How Does Hypoventilation Cause Hypoxemia?

I often find that my students sometimes confuse oxygenation and ventilation as the same process. In reality they are really very different. Ventilation exchanges air between the lungs and the atmosphere so that oxygen can be absorbed and carbon dioxide can be eliminated. Oxygenation is simply the addition of oxygen to the body. You must understand the difference to understand how hypoventilation causes hypoxia.

If you hyperventilate with room air, you will lower your arterial carbon dioxide content (PaCO2) significantly, but your oxygen levels won’t change much at all. On the other hand, if  you breathe a high concentration of oxygen, but don’t increase or decrease your respiratory rate, your arterial oxygen content (PaO2) will greatly increase, but your PaCO2 won’t change.

Ventilation changes PaCO2. Oxygenation changes PaO2.

Why do we need to understand this? Let’s look at some common examples. Along the way we will painlessly use the Alveolar Gas Equation to explain two common scenarios:

  • how hypoventilation causes hypoxia,
  • why abruptly taking all supplemental oxygen away from a carbon dioxide retainer will hurt them.

How Does Hypoventilation Cause Hypoxemia?

Hypoventilation is a common cause of too little oxygen in the blood. When breathing room air, CO2 takes up space in the alveoli, leaving less room for oxygen. Let’s see how big an effect this is. The concentration of oxygen in the alveoli can be calculated using the Alveolar Gas Equation:

PAO2 = FiO2 (PB – PH2O) – PACO2/ R

  • Where: PAO2 = partial pressure of oxygen in the alveoli
  • FiO2 = concentration of inspired oxygen
  • PB = the barometric pressure where the patient is breathing
  • PH2O = the partial pressure of water in the air (usually 47 mmHg)
  • PACO2 = alveolar carbon dioxide tension
  • R = respiratory quotient, a constant usually assumed to be 0.8

Let’s say that our emergency room patient with a narcotic overdose, at sea level and breathing room air, has an alveolar PACO2 of 80 mmHg, or twice normal. That carbon dioxide takes up space and leaves less room for oxygen.

Using the Alveolar Gas Equation, that PAO2 calculation is:

PAO2 = 0.21 (760 – 47) – 80/0.8 = 49 mmHg

Normal PAO2 is about 100 mmHg, so this is quite hypoxic, especially since the alveolar PAO2 is always a little higher than the arterial PaO2. If it weren’t, oxygen would not flow out of the alveoli into the blood — it would stay in the alveoli.

Now let’s treat this patient with 50% oxygen and see what happens:

PAO2 = 0.5 (760 – 47) – 80/0.8 = 256 mmHg

That’s a five-fold increase in alveolar oxygen without changing ventilation at all. Putting the patient on oxygen will buy you time for treatment. If this is a quickly reversible process, such as a narcotic overdose, you may not need to intubate. However, if this is not quickly reversible, then oxygen protects brain and heart while you manually ventilate or intubate.

This is also a good time to point out that a patient can have a normal oxygen saturation and even a normal arterial oxygen concentration and still be in respiratory distress or failure because ventilation and CO2 elimination is failing. In the above example our treated patient’s O2 saturation would be 100%, but with a PaCO2 of 80 mmHg, the pH would be about 7, a dangerous and potentially life-threatening respiratory acidosis. Don’t be lulled into missing a patient’s tenuous status just because the oxygen saturation looks good. Hypoventilation can eventually cause hypoxia.

The Challenge of the CO2 Retainer

Now let’s look at a CO2 retaining emphysema patient relying on hypoxic drive — which by the way, is only a very small minority of patients with end stage pulmonary disease. This patient was in respiratory distress from pneumonia with an arterial PaO2 of 65 mmHg upon arrival to the hospital. The nurse placed her on 50% oxygen.

After oxygen therapy, her blood gas shows her PaO2 is now 256 (good) and her PaCO2 is now 80 (bad) and she’s getting sleepy, probably from the high CO2. The high oxygen levels have decreased this particular patient’s drive to breathe.

Seeing CO2 retention, the nurse might be tempted to take all the oxygen off this patient in order to stimulate her breathing and get her CO2 down — but that would be the wrong thing to do. Why?

As we saw in the calculation above, we’d expect the alveolar PAO2 to abruptly drop to 49 with this change. A better way to deal with this situation would be to wean the oxygen back slowly, maintaining a good oxygen level while allowing the respiratory drive to improve. Keep reminding the patient to take deep breaths. Intubation might still be needed so watch the patient carefully.

Never let the fear of CO2 retention stop you from treating a COPD patient with oxygen in an emergency. The vast majority of patients with COPD do not retain CO2. And even if the patient you happen to be treating does retain CO2, the worst-case scenario is that you relieve their hypoxia and protect their brain and heart (good) but might have to temporarily assist ventilation.

May The Force Be With You

Christine E. Whitten MD
author of Anyone Can Intubate: A Step By Step Guide, 5th Edition &
Pediatric Airway Management: A Step-by-Step Guide

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20 thoughts on “How Does Hypoventilation Cause Hypoxemia?”

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  3. Thank you for all of,them but i need much more to understanding.Iam Tabriz univercity in Iran.

    1. Ventilation and oxygenation are two different processes, both essential. Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. A patient with opioid overdose, for example, will have respiratory failure with hypoventilation, but if provided supplemental oxygen may still maintain an adequate or even normal oxygen saturation for a while before it too starts to fail. Check out this article on my site for a more full explantation:

    2. Ventilation and oxygenation are different. Oxygenation is adding oxygen to the system. Ventilation is exchanging gas and removing CO2. Starting with the most extreme example, if the patient’s lungs have been completely preoxygenated and filled with oxygen, but they are apneic, then there will be a period of time when CO2 is rising, but there is still enough oxygen in the lungs to maintain an oxygen saturation above 100%. Remember that you can have an oxygen saturation of 100% if the PaO2 is 100 or if it is 500. It’s an insensitive measure. Only once the amount of oxygen in the lungs falls far enough so that saturation starts to fall will we see the problem. That’s why we have to keep a close eye on patients who are predisposed to respiratory compromise.

  4. Why does the CO2 in the alveoli “take up the room” of the O2, and not the other way around? And does the H2O in the alveoli displace both CO2 and O2, as suggested by the fact that we always subtract 47 mmHg (at 37 degrees C) from the barometric pressure first, before doing further calculations?

    1. The volume of each the gases in the alveoli contribute to the total volume of as in the alveoli. CO2, H20 AND O2, and even Nitrogen, when breathing room air, all take up room. As oxygen is absorbed from the alveoli into the bloodstream, the volume of oxygen goes down. As CO2 is transferred from blood to the alveoli, its volume goes up. As the alveoli empty during exhalation, we are exhaling the combination, which at the time of exhalation usually contains more CO2 than oxygen. When we then inhale, we are bringing in more oxygen than CO2. the relative volumes are constantly in flux as we inhale and exhale.
      For example, when we inhale room air, we are inhaling an FiO2 of 21% and exhaling at rest on average an FiO2 of about 17%.If we are doing mouth to mouth ventilation, the breath we give our victim contains about 17% FiO2- which is why its so important that the rescuer take a deep breath breath themselves between rescue breaths- otherwise the FiO2 of the second breath will be lower still.
      With atelectasis, alveoli are blocked and all of the oxygen gets absorbed, allowing collapse of those alveolus.

      1. Dr. Whitten, just found your site and am currently struggling with A&P respiratory physiology. Thank you for this resource! quick question on the last part of your comment, why would it be so important to take a deeper breath when providing rescue breathing besides the lower FiO2? Is it because the mixture of gases at the upper portions of the lungs would contain more CO2?

        Thank you!

      2. Thank you for your question. The tidal volume of a manual breath must be big enough to provide alveolar ventilation, and this means it must include a volume bigger than that patient’s anatomic dead space as well as the volume of dead space of the equipment you are using at the time. If not, then the air in the provided breath simply moves back and forth within a space that cannot absorb oxygen (i.e. the nose, mouth, trachea, mask and any attachments) and the patient will hypoventilate. A larger than average tidal volume also helps prevent alveolar collapse from atelectasis. On the other hand, the breath must be small enough to avoid over-filling the lungs and producing potential barotrauma.
        For a more detailed discussion of these topics see these prior articles on anatomic dead-space, equipment dead space, and ventilation perfusion mismatch:

  5. Found your page here looking for data on the effects on carbon dioxide elimination caused by the masks everyone is wearing. I can’t imagine it’s healthy to restrict airflow. I saw some guy jogging wearing one!

    1. I have worn a mask in the OR almost daily for the last 40 years. One gets used to wearing a mask and in time you don’t even notice it’s on. Don’t worry. It will not effect your oxygen or carbon dioxide levels. Stay safe.

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