Acid base balance Flashcards
Range blood pH must be maintained
7.35-7.45
<7.35
acidosis
> 7.45
alkalosis
H+ input due to
Diet (fatty acids, amino acids) and respiration (CO2, lactic acids, ketoacids)
Regulate pH by
ventilation: fast, changes level of CO2
Renal: slow, Retaining/ losing HCO3- ions
pH buffers
HCO3- in extra celullar fluid
Proteins, haemoglobin, phosphates in cells
Phosphates, ammonia in urine
Carbonic anhydrase
Catalyses carbonic acid equation both ways
Carbonic acid equation
CO2 + H2O –> H2CO3
–> HCO3- + H+
Transport of CO2 in the blood at the tissue
Diffuses from cell where it is produced into erythrocyte Dissolved CO2 carried 3 different ways: stays as dissolved CO2 or dissolved CO2 + Hb = HbCO2 or CO2 and H2O --> H2CO3 --> HCO3- + H+
Total blood CO2
Dissolved CO2, HCO3- and HbCO2
CO2 diffusion at the lungs
HbCO2–> Hb + CO2
H2CO3 –> H2O + CO2
CO2 produced diffuses into the alveolus and is expired
Blood CO2> Alveolar CO2 = net diffusion into alveolus
What happens to H+?
when O2 is released into the cell from the erythrocyte, affinity for H+ increases
What happens if someone hypoventilates?
Prevents normal elimination of CO2
arterial PCO2 and H+ conc would increase
= respiratory acidosis
Hyperventilation?
Low arterial PCO2 and decr H+
= respiratory alkalosis
Changes in PCO2 and chemoreceptors recap
Peripheral chemoreceptors respond to incr in arterial H+ due to incr in PCO2
Incr in brain PCO2 leads to incr in brain extracellular H+ conc that stimulates central chemoreceptors
Both central and peripheral chemoreceptors stimulate medullary inspiratory neurones to incr ventilation
Non-CO2 dependent changes in pH
eg incr in lactic acid
H+ can’t cross BBB so originally only activate peripheral chemoreceptors
Therefore changes in respiratory activity almost entirely due to stimulation of peripheral chemoreceptors
Bicarbonate regulation in the kidneys
HCO3- filtered completely at renal corpuscle and lots absorbed at PCT, loop of henle and CCT (cortical collecting duct)
CCT can also secrete HCO3-
Renal HCO3- secretion =
Filtered + secreted - absorbed
HCO3- reabsorption in PCT
Epithelial cells secreting H+ ions into lumen of PCT
Combines with HCO3- to form H2CO3 then to H2O and CO2, which can diffuse across into the epithelial cell where they reform H2CO3
This H2CO3 produces H+ and HCO3-, HCO3- moves into ISF by facilitated diffusion and H+ pumped into lumen (back to 1st step)
Net result reabsorption of HCO3-
Enzymes/ pumps behind reabsorption
ATPase and Na/H+ pump (antiporter) releasing H+ into tubule
CAIV extracellular form attached to epi CSM
CAII intracellular form
HCO3- moves into ISF by NBCe1-a pathway
Collecting duct: acidosis
Kidney secretes H+ and reabsorbs HCO3-
collecting duct: alkalosis
Kidney secretes K+ and HCO3- and reabsorbs H+
What happens when all filtered bicarbonate has been reabsorbed?
Additional buffering with ‘new’ bicarbonate ions, synthesised in the tubule cells, as long as a ‘sink’ for H+ (here HPO4 2- ) is available
Net gain HCO3-
diagram is useful here
Glutamine
New bicarbonate ions synthesised from catalysis of glutamine
Metabolised in the cell to make NH4+ and HCO3-
HCO3- moves into bloodstream by sodium dependent pathway and NH4+ moves into lumen, secreted
Glutamine moves in form tubular lumen because been filtered
Overall renal response to acidosis
Sufficient H+ secreted to reabsorb all HCO3-
More H+ secreted and adds new HCO3- in the plasma due to nonbicarbonate urinary buffers
Net result: HCO3- in blood incr, compensates for acidosis
Overall renal response to alkalosis
Amount of H+ secretion not enough to reabsorb all filtered bicarbonate so this is excreted in urine
Little or no excretion of H+ on nonbicarbonate buffers
Decr tubular glutamate metabolism and ammonium secretion
Net result: plasma bicarbonate decr and compensates for alkalosis
