Metabolic Acidosis/Alkalosis Jason Corbeill PA-C.

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


Uremic acidosis– Occurs in severe renal failure with GFR <20%– Kidneys unable to excrete H+ – Treatment:

dialysis


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


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


Paraldehyde intoxication– Used in the production of resins– Anti-seizure drug not used much any more


Alcohol (Ethanol) intoxication– Starvation + ethanol = ketogenesis– Occurs after long binge periods– n/v/ abdominal pain– Dehydration, hypoglycemia, GI bleed, pancreatitis


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


Lactic acidosisA—hypotension/tissue hypoxemia

B—sepsis, liver disease, DM, cancer


Lactic Acidosis-treatment– Treat underlying cause– Bicarb, especially if less than 7.10

Lactic acid will convert to HCO3-


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


Ethylene glycol ingestion treatment– Ethanol– Dialysis– Bicarb


Salicylate intoxication (aspirin)– Affects respiratory center and initially causes

respiratory alkalosis– Salicylates causes accumulation of acids

including lactic acid and ketoacids which cause 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


Type I Distal RTA treatment– Treat underlying cause– Replace K– Replace bicarb


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


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


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!


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

Metabolic Acidosis/Alkalosis Jason Corbeill PA-C.

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