EtCO2 vs PaCO2: Why the Two Numbers Differ

EtCO2 vs PaCO2 is one of the most useful things to understand in capnography, because it explains both why end-tidal CO2 is so valuable and where it can mislead you. The two numbers measure the same gas in different places, and the gap between them is not an error. It is a clue.

This page explains what each number is, why they differ, what sets the size of the gap, and when that gap widens or narrows. It is a reference, so keep it to hand alongside the glossary.

Key takeaways

• PaCO2 is the arterial CO2 from a blood gas. EtCO2 is the end-tidal CO2 from the breath.
• EtCO2 normally sits 2 to 5 mmHg below PaCO2.
• The gap is caused by alveolar dead space, lung that is ventilated but not perfused.
• The gap widens when perfusion falls: shock, embolism, trauma, cardiac arrest.
• The gap narrows, and can reverse, in pregnancy.

The two numbers

Start with what each one actually measures.

PaCO2 is the partial pressure of carbon dioxide in arterial blood. It is measured from an arterial blood gas sample, in a laboratory or on a blood gas analyser. It is the reference standard for a patient’s true carbon dioxide level, but it is invasive, intermittent and takes time.

EtCO2 is the partial pressure of carbon dioxide at the very end of exhalation, measured continuously and non-invasively by a capnograph. At the end of a breath, the gas leaving the lungs is alveolar gas, which has exchanged with the blood, so EtCO2 closely approximates the arterial value. See what is EtCO2.

In short: PaCO2 is the accurate but slow and invasive number. EtCO2 is the instant, continuous, non-invasive estimate of it. For why that estimate is so useful, see the benefits of EtCO2 over PaCO2.

Why they differ: the normal gradient

In a healthy adult, EtCO2 reads about 2 to 5 mmHg lower than PaCO2. This difference is called the arterial-to-end-tidal CO2 gradient, or the a-ET gradient. It is normal, and it has a specific cause.

Not every part of the lung contributes equally to the exhaled breath. Some alveoli are ventilated with air but receive little or no blood flow. These alveoli take almost no CO2 from the blood, because there is little blood there to give it up. When their CO2-poor gas mixes with the CO2-rich gas from well-perfused alveoli, it dilutes the exhaled sample slightly, so the measured end-tidal value comes out a little below the true arterial value.

That CO2-poor, ventilated-but-not-perfused lung is called alveolar dead space, and it is the reason the gradient exists.

Dead space, the key idea

Dead space is any part of a breath that does not take part in gas exchange. It comes in three forms.

Anatomical dead space is the conducting airways, the trachea and bronchi, which carry air but do no exchange.

Alveolar dead space is alveoli that are ventilated but not perfused. This is the part that sets the a-ET gradient.

Apparatus dead space is volume added by equipment, such as airway adapters and connectors. It matters most in small patients, where it is a large share of each tiny breath. See paediatric capnography.

The single rule that ties it together: more dead space means a bigger gap between EtCO2 and PaCO2, and a lower measured EtCO2.

When the gap widens

This is where the gradient becomes diagnostic, because anything that reduces blood flow to the lungs increases alveolar dead space and widens the gap.

Falling perfusion. Shock, severe hypotension, haemorrhage and cardiac arrest all reduce the blood reaching the lungs. Less CO2 arrives to be exhaled, so EtCO2 falls and the a-ET gap widens. In these states EtCO2 understates the true PaCO2, sometimes markedly. See EtCO2 in trauma and what does low EtCO2 mean.

Pulmonary embolism. A clot obstructs pulmonary blood flow, creating ventilated-but-not-perfused lung, the definition of alveolar dead space. The gap widens, while the waveform often stays a normal shape.

Lung disease. Emphysema, ARDS and significant ventilation-perfusion mismatch all widen the gradient.

The practical consequence: in an unstable patient, do not assume EtCO2 equals PaCO2. It understates it, and the sicker the patient, the wider the gap. Confirm with a blood gas when it matters.

When the gap narrows, and even reverses

Pregnancy is the striking exception, and it runs the opposite way.

In pregnancy the a-ET gradient narrows to almost nothing, and can even become negative, with EtCO2 reading equal to or above PaCO2. The altered chest mechanics, increased cardiac output and increased CO2 production of pregnancy change how the lung empties, so end-tidal gas reflects arterial CO2 unusually closely. This makes EtCO2 an unusually reliable guide in pregnancy, the reverse of the trauma situation. See EtCO2 in pregnancy.

Putting it together

The lesson in one line: EtCO2 is an excellent continuous guide to PaCO2, and the size of the gap between them is itself a measure of how well the lungs are being perfused.

A note on the device

This reference is published by Brainiac Healthcare, makers of RespiCOz, a portable mainstream capnograph. To see EtCO2 monitoring in practice, see the best handheld EtCO2 monitor guide, or start with the normal EtCO2 range.

Frequently asked questions

What is the difference between EtCO2 and PaCO2? PaCO2 is the arterial CO2 measured from a blood gas, the reference standard. EtCO2 is the end-tidal CO2 measured non-invasively from the breath. EtCO2 normally sits 2 to 5 mmHg below PaCO2.

Why is EtCO2 lower than PaCO2? Because of alveolar dead space, lung that is ventilated but not perfused. Its CO2-poor gas dilutes the exhaled sample, so the end-tidal value reads slightly below the true arterial value.

When does the gap between EtCO2 and PaCO2 widen? When blood flow to the lungs falls: shock, haemorrhage, cardiac arrest, pulmonary embolism and significant lung disease. In these states EtCO2 understates PaCO2.

Is EtCO2 ever higher than PaCO2? Rarely, but yes, notably in pregnancy, where the gradient can narrow to zero or reverse, so EtCO2 reads equal to or above PaCO2.

Can EtCO2 replace an arterial blood gas? No. It is an excellent continuous, non-invasive guide and trend, but in unstable patients the gap to PaCO2 widens unpredictably, so a blood gas remains the reference when the precise value matters.

Conclusion

EtCO2 vs PaCO2 is not a question of which number is right. Both are right, measured in different places, and the gap between them is caused by alveolar dead space. In a healthy patient that gap is small and steady, so EtCO2 tracks PaCO2 well. When perfusion falls, the gap widens and EtCO2 understates the truth; in pregnancy it narrows and tracks closely.

Understand the gradient, and you understand both why EtCO2 is so useful and exactly where to be cautious with it. For the vocabulary behind this, see the capnography glossary.