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Understanding Respiration: Why Real Numbers Can Mean Debility and Death


Editor’s note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that’s because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News & Views is delighted to present this series, “The Designed Body.” For the complete series, see here. Dr. Glicksman practices palliative medicine for a hospice organization.

The trillions of cells in your body are made up of matter and must therefore follow the laws of nature. These laws demand that to do what it needs to do to survive, our body needs sufficient energy. And one of the main things it needs to get that energy is oxygen (O2). The body gets O2 by breathing it in through the lungs. The respiratory center in the brain monitors the levels of O2, carbon dioxide (CO2) and hydrogen ion (H+) and orders the muscles of respiration to contract at the proper rate and depth to keep these chemicals where they need to be for survival.

the-designed-body4.jpgIn my last article in this series I showed that the respiratory system has the capacity to provide the body with the amount of O2 it needs to perform the kinds of activities our ancient ancestors would have needed to survive. But what happens when it can’t? That’s when real numbers unfortunately result in debility and even death.

A car’s performance is related to at least three things: the speed at which air and gas enter the engine, the size and number of the cylinders, and the efficiency of the transmission and differential, resulting in wheel rotation. Similarly, the functional capacity of the respiratory system is determined by the speed of airflow into and out of the lungs, the effective lung volume, and the efficiency of gas exchange. Just as a car needs all three of these factors to be at a certain level to meet certain performance standards, so too the respiratory system must have each of its three within a certain range to provide the body with enough O2, get rid of enough CO2, and control the H+ ion level.

Medical science has developed lung function tests that allow it to determine how these three factors may affect performance. A person takes in a maximal breath and then blows out as fast as they can. The air expired within one second is a measure of airflow speed and is called the FEV1 (Forced Expiratory Volume in 1 second). A normal FEV1 is about 3-4 liters. The total air expired (usually within 2-3 seconds) measures the effective lung volume and is called the FVC (Forced Vital Capacity). A normal FVC is about 4-5 liters. Note that the total lung volume is normally about 5-6 liters, but the lungs don’t fully deflate, usually leaving about one liter of residual air. Breathing in air with a small amount of carbon monoxide (CO) and measuring how much CO is in the air that is breathed out determines the DLCO (Diffusion capacity of the Lung for CO). This is a measure of the efficiency of gas exchange between the alveoli and the capillaries. The expected DLCO is 100 percent of normal.

When the body is at complete rest it uses 250 mL/min of O2. Slow walking requires 500 mL/min, fast walking 1,000 mL/min, and moderate running about 2,000 mL/min. To be maximally active, the body needs to use at least 3,500 mL/min of O2.

All things being equal, a person with a normal FEV1, FVC, and DLCO should be able to acquire enough O2 to reach the above levels of activity. But, a deficiency in one or more of these functional parameters will result in our not being able to obtain the required level of O2 to maintain high levels of activity. For example, people who smoke often develop COPD (chronic obstructive lung disease). The mucosal lining of the airways thickens, producing more mucus, and the muscles surrounding the airways tend to contract, causing bronchospasm. Together these actions reduce the opening in the airway and with it the speed of airflow.

Early in COPD, an FEV1 that has dropped to 2-3 liters (normal is 3-4 liters) will cause mild physical impairment. This means significant shortness of breath when trying to be very active, like suddenly running to catch a bus. An FEV1 of 1-2 liters will cause moderate physical limitation, having to rest intermittently while walking slowly and having problems going up stairs. A drop in the FEV1 below 1 liter causes severe physical impairment — severe shortness of breath when slowly walking just a few feet and sometimes even when talking.

All of this happens because a reduced FEV1 means that the lungs can’t move air in and out fast enough to match the O2 needs of the body for that level of activity. Depending on the degree, similar levels of physical impairment occur when the FVC or DLCO is reduced. People with neuromuscular disease (e.g., multiple sclerosis, Lou Gehrig’s disease, muscular dystrophy) aren’t able to move their lungs very well, due to weakness, so their effective lung volume (FVC) is reduced. And people with conditions that cause damage to the alveoli (e.g., emphysema, pulmonary fibrosis) have a reduced DLCO and therefore a reduced efficiency in gas exchange. Many people, particularly those who smoke, have a reduction in all three of these pulmonary function parameters, which explains why they have so much physical debility.

An acute insult, such as pneumonia, on top of a chronically impaired respiratory system, can place a person into acute respiratory failure. This usually means that ventilation of the lungs and gas exchange are severely impaired, which causes the O2 level to drop, and the CO2 and H+ ion levels to rise, to dangerous levels. As the O2 level drops below 50 units, problems with concentration, lethargy, and confusion begin. If it continues to drop past 40 units and beyond, then stupor, coma, and ultimately death takes place due to permanent brain injury and respiratory arrest.

Likewise, when the CO2 and H+ levels rise over 50 units and continue toward 90 units or more, the same phases of brain malfunction and death are the result. It’s important to keep in mind that, quite often, all three of these life-threatening changes take place at the same time, delivering three separate chemical blows to the cells, and so sometimes in this situation cardiac function succumbs first. Either way, the final result is cardiopulmonary arrest and brain death.

Now may be a good time for you to consider what’s needed for you to be able to get enough O2 to your cells. How well has evolutionary biology explained their gradual development within intermediate organisms that were able to reproduce?

First, the chemoreceptors are placed exactly where they need to be to detect O2, CO2, and H+ ion. Second, the respiratory center, with its knowledge of what the levels of O2, CO2 and H+ ion should be for survival, integrates the data and sends out orders to the muscles of respiration. And third, there are all of the working parts of the respiratory system. But is that really enough?

We’ve seen that, as with a car and other machines, certain specifications — in this case relating to airflow speed (FEV1), effective lung volume (FVC), and the efficiency of gas exchange DLCO) — must be met as well. However, getting enough O2 to pass from the lungs into the bloodstream really only solves half of the problem. For, the laws of nature present a further obstacle for which the body must come up with another innovation. That’s what we’ll look at next time.

Image by Hans Rudi Erdt (1883-1925) [Public domain], via Wikimedia Commons.