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By Ian Halim

Decades before Tenzing Norgay and Edmund Hillary achieved the first known summit of Mount Everest, disused oxygen tanks began to litter its rarefied slopes. During a 1922 attempt, one intrepid duo tossed the empties down the mountain, recalling later how each canister would ring out, “like a church bell. There goes another 5 lbs. off our backs.”

As mountaineers ascend, the air grows thinner and thinner. The air pressure drops. A breath drawn on the summit of Everest – at 29,032 feet – supplies just one-third of the oxygen found at sea level. As we climb, particularly above 10,000 feet or so, the oxygen level in our body starts to drop. We compensate by breathing faster. But as we climb higher, this isn’t enough. Without supplemental oxygen, we can suffer headaches, weakness, confusion – even death.

Altitude sickness may seem like an obscure topic, but – as we’ll see – it’s a good starting point for understanding how breathing can get disrupted in sleep. When we sleep, our muscles become less active, including some of the muscles that help us breathe. The flaccid tongue can loll back in our throat, and the flesh around our necks can press down upon our airway. When our soft tissues collapse, the passage of air can get blocked up – a bit like fingers pressing on a plastic straw. This is called obstructive sleep apnea. If the soft tissue obstruction is bad enough, our oxygen level dips. So, when some people go to sleep, it’s almost as if they’re up in the mountains.

Summiting Everest without supplemental oxygen is very dangerous. The final three thousand feet of the ascent is within the so-called Death Zone. Oxygen is so scarce here that humans can’t survive for more than a short time without supplemental oxygen. In 1978, an Italian named Reinhold Andreas Messner and an Austrian, Peter Habeler, became the first to conquer Everest unaided by concentrated oxygen.

Similar perils face pilots. As an aviator rises in an open cockpit, temperature and air pressure drop. Oxygen makes up about 21% of the gas in our atmosphere, and nitrogen about 78%. But, as the air grows thinner with rising altitude, there is less and less total gas, and therefore less and less total oxygen, per unit of volume. Early fighter aircraft, like the World War II Royal Airforce plane, the Spitfire, were outfitted with oxygen tanks and masks. And modern jet liners have airtight pressurized cabins, allowing passengers to inhale thicker, more oxygen-rich air, mimicking the conditions at a much lower altitude, even as the plane climbs skyward.

An apnea (pronounced ‘ap·nē·a, with the accent on “app”) is a pause in one’s breathing, from the Greek roots a- “not” and pneō “breathe” (from which we also get “pneumonia” and “pneumatic”). In obstructive sleep apnea, soft tissue collapse within the airway slows or arrests the stream of air again and again during a night’s sleep. Apnea refers not just to the illness, but also to each such pause in our breathing. Too many apneas over the course of a night, and you may wake up feeling unrefreshed, with a headache, or both. It’s easy to think of oxygen dips, which occur during an apnea, as stimulating further breathing.

However, another gas is usually a more important signal telling our body that we must breathe. As we use oxygen to burn up carbon-rich fats and sugars for energy, we’re constantly generating carbon dioxide as a kind of waste product – known to chemists as CO2. Each time we exhale, we “blow off” some of that carbon dioxide gas. And, since we’re always making CO2, but also always exhaling it, its concentration in our blood usually stays fairly steady. CO2 isn’t just a waste product, though. It also acts as a signal telling us to breathe. When we stop breathing for some reason, our oxygen level not only dips, we also stop exhaling CO2. The level of CO2 in our blood rises. Both these changes act like alarm bells – increasing our drive to breathe.

Carbon dioxide is so critical in this way that if we breathe too fast for too long, we can exhale so much CO2, and its level can drop so much, that we actually lose our drive to breathe. For some moments, we stop breathing. Anytime our brain doesn’t tell us to breathe, such as because of low blood CO2, this is known as a central apnea (so called for the central nervous system, which includes the brain and spinal cord).

If all of this sounds a mite abstract, you can imagine carbon dioxide and oxygen as a pair of coxswains, positioned at the front of a racing shell, facing the athletes arrayed at their oars. They call out “breathe! breathe!” resounding across the open water. CO2 is usually more important than oxygen in driving our breathing, so you can imagine that coxswain as larger and louder – with CO2 emblazoned on her jersey.

We can use the image of the two coxswains to understand what happens in obstructive sleep apnea. Each time our airway gets blocked, we stop inhaling. The level of oxygen in our blood falls, and the voice of the smaller coxswain gets louder. At the same time, we also stop exhaling, so CO2 rises, and the voice of the larger coxswain gets louder, yelling, “Breathe! Breathe!” As a result of the two shouting coxswains, we work harder to breathe against the collapsed airway, and we may even be able to force it open again, restoring our blood oxygen level, and lowering our CO2.

But this system has a kind of loophole that can work against us during sleep or at high altitude. Sometimes, when the air is very thin at high altitude, or when a collapsing airway triggers a drop in oxygen, this can cause a series of rapid breaths. Although this can help restore blood oxygen, a person may also “blow off” so much carbon dioxide that they lose the drive to breathe entirely. If CO2 drops too low, the voice of the bigger coxswain goes silent. The drive to breathe falters and our brain stops telling us to breathe – the central apnea we’ve already talked about.

Sometimes, this cycle can repeat over and over. Each time, low oxygen triggers a burst of rapid breaths, lowering CO2 and causing a central pause in our breathing. During this pause, oxygen dips, and can trigger another series of rapid breaths. And so on. This is known as periodic breathing. It can be a complication of obstructive sleep apnea, or of heart failure. It’s also common at high altitude, or it can be a primary genetic problem.

Obstructive sleep apnea with this kind of cyclical pattern of rapid breaths and central pauses in our breathing is a double hit. We stop breathing over and over again during the course of the night – sometimes when our airway collapses, sometimes because our brain interprets dips in CO2 as a signal to pause breathing. Both obstructive and central apneas awaken us partly or fully, and both degrade our sleep quality. Some people with obstructive sleep apnea say they wake up in the morning feeling worse than when they went to bed.

Thankfully, all is not lost. In fact, some of the management is similar for periodic breathing at high altitude and in obstructive sleep apnea. A medicine called acetazolamide helps prevent our body from interpreting low carbon dioxide as a signal not to breathe. This helps keep us from having central pauses, including the central apneas that punctuate cycles of rapid breaths in periodic breathing.

Another approach is to directly increase the level of carbon dioxide in the body. Dr. Robert Thomas at Beth Israel Deaconess’s sleep medicine clinic (where I trained over the past year) has pioneered just such controlled delivery of carbon dioxide during sleep. This approach stabilizes and slightly increases the blood carbon dioxide, by allowing someone to inhale some of their own exhaled carbon dioxide. Or, in another approach, a small, controlled stream of carbon dioxide is actually channeled into a patient’s inhalations from an external source. This helps nudge the larger coxswain to keep calling out, “Breathe! 2, 3 Breathe! 2, 3”