Crit Care: Acid-Base in ICU — The Stewart Approach (MRCP Part 1)
- Crack Medicine

- 3 hours ago
- 5 min read
TL;DR
The Stewart approach explains acid–base balance using three independent variables: PaCO₂, strong ion difference (SID), and total weak acids. For MRCP Part 1, this model is particularly useful in ICU physiology because it clarifies saline-induced acidosis, lactate-related disturbances, and the effects of hypoalbuminaemia. Candidates should understand how Stewart physiology complements standard ABG interpretation rather than replacing it.
Why the Stewart Approach Matters
Traditional acid–base analysis works well for many common disorders, but critically ill patients often develop multiple simultaneous abnormalities.
Examples include:
Septic shock with elevated lactate
Massive saline resuscitation
Renal failure with hyperphosphataemia
Ventilated patients with respiratory compensation
Hypoalbuminaemia masking severe acidosis
The Stewart model helps explain these mixed disturbances by identifying the true independent determinants of plasma pH.
In ICU medicine, this framework is especially useful because critically ill patients frequently receive large volumes of intravenous fluids, vasopressors, renal replacement therapy, and mechanical ventilation — all of which influence acid–base balance.
The Core Stewart Concept
According to Peter Stewart, plasma pH is determined by three independent variables:
Variable | Meaning | Clinical Relevance |
PaCO₂ | Respiratory component | Controlled by ventilation |
Strong Ion Difference (SID) | Difference between strong cations and anions | Influenced by fluids and electrolytes |
Total Weak Acids (Atot) | Mainly albumin and phosphate | Important in ICU patients |
1. PaCO₂
This behaves similarly to the traditional model.
Increased PaCO₂ → respiratory acidosis
Reduced PaCO₂ → respiratory alkalosis
In ICU settings, ventilator adjustments frequently alter PaCO₂ rapidly.
Example
A patient with COPD exacerbation and hypoventilation develops:
Raised PaCO₂
Low pH
Respiratory acidosis
This aspect remains unchanged in Stewart physiology.
2. Strong Ion Difference (SID)
SID is the most important Stewart concept for MRCP candidates.
Simplified formula:
SID≈(Na++K+)−(Cl−+lactate−)SID \approx (Na^+ + K^+) - (Cl^- + lactate^-)SID≈(Na++K+)−(Cl−+lactate−)
A normal SID is roughly 38–42 mEq/L.
Key principle
Reduced SID → metabolic acidosis
Increased SID → metabolic alkalosis
Why Normal Saline Causes Acidosis
One of the classic ICU physiology questions concerns saline-induced acidosis.
0.9% saline contains:
Sodium = 154 mmol/L
Chloride = 154 mmol/L
When large volumes are infused:
Chloride rises disproportionately
SID decreases
Hyperchloraemic metabolic acidosis develops
This explains why critically ill patients can become acidotic even without elevated lactate.
Important exam point
Normal saline is not physiologically “neutral”.
Balanced crystalloids such as Hartmann’s solution and Plasma-Lyte have electrolyte compositions closer to plasma and are therefore less likely to produce hyperchloraemic acidosis.
Further reading on balanced crystalloids from the Intensive Care Society:https://ics.ac.uk/
3. Total Weak Acids (Atot)
Weak acids include:
Albumin
Phosphate
Key principle
Increased weak acids → acidosis
Reduced weak acids → alkalosis
This is highly relevant in ICU patients because severe illness commonly causes hypoalbuminaemia.
Clinical implication
A septic patient with:
High lactate
Severe hypoalbuminaemia
may have a near-normal pH because the alkalinising effect of low albumin partially offsets the lactic acidosis.
This is a common examination trap.
The 5 Most Tested Stewart Topics in MRCP Part 1
1. Hyperchloraemic Metabolic Acidosis
Excess chloride lowers SID.
Common causes:
Large-volume saline
Renal tubular acidosis
Gastrointestinal bicarbonate loss
Key point
Normal anion gap acidosis can still represent significant pathology.
2. Lactic Acidosis
Lactate behaves as a strong anion.
Raised lactate lowers SID and produces metabolic acidosis.
Common ICU causes
Septic shock
Tissue hypoperfusion
Severe hypoxaemia
Seizures
Mesenteric ischaemia
The UK Sepsis Trust provides updated sepsis resources:https://sepsistrust.org/
3. Hypoalbuminaemic Alkalosis
Albumin acts as a weak acid.
Reduced albumin decreases Atot and shifts the balance toward alkalosis.
Exam trap
A “normal” bicarbonate or pH does not exclude severe disease.
Always interpret ABGs alongside albumin and chloride levels.
4. Mixed Acid–Base Disorders
Critically ill patients often develop several abnormalities simultaneously.
Example
A ventilated septic patient may have:
Lactic acidosis
Hypoalbuminaemia
Respiratory alkalosis from hyperventilation
Hyperchloraemia after saline resuscitation
The Stewart model helps explain these interacting disturbances more effectively than bicarbonate-centred interpretation alone.
5. Fluid Choice in Critical Care
Balanced crystalloids preserve SID more effectively than normal saline.
Examples
Hartmann’s solution
Plasma-Lyte
Several ICU studies suggest balanced solutions reduce hyperchloraemia and may improve renal outcomes in selected patients.
Further reading from the National Institute for Health and Care Excellence (NICE):https://www.nice.org.uk/
Stewart vs Henderson–Hasselbalch
Feature | Traditional Model | Stewart Model |
Main focus | Bicarbonate | Independent ions |
Simplicity | Easier | More advanced |
Best use | Routine ABGs | Complex ICU disorders |
Explains saline acidosis | Limited | Excellent |
Explains albumin effects | Poorly | Well |
Practical MRCP approach
For MRCP Part 1:
Interpret the ABG conventionally first
Use Stewart physiology to explain mechanisms
Focus especially on chloride, lactate, and albumin
10 High-Yield Stewart Revision Facts
SID is central to Stewart physiology.
Reduced SID causes metabolic acidosis.
Chloride excess is a major ICU cause of acidosis.
Lactate behaves as a strong anion.
Albumin is a weak acid.
Hypoalbuminaemia causes alkalosis.
Balanced crystalloids reduce chloride-related acidosis.
Stewart interpretation complements ABG analysis.
Mixed disorders are common in ICU patients.
Stewart concepts are increasingly examined in postgraduate medicine.
Practical Mini-Case
A 68-year-old man with septic shock receives 6 litres of normal saline during resuscitation.
Repeat blood gas:
pH: 7.28
PaCO₂: 36 mmHg
HCO₃⁻: 16 mmol/L
Lactate: 2.1 mmol/L
Chloride: 119 mmol/L
What is the most likely mechanism?
Answer
Hyperchloraemic metabolic acidosis due to reduced SID.
Explanation
Although lactate is only mildly elevated, the large chloride load lowers the strong ion difference and produces metabolic acidosis.
MRCP-Style MCQ
A ventilated ICU patient has:
Severe hypoalbuminaemia
Elevated lactate
Near-normal pH
Which Stewart principle best explains this?
A. Increased bicarbonate generationB. Respiratory compensation aloneC. Reduced weak acids offsetting acidosisD. Increased SID from chloride retentionE. Renal bicarbonate conservation
Correct answer: C
Explanation
Albumin is a weak acid. Severe hypoalbuminaemia reduces total weak acids (Atot), producing an alkalinising effect that may partially offset lactic acidosis.
Practical Study Checklist
Before the examination, ensure you can:
Interpret standard ABGs confidently
Recognise hyperchloraemic acidosis
Explain why saline lowers SID
Understand lactate as a strong anion
Identify albumin’s role in acid–base balance
Recognise mixed ICU acid–base disorders
Apply Stewart concepts clinically
Distinguish respiratory from metabolic abnormalities
For structured revision and timed practice, explore:
MRCP lectures: https://www.crackmedicine.co.uk/lectures/
Mock tests: https://www.crackmedicine.co.uk/mock-tests/
Revision notes: https://www.crackmedicine.co.uk/notes/

Common Pitfalls
Confusing bicarbonate as an independent Stewart variable
Assuming normal saline is physiologically neutral
Forgetting albumin behaves as a weak acid
Ignoring chloride levels when interpreting acidosis
Missing mixed acid–base disorders in ICU scenarios
Related MRCP Revision Topics
Candidates studying Stewart physiology should also revise:
ABG interpretation strategies
Shock physiology
Ventilation and respiratory compensation
Sepsis and lactate metabolism
Renal tubular acidosis
Suggested companion reading from the Crack Medicine blog:https://www.crackmedicine.co.uk/blog/
FAQs
Is the Stewart approach essential for MRCP Part 1?
Candidates are usually expected to understand the principles rather than perform advanced calculations. The exam focus is commonly on saline-induced acidosis, lactate, chloride balance, and albumin effects.
Why does normal saline cause metabolic acidosis?
Normal saline contains a high chloride concentration. Excess chloride lowers the strong ion difference, producing hyperchloraemic metabolic acidosis.
What is the strong ion difference?
SID refers to the difference between fully dissociated cations and anions in plasma. Reduced SID promotes acidosis, whereas increased SID promotes alkalosis.
Why does hypoalbuminaemia cause alkalosis?
Albumin behaves as a weak acid. Reduced albumin lowers the total weak acid concentration, producing a relative alkalinising effect.
Should Stewart replace traditional ABG interpretation?
No. In clinical practice, Stewart physiology complements traditional interpretation and is most useful in complex ICU acid–base disorders.
Ready to start?
The Stewart approach offers a deeper physiological understanding of acid–base disturbances in critically ill patients. For MRCP Part 1, candidates should focus on the clinically relevant concepts: SID, chloride-related acidosis, lactate physiology, and albumin effects.
Rather than replacing traditional ABG interpretation, Stewart physiology provides an additional framework that becomes particularly valuable in ICU medicine and mixed acid–base disorders.
For further MRCP revision resources, visit:
MRCP Part 1 Hub: https://www.crackmedicine.co.uk/mrcp-part-1/
Mock Tests: https://www.crackmedicine.co.uk/mock-tests/
Sources
MRCP(UK) — Official MRCP(UK) examination syllabus and curriculum guidance
Intensive Care Society — Critical care education resources and ICU physiology guidance
National Institute for Health and Care Excellence — NICE guidance on intravenous fluid therapy and critical care management



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