(Updated for 2025)
When we have too much Carbon Dioxide (CO2) in our body, that’s referred to as Hypercapnia. Elevated CO2 levels can happen from several causes, but the one we want to focus on in this article is rebreathing our own exhaled CO2. This can typically happen when a patient is on a traditional oxygen mask like a simple mask or a non-rebreather mask and the respective mandatory minimum oxygen flow rates of 5lpm or 10lpm respectively are not being maintained.
When flow rates are set below these mandatory minimums, then there’s not enough flow to wash out the CO2 from a patient’s last exhaled breath out of the mask before they need to take their next inhalation, and therefore, they rebreathe part of that CO2 remnant left in the mask cavity. Rebreathing CO2 can have a number of both acute and chronic effects on a patient’s cardiovascular and respiratory health, causing different levels of cognitive impairment, and cellular and metabolic changes.
In this article, we’ll investigate all these effects in greater detail, but first, we need to establish how CO2 fits in terms of how our body works, so we can see how too much of it can have harmful consequences.
Carbon Dioxide Production
Carbon Dioxide (CO2) is formed intracellularly in the human body as a metabolism byproduct. We breathe in Oxygen (O2) to fuel organs and tissues. When cellular respiration occurs at the tissue level using nutrients such as Glucose (C6H12O6) and O2 to produce energy, a byproduct of that energy reaction is CO2.1
C6H12O6 + 6O2 → 6CO2 + 6H2O + ATP
The bloodstream then transports CO2 to the lungs, where it normally is removed from the body as a waste product during exhalation. CO2 affects various body processes, including blood pH, respiration, metabolic responses, perfusion, and the hemoglobin’s affinity for O21. Fluctuations in CO2 therefore can cause significant disturbances in many of the body’s processes.
Normally, a patient’s arterial CO2 levels ( PaCO2 ) = 35-45mmHg. Technically, any PaCO2 > 45mmHg could be considered Hypercapnic, and even at mildly elevated levels, this could cause symptoms like headache, shortness of breath, flushed appearance and increased heart rate (HR) and blood pressure (BP)3. When PaCO2 levels get > 60mmHg, especially for patients with chronic respiratory conditions like chronic obstructive pulmonary disease (COPD), then the effects of Hypercapnia become more pronounced and can cascade into severe adverse events that can include conditions such as respiratory failure or even coma, causing an increased risk of mortality.
What really happens when a patient becomes Hypercapnic?
Cardiovascular Effects:
- Increased CO2 can cause a “sympathetic activation” which will increase HR and BP initially, but if prolonged, could lead to arrhythmias, decrease myocardial contractility and possible Cardiac Arrest.
- Hypercapnia will increase pulmonary vasoconstriction, which will cause increased right-sided heart pressure.2
Neurological Effects:
- CO2 is a potent cerebral vasodilator, thereby increasing cerebral blood flow and potentially increasing intracranial pressure.
- This can cause everything from mild to major headaches, confusion, dizziness, lethargy and agitation, impaired fine motor control and in severe cases can lead to seizures or coma.
- Hypercapnia will also cause an initial increase in respiratory drive from increased stimulation of H+/CO2 increases to the medulla’s central respiratory centre’s chemoreceptors; with an eventual depressed respiratory drive as severity/duration causes decreased consciousness.2
Respiratory Effects:
- When CO2 levels are increased, there is a right shift in the bicarbonate-carbon dioxide buffering system that normally helps the body maintain normalized pH:
CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3–
- This right shift increases production of bicarbonate, but also increases hydrogen ion concentrations which lowers blood pH – resulting in a Respiratory Acidosis
- Respiratory Acidosis will cause the body to respond by increasing respiratory rate (RR) and minute ventilation (hyperventilation) in an attempt to compensate. If the Acidosis continues however, this ineffective dyspnea will lead to Hypoxemia and Respiratory Failure.
- Respiratory Acidosis can also impede cellular enzyme function and other cellular activities.
- Elevated CO2 levels in the blood and acidity in the blood also creates a right shift in the oxyhemoglobin dissociation curve, which causes a decreased affinity for O2 to bind to hemoglobin and an unloading of oxygen to the tissues.2 (Bohr effect) If O2 has a tougher time binding to hemoglobin, this will accentuate the hastening of Hypoxemia.
- With less O2 binding to hemoglobin, then CO2 can more readily bind tighter to the hemoglobin, thus potentially further increasing PaCO2 and worsening the acidotic state. (Haldane effect)
Other effects:
- Flushed appearance; muscle twitching/spasm; fatigue, organ damage
- Accelerated immunosuppression in some cases and potential for bacterial proliferation in patients already septic.4
So it’s pretty clear that the effects of CO2 rebreathing are both widespread throughout multiple body systems, with potentially severe consequences. But how can we prevent CO2 rebreathing, and hence, this cascade of extreme events, from occurring? One way is to ensure that the right mask will always be chosen for the right patient at every moment in their acuity journey while in a Hospital’s care. And every time a patient uses an oxygen mask, that oxygen flows are set according to the instructions for use, and that errors in titrating oxygen never happen.
Well, we know that’s not realistic and traditional oxygen masks are both limiting in how much oxygen they can deliver, and error prone for many disciplines of clinicians to never, ever make a mistake in titrating someone’s oxygen below a mandatory minimum setting for every type of device. So there needs to be a better way…
And there is!
The Solution to the Decades-old Problem of CO2 Rebreathing
That’s where Oxy2Mask comes in! With Oxy2Mask we’ve engineered-out CO2 re-breathing—without engineering-in new errors.
For six decades we’ve accepted that delivering oxygen means juggling multiple mask types, memorizing minimum-flow rules, and hoping no one forgets to turn the dial up far enough to flush CO2.
That compromise stops here.
Oxy2Mask flips the script by starting with a single, open-design interface that vents every exhale, adapts to any flow, and all but eliminates the two things we clinicians dread—rebreathing-induced hypercapnia and device-swap errors.
Here’s why it’s the better oxygen mask in practice, not just in theory:
Open Mask Design
Oxy2Mask’s open mask design vents every exhale instantly, so CO2 never pools in the mask—dramatically cutting rebreathing risk while keeping patients clear-headed and safe. The feather-light frame uses no valves or reservoir bag, letting prescribed oxygen blend naturally with entrained room air; your flow-rate setting and the patient’s own inspiratory demand determine the final FiO2 without swapping devices. One mask, fewer parts, better breaths.
1–15 + L min-1 flow range, 24–90% FiO2
One mask now covers nasal-cannula to NRB territory. Clinicians dial in any acuity—from chronic COPD titration up to pre-intubation pre-oxygenation—without changing interfaces.
Error-proof oxygen therapy
Because there is no mandatory minimum flow, accidental under-flow can’t trigger hypercapnia. Mixed-skill teams (EMS, wards, PACU) get the same simple rule: set the flow your patient needs, period.
Better for patients
- Easier to talk and drink: The open design lets patients communicate and sip fluids, boosting compliance and reducing claustrophobia.
- Cooler, lighter, kinder to skin: No heavy plastic shell, fewer pressure points.
Better for hospitals & our planet
One Oxy2Mask often replaces three legacy devices across an admission, cutting procurement SKUs, training burden, and single-use plastic waste.
Let’s Put an End to CO2 Rebreathing
Traditional oxygen masks solved a 1960s problem—and baked hypercapnia risk into every low-flow setting. Oxy2Mask solves a 2025 reality: complex patients, tight staffing, and zero tolerance for preventable harm.
By venting exhaled CO2, eliminating minimum-flow rules, and spanning the full FiO2 spectrum, Oxy2Mask gives clinicians one simple, safer interface and gives patients the comfort and confidence they deserve. Discover the better oxygen mask at thebetteroxygenmask.com.
References:
- Patel, S., et al; Physiology, Carbon Dioxide Retention ; StatPearls – National Library of Medicine, 2022
- Feller-Kopman, DJ, et al; Mechanisms, causes and effects of Hypercapnia; Uptodate.com, 2025
- Snow, S., et al; Exploring the physiological, neurophysiological + cognitive effects of increased carbon dioxide concentrations indoors; Building + Environment, Vol 156, pg. 243-252, 2019
- Marhong, J.; Carbon Dioxide in the Critically Ill: too much or too little of a good thing?; Respiratory Care 59(10 ), pg. 1597-1605, 2014