Ch. 26 Fluid Acid-Base Balance

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diff in water content b/w Ms and Fs; why: 60% vs. 50%

Fs have higher avg body fat content
smaller rel amount of skel muscle
subdivisions of extracellular fluid: plasma - fluid portion of the blood
interstitial fluid - in spaces b/w cells (80% of ECF)
what regulates exchange between ICF and ECF: osmotic and hydrostatic pressures
net fluid movement is in what direction: blood to interstitial space; then taken up from interstitial space by lymphatic vessels and returned to the bloodstream
sources of obligatory water loss; effect: from lungs and skin; water that accompanies undigested food residues in feces

kidneys must excrete 900-1200 mOsm of solutes to make up for this
effect of : decrease in plasma volume decrease in plasma osmolality: stim thirst center
inhibit
what stimuli stimulate the hypothalamic thirst center: baroreceptors
angiotensin II
feedback signals that inhibit the thirst center: moistening of mucosa of mouth and throat
activation of stomach and intestinal stretch receptors
effect of low ADH levels on urine and body fluids: dilute urine (increased vol)
reduced body fluid volume
prolonged dehydration may cause what: fever
mental confusion
what triggers ADH rel; effect of high ADH: fever, excessive sweating, vomiting, or diarrhea, severe blood loss, traumatic burns

concentrated urine (decreased vol)
what is hypotonic hydration; how does it develop: cellular overhydration

ECF is diluted from excess water --> hypnatremia --> net osmosis into tissue cells --> swelling --> brain damage b/c of compressed b. vessels --> decreased blood flow to brain
effect of increased flow of fluids out of bloodstream: increase in fluid in interstitial space --> edema
effect of increased blood pressure on fluid balance: more fluid flows out of bloodstream --> edema
effect of congestive heart failure on fluid balance: edema
effect of blocked lymph vessels on fluid balance: edema (increased fluid in interstitial space)
impact of chronic interstitial fluid accumulation: low blood pressure (b/c the fluid is in interstitial space instead of blood)
what is the most abundant ECF cation: Na
effect of high aldosterone levels on fluid balance: Na actively reabsorbed in DCTs and collecting ducts
then IF collecting duct permeability has been increased by ADH, water follows Na (to interstitial fluid?)
what mechanism regulates aldosterone release; what general condition causes it: renin-angiotensin mechanism
nephron's JG apparatus mediates its release from the adrenal cortex

basically when BP is too low aldosterone is rel to increase fluid pressure (systemic and glomerular)
compare response to ADH vs. response to aldosterone: fast, since no protein synthesis is necessary

slow, since new transporters that increase Na reabsorption in collecting ducts must be prod
effect of excessive ECF K concentration: decreased membrane potential (too little positive ions inside cell) --> hypopolarization --> hyperresponsiveness
where is regulatory site of renal K balance: collecting ducts
what stimulates K secretion: aldosterone --> for each Na reasborbed, one K is secreted

rel of aldosterone occurs with high K ECF
major anion in the ECF major cation in the ECF: Cl
Na
comparison of reabsorption of Cl with other anions (phosphates, sulfates): 99% Cl reabsorbed
others have transport maximums so excess can't be reasborbed and is excreted
definition alkalosis: alkalemia --> arterial blood pH above 7.45
definition acidosis: arterial blood pH below 7.35
compare pH of arterial blood, venous blood, intracellular fluid, interstitial fluid: basic to acidic

arterial
venous, interstitial
intracellular
source of H ions in body: mostly from cellular metabolism --> phosphoric acid, sulfuric acid from macromolecule breakdown

lactic acid from glucose breakdown
organic acids from fat metabolism

transporting CO2 as bicarbonate releases H ions
sequence of systems regulating H+ concentration: chemical -- seconds
pulmonary -- 1 min (resp center in brain)
renal -- hours to days
diff b/w the diff systems of H+ regulation: only the renal mechanism can achieve balance without hyperventilation or causing disequilibrium --> physically removes the H+ imbalance
list the subtypes of chemical buffer systems to regulate H+: bicarbonate
phosphate
protein (b/c of carboxylic acid and amino groups in proteins)
bicarbonate buffer system response to adding of acid: H+ ions combine with bicarbonate --> shifts eqn L, to H2CO3
when would more bicarbonate be produced to regulate H+: if H+ was too low --> eqn shifts R to produce more H+ and HCO3-
molecules of the phosphate buffer system to regulate H+: H2PO4-; HPO42-
where is phosphate buffer system to regulate H+ most effective: in urine and intracell fluid (concen of buffer molecules is highest here)
body's most powerful and plentiful buffers are what? where?: proteins; in plasma and intracell fluid
how does respiratory buffer system respond to acidosis: deeper, more rapid breathing --> expel more CO2 --> eqn shifts L away from H+ and HCO3- to H2CO3 and CO2 + H2O --> decreased H+
respiratory buffer system response to alkalosis: slower, more shallow breathing --> retain more CO2 --> shifts eqn R to carry more CO2 as HCO3, which increases H+
how does renal buffer system regulate acid-base balance: changing bicarbonate concentration (reabsorb from filtrate to increase its levels in blood or let it be excreted)
should bicarbonate be excreted or reabsorbed to stop acidosis: reabsorbed (gaining bicarbonate is like losing H+)
what happens after carbonic acid is formed in filtrate to change H+ balance: it dissociates to release CO2 and water in the filtrate --> CO2 diffuses from filtrate into tubule cells --> here it forms H2CO3 and then H+ and HCO3- to trigger further H+ secretion (the H+ flow out of tubule cells into filtrate)
how do kidneys generate more bicarbonate ions? effect?: increasing respiration in the tubule cells --> increased CO2 --> forms H2CO3 --> then H+ and HCO3- --> H+ leaves tubule cells and is added to filtrate
transport of H+ ions in urine; why: must bind to buffers in urine (phosphate buffer system and ammonia sys)

since lowest pH that urine can have is around 4.5
source of ammonium ions for ammonium buffer system: ammonium ions prod by metabolism of glutamine in PCT cells --> each produces 2 ammonium ions and 2 bicarbonate ions
fate of bicarbonate and ammonium prod by glutamine metabolism: moves to blood

moves to urine
def. respiratory alkalosis/acidosis; cause: pH imbalance from failure of respiratory buffer sys
what is most important indicator of respiratory inadequacy; what is condition for acidosis? alkalosis?: P Co2

too high --> acidosis
too low --> alkalosis
hyperventilation causes what respiratory imbalance: alkalosis
metabolic acidosis is caused by what: too low bicarbonate levels
causes of metabolic acidosis: ingestion of too much alcohol
excess loss of bicarbonate
accumul of lactic acid
shock
ketosis in diabetic crisis
starvation
kidney failure
what indicates metabolic alkalosis: increased blood pH
increased bicarbonate levels
causes of metabolic alkalosis: vomiting
intake of excessive base (ex. antacids)
constipation (fecal matter stays in body --> increased blood bicarbonate levels)
what happens if one buffer system is not working properly: the other systems work harder to compensate
ex. of how respiratory system works to compensate for metabolic acidosis: increase rate and depth of breathing --> to decrease blood CO2
causes eqn shift toward prod of CO2 --> causes decrease in H+

PCO2 falls below normal as the resp sys works to compensate
ex. of how respiratory buffer system works to compensate for metabolic alkalosis: slow, shallow breathing --> CO2 accumulates in blood
shifts eqn R toward prod of HCO3-, H+

causes increased pH and increased bicarbonate levels, as well as rising PCO2
char of compensated respiratory acidosis: high PCO2 (cause of acidosis)
high bicarbonate --> by kidneys retaining bicarbonate to offset the acidosis
char of compensated respiratory alkalosis: low PCO2 --> cause
low bicarbonate --> kidneys eliminate it in order to lower the pH

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Created By bschneider1590