Acid Base Flashcards
Metabolism of carbohydrates, phospholipids, and proteins results in:
Carbohydrates = Carbonic Acid, Lactic Acid* Phospholipids = carbonic acid, phosphoric acid* Proteins = carbonic acid, sulfuric acid*, and HCl*
3 types of buffers in the body
HCO3
Phosphate
Proteins (albumin)
How does bicarb serve as a buffer?
present in 5x10^6 times greater conc. than H+ concentration
How does phosphate serve as a buffer? where is it normally stored?
What happens if there is chronic acidosis?
stored mostly in the mineral matrix of bone; therefore buffering of acids by phosphate (acidosis) can force the body to release phosphate from the skeleton as a buffer, leading to bone mineral loss over time.
How does albumin serve as a buffer?
What happens during acidemia? alkalemia?
- Negatively charged; contains exposed amine groups that complexes with Na, Ca, Mg (main extracellular cations)
- With significant acidemia, albumin binds H+ and releases Ca, resulting in incr. free Ca.
- During periods of alkalemia, Ca is bound to albumin and symptomatic hypocalcemia can develop.
How to calculate anion gap?
What is NOT measured routinely in an AG?
Anion Gap = Na – (Cl + HCO3)
Albumin, sulfate, and phosphate are (-) charged and are not measured during a routine metabolic panel
What is the normal AG? What is it primarily attributed to?
normal AG = 12mEq/L; primarily due to albumin
How does albumin affect the AG?
hypoalbuminemia causes decr. AG (1 g/dL decr. albumin = AG decr. by 2.5)
What happens if the AG increases?
presence of an non-HCl acid load ie lactic acid, ketoacid, acetic acid; even if HCO3/CO2 is normal!!.
What causes increased AG?
o Methanol o Uremia o DKA o Paraldehyde o INH o Lactic acidosis o Ethylene glycol o Salicylates
Calculation for osmolar gap?
2xNa + glucose/18 + BUN/2.8 + 1/amount ingested
What does it mean if the calculated osmolar gap is greater than the expected osmolar gap?
there is an unmeasured osmole present!
What are some toxins that can can incr. osmolar gap with acidosis?
- Etylene glycol
- Methanol
- Ketoacidosis
- Uremia
- Paraldehyde
- Lactic acidosis
What are some toxins that can can incr. osmolar gap w/o acidosis?
- Ethanol
- Isopropanol
- Mannitol
- Diethyl ether
- Severe hyperlipidemia
- Hyperproteinemia
- Severe Li+ toxicity
AG = 16 and HCO3 = 10
what is the ∆AG and ∆HCO3?
What does this mean?
Δ[anion gap] = 16 – 12 = 4
Δ[HCO3-] = 24 – 10 = 14
[HCO3-] has changed more than AG (ΔAG-Δbicarb = -10)
- both a hyperchloremic acidosis and a incr. AG acidosis are present
- the concurrent hyperchloremic acidosis makes the overall acidosis WORSE than the gap acidosis alone
AG = 20 and HCO3 = 20
what is the ∆AG and ∆HCO3?
What does this mean?
Δ[anion gap] = 20 – 12 = 8
Δ[HCO3-] = 20 - 24 = 4
[HCO3-] has changed less than AG (ΔAG-Δbicarb = +4)
- both a metabolic alkalosis and a AG acidosis are present
- the concurrent metabolic alkalosis makes the acidosis IMPROVED compared to the gap acidosis alone;
AG = 16 and HCO3 = 30
what is the ∆AG and ∆HCO3?
What does this mean?
Δ[anion gap] = 16 – 12 = 4
Δ[HCO3-] = 24 – 30 = -6
Anion[HCO3 (ΔAG – Δbicarb = +10)
Again, both a metabolic alkalosis and a incr. AG acidosis are present
This time the metabolic alkalosis is the dominant process, but they co-exist, nonetheless!
How to calculate ∆∆?
What is the normal ∆∆ you should expect?
What if it is not proportional?
Delta-Delta Gap (∆∆) = ∆AG - ∆HCO3
for every incr 1 mEq in AG = decr 1 mEq/L HCO3
ie expected AG = 12, expected HCO3 = 24
if ∆AG ≠ ∆HCO3, then an additional acid-base d/o is may be present.
Note: ∆anion gap and ∆HCO3 are not mutually exclusive.
If there is incr. AG, measure ∆∆ to determine if there is an concurrent metabolic disorder.
What does it mean if:
ΔAG > Δbicarb
ΔAG < Δbicarb
ΔAG = Δbicarb
ΔAG > Δbicarb = metabolic alkalosis (AG rise is more than the fall in HCO3) + AG acidosis. Need less HCO3 to buffer it, which is why it’s greater in presence.
ΔAG < Δbicarb = hyperchloremic metabolic acidosis (AG rise is less than the fall in HCO3) + AG acidosis - bicarb has changed less because a lot of HCO3 is req’d to buffer it
ΔAG = Δbicarb, incr. AG acidosis is the sole metabolic disorder.
Urinary AG calculation?
When do you calculate it?
Urine Anion Gap (UAG) = Urinary ([Na+] + [K-]) – [Cl-]
when the pH is abnormal.
How does kidneys excrete acid?
as NH4Cl
NH3 is volatile and is difficult to measure accurately because it can diffuse freely across membranes, but in the distal tubule, NH3 is “trapped” by H+ as NH4 for excretion.
NH4+ is polar and lipid-insouble and since Cl- must accompany NH4 for electroneutrality, urine Cl can be used to infer urinary acid excretion
Metabolic acidosis = if UAG is +, what does this mean? If UAG is -??
Metabolic alkalosis = if UAG is +, what does this mean? If UAG is -??
Acidosis
(–) UAG = appropriate renal response/excretion of acid
(+) UAG = renal disorder (ie distal renal tubular acidosis)
Alkalosis
(–) UAG = renal d/o (incr. CL excretion)
(+) UAG = appropriate renal response (less Cl excretion)
Remember: Urine Anion Gap (UAG) = Urinary ([Na+] + [K-]) – [Cl-]
How do kidneys compensate for respiratory acidosis?
Respiratory Alkalosis?
renal compensation: incr. HCO3 production and retention to restore pH towards normal
resp. acidosis
- acute: limited response (min-hours); rate: incr. 1 mEq HCO3 for every 10mmHg CO2
- chronic: more robust (2-3days); rate: incr. 3-4 mEq for every 10mmHg CO2
resp. alkalosis:
- Acute: decr. 2 mEq/L HCO3 = decr. 10 mmHg pCO2
- Chronic: decr. 4 mEq/L HCO3 = decr. 10 mmHg pCO2
What characterizes metabolic acidosis?
how is it compensated?
decr. HCO3
decr. pH
incr. AG and/or Hyperchloremic Acidosis*
compensation: respiratory
What causes Hyperchloremic acidosis?
HCO3 loss via gut - - incr. Cl intake (occurs at the expense of HCO3)
- examples: saline resuscitation or hyperailmentation, as evidenced by history and review of IV fluids
H+ retention via kidneys - distal renal tubular acidosis -> impaired H+ excretion -> incr HCl
how does aspirin OD usually present?
What is the mxn behind this?
1˚ respiratory alkalosis with an incr. AG acidosis
salicyclate produces an incr. AG metabolic acidosis; the body responds by incr. minute ventilation, thus lowering pCO2.
Aspirin also directly stimulates the respiratory center, furthering lowering pCO2 and causing a superimposed respiratory alkalosis.
Type I RTA
cause?
Labs?
Urine pH? UAG?
trmt?
RTA I (distal) - ICCs are unable to secrete H+ or H+ leaks back into the cell from the lumen
causes: autoimmune, small things (ie Ca excess, drugs (ifosfamide, amphotericin, lithium, toluene)
Serum Labs:
decr. HCO3 (5.5
(+) UAG
Trmt:
HCO3
Type II RTA
cause?
Labs?
Urine pH? UAG?
trmt?
RTA II (proximal): defect in HCO3 reabsorption in PCT -> bicarbonaturia
Causes: “best one to have”; caused by large things “amyloidosis, light chain myeloma, PNH, heavy metals, drugs (ifosfamide, tenovfir, aminoglycosides, Ca inhibitors)
Labs
decr. HCO3 (12-18mEq/L)
decr. K - due to incr Na/bicarbonate delivery to principal cells and incr Na delivery, which incr K secretion
Urine
pH = <5.5 - distal acidification mechanisms are still intact
(–) UAG, steady state
Trmt:
HCO3
Type IV RTA
cause?
Labs?
Urine pH? UAG?
trmt?
Type IV RTA - hypOaldosteronism or aldosterone resistance (via ACEi/ARB): net effect: limited H,K excretion
Serum Labs
- decr. HCO3
Should be suspected in any case of hyperchloremic acidosis with hyperkalemia with normal or near-normal creatinine
Urine
decr. K (despite hyperkalemia)
Trmt:
hypOaldosteronism: fludrocortisone
HCO3 supplements
K restriction
Hyperchloremic acidosis - what is it?
NORMAL AG, but the ratios of Cl and HCO3 has changed (usually due to HCO3 loss via gut or H+ retention via kidneys)
Osmolar gap - what is normal?
What if it deviates from normal?
10-15 mOsms/L
if measured»_space; calculated, then there is an unmeasured osmole pressent.
2 types of metabolic acidosis. what are they and what does it mean?
AG acidosis - non-HCl acid (ie lactic acid, ketoacids)
Hyperchloremic acidosis - HCl retention or HCO3 loss (ratio of HCO3/HCl changes, but AG does not change), ie RTA I, II, IV, diarrhea
Volume depletion does what to acid/base balance?
results in contraction ALKALOSIS because it results in RAAS activation ->
AII stimulates Na/HCO3 uptake in PCT
Aldosterone stimulates Na uptake, H/K secretion in CD
