You look at the ABG:

pH 7.20
PaCO₂ 40 mmHg
HCO₃⁻ 15 mmol/L

The diagnosis seems straightforward:

Metabolic acidosis.

But then comes the more important question:

Why is the bicarbonate low?

Is it lactate?
Too much chloride?
Hypoalbuminemia masking the acidosis?
Renal dysfunction?
Ketones?
Unmeasured anions?
Or a combination of several processes occurring simultaneously?

This is where the Stewart approach becomes useful. Not because the traditional Henderson–Hasselbalch approach is wrong.

But because sometimes:

Henderson–Hasselbalch tells you what is happening. Stewart helps you understand what is driving it.

Don’t throw away the traditional ABG approach

For most patients in the ED, start conventionally as we discussed in the previous post ABG Series #4

pH → PaCO₂ → HCO₃⁻ → anion gap → compensation → clinical context

This is fast, familiar and clinically useful.

The problem arises when the patient has multiple simultaneous processes.

A critically ill patient may have:

• lactic acidosis from shock

• hyperchloremia from saline

• hypoalbuminemia

• renal dysfunction

• unmeasured anions

• and a respiratory disorder

…and these processes can partially cancel each other out. The ABG may therefore look deceptively simple. This is exactly where a quantitative approach can add another layer of understanding.

The Stewart idea: What actually determines pH?

Stewart’s approach starts with a different question. Instead of treating bicarbonate and hydrogen ions as independent causes of acid–base disturbance, it considers three major independent variables:

1️⃣ PaCO₂

The respiratory component.

2️⃣ Strong Ion Difference — SID

The difference between fully dissociated cations and anions.

3️⃣ Total concentration of weak acids — Aₜₒₜ

Primarily albumin and phosphate in plasma.

In the full Stewart model, these variables interact through the principles of mass conservation, electrical neutrality and chemical equilibrium. As Story explains, H⁺ and HCO₃⁻ are dependent variables in this framework; their concentrations are determined by PaCO₂, SID and Aₜₒₜ. (Story, 2016). modified abg (1)(4)

That sounds intimidating. Fortunately, you don’t need six simultaneous equations to use the concept at the bedside.

The Physician-friendly version

David Story proposed a simplified bedside approach that translates the Stewart concept into something much more practical. (Story, 2016).

The idea is to deconstruct the base excess (BE) into clinically recognizable components. Think of BE as the net metabolic effect.

Then ask:

What is making the patient acidotic, and what is simultaneously pushing the pH in the opposite direction?

Story’s simplified approach breaks this into:

1. Na⁺–Cl⁻ effect

2. Lactate effect

3. Albumin effect

4. Other ions* - most important component

And together:

BE = Na–Cl effect + Lactate effect + Albumin effect + Other ions

Let me explain simply

Total metabolic component = NAGMA + HAGMA + Met. Alkalosis

Total Metabolic component = Base Excess

NAGMA plus Met. Alkalosis = Na- Cl Component - SID

HAGMA = lactate plus ketones plus urea and other unmeasured causes

and Albumin effect

1. The Na⁺–Cl⁻ component

This is one of the most clinically useful Stewart concepts in the ED. For the simplified bedside calculation:

NAGMA and Metabolic alkalosis component = (Na − Cl) − 35

Na - Cl > 35 - Met alkalosis

Na- Cl < 35 - NAGMA

The reference Na−Cl difference is approximately 35 mEq/L.

If the difference becomes smaller, the effect is acidifying.

Example

Na = 140
Cl = 115

Na − Cl = 25

Therefore:

25 − 35 = −10 mEq/L

That’s a substantial acidifying effect. And this is where the familiar ED scenario becomes relevant:

Large-volume normal saline.

Normal saline contains a relatively high chloride concentration. As chloride accumulates, the Na−Cl difference narrows → SID decreases → metabolic acidosis develops.

This is the physiological basis behind hyperchloremic metabolic acidosis.

The clinical example also highlights how fluid choice can influence this component: a lower-chloride fluid would be expected to widen the Na−Cl difference and reduce this acidifying effect.

So instead of simply saying:

“The patient has NAGMA.”

Stewart lets you ask:

“Is chloride actually driving part of this acidosis?”

That’s a much more actionable question.

2. Lactate

The next component is easier.

Lactate effect = 1 − measured lactate

with 1 mmol/L as the reference value.

So if lactate = 5:

1 − 5 = −4 mEq/L

That’s an acidifying effect. This immediately links the physiology to the clinical picture:

Shock → tissue hypoperfusion → increased lactate → increased strong anion burden → metabolic acidosis.

But here’s an important point:

Lactate may not explain the entire acidosis.

A patient with lactate 5 may have:

• lactate-driven acidosis

• hyperchloremic acidosis

• hypoalbuminemic alkalinization

• and another unidentified acidifying process

all at the same time. And that’s where the next component becomes important.

3. Albumin: the hidden alkalinizer

This is probably one of the most clinically useful lessons from the Stewart framework. Albumin is a weak acid. Therefore:

Lower albumin → less weak acid → alkalinizing effect.

Story’s simplified calculation is:

Albumin effect = 0.25 × (42 − albumin in g/L)

with 42 g/L as the reference albumin concentration.

For example:

Albumin = 22 g/L

0.25 × (42 − 22)
= +5 mEq/L approximately

That’s an alkalinizing effect. And this matters enormously in critically ill patients. Because a patient can simultaneously have:

Lactic acidosis + hyperchloremia while hypoalbuminemia is partially masking the severity of the metabolic acidosis.

So a “not too bad” pH does not necessarily mean a mild metabolic disturbance. The patient may have several opposing processes.

4. And then comes the most interesting component:

“Other ions”

This is where Stewart becomes particularly interesting clinically.

After accounting for:

• Na–Cl

• lactate

• albumin

there may still be an unexplained component of the base excess. Story refers to this as other ions, encompassing measured and unmeasured cations and anions. Ketoacids, Phosphate, sulfate and other unmeasured ions may become particularly relevant in organ dysfunction.

You can calculate it as a residual:

Other ions = BE − (Na–Cl effect + lactate effect + albumin effect)

And this is where the calculation can become a clinical clue.

What if “Other ions” is −6?

Imagine:

Other ions = −6 mEq/L

after accounting for lactate and albumin.

That means:

Your currently identified causes don’t completely explain the metabolic acidosis.

And this is the key clinical interpretation:

The “other ions” component doesn’t tell you what the diagnosis is. It tells you that your current explanation is incomplete.

Now broaden the differential.

Could there be significant renal dysfunction with retention of acidifying ions such as urate, sulfate, phosphate and other organic anions?

Could there be ketones?

Could there be another unmeasured anion?

And if those explanations don’t fit, particularly in the right clinical context, could this represent a toxic ingestion?

For example:

• methanol

• ethylene glycol

• other toxic causes of high-anion-gap metabolic acidosis

The ED may not immediately have access to every specific toxin assay. But the physiology can tell you:

“There is something here that I haven’t accounted for.”

That should trigger targeted investigation rather than premature closure. And importantly, a negative “other ions” residual does not diagnose a toxin. It is a signal to reconsider the differential using the history, renal function, ketones, lactate, anion/osmolal gaps and clinical context.

Let’s put everything together

A worked example makes this much easier to understand.

Patient:

• Na⁺ = 133 mmol/L

• Cl⁻ = 110 mmol/L

• Albumin = 22 g/L

• Lactate = 5 mmol/L

• pH = 7.20

• PaCO₂ = 40 mmHg

• HCO₃⁻ = 15 mmol/L

• BE = −11.5 mmol/L

At first glance:

Metabolic acidosis.

But Stewart asks:

What all is contributing to that BE = − 11.5?

a. Na–Cl ( sum of NAGMA plus Met. Alkalosis component)

(133 − 110) − 35 = −12 mEq/L

Strong acidifying effect.

b. Lactate

1 − 5 = −4 mEq/L

Another acidifying effect.

c. Albumin

0.25 × (42 − 22) = +5.5 mEq/L

An alkalinizing effect.

d. Other ions

We already know:

BE = −11.5

So:

Other ions = −11.5 − [−12 + (−4) + 5.5] = approximately −1 mEq/L

Put everything together:

BE = −12 − 4 + 5.5 − 1

BE ≈ −11.5 mEq/L

Exactly matching the measured BE.

Now the ABG is no longer simply:

“Metabolic acidosis.”

We can tell a much richer story:

Hyperchloremic/low Na–Cl contribution

• lactic acidosis

• hypoalbuminemic alkalinization

• small residual other-ion effect

And there is another important observation.

With HCO₃⁻ around 15 mmol/L, expected PaCO₂ by Winter’s formula would be approximately 30–32 mmHg.

But PaCO₂ is 40 mmHg.

So this patient also has a respiratory acidosis.

Now the physiology starts making sense:

Multiple disorders are occurring simultaneously—and some are masking others.

Why does this matter in the ED and acute care?

Because ED patients rarely arrive with a single textbook disorder. Consider the septic patient who has:

Lactate ↑
Normal saline resuscitation
Albumin ↓
AKI developing
Possible ketosis
Respiratory fatigue

The traditional approach may tell you:

“Mixed metabolic acidosis.”

Useful - but incomplete. The Stewart lens asks:

Which processes are actually pushing the pH in each direction?

That distinction matters because the answer may influence what you do next.

If chloride is the problem:

Think about ongoing chloride-rich fluid exposure.

If lactate dominates:

Treat the underlying perfusion problem.

If hypoalbuminemia is substantial:

Recognize that it may be masking part of the metabolic acidosis.

If renal dysfunction is present:

Think beyond urea alone—the acidifying effect is related to retention of sulfate, phosphate and other acids/anions.

If a significant unexplained residual remains:

Look for ketones, unmeasured anions and—when clinically appropriate—toxic causes.

The point isn’t to calculate numbers for the sake of calculation.

The point is to connect the ABG to the patient’s physiology.

Why is it particularly relevant in acute care?

Because acute-care medicine is full of rapidly changing iatrogenic physiology. The patient’s acid–base status is not static. Fluids change chloride. Blood products and medications alter the ionic environment. Resuscitation changes lactate. Renal function evolves. Albumin changes. Ventilation changes PaCO₂.

And the patient may move from one dominant process to another within hours.

Story specifically emphasizes that the simplified Stewart approach can help understand the patient’s current acid–base status and anticipate the acid–base consequences of future fluids and therapies. modified abg (1)(4)

That makes it particularly relevant to:

Resuscitation → ICU transfer → ventilation → renal replacement → ongoing fluid therapy

rather than being merely an academic alternative to Henderson–Hasselbalch.

But is Stewart better than the traditional approach?

This is where we need to be honest.

Not necessarily.

The Stewart approach provides a mechanistic framework and can make complex mixed disorders easier to understand.

But it is more cumbersome. Studies comparing Stewart-based approaches with traditional methods have often found that much of the additional information can also be obtained using albumin-corrected anion gap and conventional acid–base analysis.

Rastegar (2009), for example, concluded that Stewart’s method offers a mechanistic explanation but did not demonstrate clear superiority in diagnostic, management or prognostic performance over traditional approaches.

More recent work continues to support a pragmatic position: conventional approaches work well for many patients, while a simplified Stewart approach becomes particularly useful when multiple metabolic processes coexist or appear to be offsetting each other.

So the message isn’t:

❌ “Forget Henderson–Hasselbalch.”

It is:

✅ “Know when the traditional framework isn’t telling you enough.”

The take-home message

Stewart can initially feel unnecessarily complicated.

But at the bedside, its most useful lesson is actually quite simple:

Acid–base disorders are often not one problem. They are several processes happening simultaneously.

A patient can be:

acidotic from chloride
acidotic from lactate
acidotic from unmeasured ions
while being
alkalotic from hypoalbuminemia

—all at the same time.

And the final pH is simply the result of those competing forces.

So remember:

—> Henderson–Hasselbach tells you WHAT is happening.

—> Base excess tells you the NET metabolic effect.

—> Stewart helps you understand WHAT is DRIVING that effect.

And perhaps the most useful lesson of all:

When the “other ions” component is abnormal, don’t immediately ask, “What toxin is this?”

Ask, “What have I not explained yet?”

Because in acute care, an unexplained residual is often more valuable than a falsely reassuring explanation.

Preferred Reads -

1. Story DA. Stewart acid-base: a simplified bedside approach. Anesth Analg. 2016;123(3):511-515. doi:10.1213/ANE.0000000000001261

2. Rastegar A. Clinical utility of Stewart’s method in diagnosis and management of acid-base disorders. Clin J Am Soc Nephrol. 2009;4(7):1267-1274. doi:10.2215/CJN.01870309

3. Duška F, Krbec M, Heldeweg M, Elbers PWG, Giosa L. A pragmatic approach to complex acid base disturbances of critical illness: the “Stewart light.” Intensive Care Med. 2026;52(6):1322-1325. doi:10.1007/s00134-026-08416-3.

A patient arrives tachypneic.

ABG:

pH 7.21
PaCO₂ 24 mmHg
HCO₃⁻ 10 mmol/L

You say:

“Metabolic acidosis.”

But is that the whole diagnosis?

What does acidemia actually mean?
Is acidosis the same thing?
What does the base excess tell you?
Is this HAGMA or NAGMA?
Is the respiratory response appropriate?
Could there be a second metabolic disorder hiding underneath?

And importantly:

Can a patient have a normal pH and still have a major acid–base disorder?

This is where we move beyond simply reading the bicarbonate.

1. Acidemia ≠ Acidosis

This should be the first major teaching point.

Acidemia

A state of the blood in which:

pH < 7.35

Acidosis

A physiological process that tends to lower pH.

Similarly:

Alkalemia

pH > 7.45

Alkalosis

A physiological process that tends to raise pH.

Why does this distinction matter?

Because a patient can have multiple simultaneous processes. For example:

Metabolic acidosis + metabolic alkalosis

may produce a near-normal pH.

So:

A normal pH does not exclude an acid–base disorder.

And:

Acidemia tells you the net result. Acidosis tells you about one of the processes producing that result.

2. Where does the metabolic component fit?

Once you identify the pH, look at:

PaCO₂ + HCO₃⁻

Metabolic acidosis

HCO₃⁻ ↓

Metabolic alkalosis

HCO₃⁻ ↑

But don’t immediately label the disorder.

First ask:

Is the change appropriate compensation, or is another disorder present?

3. Base Excess: the often-underused number on the ABG

Base excess summarises the complete metabolic component of an acid–base disorder, independent of the respiratory component.

Base excess is the amount of strong acid or base required to return blood to pH 7.40 under standardized conditions, with a normal range around −3 to +3 mmol/L. modified abg (1)(3)

Think of it simply:

Negative BE → metabolic acidosis
Positive BE → metabolic alkalosis

For example:

BE −12 → significant metabolic acid load / base deficit.

BE +8 → metabolic alkalosis.

Base deficit vs base excess

Be careful with terminology:
Base excess −10
and
Base deficit +10

describe the same direction of metabolic disturbance but use opposite signs.

Practical message

HCO₃⁻ tells you the bicarbonate concentration. Base excess helps quantify the metabolic component.

4. Metabolic Acidosis

Now build the actual framework.

Typical ABG:

pH ↓
HCO₃⁻ ↓

The PaCO₂ should fall as respiratory compensation develops.

But we need to determine:

1. Is compensation appropriate?

2. Is there an anion gap?

3. If there is an anion gap, is there another metabolic disorder?

5. Step 1 — Check respiratory compensation

Winter’s formula

Expected PaCO₂ = 1.5 × HCO₃⁻ + 8 ± 2

Example

HCO₃⁻ = 12

Expected:

1.5 × 12 + 8 = 26

Expected PaCO₂:

24–28 mmHg

If actual PaCO₂ is:

26

→ appropriate compensation

40

→ metabolic acidosis + respiratory acidosis

18

→ metabolic acidosis + respiratory alkalosis

So:

Compensation should be calculated, not assumed.

6. Step 2 — Find the Anion Gap

AG = Na⁺ − (Cl⁻ + HCO₃⁻)

12 ± 4 mEq/L as the conventional normal range. (Confirm with your own lab)

The conceptual question is:

Why has bicarbonate fallen?

7. HAGMA (High-Anion-Gap Metabolic Acidosis)

Here, acids accumulate and their accompanying anions are not routinely measured.

Think:

“New unmeasured anions have appeared.”

GOLD MARK

G — Glycols
O — Oxoproline
L — L-lactate
D — D-lactate
M — Methanol
A — Aspirin
R — Renal failure
K — Ketoacidosis

Then add the clinical context:

• DKA

• Alcoholic ketoacidosis

• Starvation ketoacidosis

• Lactic acidosis

• Renal failure

• Toxic alcohols

• Salicylates

8. Don’t forget albumin

Albumin is an important unmeasured anion.

Therefore:

Hypoalbuminemia can make the anion gap look deceptively normal.

Corrected AG

Corrected AG = measured AG + 2.5 × (4 − albumin g/dL)

Your source gives this correction explicitly. modified abg (1)(3)

Example

AG = 14
Albumin = 2 g/dL

Corrected AG:

14 + 2.5 × (4−2) = 19

So what initially looked like a modest AG may actually represent a significant HAGMA.

9. NAGMA (Normal-Anion-Gap Metabolic Acidosis)

Also called:

Hyperchloremic metabolic acidosis

Here:

HCO₃⁻ ↓ but:

Cl⁻ ↑

maintains electrical neutrality.

Major causes

GI bicarbonate loss

• Diarrhea

• High-output intestinal losses

Renal

• Renal tubular acidosis

Drugs

• Acetazolamide

Iatrogenic

• Large-volume 0.9% saline

The key mental model:

HAGMA = addition of unmeasured acid/anions
NAGMA = bicarbonate loss/reduction with relative chloride increase

10. But what if the patient has TWO metabolic disorders?

This is where the article becomes more interesting.

Delta gap / Delta ratio

Once you identify HAGMA:

ΔAG

AG − 12

ΔHCO₃

24 − measured HCO₃

Then:

Delta ratio = ΔAG / ΔHCO₃

<1 - HAGMA + NAGMA
1–2 - Predominantly HAGMA
>2 - HAGMA + metabolic alkalosis

11. Why is this useful?

Imagine: AG = 30

Therefore: ΔAG = 18

And: HCO₃⁻ = 18

Therefore: ΔHCO₃ = 6

Delta ratio:

18 / 6 = 3

That’s too high for a pure HAGMA.

It suggests:

HAGMA + metabolic alkalosis

This is exactly the type of patient we miss if we stop at:

“The patient has DKA.”

12. Metabolic Alkalosis

the other side of the metabolic spectrum.

Typical pattern:

pH ↑

HCO₃⁻ ↑

The respiratory response should be:

PaCO₂ ↑

because hypoventilation provides respiratory compensation.

A useful approximation:

Expected PaCO₂ ≈ 0.7 × (HCO₃⁻ − 24) + 40 ± 2

Again:

If the PaCO₂ is substantially outside the expected range, think:

Metabolic alkalosis + a second respiratory disorder.

13. Causes of metabolic alkalosis

I’d keep this clinically oriented rather than getting too deep into renal physiology.

Vomiting / gastric losses

Loss of:

H⁺ + Cl⁻

→ metabolic alkalosis

Nasogastric suction

Same principle.

Diuretics

Especially:

• Loop diuretics

• Thiazides

Volume/chloride depletion

The alkalosis can be maintained by continued volume and chloride depletion.

Mineralocorticoid excess

Think:

• Primary hyperaldosteronism

• Cushing physiology

• Other mineralocorticoid states

Hypokalemia

Can contribute to maintenance of alkalosis.

14. Chloride-responsive vs chloride-resistant

Chloride-responsive

Think:

Vomiting | NG suction | prior diuretic use | volume depletion

Chloride-resistant

Think:

Mineralocorticoid excess | ongoing renal causes | severe hypokalemia

This gives the reader a practical next step after simply identifying metabolic alkalosis.

15. Mixed metabolic disorders

Example 1

DKA + diarrhea

→ HAGMA + NAGMA

Example 2

DKA + vomiting

→ HAGMA + metabolic alkalosis

Example 3

Diarrhea + vomiting

→ NAGMA + metabolic alkalosis

Example 4

Sepsis + lactic acidosis + vomiting

→ HAGMA + metabolic alkalosis

And these can coexist with a respiratory disorder as well.

16. The “normal pH” trap

pH 7.40 does not mean normal.

look at the anion gap, normal pH with increased anion gap, might mean it is mixed disorder

look at base excess/deficit if abnormal , it is mixed disorder (respiratory plus metabolic)

A patient may have:

Metabolic acidosis + metabolic alkalosis

with the two processes partially cancelling each other.

(to look at elevated anion gap for this)

Or:

Metabolic acidosis + respiratory alkalosis

producing a relatively normal pH.

(To look at anion gap and base excess for this)

Final message of the article

Don’t let the pH fool you.

Acidemia is a state. Acidosis is a process.

Base excess tells you about the metabolic component.

The anion gap tells you where to look.

The delta ratio tells you whether one metabolic process is enough.

And compensation tells you whether the lungs are responding appropriately — or whether another respiratory disorder is hiding underneath.

The goal isn’t to name the abnormal number.

The goal is to explain the entire acid–base picture.

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We often learn a simple rule:

PaCO₂ 35–45 mmHg = normal ventilation.

But physiology doesn’t always follow the reference range.

PaCO₂ has to be interpreted in context.

Here are 3 patients who can make a “normal” PaCO₂ look very different.

CASE 1 — The acidotic patient with a PaCO₂ of 30

A 24-year-old man with severe DKA arrives tachypnoeic and dehydrated.

ABG:

pH 7.10
HCO₃⁻ 8 mmol/L
PaCO₂ 25 mmHg

At first glance:

“PaCO₂ is low. He’s ventilating well.”

But here’s the important question:

Is PaCO₂ of 25 actually appropriate for this degree of metabolic acidosis?

Use Winter’s formula:
Expected PaCO₂ = 1.5 × HCO₃⁻ + 8 ± 2

= 1.5 × 8 + 8
= 20 ± 2 mmHg

His PaCO₂ is 25 mmHg.

So despite the fact that his PaCO₂ is low, it is higher than expected. He is not compensating adequately.

There may already be an additional respiratory acidosis. This is one of the most important concepts when assessing ventilation:

The “normal” PaCO₂ is not necessarily 40.
The appropriate PaCO₂ depends on the metabolic disturbance.

In severe metabolic acidosis, the patient’s low PaCO₂ is part of the compensatory response. The ventilatory response can become so important that losing it during intubation may cause a rapid rise in PaCO₂ and worsening acidemia.

I wrote about this in detail here:

Ventilating the Acidotic Patient: VCV Strategies to Preserve Compensation

The key lesson:
Don’t ask:

“Is the PaCO₂ normal?”

Ask:

“Is the PaCO₂ appropriate for this patient’s metabolic state?”

CASE 2 — The pregnant patient with a PaCO₂ of 40

A 30-year-old woman in her third trimester presents with dyspnea.

ABG:
pH 7.40
PaCO₂ 40 mmHg
HCO₃⁻ 24 mmol/L

Looks completely normal. Right?

Not necessarily.

Pregnancy changes the baseline. Progesterone increases respiratory drive, producing increased minute ventilation and a physiological respiratory alkalosis.

Typical pregnancy values are approximately:

PaCO₂: 28–32 mmHg
HCO₃⁻: 18–21 mmol/L
pH: ~7.40–7.47

So in a pregnant patient:
PaCO₂ of 40 mmHg is not reassuring.

It may represent relative hypoventilation compared with the expected pregnancy baseline. In fact, literature describing obstetric critical illness notes that a PaCO₂ of 35–40 mmHg during pregnancy can indicate respiratory compromise.

Why does this matter? Because maternal CO₂ needs to remain lower than fetal CO₂ to maintain the maternal–fetal CO₂ gradient and facilitate fetal CO₂ elimination.

So remember:

A “normal” PaCO₂ in pregnancy may actually be abnormal.

Reference ranges are not universal truths.

They are population-dependent.

CASE 3 — The patient with hypercapnia

Now let’s say the PaCO₂ really is high. PaCO₂ 65 mmHg

What do you do? Don’t immediately write:

“Hypercapnic respiratory failure.”

Instead ask:

WHY is the CO₂ high?

Because hypercapnia is a physiological signal, not a diagnosis.

My previous Life on the Frontline post frames it beautifully:

Hypercapnia means alveolar ventilation is inadequate relative to CO₂ production.

And that can happen through several mechanisms.

Quick link : Acute Hypercapnia: A Mechanistic Approach to Ventilator Troubleshooting

1. The patient WON’T breathe

Central / drive problem

The respiratory drive is inadequate.

Think:

• Opioids

• Sedatives

• CNS disease

• Brainstem injury

• Central hypoventilation

• Inadequate ventilatory response to metabolic demand

The lungs may actually be structurally normal.

The problem is control.

2. The patient CAN’T breathe

Mechanical / pump problem

The patient has respiratory drive — but effective ventilation is limited.

Think:

• COPD

• Asthma

• Airway obstruction

• Dynamic hyperinflation

• Intrinsic PEEP

• Increased dead space

Here, simply increasing the respiratory rate may actually make things worse if it further reduces expiratory time and increases air trapping.

3. The patient is being asked to do more than they can

This is an under-appreciated mechanism.

For example:

Severe metabolic acidosis

The metabolic demand for CO₂ elimination is enormous.

The patient may be breathing at 30–40/min and generating huge minute ventilation just to maintain the compensatory PaCO₂.

If that compensation becomes inadequate:

PaCO₂ rises → pH falls further → physiology deteriorates.

This is why a rising PaCO₂ in severe metabolic acidosis can be particularly dangerous.

So how should we read ventilation on an ABG?

Don’t use:

PaCO₂ = 35–45 → “normal ventilation”

as your only rule.

Instead:

STEP 1

Look at PaCO₂.

Is it high, low or apparently normal?

STEP 2

Ask whether it is appropriate for the metabolic state.

In metabolic acidosis:

Use Winter’s formula.

STEP 3

Know the patient’s physiological baseline.

Pregnancy is a classic example.

STEP 4

If PaCO₂ is elevated:

Find the mechanism.

Won’t breathe?
Can’t breathe?
Or simply can’t meet the metabolic demand?

Read next

For a deeper dive into the mechanisms behind rising PaCO₂ and how to troubleshoot hypercapnia:

Acute Hypercapnia: A Mechanistic Approach to Ventilator Troubleshooting

And for the special problem of preserving respiratory compensation in severe metabolic acidosis:

Ventilating the Acidotic Patient: VCV Strategies to Preserve Compensation

Next in ABG Series → Deep dive into metabolic problems

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Before asking “What is the acid–base disorder?”, first ask:

Was this ABG collected, handled and processed correctly?

And then:

Is the ABG internally consistent?

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1. Why do we perform an ABG?

An arterial blood gas can help assess:

Oxygenation
→ PaO₂, SaO₂

Ventilation
→ PaCO₂

Acid–base status
→ pH, PaCO₂

Oxygen-carrying capacity
→ PaO₂, Hb, total Hb and dyshemoglobins

Electrolytes, Hb, Hct, Osmolality, etc.

It can also be used to assess response to interventions such as oxygen therapy and to monitor the severity or progression of disease.

2. Getting the sample right

Before puncture

• Allen’s test as a prerequisite

• Slight wrist extension for radial artery sampling

• Clean the site with 70% alcohol

• Use an appropriate heparinised syringe

• Enter the skin at approximately 45° for radial artery sampling

• Obtain approximately 1 mL of blood

• Do not pull back the syringe plunger

If an air bubble enters the syringe:

Remove it immediately.

Then apply firm pressure to the puncture site for at least 5 minutes.

3. The sample can be wrong even when the puncture was right

Several pre-analytical errors can alter the ABG:

Too much or too little anticoagulant

The source highlights the potential effects of excess/inadequate anticoagulant, including electrolyte binding.

Venous contamination

Mixing venous and arterial blood during puncture can produce misleading values.

Air bubbles

Air exposure can:

↑ PaO₂
↓ PaCO₂

Inadequate mixing

Can cause RBC stacking and compromise the sample.

4. Time matters

Analyse within 5 minutes
Maximum: 15 minutes

If a delay of >30 minutes is expected, it is recommended to keep in a glass syringe with an ice slurry, with iced-sample analysis possible for up to approximately 1 hour.

Practical takeaway:

Don’t let a good arterial puncture become a bad ABG because of poor handling.

5. When should you avoid a particular puncture site?

These cautions:

• Negative Allen’s test

• Surgical shunt/fistula or bypass graft

• Infection at the site

• Limb ischemia/Raynaud’s disease

• Bleeding diathesis — described as a relative contraindication in the post-thrombolysis setting

6. Complications of ABG sampling

Even a routine ABG is an arterial puncture. Potential complications include:

Arterial spasm
Hematoma
Arterial occlusion
Air/thrombus embolism
Local infection
Nerve or vessel injury
Vasovagal response
Needle-stick injury

7. Now comes the part most people skip…

CHECK THE ABG BEFORE INTERPRETING IT

Before jumping to:

❌ “It’s metabolic acidosis.”
❌ “It’s respiratory alkalosis.”
❌ “The patient is hypoxic.”

First ask:

Does the ABG make physiological sense?

The modified Henderson–Hasselbalch relationship

[H⁺] = 24 × PaCO₂ / HCO₃⁻

Use the reported PaCO₂ and HCO₃⁻ to estimate the corresponding hydrogen ion concentration.

Then compare it with the reported pH.

If the pH and calculated H⁺ are inconsistent:

Question the validity of the ABG.

A corresponding pH–H⁺ table as a bedside reference.

The Frontline Takeaway

Don’t interpret the numbers before validating the sample.

Good ABG interpretation begins before the ABG reaches the analyser.

Collect correctly → Handle correctly → Process promptly → Check consistency → Then interpret.

Coming next…

ABG series #2 — Oxygenation

Hypoxemia ≠ Hypoxia

We’ll start with:

PaO₂ → SaO₂ → FiO₂ → P/F ratio → A–a gradient

And then ask the more important question:

Why is this patient hypoxemic?

Follow @humans.of.em for the next part of the ABG series.

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