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Flashcards in Acid/base Deck (41):
1

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-

2

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

3

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

4

Respiratory compensation for metabolic alkalosis

Decreased ventilation
Not able to fully compensate for alkalosis

5

Renal compensation for respiratory acidosis

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

6

Renal compensation for respiratory alkalosis

increased ventilation --> decreased pCO2
increased excretion of bicarbonate

7

Henderson-Hasselbach

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

8

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

9

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

10

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

11

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

12

Renal excretion of H+

Combination of H+ + titratable acids
Generation of ammonium

13

Excretion of H+ with titratable acids

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

14

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

15

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

16

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

17

pH threshold

7.4 - above: alkalosis, below: acidosis

18

Bicarbonate threshold

Low <12

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

19

anion gap

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

20

Clinical utility of AG

differentiating between different causes of metabolic acidosis

21

Anion-gap metabolic acidosis causes

MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde/metformin
Iron/isoniazid
Lactic acidosis
Ethylene glycol, ethanol
Salicylates

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

22

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

23

Sx of metabolic alkalosis

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

24

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

25

Presentation of metabolic alkalosis

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

26

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

27

Initiation of metabolic alkalosis

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

28

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


29

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

30

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

31

Alkali administration

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

32

Contraction alkalosis/Cl-depletion alkalosis

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

33

Most common initiators of metabolic alkalosis

Diuretics
GI loss
Post-hypercapnia
Bicarb administration

34

Maintenance of met alk

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

35

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

36

Hypokalemia - maintenance

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

37

Chloride depletion - maintenance

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

38

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

39

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

40

Cortisol in acid-base

release stimulated by acidosis
H+ secretion, HCO3- retention

41

PTH in acid-base

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