• due to large change in solute concentration
• could damage cells
hypotonic plasma
• decreased ECF osmotic concentration
• H2O moves from ECF to cells
hypertonic plasma
• increased ECF osmotic concentration
• H2O moves from cells to ECF
• H2O depletion: lossess exceed gains
• results in low BP-can cause shock
• hypernatremia
• abnormally high concentration of Na ions in the plasma
• gain exceed losses
• hyponatremia
• cell size inceases due to hypotonic ECF
• enzymes in ICF diluted
• abnormally low level of Na in the blood
electrolyte imbalance
• can greatly disturb nerve and muscle funcion-may be fatal
• ICF and ECF levels effect cell function
• Na highest amt in ECF, more common issues
• Na / K / Mg / Ca
• Cl / HPO4 / HCO3
Sodium (Na)
• H2O follows
• mostly in ECF
Na regulation via negative feedback
• hypernatremia > osmoreceptors detect high Na level > release ADH > decrease H2O loss at kidneys and stimulate thirst > increased H2O gain > ECF diluted and Na concentration lowered
Potassium (K)
• mostly in ICF
• more dangerous if imbalance
• cells expend energy to recover ions diffused from cytoplasm to ICF
Regulation of Fluids and Electrolytes
1. homeostatic mechanisms monitor and adjust fluid comp. in response to changes in ECF, not ICF
2. receptors do not directly monitor fluid or electrolyte balance
3. cells cannot move water molecules by active transport
4. H2O / electrolyte content will rise if dietary gains exceed environmental losses and will fall if losses exceed gains
primary regulatory hormones
• Aldosterone
• Natriuretic peptides
K regulation
• regulated by ECF concentration at kidneys
• pH-low pH causes tubules to secrete H+ which will increase levels
• Aldosterone
• low concentration of plasma K (below 2mEq/L)
• causes muscular weakness, paralysys and potentially death
• may be caused by aldosteronism, diuretics, chronically low fluid pH, kidney failure and drugs block Na reabsorption
Calcium (Ca)
• mostly in bone
• assists with muscular / neural activities
• blood clotting / enzymatic reactions / second messengers
calcium managment
• PTH / Calcitriol raise levels
• Calcitonin lowers levels
• too much Ca: very dangerous to heart
• usually caused by hyperparathyroidism > oversecretion of PTH
• also from Cx, excessive supplementation
• too little Ca: very dangerous to heart
• usually caused by chronic renal failure
• may be caused by hypoparathyroidism > undersecretion of PTH or Vit D deficiency
• raises cacium plasma levels
• lowers calcium plasma levels
• raises calcium plasma levels
acid - base balance
• body tends to create acidosis due to metabolic activity
• may also create alkalosis
• strong acids and bases completely dissociate into anion or cation plus H+ or OH-
• weak acids or bases
• don't completely dissociate
• can accept or lose H+ or OH- depending on need
• low plasma pH
• disturbs all functions, especially nerve and cardiac
metabolic acidosis
• production of many fixed / organic acids
• impaired H+ excretion at kidneys (renal failure)
• severe bicarbonate loss (chronic diarrhea)
lactic acidosis
• anerobic cellular respiration
• burning fats instead of carbs
• high plasma pH
• disturbs all functions, especially nerve and cardiac
metabolic alkalosis
• caused by elevated HCO3 concentrations-accept too many H+ > raise pH
• bicarbonate ions interact with H+ in solution: form H2CO3
> prolonged vomiting
homeostatic response to alkalosis
• decreased respiratory rate
• H+ ions generated at kidneys
• buffer systems donate H+ ions
detection of acidosis / alkalosis
• blood tests for pH, PCO2 and HCO3
• carbonic acid
• carbon dioxide partial pressure
• bicarbonate
volatile acids
• out of solution and into air
> carbonic acid forming CO2 and leaving alveoli
fixed acids
• remain in solution
• must be eliminated at kidneys
> sulfuric and phosphoric acid
organic acids
• involved in metabolism
> lactic acid: anerobic metabolism
> ketone bodies: burning fats instead of carbs
buffer systems
• use weak acids and bases to regulate pH temporarily
> pH normally regulated at kidneys and lungs
important buffers
• amino acids
• carbonic acid
• phosphoric acid
3 methods of H2CO3 removal
• carbonic acid-bicarbonate buffer system
• phosphate buffer system
• amonia buffer system
carbonic acid-bicarbonate buffer system
• H+ ions added to system > pH lowered > HCO3 ion accepts H+ > becomes CO2 and H2O > CO2 excreted via lungs and kidneys
amino acid buffer system
• donates or accepts H+ to lower or raise pH
respiratory response to acidosis
• increased rate lowers PCO2
• converts H2CO3 to H2O and CO2
renal response to acidosis
• kidney tubules secrete H+ ions
• remove CO2
• reabsorb HCO3 to replenish bicarb reserve
respiratory compensation
• low pH: rate increases > more CO2 released > H2CO3 produced
• high pH: rate decreases > retains CO2 > make more carbonic acid
renal compensation
• low pH: tubules secrete H+ into urine-also must secrete HCO3-, PO4 and ammonia as buffers to keep urine pH from lowering
• high pH: tubules secrete less H+ and reclaim less HCO3-
contributing factors of acidosis / alkalosis
• renal, respiratory, cardiac, CNS and metabolic disorders
• disrupt rates of productions / excretion of acids, bases & buffers
respiratory acidosis
• system cannot effectively eliminate CO2 (hypoventilation)
• causes hypercapnia and low pH
> emphysema, asthma, CHF, pneumonia
respiratory alkalosis
• breathing out too much CO2 (hyperventilation)
• causes hypocapnia and high pH
> anxiety attack