hypoventilation; generation of H+ from CO2 via carbonic acid buffering system
H+ gain
production of nonvolatile acids from the metabolism (catabolism) of proteins and other organic molecules
H+ gain
losing H+ buffering capacity due to loss of HCO3- in diarrhea or other nongastric GI fluids (look at carbonic acid buffering system)
H+ gain
more H+ due to loss of HCO3- in the urine
H+ gain
utilization of H+ in the metabolism of various organic anions; anabolism
H+ loss
loss of H+ in vomitus; stomach acid = HCl
H+ loss
loss of H+ (primarily in the form of H2PO4- and NH4+) in the urine
H+ loss
hyperventilation (look at carbonic acid buffering system = CO2 + H2O <-> H2CO3 <-> HCO3- + H+)
H+ loss
most individuals reabsorb __% of bicarbonate at rest due to net acid load
100%
for every 1 bicarbonate filtered, there is 1 bicarbonate __________
reabsorbed
in a typical human, there is a trend toward
acidosis and excess plasma [H+]
(1ST METHOD) after all filtered HCO3- is reabsorbed...
secreted H+ combines with non-bicarbonate buffer molecules like HPO42-; net gain of "new" HCO3- and goes back to normal pH
(2ND METHOD) after all filtered HCO3- is reabsorbed...
secrete H+ via ammonium from breakdown of glutamine; net gain of "new" HCO3- and goes back to normal pH
ammonium = NH4+
sufficient H+ is secreted to reabsorb all the filtered HCO3-
renal response to acidosis
still more H+ is secreted, and this contributes new HCO3- to the plasma as the H+ is excreted bound to nonbicarbonate urinary buffers such as HPO4(2-)
renal response to acidosis
tubular glutamine metabolism and ammonium excretion are enhanced, which also contributes new HCO3- to the plasma
renal response to acidosis
more new HCO3- than usual is added to the blood, and plasma HCO3- is increased, thereby compensating for the acidosis. the urine is highly acidic (lowest attainable pH = 4.4)
netresult of renal responses to acidosis
rate of H+ secretion is inadequate to reabsorb all the filtered HCO3-, so significant amounts of HCO3- are excreted in the urine, and there is little or no excretion of H+ on nonbicarbonate urinary buffers
renal response to alkalosis
tubular glutamine metabolism and ammonium excretion are decreased so that little or no new HCO3- is contributed to the plasma from this source
renal response to alkalosis
plasma HCO3- concentration is decreased, thereby compensating for the alkalosis; the urine is alkaline (pH > 7.4)
netresult of renal responses to alkalosis
cause: ^ CO2 (hypoventilation)
result: ^ H+
compensation: renal compensation to ^ HCO3- (new bicarb.)
respiratoryacidosis
cause: decreased CO2 (hyperventilation)
result: decreased H+
compensation: renal compensation to decrease HCO3- (excrete bicarb.)
respiratoryalkalosis
cause: ^ H+ (^ lactic acid in exercise; loss of bicarb. in diarrhea)