Chapter 27: Fluid, Electrolyte and Acid-Base Balance

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pH range of ECF and ICF

• 7.35-7.45

ICF

• Intracellular Fluid
• largest component of fluid

ECF

• 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)

electrolytes

• 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

ADH

• 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

Aldosterone

• 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

diuresis

• increased secretion of urine

result of natriuretic peptide release

• increased thirst
• diuresis

edema

• 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

dehydration

• H2O depletion: lossess exceed gains
• results in low BP-can cause shock
• hypernatremia

hypernatremia

• abnormally high concentration of Na ions in the plasma

overhydration

• gain exceed losses
• hyponatremia
• cell size inceases due to hypotonic ECF
• enzymes in ICF diluted

hyponatremia

• 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

Cations

• Na / K / Mg / Ca

Anions

• 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

• ADH
• Aldosterone
• Natriuretic peptides

K regulation

• regulated by ECF concentration at kidneys
• pH-low pH causes tubules to secrete H+ which will increase levels
• Aldosterone

hypokalemia

• 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

hypercalcemia

• too much Ca: very dangerous to heart
• usually caused by hyperparathyroidism > oversecretion of PTH
• also from Cx, excessive supplementation

hypocalcemia

• 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

PTH

• raises cacium plasma levels

Calcitonin

• lowers calcium plasma levels

Calcitriol

• 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-

buffer

• weak acids or bases
• don't completely dissociate
• can accept or lose H+ or OH- depending on need

acidosis

• 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

ketoacidosis

• burning fats instead of carbs

alkalosis

• 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

H2CO3

• carbonic acid

PCO2

• carbon dioxide partial pressure

HCO3

• 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

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