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.
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.
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