Metabolic Acidosis/Alkalosis
Jason Corbeill PA-C
Normal values
From serum (venous) blood:– CO2 (bicarb) 22-32 mmol/L
– Na 135-146 mmol/L– Cl 98-111 mmol/L
From ABG:– pH 7.35-7.45– pCO2 35-45
– Bicarb 21-29
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
-
Metabolic Acidosis
Gain of H+ Loss of HCO3
-(bicarb)
Causes of metabolic acidosis due to gain of acid
Endogenous hydrogen ion production:ketoacidosis
lactic acidosissalicylate overdose
Metabolism of toxinsmethanolethylene glycol
Decreased renal excretionuremiarenal tubular acidosis (type 1) distal
Causes of metabolic acidosis due to loss of bicarb
--Renal tubular acidosis type II (proximal)
--GI loss (diarrhea)
Metabolic Acidosis
Metabolic acidosis can be characterized based on anion gap– High anion gap >20– Normal anion gap 7-15 meq/L
AG=Na – (Cl + HCO3-)
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
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
Elevated anion gap acidosis
Uremic acidosis– Occurs in severe renal failure with GFR <20%– Kidneys unable to excrete H+ – Treatment:
dialysis
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
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
Elevated anion gap acidosis
Paraldehyde intoxication– Used in the production of resins– Anti-seizure drug not used much any more
Elevated anion gap acidosis
Alcohol (Ethanol) intoxication– Starvation + ethanol = ketogenesis– Occurs after long binge periods– n/v/ abdominal pain– Dehydration, hypoglycemia, GI bleed, pancreatitis
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
Elevated anion gap acidosis
Lactic acidosisA—hypotension/tissue hypoxemia
B—sepsis, liver disease, DM, cancer
Elevated anion gap acidosis
Lactic Acidosis-treatment– Treat underlying cause– Bicarb, especially if less than 7.10
Lactic acid will convert to HCO3-
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
Elevated anion gap acidosis
Ethylene glycol ingestion treatment– Ethanol– Dialysis– Bicarb
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
Elevated anion gap acidosis
Salicylate intoxication-treatment– Alkalinize the urine with bicarb– May require dialysis
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
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
Normal Anion Gap Acidosis
Type I Distal RTA treatment– Treat underlying cause– Replace K– Replace bicarb
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
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.
Metabolic Alkalosis
Results from loss of H+ Results from impaired excretion of HCO3
-
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
Metabolic Alkalosis
Treatment of metabolic alkalosis– Dehydration—NSS IV– Hypokalemia—potassium– Mineralocorticoid excess—treat underlying
disorder. No NSS as already fluid overloaded and hypertensive.
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
Approach to acid/base problems
2. Calculate expected compensation For metabolic acidosis..
– Expected pCO2 =1.5 x (HCO3-) + 8
For metabolic alkalosis…– Expected pCO2 =40 + 0.7 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!
Approach to acid/base problems
3. Calculate anion gap AG = Na – (Cl + HCO3
-)
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?
Cases
2. 20 y/o woman with protracted vomiting, lethargy, tachypnea, tachycardia, BP 150-98. 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
Cases
Other labs? How would negative serum ketones and a
creatinine of 12 change your diagnosis?
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
Cases
Other labs? Urine shows calcium oxalate crystals High osmolal gap is present
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
Cases
5. ABG: pH 7.08, HCO3- 10, pCO2 35
1. Problem
2. Expected pCO2 : 23
3. AG: 14
Cases
6. ABG: pH 7.49, HCO3- 35, pCO2 48
1. underlying problem: 2. expected pCO2 : 48 which equation? 3. AG: 16
Cases
7. ABG: pH 7.68, HCO3- 40, pCO2 35
1. underlying disorder: 2. expected pCO2 : 51 equation? 3. AG: 14