Metabolic Acidosis/Alkalosis Jason Corbeill PA-C

Normal values From serum (venous) blood: From ABG: 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 acidosis salicylate overdose Metabolism of toxins methanol ethylene glycol Decreased renal excretion uremia renal 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 acidosis A—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 Problem 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