Lect 10 Flashcards
how is respiration regulated by plasma CO2
- CO2 diffuses across BBB, forms with water, and the dissociated H+ stimulates the chemosensitive areas of the medulla
- elevated PCO2 stimulates respiration to blow off more CO2
what is the basic role of the kidney in control of bicarbonate
stabilize [HCO3-] at 22-26 mEq/L
how does the kidney control bicarbonate (3 mechanisms)
- complete “recovery” of filtered bilcarbonate when plasma [HCO3-] is < 26 mEq/L
- synthesize new HCO3- above and beyond that entering in the glomerular filtrate
- excrete HCO3- when present in excess
describe the process of how HCO3- is recovered by the kidney
- H2O + CO2 -> H2CO3 inside tubular cells (carbonic anhydrase required).
- H2CO3 dissociates into H+ and HCO3-
- H+ is secreted (drives process)
- HCO3- enteres blood
- secreted H+ reacts with HCO3- in urine; HCO3- does not cross apical membrane to be reabsorbed
where in the nephron, is the most amount of bicarbonate reabsorbed
- proximal tubule: 85%
- **99.9% of all filtered HCO3- is generally reabsorbed
what happens to H2CO3 once it is formed in the tubule fluid from filtered bicarb and secreted H+
- H2CO3 is acted on by carbonic anhydrase to form H2O and CO2.
- CO2 can either be excreted or be reabsorbed into the tubule cell to help form more bicarbonate in the cell
via what mechanisms is H+ secreted in the proximal tubule
- sodium-proton antiport
- actively secreted (requires ATP)
via what mechanisms is HCO3- transported from tubule cell into ECF in the proximal tubule
- HCO3-, Na+ symport (driven by bicarb conc)
- HCO3-,Cl- antiport
via what mechanisms is H+ transported from tubule cell into tubule fluid in collecting duct (type A intercalated cell)
- proton ATPase
- potassium proton antiport (requires ATP)
one HCO3- is released into the peritubular capillaries for every X HCO3- neutralized in the tubule
for every 1 HCO3-
- 1:1
what causes net H+ extrusion to stop
- when HCO3- is gone from the filtrate
- luminal pH falls to 4.5 (pH gradient from 7.4 to 4.5 is 1000 fold)
what is titratable acidity
- primarily filtered phosphate
- pK for phosphate = 6.8 is excellent for buffering
- H+ picked up by phosphate allows synthesis of additional HCO3-
explain why the proxmal tubule metabolizes glutamine from blood
- glutamine metabolized to yeild NH3 and a-ketoglutarate
- NH3 enters tubular fluid and is protonated -> NH4 (diffusing trapping)-> urine
- a-ketoglutarate metabolized to HCO3- -> blood
- Each glutamine -> 2 HCO3- and 2 NH4+
synthesis of NH4 from glutamine is regulated by
intracelluar pH
- acidosis stimulates glutamine catabolism -> allows HCO3- to be returned to the blood to neutralize the H+
what effect does [K+] have on NH4+ synthesis
- hypokalemia stimulates NH4+ synthesis and hyperkalemia inhibits NH4+ synthesis
- related to H+/K+ exchange across cell membrane
the majority of fixed acids will be handled by what compound
- NH4+; stimulated by acidosis
- titratable acid is limited
what is the mass action rule
- when PCO2 changes (either as a primary problem or secondary compensation), it causes a small change in HCO3- due to mass action
- CO2 + H2O <-> H2CO3 <-> H+ + HCO3-
- every 10 mmHg increase in PCO2 results in 1 mEq/L increase in HCO3-
- every 10 mmHg decrease in CO2 results in a 2 mEq/L decrease in HCO3-
how do you classify acid-base disturbances
- determine whether the condition is normal (pH = 7.4), acidosis, or alkalosis
- range: 7.35-7.45
- determine whether condition has a respiratory or metabolic cause
- is there any compensation; has the ratio been adjusted to reduce pH change
- partial or complete
ex:
- a patient ingests acid until HCO3- = 15 (PaCO2 = 40 mmHg)
- patient starts hyperventilating and PaCO2 falls to 30 mmHg
- what is the new HCO3- and pH?
- PaCO2 decreased 10 mmHg -> estimated decrease in HcO3- = 2 mEq/L (mass action)
- new HCO3- = 13 mEq/L
-
pH = 6.1 + log [HCO3-] / 0.03 PCO2
- log[13/0.9]
- 6.1 + 1.16 = 7.26
- partially compensated metabolic acidosis
what is the pH equation you use when determining pH for changes in HCO3-
pH = 6.1 + log [HCO3-] / 0.03 PCO2
what is the normal value of bicarbonate
HCO3- = 24 mEq/L
ex:
- a person has a chronic obstructive lung disease
- PaCO2 = 60mmHg
- HCO3- = 26 mEq/L
- has renal compensation occured?
- what is the pH?
- PaCO2 increased by 20 mEq/L -> mass action means that there should be a 2 mEq/L increase in HCO3-; which accounts for the value of 26 mEq/L
- therefore, no renal compensation has occured
- pH= 6.1 + log (26/1.8) = 7.26
ex:
- a person has a chronic obstructive lung disease
- PaCO2 = 60mmHg
- HCO3- = 35 mEq/L
- has renal compensation occured?
- what is the pH?
- HCO3- > 26 mEq/L, the expected value due to mass action; thus renal compensation has occured
- pH=6.1 + log 35/1.8 = 7.39 (in normal range)
- completely compensated respiratory acidosis
what is pure (uncompensated) metabolic acidosis
- HCO3- low
- addition of acid with no change in PCO2
what is pure (uncompensated) metabolic alkalosis
- HCO3- high
- addition of a base with no change in PCO2
what is pure (uncompensated) respiratory acidosis
- addition of CO2 with no renal compensation
what is pure (uncompensated) respiratory alkalosis
- removal of CO2 with no renal compensation
what is partly compensated metabolic acidosis
- a primary acid load
- secondary respiratory alkalosis
- pH below 7.35
what is completely compensated metabolic acidosis
- a primary acid load
- secondary respiratory alkalosis
- pH = 7.35-7.40
what is partly compensated metabolic alkalosis
- a primary base load
- secondary respiratory acidosis
- pH > 7.45
what is completely compensated metabolic alkalosis
- primary base load
- secondary respiratory acidosis
- pH from 7.40-7.45
in general, the lungs are only capable of compensation and the kidneys are capable of
- lungs: partial compensation
- kidneys: complete compensation for chronic disturbances originating outside the renal system
what is partly compensated respiratory acidosis
- primary respiratory acid load
- secondary renal increase in HCO3-
- pH < 7.35
what is completely compensated respiratory acidosis
- a primary respiratory acid load
- secondary renal increase in HCO3-
- pH: 7.35-7.40
what is completely compensated respiratory alkalosis
- primary respiratory alkalosis
- secondary renal decrease in HCO3-
- pH = 7.40-7.45
what is partly compensated respiratory alkalosis
- primary respiratory alkalosis
- secondary renal decrease in HCO3-
- pH>7.45
what is mixed acidosis
- metabolic acidosis + respiratory acidosis
- bicarb decreased while PCO2 increased
- low pH
what is mixed alkalosis
- metabolic alkalosis + respiratory alkalosis
- bicarb increased while PCO2 decreased
- high pH
look at acid-base workshop
