1. Metabolic Acidosis/Alkalosis
Jason Corbeill PA-C

2. Normal values From serum (venous) blood: From ABG:
CO2 (bicarb) mmol/L
Na mmol/L
Cl mmol/L
From ABG: pH
pCO
Bicarb

3. Metabolic Acidosis HCO3- excretion is controlled by the kidney
H+ excretion is controlled by the kidney
One H+ buffers one HCO3-
So, an increase in H+ can cause a decrease in HCO3-

4. Metabolic Acidosis
Gain of H+
Loss of HCO3-(bicarb)

5. Causes of metabolic acidosis due to gain of acid
Endogenous hydrogen ion production:
ketoacidosis
lactic acidosis
salicylate overdose
Metabolism of toxins
methanol
ethylene glycol
Decreased renal excretion
uremia
renal tubular acidosis (type 1) distal

6. Causes of metabolic acidosis due to loss of bicarb
--Renal tubular acidosis type II (proximal)
--GI loss (diarrhea)

7. Metabolic Acidosis
Metabolic acidosis can be characterized based on anion gap
High anion gap >20
Normal anion gap meq/L
AG=Na – (Cl + HCO3-)

8. Diff Dx of elevated anion gap acidosis
Methanol intoxication (denatured alcohol)
Uremic acidosis
Diabetic ketoacidosis
Paraldehyde intoxication/alcohol intoxication
I INH, infection
Lactic acidosis
Ethylene glycol intoxication
Salicylate intoxication

9. Elevated anion gap acidosis
Methanol intoxication
Ingested methanol is converted in the body to formic acid leading to metabolic acidosis and high anion gap
Also will have increased osmolal gap
Antifreeze, de-icing solutions, cleaners, solvents
Symptoms include optic neuritis, blindness, pancreatitis
Treatment:
Give ethanol IV to stop methanol conversion to formic acid
Fomepizole
Dialysis
bicarbonate

10. Elevated anion gap acidosis
Uremic acidosis
Occurs in severe renal failure with GFR <20%
Kidneys unable to excrete H+
Treatment:
dialysis

11. Elevated anion gap acidosis
Diabetic ketoacidosis
Production of ketoacids due to incomplete fatty acid oxidation
Presentation
Acidemia pH 7.15
Hyperglycemia
dehydration
Low k-even if levels appear normal
Urine ketones
Serum ketones (more sensitive)
Tachypnea, polydipsia, polyuria

12. Elevated anion gap acidosis
Treatment of DKA
Insulin
NSS with KCl (250mL/hr)
KCl bolus
No bicarb unless pH less than 7.10
Ketoacids will be converted to bicarb
Watch K closely
Serum K driven into cells by insulin in setting of hyperglycemia

13. Elevated anion gap acidosis
Paraldehyde intoxication
Used in the production of resins
Anti-seizure drug not used much any more

14. Elevated anion gap acidosis
Alcohol (Ethanol) intoxication
Starvation + ethanol = ketogenesis
Occurs after long binge periods
n/v/ abdominal pain
Dehydration, hypoglycemia, GI bleed, pancreatitis

15. Elevated anion gap acidosis
Treatment of ethanol intoxication/acidosis
Do not give glucose until first given thiamine
Reduces chances for Wernicke’s encephalopathy
“banana bag” or “rally pack” over 4 hrs
100mg thiamine x 3
Folate 5mg in IVF
MVI in IVF
Mag sulfate 2g
No need for bicarb unless pH < 7.10

16. Elevated anion gap acidosis
Lactic acidosis
A—hypotension/tissue hypoxemia
B—sepsis, liver disease, DM, cancer

17. Elevated anion gap acidosis
Lactic Acidosis-treatment
Treat underlying cause
Bicarb, especially if less than 7.10
Lactic acid will convert to HCO3-

18. Elevated anion gap acidosis
Ethylene glycol ingestion
Similar to methanol intoxication
Usually hx alcohol abuse
Drinking antifreeze/radiator fluid
Causes production of toxic acids
Acute renal failure
Osmolal gap
Calcium oxalate crystals in urine (oxalic acid)
CNS dysfunction
Ataxia, confusion, seizures, coma

19. Elevated anion gap acidosis
Ethylene glycol ingestion treatment
Ethanol
Dialysis
Bicarb

20. Elevated anion gap acidosis
Salicylate intoxication (aspirin)
Affects respiratory center and initially causes respiratory alkalosis
Salicylates causes accumulation of acids including lactic acid and ketoacids which cause acidosis

21. Elevated anion gap acidosis
Salicylate intoxication-treatment
Alkalinize the urine with bicarb
May require dialysis

22. Differential Diagnosis of normal anion gap acidosis
Mild renal failure
GI loss of bicarb via diarrhea
Type I (distal) renal tubular acidosis
Type II (proximal) renal tubular acidosis

23. Normal Anion Gap Acidosis
Type I Distal RTA
May be caused by…
Hyperparathyroidism
Sjorgren’s syndrome
Amphotericin B
Renal tubule unable to eliminate H+
Results in urine pH > 5.3
Calcium phosphate stones

24. Normal Anion Gap Acidosis
Type I Distal RTA treatment
Treat underlying cause
Replace K
Replace bicarb

25. Normal Anion Gap Acidosis
Type II (proximal) RTA
Causes include: multiple myeloma, mercury, lead
Impaired proximal tubular reabsorption of bicarb
May also have a defect in reabsorption of other solutes such as amino acids, phosphorus, urate, glucose (Fanconi Syndrome)
Urine pH able to be less than 5.3

26. Normal Anion Gap Acidosis
Type II (proximal) RTA treatment
May require lots of bicarb (K citra)
Replace potassium
Difficult to maintain bicarb levels as reabsorption threshhold set too low.

27. Metabolic Alkalosis Results from loss of H+
Results from impaired excretion of HCO3-

28. Metabolic Alkalosis Causes of metabolic alkalosis: Potassium depletion
Mineralocorticoid excess (aldosteronism)
Increases H+ secretion into tubule, loss of K
Dehydration
Vomiting/NGT suction
Diuretics
Chronic diarrhea

29. Metabolic Alkalosis Treatment of metabolic alkalosis
Dehydration—NSS IV
Hypokalemia—potassium
Mineralocorticoid excess—treat underlying disorder.
No NSS as already fluid overloaded and hypertensive.

30. Approach to acid/base problems
1. Identify most obvious disorder
Look at pH, pCO2 (H+ ) and HCO3- on ABG
If multiple abnormalities, look at which is MORE abnormal

31. Approach to acid/base problems
2. Calculate expected compensation
For metabolic acidosis..
Expected pCO2 =1.5 x (HCO3-) + 8
For metabolic alkalosis…
Expected pCO2 = x [(measured HCO3-) – (normal HCO3-)]
If the degree of compensation is not what is expected by the above calculation, then there is a respiratory component involved!

32. Approach to acid/base problems
3. Calculate anion gap
AG = Na – (Cl + HCO3-)

33. CASES: 1. 40 yo male with shallow respirations, tachypnea.
Serum Na 142, K 3.6, Cl 100, bicarb 12
ABG: pH 7.28, pCO2 26, HCO3- 12
1. metabolic acidosis (pH and HCO3- both low)
2. calculate compensation: exp pCO2 = 26
3. AG = 30
Other labs, questions?

34. Cases
y/o woman with protracted vomiting, lethargy, tachypnea, tachycardia, BP Hx IDDM not taking her insulin with variable glucoses at home. Not eating well.
Serum Na 142, K 3.6, CL 106, bicarb 16, glu 230, BUN 70, CR 1.2
ABG pH 7.28, pCO2 34, HCO3- 16

35. Cases
Other labs?
How would negative serum ketones and a creatinine of 12 change your diagnosis?

36. Cases 3. 50 y/o male with tachypnea, tachycardia, BP 90/60
Serum Na 142, K 3.6, Cl 100, bicarb 12, glu 180, bun 28,
ABG pH 7.28, pCO2 26, HCO3- 12
1. problem:
2. expected pCO2 : 26
3. Anion gap: 30

37. Cases Other labs? Urine shows calcium oxalate crystals
High osmolal gap is present

38. Cases
4. Serum Na 135, Cl 114, K 4.5 Bicarb 6 ABG pH 7.15, HCO3- 6, pCO2 18
1. underlying problem
2. expected pCO2? 17
3. AG? 15

39. Cases 5. ABG: pH 7.08, HCO3- 10, pCO2 35 Problem Expected pCO2 : 23
3. AG: 14

40. Cases 6. ABG: pH 7.49, HCO3- 35, pCO2 48 1. underlying problem:
2. expected pCO2 : 48 which equation?
3. AG: 16

41. Cases 7. ABG: pH 7.68, HCO3- 40, pCO2 35 1. underlying disorder:
2. expected pCO2 : 51 equation?
3. AG: 14