Jan10 M1-Acid Base Physiology Flashcards
lower and upper limit of pH before death
6.8 to 8.0
pH formula
-(log H+)
blood pH formula
6.1 + log (bicarb/0.03PCO2) = pH
3 values to check for acid base balance
pH, CO2, bicarb
rule in HCO3 and CO2 variation
always move in the same direction, no matter which one is the primary problem
how to know if problem is primarily respiratory or metabolic
if pH and CO2 change in same direction, metabolic
if pH and CO2 change in opposite direction, respiratory
how much CO2 prod daily and how
15000 mmol. because of the Krebs cycle
2 types of acids in the body and what they correspond to
carbonic acid (volatile): CO2 non-carbonic acid (non-volatile): lactic, phosphoric, sulfuric
non-carbonic acids source and how much produced daily
from a.a metabolism. 50-100 mmol
buffer def
any substance that can reversibly bind H+ ions
how H+ ions are buffered in the body
by extracellular (HCO3, etc.) and intracellular buffers
major intracellular buffers
phosphates, proteins and carbonate (CO3) in bone
2 steps to acid metabolism in the body
- buffering
2. excretion
how much acid do the kidneys and the lungs excrete daily
lungs: 15000mmol
kidneys: 50-100 mmol
in the kidney, excreting acid is the equivalent of what
generating bicarb (50-100 mmol daily)
minimal tubular pH and what takes care of buffering there
4.5
ammonium (NH4+) and hydrogen phosphate (HPO4 2-)
where are acids handled in the tubules
PCT, loop of Henle, CD
main thing kidney does to keep the serum bicarb
reabso of filtered bicarb
how is bicarb reabsorbed at the tubules (PCT)
- H+ pumped out via Na-H exchanger
- H+ and bicarb form CO2 (via luminal CA)
- CO2 enters membrane and becomes H+ and bicarb via cellular CA
- bicarb in blood via Na-3bicarb cotransporter
- H+ out again
CA inhibitors inhibit what CAs and consequence on urine, what is excreted
CA in and out of the cell inhibited. No more H+ made so Na-H exchanger stops working. Pee NaHCO3
CAi used for what (2)
glaucoma and mountain sickness
principle of using CA in mountain sickness
you hyperventilate because of the hypoxia so lose a lot of CO2, become alkalotic. CA stops that by inhibiting PCT reabso of bicarb
can you induce alkalosis by ingesting too much bicarb?
no, excess filtered at kidney is excreted
2 ways for the kidney to generate new bicarb and why must do that
- urine buffering by H-HPO4 adds 1 bicarb to plasma
- urine buffering by ammonium adds 1 bicarb to the plasma
* necessary bc need NEW bicarb to buffer the NEW acid. (good to reabso bicarb but need new)
when does the kidney start to use H-HPO4 urine buffering (one method to make new bicarb)
when there is no more bicarb available in the tubule and all has been reabso
Urine buffering by H-HPO4: how it works to generate a bicarb
CA in the cell makes H+ and HCO3- from H2O and CO2. H+ out to bind HPO4 and form H2PO4. bicarb in
Urine buffering by ammonium: how it works to add 1 bicarb to the plasma
- glut reabso at PCT via Na-a.a cotransporter
- glut forms NH4+ + bicarb and bicarb taken in
- NH4+ out via Na-H exchanger (takes H+’s spot)
main adaptive response to an acid load and how much bicarb it produces daily
NH4+ excretion. makes 30-40 mmol daily
other way to secrete NH4+ coming from glutamine than Na-H cotransporter
NH3 in the cell diffuses in the lumen and binds an H+ to make ammonium
other place in the tubule where there is acid handling and what mechanism is used
loop of Henle. 1st mech for new bicarb. H2O and CO2 make HCO3 and H+ via CA. HCO3 in via Na-HCO3 cotransporter. H+ out via Na-H exchanger
what is the main determinant of acid excretion and how it works (acts on what)
low extracellular pH acts on 2 mech for new bicarb bc low pH = acid load
- revs up Na-H antiporter in PCT
- increases glut uptake and metab by PCT
- revs up Na-3 bicarb cotransporter in PCT
- revs up H-K activity in CD (alpha-int)
- promotes ammonium excretion
H+ handling in the CD (2 things)
- alpha-int cells have H+ (out) K (in) exchanger ATPase (and then bicarb-Cl exchanger)
- NH3 that diffused out into the tubule lumen becomes NH4+ bc of that acid and goes out
how to maintain acid base balance in renal failure
IV D5W + bicarb (hypertonic but sugar quickly metab)
normal arterial and venous pH, H+, CO2 and bicarb values
arterial: 7.4, 40, 40, 24
venous: 7.45, 45, 45, 25
causes of metabolic acidosis
diarrhea (loss of bicarb), renal failure, poisoning, diabetic ketoacidosis, lactic acidosis
2 responses to metabolic acidosis
- buffering by IC and EC buffers
2. compensatory rise in ventilation
2 causes of metabolic alkalosis
vomiting, hyperaldo (increased H secretion in DCT and CCD bc revs up H-K ATPase in alpha int)
2 causes of respiratory acidosis
acute respiratory failure (morphine)
COPD (chronic)
compensation to metabolic alkalosis
less bicarb reabso
compensation to resp acidosis
kidney increases acid (mostly NH4+ excretion)
4 causes of resp alkalosis
pneumonia, anxiety, pregnancy, mountaineering
why pregnancy causes resp alkalosis
medulla stimulated at lower CO2 (stimulates breathing at lower CO2)
contraction alkalosis def
volume contraction state where all bicarb is retained
ions left and ions reabsorbed in contraction alkalosis + their urine amount
Na and bicarb all reabsorbed (PCT important)
Cl low in serum and low in urine bc is lost in the fluid loss
why can’t excrete bicarb in contraction alkalosis
because Na reabsorbed at PCT so bicarb too. if euvolemic, less Na-H exchanger work so more H left in the cell and unavailable to bind bicarb in urine to make it enter the PCT so bicarb stays in the urine
how to treat contraction alkalosis
give NS so that Na not too retained anymore
