Acid base disorders Flashcards
Difference between respiratory and metabolic disturbances.
respiratory acidosis: ↑ CO2
respiratory alkalosis: ↓ CO2
Metabolic acidosis: ↓ HCO3-
Metabolic alkalosis: ↑ HCO3-
What direction is compensation?
It is always in the same direction as the primary change and with the corresponding molecule.
Ie: respiratory alkalosis initial change = ↓ PCO2
- compensation is ↓ [HCO3-]
Ie: Metabolic alkalosis initial change = ↑ [HCO3-]
- compensation is ↑ [CO2]
In acute respiratory alkalosis, the HCO3- is expected to fall by _____ meq/l for every ___ fall in PCO2-
↓2 HCO3-, ↓ 10 pCO2
2:10
In chronic respiratory alkalosis, the HCO3- is expected to fall by _____ meq/l for every ___ fall in PCO2-
↓4 HCO3-, ↓ 10 pCO2
4:10
During respiratory alkalosis, how is compensation with ↓ HCO3 achieved?
- cell H+ release (acute)
- renal H+ retention (chronic)
- either way, H+ binds to HCO3- which lowers it and drives CO2 formation
During respiratory acidosis, how is compensation with ↑ HCO3- achieved?
- cell buffering (acute)
2. Renal H+ EXCRETION (HCO3- resorption) (Chronic)
In acute respiratory ACIDOSIS, the HCO3- is expected to INCREASE by _____ meq/l for every ___ INCREASE in PCO2-
↑ 1 HCO3-, ↑10 pCO2
1:10
In chronic respiratory ACIDOSIS, the HCO3- is expected to INCREASE by _____ meq/l for every ___ INCREASE in PCO2-
↑ 4 HCO3-, ↑10 pCO2
4:10
Metabolic alkalosis requires generation and maintainance,
How does generation of met alk occur?
- addition of HCO3-
- loss of H+
- Loss of Cl- rich fluids (contraction alkalosis)
- post hypercapnea
- hypokalemia
Ways that loss of H+ can occur leading to metabolic alkalosis?
- GI loss
- Renal loss: loop/thiazide diuretics, mc excess
- inhibit N+ resorption→ increase Na+ delivery to distal tubule → resorbs Na+ → generates (-) charged tubular lumen → FAVORS H+ SECRETION →metabolic alkalosis
maintenance of metabolic alkalosis is ALWAYS due to what?
the inability to excrete excess HCO3-
met alk is due to primary increase in HCO3-
How does chloride depletion result in maintaining met alk?
it results in the resorption of HCO3- via Cl-/HCO3- exchanger on basolateral mem.
- note that Cl- depletion is frequently accompanied by volume depletion
(remember that maintenance of met alk is always due to inability to excrete excess HCO3-)
Why does increased mineralocorticoid activity result in maintaining met alk?
They stim the H+-ATPase pump leading to secretion of H+ into the lumen.
This is accompanied by bicarb resorption.
Aldosterone and mineralocorticoids effects on H+-ATPase activity. What significance does this have on metabolic disturbances?
Increase H+-ATPase pump, eventually reabsorbing HCO3- and maintaining metabolic alkalosis
Metabolic alkalosis is divided into 2 categories:
chloride responsive (saline responsive) - UCl 20 meq/L