Lecture 17: Acid Base 2 Flashcards
Three step approach to interpreting acid base data
- Acidosis or alkalosis
- metabolic or respiratory
- compensated or not (looking at non/primary component)
- inappropriate compensation –> hint at mixed disorder
.. - anion gap (yes = metabolic acidosis)
- change in anion gap (yes = co-existing metabolic alkalosis and acidosis)
Base excess BE
Calculated measure/parameter (experimental construct = reflects metabolic change) –> pH, pCO2, and Hb haemaglobin
The amount of acid or base needed to restore pH to 7.4
Normal Base excess = 0 (-2 2)
BE = base excess =
1. +ve in alkalosis (too +ve, needs more acid to restore to normal)
2. -ve in acidosis (too -ve pH, needs more base to restore to normal)
Chronic lung disease + ventilator
- Admitted –> High HCO3- + High BE –> w. Respiratory acidosis + Renal compensation
Chronic lung disease –> COPD –> obstruction causes decreased CO2 expiration –> admitted as respiratory acidosis
Renal compensation = +10 BE - –> Ventilator –> increase minute ventilation –> increased CO2 expiration –> respiratory acidosis fixed
Note: still have BE +10 –> Metabolic alkalosis remains –> POST HYPERCAPNIC ALKALOSIS
Note 2: Kidneys take a longer time course to begin compensating –> therefore if renal compensation is occurring is a chronic condition –> post hypercapnic (respiratory acidosis) alklaosis
Meaning of Post Hypercapnic Alkalosis
COPD:
Post (after) Hypercapnic (High H+ acid from respiratory acidosis) Alkalosis (high BE from renal compensation, which remains after acidosis is fixed by ventilator-increased-minture-ventilation-expiration-of-CO2)
Anion Gap AG
AG = difference b/w Cations and anions in blood
(calculated parameter)
Normally reflects unmeasured Protein anions
Normal conditions= cation and anion difference EXCLUDING PROTEINS is equal as reflects ELECTRO NEUTRALITY –> therefore normal range is 14-18 as Protein charge tends to be 16
AG = (cations) - (anions) = (Na + K) - (Cl + HCO3-)
= (140 + 4) - (104 + 24) = 16 = Protein difference = electronuetrality of 0 as Proteins compensate/balance to 0 difference when included in equation
(Na + K) = EQUAL/0 difference = (Cl- + HCO3- + Protein)
Acid in blood –> dissociates in Anion + H+ –> increased difference b/w cations and anion in blood –> increased anion gap
Therefore: out of/above normal AG range = Presence of UNMEASURED ANIONS –> presence of added acid –> Metabolic ACIDOSIS
e.g. Na+ + K+ = Cl- + HCO3- + Protein + Lactate
Note: Lactic acid has dissociated into H+ and a Anion –> therefore contribute to the Anion side of the electroneutrality equation
Why dont you want a change in the Anion Gap?
As you want blood to be ELECTRONEUTRAL (want a balance b/w acids and bases in blood) so can have SAME pH
What is the main protein which causes Proteins to have an anion charge of 16
Albumin concentration
- can be a major determinant if protein anion charge changes
- therefore different reference ranges to compensate for this
What is AG useful for?
Metabolic Acidosis
As it is only an increase in metabolic acid forms which increases the concentration acid which dissociates into anions and H+
With the addition of Metabolic acid, what causes the changes in HCO3- and Protein levels?
Want to return to 16 balance –> need to decrease anion side of equation –> composed of Cl- and HCO3- and Protein and new metabolic acid –> HCO3- and Protein levels decrease acting as protein buffers –> balances out sides of equation to remain equal = keeps electroneutrality of 0 = keeps pH of 7.4
Electronuetrality equation vs Anion gap equation
- Anion gap uses the values of Meaurable substances –> forming a value which shows presence of immeasurable substances
AG = (cations) - (anions) = (Na + K) - (Cl + HCO3-)
= (140 + 4) - (104 + 24) = 16 = Protein difference - Electroneutrality equation shows the compensation by both the measurable and immeasurable substances
Electroneutrality of 0 –> illustrates renal compensation by body = (cations) - (anions + proteins + Metabolic acid) = (Na + K) - (Cl + HCO3- + Proteins + Metabolic acid)
= (140 + 4) - (104 + 24) = 16 = Protein difference
Causes of Acidosis
- Lactic Acidosis: hypoxia, poor diffusion, drugs
- Ketoacidosis: Beta-hydroxbutyrate (ketone body) as main anions (diabetic/alcohol/starvation)
- Renal Failure: retention of phosphate and sulphate –> slightly increased AG
… - Methanol poisoning (formate anion) e.g. moonshine
- Ethylene glycol poisoning (glycolate anion, lgyoxylate, oxalate anions) e.g. suicide attempt via antifreeze poisoning
- Salicylate (aspirin) overdose –> causes respiratory acidosis
- Organic acidurias (children) e.g. methylmalonic aicduria (inheritable)
- Pyroglutamic aciduria (adults)
- Toxic ED
What is the causative pathway of lactic acid production?
Lactic acid is produced due to occurrence of ANAEROBIC METABOLISM
Hypoxia/poor tissue diffusion/drug –> decrease in O2 –> anaerobic metabolism –> Lactic acid production –> dissociates into lactate + H+ –> increase in anion gap (immeasurable protein and metabolic anions) –> greater difference b/w cations Na + K and main measurable anions Cl- and HCO3-
Metabolic acidosis with respiratory compensation vs renal compensation
Metabolic acidosis = too much acid = -ve BE
Respiratory compensation = Change in CO2 (decrease) –> Know is primarily Metabolic as has biggest change
Renal compensation = change in HCO3- (decrease due to attempted buffer)
Continued tests on semicomatos, seizuring, metabolic acidosis patient
Normal lactic acid (not due to hypoxia/poor tissue diffusion induced anaerobic metabolism)
Normal batehydroxybuturate (not due to diabetic ketoacidosis)
Ethylene glycol poisoning (suicide attempt ia drinking ANTIFreeze
Treatment:
1. Ethanol: inhibits alcohol dehydrogenase metbaolism of ethylene glycol into toxic substances
2. Dyalisis: especially if toxic metabolites are all through the body and need removal
Ethylene glycol
Non-toxic shelf substance –> alcohol dehydrogenase –> metabolised to Glycolic and OXALIC acids –> metabolic acidosis –> attempted suicide –> treat with ethanol –> inhibition of alcoholic ehydrogenase –> ethelyene glycol
Good: enzyme alcohol dehydrogenase normally metabolises alcohol –> dont get hangover
Bad: alcohol dehydrogenase metabolises ethylene glycol –> glycolic acid + oxalic acid –> metbaolic acidosis
Note: Ethanol and FOMEPRIZOLE competitively inhibit ethanol dehydrogenase enzyme –> treatment –> toxic products not formed from non-toxic ethylene glycole
Child with Rickets and Failure to thrive (growth delay)
Bow legged + Ineffective metabolism (failure to grow/thrive) –> potentially and increase in ENDOGENOUS acid
- normal Na + K
- Increase Cl (HYPERCHLOERMIC) -> not pumped out
- lower acidemic pH
- decreased CO2 (smaller decrease = respiratory compensation)
- biggest decrease bicarbonate (primary metabolic acidosis)
- -ve base excess
Anion gap = 17 (increase in metabolic acid)
Causes for relatively Normal Anion Gap + Hyperchloremic acidosis
- Renal Tubular Acidosis
- Aldosterone deficiency or resistance (RTA type 4) (Addison’s disease)
- GI bicarbonate loss
- Glus/Paint sniffing
Renal tubular acidosis
Kidney/Renal Defects –> decreased acid excretion
- increased pH or urine
- SAME urine AMMONIUM (not increased –> therefore not metabolic acidosis)
- INCREASED CL- (not pumped out)
- proximal and distal
- assoc. with rickets and hyperkalemia
- potentially also associated with other renal tubular defects such as PT tubular defect in Fanconi sydrome
Aldosterone deficiency or resistance (RTA type 4)
ADDISONS DISEASE
- congenital adrenal hyperplasia syndrome –> enzyme blocking aldosterone production
- Renin deficiency –> diabetic neuropathy
- Aldosterone resistance (pseudohypoaldosteronism)
GI bicarbonate loss
Diarrohea/Intestinal/fistula/ileostomy
Acute –> decrease in Na /HCl
Chronic –> decrease in Bicarbonate
Glue/paint sniffing
Toulene metabolized to hippuric acid –> Hypercalemic acidosis
Meaning of Ammonium levels
Metabolic acidosis: UAG NEGATIVE –> INCREASED presence of AMMONIUM –> inappropriate acidification
RTA: UAG positive: same NH4 (SAME) –> RTA renal tubular acidosis –> as ammonium not effected –> rickets
Normal anion gap acidoses reason for being hyperchloremic
Low HCO2- –> Extra Cl- absorbed –> maintained Na balance –> pH/osmolality maintained within 1-2% range
Link between potassium and Acid-base. First link via shift of H+ and K+ into and out of cells
Relationship b/w H+ ions (move into cells) and K+ ions moving out of cell
Acidosis –> Hyperkalemia (+ increased H+ and decreased pH)
Alkalosis –> Hypokalemia
1: Primary Acidosis –> H+ START moving into cell to try buffer/decreased acid H+ levels –> Causes Secondary Hyperkalemia –> drives an increased K+ movement out of cell
2. Primary Hyperkalemia –> Increased K+ movements out of cell –> Secondary Acidosis –> H+ START moving into cell
3. Primary alkalosis –> H+ START moving out of cell into plasma to buffer/increased alkalotic H+ levels –> causes Secondary hypokalemia –> drives K+ into cell to balance H+ loss inside
4. Primary Hypokalemia –> K+ start moving out of cell to increase plasma K+ concentration –> Causes Secondary Alkalosis –> H+ movement driven into cell to try and balance K+ loss inside cell
Link between potassium and acid base: Second link via H+ and K+ competing with each other for secretion
When one is slightly high –> the other is preferentially secreted
Na out –> compensated by either H and K in –> relatively more in by the one more out of balance –> Electronuetrality
Overall link b/w Potassium and acid base balance
- Shift of H+ and K+ into and out of cells
- Relationship of H+ and K+ pumping opposite way of Na+ –> trying to maintain within 1-2% stable osmolality range –> preferentially secretion which every ion (H+ or K+ is relatively more our of balance) –> maintained electroneutrality and hence pH and hence osmolality
Exceptions: - Diarrohia (Bicarbonate AND K+ loss)
- Renal Tubular Acidosis (DT and PT types –> both associated with Hypokalemia)
