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ABG Interpretation: A Nurse's Guide to Reading Blood Gases

William Kelly, MSN, FNP-C
Updated June 2026 · Medically reviewed for nurses
11 min read

Arterial blood gases — the ABG — are one of the fastest ways to see what's really happening inside a sick patient: their acid-base balance, their ventilation, and their oxygenation, all in one draw. Learn a systematic approach and they stop being intimidating.

This guide breaks down every value on the panel, walks through the four acid-base disturbances, and gives you a step-by-step method to interpret any gas with confidence — whether you're on a med-surg floor, in the ED, or at an ICU bedside.

What Are ABGs or a Blood Gas?

An ABG — Arterial Blood Gas — is a blood sample drawn from an artery, usually in the wrist (radial artery). That's different from routine labs, which come from a vein. The arterial sample is typically obtained by a respiratory therapist, a critical care nurse, or a provider.

Arterial blood gives a better picture of oxygen and carbon dioxide levels than venous blood, and the ABG also reports the blood's acidity and bicarbonate. In short, a blood gas is used to evaluate acid-base disturbances and the adequacy of oxygenation and ventilation. Four core values are reported:

Oxygen
Oxygen
Reported as PaO2 (partial pressure) and SaO2 (saturation).
Carbon dioxide
Carbon Dioxide
Reported as PaCO2 — the respiratory acid.
pH
pH
The acidity of the blood — the headline number.
Bicarbonate
Bicarbonate (HCO3)
The metabolic buffer that offsets acid.
The three that matter most: when you're determining acid-base balance, focus on the pH, the PaCO2, and the HCO3. Oxygenation (PaO2/SaO2) is read separately.

When Are ABGs Ordered?

ABGs shine when you need to evaluate an acid-base problem or a ventilation/oxygenation problem. The patients who get them are usually sick — often ICU-bound. Common scenarios include:

Respiratory failure
Acute Respiratory Failure
Often heading toward intubation.
Ventilated patient
Ventilated Patients
To confirm settings are matching the patient's needs.
COPD and CHF
COPD / CHF with AMS
Altered mental status raises concern for CO2 retention.
Diabetic ketoacidosis
DKA
Diabetic ketoacidosis — though a VBG often suffices.

Things to Keep in Mind with ABGs

A few principles make interpretation far less confusing.

Things Aren't Always Simple

Patients can have mixed acid-base disturbances at once, which muddies the picture. Final interpretation is ultimately the provider's call, especially in complex critical-care cases.

Compensation

The body is always chasing homeostasis. The respiratory system will try to compensate for a metabolic problem, and the kidneys (metabolic) will try to compensate for a respiratory one.

Always treat the underlying cause. The ABG tells you what is wrong; fixing the patient means addressing why.

The ABG Measurements

Let's go value by value and unpack what each one means.

The pH

pH is the "potential of Hydrogen" — a measure of how acidic the blood is. The more hydrogen ions, the more acidic.

Normal
7.35–7.45
pH
Acidemia
< 7.35
acidosis
Alkalemia
> 7.45
alkalosis

pH can be normal or near-normal in chronic disturbances because of compensation, or when a patient has more than one acid-base process happening at once.

The PaCO2

PaCO2 is the partial pressure of carbon dioxide in arterial blood — essentially how much CO2 is dissolved in the blood. The lungs deliver oxygen to the cells; the cells make energy (ATP) and produce CO2 as a byproduct, which is then exhaled.

CO2 isn't acidic on its own, but in blood it forms carbonic acid, which is. So retaining CO2 drives acidosis, and blowing off too much CO2 drives alkalosis. That makes PaCO2 the respiratory half of the equation.

How CO2 relates to acidity in the body on an ABG
CO2 and acidity in the body.

Watch the Direction

In respiratory acidosis, PaCO2 is high and pH is low — they move in opposite directions. (CO2 is an acid, so as it rises, pH falls.) A high CO2 with a low pH is your classic respiratory acidosis.

Normal
35–45
mmHg
Hypercapnia
> 45
mmHg
Hypocapnia
< 35
mmHg

"My Blood Is Boiling"

Hold your breath and eventually you feel like you have to breathe — like your blood is boiling. That's the CO2 building up and turning acidic. A handy way to remember: not breathing enough = CO2 climbs = acidosis.

The HCO3 (Bicarbonate)

HCO3 is the serum bicarbonate in the arterial blood. Bicarb is a buffer — think of it as the opposite of hydrogen ions. The less bicarb, the more acidic the blood. It's the metabolic half of the equation: bicarb reacts with H+ to form carbonic acid, which the body breaks into CO2 and water and breathes off.

Normal
22–26
mEq/L
Met. Acidosis
< 22
mEq/L
Met. Alkalosis
> 26
mEq/L

The PaO2

PaO2 is the partial pressure of oxygen in arterial blood — the actual oxygen content of the gas.

Normal
> 80
mmHg
Hypoxemia
< 80
mmHg
Over-oxygenated
> 100
mmHg

A low PaO2 is associated with respiratory failure (though severe anemia can contribute). A very high PaO2 usually reflects over-oxygenation.

Oxygen Toxicity

Too much oxygen can harm, too. High levels can generate reactive oxygen species causing cellular injury and inflammation, and excess oxygen can worsen CO2 retention in some COPD patients.

The SaO2

SaO2 is the oxygen saturation, equivalent to the pulse ox reading.

Normal
94–100%
SaO2
Low
< 90–92%
SaO2
Borderline
92–94%
SaO2

The Four Acid-Base Disturbances

When you read an ABG, you're sorting it into one (or more) of four buckets:

Respiratory acidosis
Respiratory Acidosis
High PaCO2, low pH — too little ventilation.
Respiratory alkalosis
Respiratory Alkalosis
Low PaCO2, high pH — too much ventilation.
Metabolic acidosis
Metabolic Acidosis
Low HCO3, low pH — acid gain or bicarb loss.
Metabolic alkalosis
Metabolic Alkalosis
High HCO3, high pH — acid loss or bicarb gain.

Remember a patient can have more than one disturbance at once — medicine is rarely black and white — but these four categories point you toward the underlying cause.

Respiratory Acidosis

Respiratory acidosis comes from alveolar hypoventilation: the lungs can't clear CO2 fast enough, so CO2 (and hydrogen ions) build up. PaCO2 is high and pH is low. It can be acute or chronic, and it shows up classically in COPD, where blunted response to hypoxia, increased dead-space ventilation, and a fatigued, hyperinflated diaphragm all contribute.

Acute respiratory acidosis
Acute Causes
Severe asthma/COPD/CHF, stroke or TBI, opioid or benzo overdose, and neuromuscular disease (myasthenia gravis, ALS, Guillain-Barré).
Chronic respiratory acidosis
Chronic Causes
COPD with chronic CO2 retention, obesity-hypoventilation (Pickwickian) syndrome, ALS, interstitial fibrosis, and thoracic deformities. pH may be near-normal from metabolic compensation.

COPD & Oxygen

A COPD patient on high-flow oxygen carries a real risk of hypoventilation and CO2 retention. This is the classic patient to keep picturing whenever you think "respiratory acidosis."

Treatment targets the underlying cause (for example, naloxone for an opioid overdose), but more often it comes down to BiPAP or intubation.

Respiratory Alkalosis

The mirror image: alveolar hyperventilation blows off too much CO2, producing hypocapnia (low PaCO2) and a high pH. It's common in the critically ill, but shows up in several settings:

Ventilated patients
Ventilator Settings
A set rate that's too fast can drive off CO2 and cause alkalosis.
Hyperventilation
Hyperventilation
Panic attacks, severe anxiety, or psychosis — though ABGs are rarely ordered for a simple panic attack.
Early lung disease
Early Lung Disease
Pneumonia, pneumothorax, pulmonary embolism, asthma, bronchitis — the increased rate compensating early, before later tipping into acidosis.
Numbness and tingling
Numbness & Tingling
Acute low CO2 shifts potassium and phosphorus into cells and increases calcium binding to albumin — causing the classic tingling many feel during a panic attack.

Treatment again addresses the cause — adjusting ventilator settings, treating anxiety, and so on.

Metabolic Acidosis

A bicarb < 22 mEq/L with a pH < 7.35 is metabolic acidosis: increased plasma acidity from the metabolic side. It's split by whether the anion gap is normal or elevated. A severe HCO3 < 12 almost always means true metabolic acidosis rather than mere compensation.

Normal-Gap Metabolic Acidosis

Usually accompanied by high chloride. Bicarbonate is lost through the GI tract or kidneys. Common causes:

Diarrhea
Diarrhea
Loses bicarb in the stool while sparing chloride, so the gap stays normal.
Chronic renal failure
Chronic Renal Failure
Typically as GFR falls to roughly 20–50 mL/min.
Renal tubular acidosis
Renal Tubular Acidosis
The kidneys fail to clear acid from the blood as they should.
Large-volume fluid resuscitation
Large-Volume Saline
Replacing large volumes of normal saline can cause a dilutional acidosis; lactated Ringer's, with its lactate buffer, may be gentler.

Elevated-Gap Metabolic Acidosis

The anion gap is the difference between the main measured cation (sodium) and the measured anions (chloride and bicarb). A high gap means unmeasured acids — lactate, ketones, toxins — are accumulating. Common causes:

Diabetic ketoacidosis
DKA
Diabetic ketoacidosis floods the blood with acidic ketones plus severe dehydration.
Lactic acidosis
Lactic Acidosis
Especially in sepsis, where poor perfusion drives lactate up.
Acute kidney injury
Acute Kidney Injury
Reduced ability to excrete hydrogen ions and regenerate bicarb.
Toxic ingestions
Toxic Ingestions
Toxic alcohols, salicylates, and others can each generate acid.

Treatment corrects the underlying problem. A bicarb drip may be used in severe acidosis (roughly pH < 7.1).

Metabolic Alkalosis

Caused by increased serum bicarb and decreased acidity. A bicarb > 35 mEq/L almost always reflects true metabolic alkalosis rather than compensation. Hydrogen ions are usually lost through the GI tract or kidneys:

Vomiting
Excessive Vomiting
Gastric secretions are rich in hydrogen ions, so heavy vomiting strips acid from the body.
NG tube suction
NG Tube Suction
Over time, removing gastric fluid acts like ongoing vomiting and lowers hydrogen ions.
Antacid overdose
Alkali Overload
Rare, but huge intakes of milk or antacids (milk-alkali) can tip into alkalosis.
Renal losses
Renal Losses
Certain diuretics, mineralocorticoid excess, and some rarer disorders push the kidneys to excrete too many hydrogen ions.

Steps to Interpret an ABG

A systematic approach keeps you from missing a step. Work through it in order every time:

1
Determine the pH

Is the patient acidic (pH < 7.35) or alkalotic (pH > 7.45)? This tells you the primary direction.

2
Check PaCO2 and HCO3

Which values are abnormal, and are they leaning acidic or alkalotic?

3
Correlate with the pH

Which value matches the pH? Example: pH 7.20 (acidic) with CO2 56 and HCO3 30 — the CO2 is acidic and matches, so this is respiratory.

4
Determine compensation

Look at the value that didn't match. Is it abnormal in the opposite direction? That's compensation. If the pH is still abnormal, it's only partial compensation.

5
Check the anion gap

Optional, for metabolic acidosis. A high gap points to AKI, sepsis, or DKA; a normal gap points to causes like severe diarrhea.

Clinical Pearls

1
pH and CO2 move opposite in respiratory problems. High CO2 → low pH (acidosis); low CO2 → high pH (alkalosis). The bicarb moves the same direction as pH in metabolic problems.
2
The value that matches the pH is the primary problem. The other value, if abnormal in the opposite direction, is compensation.
3
A near-normal pH with very abnormal CO2 and HCO3 suggests a chronic, well-compensated process — or a mixed disorder.
4
Always treat the cause, not the number. Naloxone, ventilator adjustments, fluids, or insulin fix the gas far better than chasing the value alone.

References

Clinical Databases & Guidelines
  1. Theodore, A. C. Arterial blood gases. UpToDate.
  2. Emmett, M., & Szerlip, H. Approach to the adult with metabolic acidosis. UpToDate.
  3. Emmett, M., & Szerlip, H. Causes of metabolic alkalosis. UpToDate.
  4. Hopkins, E., Sanvictores, T., & Sharma, S. Physiology, Acid Base Balance. StatPearls, National Library of Medicine.
  5. Sood, P., Paul, G., & Puri, S. Interpretation of arterial blood gas. Indian J Crit Care Med, 14(2), 57–64.
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