There is often a great deal of confusion about how to manage the care of a patient with COPD because of concern about inducing CO2 retention. This fear of causing CO2 retention sometimes causes providers to withhold or withdraw oxygen inappropriately. Understanding some of the respiratory physiology behind CO2 retention will allow you to make more informed decisions. Let’s start at the beginning. Some of this material comes from my book Anyone Can Intubate, 5th Edition.
What Factors Control Breathing?
Respiration varies throughout the course of the day depending on the body’s needs and on the feedback signals received by the brain. Given the importance of maintaining normal oxygen, CO2, and pH, it should not be surprising that the most important stimuli for respiration are the level of oxygen, the level of CO2, and the acid/base balance in the blood.
Breathing is controlled by 4 main centers in the body: the chemoreceptors of the central respiratory center (inside the brain), the peripheral chemoreceptors (outside the brain), the brain itself, and the lungs. A chemoreceptor is a receptor that responds to change in the chemical composition of the blood or other fluid around it. The build-up of CO2 (hypercapnia or hypercarbia) and decrease of O2 in the circulation (hypoxia) are two of the strongest stimuli to increase respiratory rate.
The respiratory “center” is found in the midbrain, comprised of sections of both the medulla and pons. Central chemoreceptors are surrounded by brain extracellular fluid, or fluid outside the cells.
You would think that PaO2 level would be the major driving force to breathe, but it’s not. Central chemoreceptors don’t respond to changes in blood oxygen, they respond to changes in pH. As CO2 diffuses out of the brain’s capillaries, it changes the pH of this extracellular fluid (fluid outside the cells). As CO2 accumulates, pH goes down, becoming more acidic. A pH more acidic (lower) than the normal pH of 7.35-7.45, stimulates ventilation. A higher (more basic) pH inhibits ventilation.
Because of its effect on the pH, the most powerful stimulus to breathe tends to be the level of carbon dioxide in the bloodstream (PaCO2). Under most conditions CO2 is tightly controlled. Small changes in arterial CO2 cause significant changes in pH and thus in respiratory drive.
The sensors detecting the oxygen tension in the arterial blood (PaO2) are peripheral chemoreceptors located in the carotid bodies at the bifurcation (first major branch point) of the carotid artery, and at the thoracic curve of the aorta. Information from the carotid and aortic bodies is believed to regulate breathing by the respiratory control center, breath by breath.
The conscious brain plays a minor role in respiratory control. We all can decide to consciously hyperventilate and then hold our breath for a while, but only for so long. Breathing is for the most part an automatic reflex. We can’t really hold our breath until we “turn blue in the face”. In fact, the reflex is so strong it’s hard to consciously stop breathing for any length of time.
Finally, the lung contains receptors that trigger protective mechanisms. Inhaling an irritating substance causes coughing, breath holding, and sneezing. Other receptors located in the smooth muscle of the airways are sensitive to stretch. The Hering–Breuer reflex actively inhibits inspiration once a certain lung stretch occurs, allowing expiration to occur and preventing over inflation.
What Is CO2 Retention
CO2 retention is a problem for a small number of COPD patients. As we all know the lungs eliminate CO2 from the body. COPD can effect how efficiently the lungs work either by having airways blocked by secretions and inflammation (chronic bronchitis) or by breakdown between the septa of alveoli thereby decreasing surface area for exchange (emphysema), or both. In severe cases, gas exchange in the lungs is impaired to the extent that CO2 builds up in the bloodstream as a chronic condition. These patients are termed CO2 retainers because quite literally their bodies retain more CO2 than normal. These patients therefore have a lower, more acidic, baseline pH. They also, by virtue of their impaired gas exchange, tend to have lower oxygen levels, often with chronic hypoxia.
COPD patients with chronic ventilatory failure clinically adapt metabolically to chronic hypercarbia and hypoxia. As we saw earlier, the main driver for breathing in the normal person is pH. In the CO2 retainer, because the body gets used to living at a chronically low pH, the driver changes to arterial oxygen level, which is a much less effective driver simply because of how the respiratory control center works. The problem with the CO2 retainer is that when you give them excess oxygen to breathe, as you might when they get sick, you can remove some of their drive to breathe. They may therefore either breathe less or stop breathing.
Knowing this, providers often fear to give oxygen to patients with COPD. However, when patients with COPD become ill, they can easily hypoventilate and develop worsened hypoxemia/hypoxia requiring oxygen therapy. To understand why it’s bad to withhold oxygen when treating a CO2 retainer with respiratory decompensation let’s look quickly (and painlessly I promise) at the alveolar gas equation.
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
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 CO2 takes up space and leave less room for O2. The PAO2 calculation is:
PAO2 = .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. 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 O2 sat and even a normal PaO2 and still be in respiratory distress or failure because ventilation and CO2 elimination is failing. In the above example our treated patient’s O2 sat 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 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 a 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 be needed so watch the patient carefully.
Now that was a fairly long discussion, but I hope it helps you see how understanding some of the physiology behind hypoventilation and CO2 retention helps you to better treat your patient. Never let the fear of CO2 retention stop you from treating a COPD patient with oxygen in an emergency. First, the vast majority of patients with COPD do not retain CO2.
If you think your patient is a CO2 retainer and that your patient needs oxygen, start slowly and monitor the effect. 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. If you think your patient is retaining more CO2, withdraw supplemental oxygen slowly while supporting ventilation as appropriate.
May The Force Be With You
Christine Whitten MD
Author Anyone Can Intubate