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Internal MedicineNephrologyAcid Base Abnormalities

Acid Base Abnormalities

Introduction to Acid-Base Physiology for MCCQE1

Understanding acid-base balance is a core competency for the Medical Expert role in the CanMEDS framework. For the MCCQE1, candidates are expected to diagnose simple and mixed acid-base disorders, identify underlying etiologies, and initiate appropriate management within the Canadian healthcare context.

Acid-base homeostasis is maintained by three mechanisms:

  1. Chemical Buffers: Immediate response (Bicarbonate, Phosphate, Proteins).
  2. Respiratory Regulation: Minutes to hours (CO2 elimination).
  3. Renal Regulation: Hours to days (HCO3- reabsorption and H+ excretion).
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Canadian Context: In Canada, arterial blood gas (ABG) results are reported in SI units.

  • pH: dimensionless
  • pCO2: mmHg
  • HCO3-: mmol/L
  • Lactate: mmol/L

Normal Reference Ranges

ParameterNormal RangeSignificance
pH7.35 – 7.45<7.35 = Acidemia; >7.45 = Alkalemia
pCO235 – 45 mmHgRespiratory component (Acid)
HCO3-22 – 26 mmol/LMetabolic component (Base)
Anion Gap8 – 12 mmol/LCalculated as Na+ - (Cl- + HCO3-)

Systematic Approach to Acid-Base Analysis

A structured approach is vital for the MCCQE1 to avoid missing mixed disorders.

Step 1: Look at the pH

Determine if the primary disturbance is acidemia or alkalemia.

  • pH < 7.35: Acidemia
  • pH > 7.45: Alkalemia
  • Normal pH: Normal balance or a mixed disorder (e.g., Metabolic Acidosis + Respiratory Alkalosis).

Step 2: Look at the pCO2

Does the pCO2 explain the pH?

  • If pH is low and pCO2 is high (>45), it is Respiratory Acidosis.
  • If pH is high and pCO2 is low (<35), it is Respiratory Alkalosis.

Step 3: Look at the HCO3-

Does the bicarbonate explain the pH?

  • If pH is low and HCO3- is low (<22), it is Metabolic Acidosis.
  • If pH is high and HCO3- is high (>26), it is Metabolic Alkalosis.

Step 4: Check for Compensation

Is the body compensating appropriately? (See formulae section below).

  • If the compensation is less or more than calculated, a second (mixed) disorder is present.

Step 5: Calculate the Anion Gap

Perform this for all metabolic acidosis cases.

  • Formula: AG = Na - (Cl + HCO3)
  • If AG > 12, an Anion Gap Metabolic Acidosis is present.
  • Note: Albumin correction is necessary in hypoalbuminemia. For every 10 g/L drop in albumin, add 2.5 to the calculated AG.

Metabolic Acidosis

Metabolic acidosis is characterized by a primary decrease in HCO3-, leading to a decrease in pH. The respiratory response is hyperventilation (lowering pCO2).

Classification

High Anion Gap Metabolic Acidosis (HAGMA) occurs due to the accumulation of organic acids.

Mnemonic: MUDPILES

  • Methanol
  • Uremia (Renal Failure)
  • Diabetic Ketoacidosis (DKA)
  • Paraldehyde (rare)
  • Iron tablets / Isoniazid
  • Lactic Acidosis (Sepsis, Ischemia)
  • Ethylene Glycol (Antifreeze)
  • Salicylates (Aspirin)

Newer mnemonic: GOLD MARK (Glycols, Oxoproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, Ketoacidosis).

Compensation: Winter’s Formula

For Metabolic Acidosis, calculate the expected pCO2:

ExpectedpCO2=(1.5×HCO3)+8±2Expected pCO2 = (1.5 × HCO3) + 8 ± 2
  • If measured pCO2 > Expected: Concomitant Respiratory Acidosis.
  • If measured pCO2 < Expected: Concomitant Respiratory Alkalosis.

Metabolic Alkalosis

Characterized by an increase in HCO3- and increased pH. The respiratory compensation is hypoventilation (increasing pCO2).

Classification: Urine Chloride

The most useful diagnostic test is Urine Chloride.

Saline Responsive vs. Resistant

Saline Responsive (Urine Cl < 20 mmol/L)

Caused by volume depletion. The kidney holds onto Cl-.

  • Vomiting / Nasogastric suction
  • Diuretic use (prior use)
  • Volume depletion

Tx: Normal Saline + K+

Saline Resistant (Urine Cl > 20 mmol/L)

Caused by mineralocorticoid excess or profound K+ depletion.

  • Hyperaldosteronism (Conn’s)
  • Cushing’s Syndrome
  • Bartter’s / Gitelman’s Syndrome
  • Severe Hypokalemia

Tx: Treat underlying cause

Respiratory Disorders

Respiratory Acidosis

  • Mechanism: Alveolar hypoventilation causing CO2 retention.
  • Causes:
    • CNS depression: Opioids, Sedatives, Stroke.
    • Neuromuscular: Guillain-Barré, Myasthenia Gravis.
    • Airway/Lung: COPD, Asthma, Pneumonia, OSA.

Respiratory Alkalosis

  • Mechanism: Alveolar hyperventilation blowing off CO2.
  • Causes:
    • CHAMPS: CNS disease, Hypoxia, Anxiety/Pain, Mechanical ventilation, Progesterone (Pregnancy), Salicylates/Sepsis.
    • Note: Early salicylate toxicity causes respiratory alkalosis directly; late toxicity causes metabolic acidosis.

Compensation Rules

Unlike metabolic disorders, respiratory compensation happens in two phases: Acute (buffers) and Chronic (renal).

DisorderPhaseExpected Change
Resp. AcidosisAcuteHCO3 increases by 1 for every 10 mmHg rise in pCO2
Resp. AcidosisChronicHCO3 increases by 4 for every 10 mmHg rise in pCO2
Resp. AlkalosisAcuteHCO3 decreases by 2 for every 10 mmHg drop in pCO2
Resp. AlkalosisChronicHCO3 decreases by 5 for every 10 mmHg drop in pCO2
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Mnemonic for Compensation: 1-4-2-5 (Acidosis Acute/Chronic, Alkalosis Acute/Chronic).

Canadian Guidelines & Clinical Management

Toxic Alcohol Poisoning

In Canada, the management of Methanol and Ethylene Glycol poisoning is a critical emergency medicine topic.

  • First-line antidote: Fomepizole (Alcohol dehydrogenase inhibitor).
  • Alternative: Ethanol (if Fomepizole is unavailable).
  • Dialysis: Indicated for severe acidosis (pH < 7.25-7.30), visual changes, renal failure, or high serum levels (>50 mg/dL or >10 mmol/L).

Indications for Urgent Dialysis (AEIOU)

  1. Acidosis: Severe metabolic acidosis (pH < 7.1) refractory to medical therapy.
  2. Electrolytes: Hyperkalemia (K > 6.5 mmol/L) with ECG changes or refractory.
  3. Intoxications: Toxic alcohols, Salicylates, Lithium.
  4. Overload: Volume overload refractory to diuretics.
  5. Uremia: Uremic pericarditis, encephalopathy.

Key Points to Remember for MCCQE1

  • Mixed Disorders: Always check Winter’s formula. If the pCO2 is not what you predict, a second respiratory disorder exists.
  • Albumin: Always correct the Anion Gap for hypoalbuminemia. A “normal” AG in a patient with albumin of 20 g/L is actually a High AG.
  • Salicylate Toxicity: Classic presentation is a mixed Respiratory Alkalosis (direct respiratory center stimulation) and Metabolic Acidosis (uncoupling of oxidative phosphorylation).
  • Vomiting: Causes hypokalemic, hypochloremic metabolic alkalosis.
  • Diarrhea: Causes non-anion gap metabolic acidosis (loss of HCO3-).

Sample Question

Clinical Scenario

A 68-year-old man presents to the emergency department with a 3-day history of severe diarrhea. He has a history of hypertension and osteoarthritis. He appears dehydrated with dry mucous membranes and reduced skin turgor.

Vital Signs:

  • BP: 100/60 mmHg
  • HR: 104 bpm
  • RR: 22/min
  • Temp: 37.1°C

Laboratory Investigations:

  • Na+: 138 mmol/L
  • K+: 3.2 mmol/L
  • Cl-: 115 mmol/L
  • HCO3-: 13 mmol/L
  • BUN: 12 mmol/L
  • Creatinine: 110 µmol/L
  • Albumin: 40 g/L (Normal)
  • Arterial Blood Gas (Room Air):
    • pH: 7.28
    • pCO2: 28 mmHg

Which of the following best describes this patient’s acid-base status?

Options

  • A. High anion gap metabolic acidosis with appropriate respiratory compensation
  • B. Normal anion gap metabolic acidosis with appropriate respiratory compensation
  • C. High anion gap metabolic acidosis with concomitant respiratory alkalosis
  • D. Normal anion gap metabolic acidosis with concomitant respiratory alkalosis
  • E. Normal anion gap metabolic acidosis with concomitant respiratory acidosis

Explanation

The correct answer is:

  • B. Normal anion gap metabolic acidosis with appropriate respiratory compensation

Step-by-Step Analysis:

  1. Check pH: 7.28 (< 7.35) → Acidemia.
  2. Check HCO3-: 13 mmol/L (Low) → Metabolic Acidosis.
  3. Check Anion Gap:
    • Formula: Na - (Cl + HCO3)
    • Calculation: 138 - (115 + 13) = 138 - 128 = 10.
    • Result: Normal Anion Gap (Normal range 8-12). This is a NAGMA. This fits the clinical history of diarrhea (loss of bicarbonate).
  4. Check Compensation (Winter’s Formula):
    • Formula: Expected pCO2 = (1.5 × HCO3) + 8 ± 2
    • Calculation: (1.5 × 13) + 8 = 19.5 + 8 = 27.5 mmHg.
    • Range: 25.5 – 29.5 mmHg.
    • Measured pCO2: 28 mmHg.
    • Result: The measured pCO2 falls exactly within the expected range. Therefore, there is appropriate respiratory compensation.

Why other options are incorrect:

  • A & C: The Anion Gap is 10, which is normal, not high.
  • D: The pCO2 is exactly what is expected for compensation. For a concomitant respiratory alkalosis to be present, the pCO2 would need to be significantly lower than predicted (e.g., < 25 mmHg).
  • E: For a concomitant respiratory acidosis, the pCO2 would need to be higher than predicted (e.g., > 30 mmHg).

References

  1. Medical Council of Canada. Objectives for the Qualifying Examination Part I. Available at: mcc.ca 
  2. Haber, R.J. (1991). A practical approach to acid-base disorders. Western Journal of Medicine.
  3. Adrogué, H.J., & Madias, N.E. (2010). Secondary responses to altered acid-base status: the rules of engagement. Journal of the American Society of Nephrology.
  4. Toronto Notes 2024. Nephrology Chapter. Toronto Notes for Medical Students, Inc.
  5. UpToDate. Simple and mixed acid-base disorders. Accessed 2023.
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