ACID/BASE AM DIDACTIC TEACHING GUIDE

Learning Objectives:
By the end of the lecture, the learner will be able to:
1. Know the differential diagnosis of metabolic acidosis with high anion gap.
2. Know the differential diagnosis of metabolic acidosis with normal anion gap.
3. Describe the expected respiratory compensatory changes in metabolic acidosis and alkalosis.
4. Describe the expected metabolic compensatory changes in respiratory acidosis and alkalosis.

Teaching Guide:
Blood pH 7.35-7.45
--Acidemia: Blood pH < 7.35
--Alkalemia: Blood pH > 7.45
--Death occurs when Blood pH <6.8 or >8.0
Homeostasis of pH is tightly regulated.
1. Use of Carbonic acid-bicarbonate buffer
system
H+ + HCO3-  H2CO3  H2O + CO2
2. pH is determined with the Henderson-
Hasselbalch equation:
pH = pK + log10 [HCO3]
0.03 x PaCO2

Metabolic Acidosis
 Bicarbonate deficiency (HCO3- < 22 mmEq/L)
o Elevated anion gap (AG), i.e.: [Na]-([Cl]+[HCO3-])=12±2mEq/L
 Due to accumulation of unmeasured anions, i.e.: other acids
 Ketoacids
o Starvation
o Diabetic ketoacidosis
 Lactic acid
o Tissue hypoxia
o Type B lactic acidosis, including inborn errors of metabolism
 Ingestions
o Methanol (will have high osmotic gap)
o Ethylene glycol (will have high osmotic gap)
o Salicylates
o Paraldehyde (will have high osmotic gap)
o Acetaminophen
o Isoniazid
 Renal failure (uremia)
 AG is falsely low in hypoalbuminemia
 Adjusted AG = Observed AG+(2.5[normal albumin-observed albumin])
o Normal AG
 Loss of bicarbonate
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 ACID/BASE AM DIDACTIC TEACHING GUIDE

 Diarrhea
 Small bowel or pancreatic fistula
 Renal dysfunction (RTA)
 Carbonic anhydrase inhibitors (acetazolamide)
 Hyperparathyroidism
 Iatrogenic hyperchloremia
 Hypoaldosteronism
o Secondary response: For every 1mEq/L decrease in [HCO3-]  1.2mmHg decrease in PCO2
 May take up to 24 hours for compensation to be complete
 If PCO2 is higher than expected responseconcurrent Respiratory acidosis
 If PCO2 is lower than expected responseconcurrent Respiratory alkalosis

Metabolic Alkalosis
 Bicarbonate excess
o Decreased bicarbonate excretion from kidney
o Increased H+ loss
 H+ loss from GI tract
 Vomiting
 High gastric tube output
 H+ loss from kidney
 Increased aldosterone secretion
 Diuretics
 Bartter and Gitelman syndromes
 Volume contraction
o Secondary response: For every 1mEq/L increase in [HCO 3-] 0.7mmHg increase in PCO2
 May take up to 24 hours for compensation to be complete
 If PCO2 is higher than expected responseconcurrent Respiratory acidosis
 If PCO2 is lower than expected responseconcurrent Respiratory alkalosis

Respiratory Acidosis
 PCO2 increase due to decreased minute ventilation or increase in CO 2 production
o Respiratory tract obstruction
o Chest wall/Lung disorders
o Neuromuscular disorders
o CNS depression
 Secondary response:
o Acute: For every 10mmHg increase in PCO21mEq/L increase in [HCO3-]
o Chronic (3-5 days): For every 10 mmHg increase in PCO23.5mEq/L increase in [HCO3-]
 If [HCO3] is higher than expected response concurrent metabolic alkalosis
 If [HCO3] is lower than expected responseconcurrent metabolic acidosis

Respiratory Alkalosis
 PCO2 decrease due to increased minute ventilation
o Medication toxicity
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 ACID/BASE AM DIDACTIC TEACHING GUIDE

o CNS disorders
o Intrinsic lung disease
o High altitude
 Secondary response:
o Acute: For every 10mmHg decrease in PCO22mEq/L decrease in [HCO3-]
o Chronic (3-5 days): For every 10 mmHg decrease in PCO24mEq/L decrease in [HCO3-]
 If [HCO3] is higher than expected response concurrent metabolic alkalosis
 If [HCO3] is lower than expected responseconcurrent metabolic acidosis

pH pCO2 [HCO3] BE
Uncompensated metabolic  N  
acidosis
Compensated metabolic acidosis N   
Uncompensated metabolic  N  
alkalosis
Compensated metabolic alkalosis N   

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