Metabolic Acidosis/Alkalosis

Jason Corbeill PA-C

Normal values

 From serum (venous) blood: – – – CO 2 (bicarb) 22-32 mmol/L Na 135-146 mmol/L Cl 98-111 mmol/L  From ABG: – – – pH 7.35-7.45

pCO 2 35-45 Bicarb 21-29

Metabolic Acidosis

  HCO 3 excretion is controlled by the kidney H + excretion is controlled by the kidney  One H+ buffers one HCO 3 – So, an increase in H + HCO 3 can cause a decrease in

Metabolic Acidosis

 Gain of H +  Loss of HCO 3 (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 + HCO 3 )

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 HCO 3 -

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 HCO 3 -

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, pCO 2 (H + ) and HCO 3 on ABG If multiple abnormalities, look at which is MORE abnormal

Approach to acid/base problems

 2. Calculate expected compensation  For metabolic acidosis..

 – Expected pCO 2 =1.5 x (HCO 3 ) + 8 For metabolic alkalosis… – Expected pCO 2 (normal HCO 3 )] =40 + 0.7 x [(measured HCO 3 ) –  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 + HCO 3 )

CASES:

 1. 40 yo male with shallow respirations, tachypnea. – – Serum Na 142, K 3.6, Cl 100, bicarb 12 ABG: pH 7.28, pCO 2  26, HCO 3 12 1. metabolic acidosis (pH and HCO 3 both low)  2. calculate compensation: exp pCO 2 = 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, pCO 2 34, HCO 3 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, pCO 2  1. problem: 26, HCO 3 12  2. expected pCO 2 : 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, HCO 3 6, pCO 2 18 1. underlying problem   2. expected pCO 2 ? 17 3. AG? 15

Cases

 5. ABG: pH 7.08, HCO 3 10, pCO 2 35 1.

Problem 2.

Expected pCO 2 : 23 3. AG: 14

Cases

 6. ABG: pH 7.49, HCO 3 35, pCO 2 48  1. underlying problem:   2. expected pCO 2 : 48 which equation?

3. AG: 16

Cases

 7. ABG: pH 7.68, HCO 3 40, pCO 2 35  1. underlying disorder:   2. expected pCO 2 : 51 equation?

3. AG: 14