The main determinant of end-tidal CO2 (ETCO2) during CPR is cardiac output, specifically how much blood flows through the lungs as a result of chest compressions. During cardiac arrest, the body’s ability to deliver CO2 from the tissues to the lungs becomes the rate-limiting step in CO2 elimination. Because ventilation is being provided mechanically, the amount of CO2 that reaches the lungs depends almost entirely on how much blood the chest compressions are pushing forward. This makes ETCO2 a real-time surrogate for the effectiveness of circulation during resuscitation.
Why Pulmonary Blood Flow Is the Limiting Factor
CO2 is constantly produced by cells throughout the body. Under normal circumstances, the bloodstream carries it to the lungs, where it’s exhaled. Three things have to happen for CO2 to show up on an exhaled breath measurement: the tissues have to produce it, the circulation has to transport it to the lungs, and the lungs have to ventilate it out. During cardiac arrest, production continues (at a reduced rate) and ventilation is being supplied by the rescuer, so the bottleneck shifts to transport. The decreased delivery of CO2 to the lungs is the major, rate-limiting determinant of the ETCO2 reading during low-flow states like cardiac arrest.
As circulation improves, whether from better compressions or from return of spontaneous circulation (ROSC), more CO2 reaches the alveoli and the ETCO2 number climbs. Once adequate cardiac output is restored, the rate-limiting factor flips back to ventilation, particularly after the initial washout of CO2 that has been accumulating in the tissues.
How Compression Quality Affects the Reading
Since ETCO2 tracks blood flow through the lungs, it responds to the quality of chest compressions. Research has examined how compression depth, rate, and chest wall recoil each contribute. Interestingly, the strongest predictor of ETCO2 among compression mechanics appears to be recoil velocity, the speed at which the chest returns to its resting position after each compression. One study found a strong linear correlation between recoil velocity and ETCO2 (r = .61), while the correlation between compression depth alone and ETCO2 was weaker (r = .23). A model incorporating rate, depth, and recoil velocity together showed excellent performance, suggesting that recoil velocity is the primary driver of stroke volume during compressions.
The relationship between compression rate and ETCO2 is not straightforward. It follows a curved (parabolic) pattern, meaning there’s a sweet spot. Compressing too fast can reduce the time for the chest to fully recoil and refill with blood, which ultimately lowers the volume of blood pushed to the lungs with each compression.
Using ETCO2 to Gauge Resuscitation Progress
Because ETCO2 reflects perfusion in real time, specific thresholds have clinical meaning. Initial values below 10 mmHg correlate with poor outcomes, while values above 20 mmHg are associated with higher blood pressures during CPR and improved survival chances. A sudden, sustained jump in ETCO2 during resuscitation often signals ROSC, as the heart begins generating its own cardiac output and flushes accumulated CO2 from the tissues into the lungs.
On the other end, persistently low readings carry prognostic weight. If ETCO2 remains below 10 mmHg after 20 minutes of CPR, resuscitation is almost universally unsuccessful. That said, the 2025 American Heart Association guidelines emphasize that ETCO2 should not be used in isolation to terminate resuscitative efforts, because several confounding factors can artificially suppress or inflate the reading.
Factors That Distort the Reading
While cardiac output is the dominant determinant, several other variables can shift ETCO2 independent of actual perfusion, making interpretation less straightforward.
Epinephrine
The effect of epinephrine on ETCO2 is inconsistent across studies. Some animal research shows that epinephrine significantly decreases ETCO2 by causing a mismatch between ventilation and blood flow in the lungs, essentially redirecting blood away from well-ventilated areas. Other studies have found no change or even a brief increase after the first dose. The most likely explanation for a drop is that epinephrine constricts pulmonary blood vessels, increasing the amount of lung tissue that receives air but no blood (dead space), which lowers the CO2 in exhaled breath even if overall circulation has improved.
Ventilation Rate
Faster ventilation dilutes the CO2 in each breath. ETCO2 decays exponentially as ventilation rate increases, meaning that hyperventilation, a common problem during the stress of resuscitation, can drive ETCO2 readings down and make perfusion appear worse than it actually is. This is one reason capnography readings must be interpreted alongside ventilation rate.
Sodium Bicarbonate
Giving sodium bicarbonate produces a dramatic and sustained spike in ETCO2. When bicarbonate reacts with acid in the blood, it generates a surge of CO2 that floods the lungs. In one study, ETCO2 doubled from a median of 15 to 41 mmHg in patients receiving CPR after bicarbonate administration. The rise began within about 17 seconds, peaked around 35 seconds, and stayed elevated above 20% of baseline for roughly 7 minutes. During that window, ETCO2 is unreliable as a perfusion indicator.
Pulmonary Embolism
When the cause of cardiac arrest is a massive pulmonary embolism, ETCO2 readings are disproportionately low because the clot physically blocks blood from reaching the gas-exchange areas of the lungs. In animal models, ETCO2 during CPR after cardiac arrest from PE was dramatically lower (around 6.5 mmHg) compared to cardiac arrest from other causes (around 34 mmHg at the same blood pressure). This means a very low ETCO2 during CPR could be a clue pointing toward PE as the underlying cause, but it also means the number underrepresents whatever cardiac output the compressions are generating.
Putting It All Together
ETCO2 during CPR is fundamentally a measure of how much blood your chest compressions are moving through the lungs. It rises when compressions are effective, spikes when the heart restarts, and stays flat when perfusion is poor. But it’s not a pure signal. Medications, ventilation technique, and the underlying cause of the arrest can all push the number up or down independently of actual blood flow. Reading ETCO2 during resuscitation means understanding that cardiac output is the main driver while accounting for the noise created by everything else happening at the same time.