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Flashcards in Acid/base Deck (41):

Sources of H+

All from metabolism
Carbonic acid (volatile, H2CO3)
- excreted at lungs
- H+ produced - need CA
-reversed at lungs

Non-carbonic acids (non-volatile, HCl, H2SO4)
- metabolism of proteins, sulfates, phosphates
- daily acid load
- 50-100 mEq/day on normal diet
- buffered by HCO3-


Buffering systems for H+

Intracellular: inorganic phosphates, cystosolic proteins, hemoglobin/RBC
Extracellular: HCO3-/CO2 (primary mechanism), plasma proteins, inorganic phosphates
Bone: important in acidosis, takes up H+, dissolve bone mineral, breaks down carbonate --> bicarb and releases bicarb as buffer


Respiratory compensation for metabolic acidosis

- due to increase in H+ or decrease in bicarb
- causes decrease in HCO3- concentration
- increased ventilation --> decrease pCO2, rectifies ([H+] is proportional to pCO2/[HCO3-])
- H+ ion concentration in plasma determined by pCO2
- should not be able to completely resolve acidosis

Kusmall breathing: fast, deep --> diabetic ketoacidosis

Rule of thumb: for every decrease in 1 unit of bicarb, should also see 1 unit of decrease in pCO2, otherwise other acid-base issue in play


Respiratory compensation for metabolic alkalosis

Decreased ventilation
Not able to fully compensate for alkalosis


Renal compensation for respiratory acidosis

decreased ventilation --> increase pCO2
increase renal retention of bicarb
reabsorption of bicarb paired with production & excretion of ammonia


Renal compensation for respiratory alkalosis

increased ventilation --> decreased pCO2
increased excretion of bicarbonate



pH = 6.1 + log [HCO3-]/0.03(pCO2)


Renal compensation for H+ load

regenerates bicarbonate by eliminating H+
for every H+ eliminated, one HCO3- added to ECF
eliminated 50-100 mEq H+ / day


Renal resorption of all filtered bicarbonate

Hydrogen ion excretion:
- not filtered at glomerulus
- HCO3- filtered at glomerulus
- H+ secreted by PT and CD into lumen

HCO3- reabsorption
- all consequence of H+ secretion
- ~4300 mEq/day filtered
- almost all reabsorbed - 90% at PT, rest at LOH, CD


Reabsorption of bicarb at PT

water --> H+ and OH- in cell
H+ secreted into lumen through Na/H exchanger (gradient by Na/K ATPase)
Lumen: H+ + HCO3- --> H2CO3 --> H2O + CO2
CO2 and H2O passively reabsorbed into cell
Cell: CO2 + OH - --> HCO3- by CA
HCO3- goes to blood by HCO3-/Na+ exchanger


Reabsorption of bicarb at CD

H2O --> OH- and H+ in cell
H+ secreted into lumen via H+ ATPase
H+ + HCO3 --> H2CO3 --> CO2 + H2O (CA)
passively resorbed into cell
CO2 + OH- --> HCO3- by CA
HCO3- moved out of cell into blood via HCO3-/Cl- exchanger


Renal excretion of H+

Combination of H+ + titratable acids
Generation of ammonium


Excretion of H+ with titratable acids

gets used up quickly
once pH < 5.5, all phosphate is in H2PO4- form
PT and CD


Excretion of H+ with phosphate in PT

water --> H+ + OH-
H+ secreted through Na+/H+ exchanger
H+ combines with titratable phosphate in lumen --> H2PO4-, excreted
OH- generated in cell combines with CO2 --> HCO3 via CA
HCO3- moves into blood via HCO3-/Na+ exchanger


Excretion of H+ with phosphate in CD

water --> OH- + H+ in cell
H+ secreted to lumen via H+ ATPase
OH- + CO2 --> HCO3- via CA in cell
HCO3- moved to blood with HCO3-/Cl- exchanger


Excretion of H+ through ammonium

Accounts for ~50% fixed acid load excretion
can increase in response to acid load
NH4+ cant get trapped right away because it isn't acidic enough
want to avoid losing NH4+ to blood

1) ammonium formation
- hydrolysis of glutamine in PT --> ammonium + alpha-KG
- ammonium excreted into lumen via Na+/NH4+ exchanger
- NH4+ in lumen is in equilibrium with NH3
- AKG --> HCO3- by CA, moved out by HCO3-/Na+ exchanger

2) ammonium reabsorption and recycling
- TAL: ammonium moved into cell in place of K+ through NKCC2
- NH4+ --> NH3 inside cell, NH3 accumulates in interstitium

3) Buffer in CD
- NH3 diffuses from interstitium --> cell --> lumen
- H2O --> OH- + H+
- H+ pumped to lumen via H+ ATPase
- lumen: H+ + NH3 --> NH4+
- NH4+ trapped in urine, excreted
- OH- in cell generates bicarbonate, moved to blood via HCO3-/Cl- exchanger


pH threshold

7.4 - above: alkalosis, below: acidosis


Bicarbonate threshold

Low <12

low pH + low bicarb = metabolic acidosis
high pH + low bicarb = compensation for respiratory alkalosis


anion gap

Anion gap = [Na+] - [Cl-] - [HCO3-]
Normal add 3 to AG (same threshold)


Clinical utility of AG

differentiating between different causes of metabolic acidosis


Anion-gap metabolic acidosis causes

Diabetic ketoacidosis
Lactic acidosis
Ethylene glycol, ethanol

Presence of acids
Lactic acidosis
- type A: impairment in tissue oxygenation
- type B: no impairment in tissue oxygenation (meds, malignancy, alcoholism, cirrhosis)
renal failure


Non-anion gap metabolic acidosis causes

Loss of bicarbonate

GI loss from diarrhea
Renal tubular acidosis
- impaired reabs at PT
- defective H+ excretion at PT
- aldosterone deficiency/resistance
Dilution acidosis due to rapid ECFV expansion


Sx of metabolic alkalosis

Confusion/change in mental status
muscle cramps/ tetany
Sx related to causes - e.g. vomiting


DDx of elevated serum bicarb

Metabolic alkalosis
Respiratory acidosis with compensatory metabolic alkalosis

Differentiate with arterial pH:
- low pH = respiratory acidosis with compensatory metabolic alkalosis
- high pH = metabolic alkalosis


Presentation of metabolic alkalosis

increased serum bicarb
increased arterial pH
increased PaCO2 (compensatory respiratory acidosis)
hypokalemia, hypochloremia, hypovolemia also often present


Kidney's role in alkalosis

Perpetuates - stimulation of H+ secretion = stimulate bicarb reabsorption, can perpetuate alkalosis

Indirect resorption via H+ secretion/Na+ resorption
- H+ secretion promoted by electronegative lumen
- Na+ resorption promoted by low ECFV, activation of RAAS
New HCO3- generated via glutamine metabolism
CCD: alpha/beta intercalated cells control bicarb resorption
- alpha: H+ secretion
- beta: HCO3- secretion


Initiation of metabolic alkalosis

1) H+ loss/HCO3- gain
2) Intracellular shift of H+
3) Alkali administration
4) contraction alkalosis


Vomiting/nasogastric irritation

- HCl lost
- parietal cells secrete H+ into stomach, HCO3- into blood
- loss of neutralization of pancreatic bicarb
- less Cl- available in urine to exchange with HCO3- in tubular lumen for excretion
- hypokalemia: alpha-intercalated cell of CCD promotes H+ secretion to take up K+ from lumen, promotes HCO3- return to blood
- volume depletion: active RAAS promotes hypokalemia - promote Na+ resorption in CCD, increase K+ secretion
- Na+ resorp --> H+ secretion --> bicarb resorption
- RAAS also promotes H+ secretion distally, promoting HCO3- resorption


renal loss of H, K, Cl

- Diuretics (most common cause of metabolic alkalosis)
- Primary aldosteronism: hypokalemia, Na+ resorption
- Bartter's and Gitelman's: diuretic-like
- Posthypercapnic alkalosis: bicarb generated by body due to chronic increase in pCO2 - once pCO2 is corrected, end up with metabolic alkalosis
- Post-correction alkalosis : give bicarb to treat severe metabolic acidosis --> bicarb load


Intracellular shift of H+

To compensate for hypokalemia: K+ shifts from ICF --> ECF
to maintain electroneutrality, H+ moves into cell, producing extracellular alkalosis
Causes intracelluar acidosis in PT, promoting HCO3- production, perpetuates metabolic alkalosis


Alkali administration

Post-correction metabolic alkalosis
Post-hypercapnic metabolic alk
Citrate excess: metabolized to bicarb in liver - massive transfusion


Contraction alkalosis/Cl-depletion alkalosis

Reduction of ECF with HCO3- staying relatively stable
Also caused by hypochloremia


Most common initiators of metabolic alkalosis

GI loss
Bicarb administration


Maintenance of met alk

1) effective circulating vol depletion
2) hypokalemia
3) chloride depletion


Effective circulating vol depletion

lowered GFR - less HCO3- filtered
RAAS activation
- AngII: upreg of H+ ATPase in PCT and CCD
- aldosterone: ENaC in CCD - electronegative lumen, H+/K+ secretion


Hypokalemia - maintenance

Leads to intracellular acidosis
increased distal resorption of K+ in CCD
- H/K ATPase
- secretion of H+


Chloride depletion - maintenance

luminal hypochloremia
- stimulates RAAS
- reduced activity of Cl/HCO3- exchanger


AII in acid-base

activated by low ECFV or reduced NaCl concentration in ultrafiltrate
increase activity of Na/H antiporter in apical PT
increased activity of Na/3HCO3- antiporter in basolateral PT
H+ secretion, HCO3- reabsorption


Aldosterone in acid-base

increase Na/K ATpase in basolateral side of DT and CD, creating Na+ gradient --> increase Na resorption
electronegative lumen = secrete K+, H+
H+ secretion, HCO3- reabsorption


Cortisol in acid-base

release stimulated by acidosis
H+ secretion, HCO3- retention


PTH in acid-base

stimulated by acidosis
increases inorganic phosphate excretion in urine, promoting H+ excretion