Understanding Cardiovascular Function: A Challenge to Evolution from Coronary Artery Disease
Howard Glicksman August 8, 2015 5:59 AM
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." Dr. Glicksman practices palliative medicine for a hospice organization.
Since the body cannot adequately store oxygen (O2) and is dependent on it for its metabolic needs, determining how much O2 is needed for a given level of activity is a way for medical science to assess functional capacity. At complete rest, the body needs about 250 mL/min of O2 just to keep its vital organs working properly. Slow walking requires 500 mL/min, fast walking 1,000 mL/min, and moderate jogging about 2,000 mL/min of O2. With maximum activity, the kind our earliest ancestors would have needed to win the battle for survival, the body requires about 3,500 mL/min of O2.
These are real numbers that reflect the real amount of O2 needed to perform these levels of activity. If you were trying to explain how the first horseless carriage evolved into a Formula 1 race car, you would not only have to explain how its parts came together to function as a method of transport, but also how it developed the power to overcome the laws of nature and move so quickly.
So too, when it comes to the development of life, providing an explanation of how it looks, as evolutionary biologists claim to have done (through chance and necessity alone), while neglecting how it actually works to overcome the laws of nature to stay alive, should be considered inadequate and frankly, unscientific.
In this series, I have shown that, regarding pulmonary function, when there is diminished airflow speed, and/or effective lung volume, and/or efficiency of gas exchange, this results in a diminished capacity of the body to obtain O2. This in turn limits the body's ability to be very active and its survival capacity as well.
So too, since it is the heart that is responsible for pumping the blood that carries O2 throughout the body, this means that diminished cardiac function likewise places limits on ability. My last article described four common conditions that are commonly responsible for problems with heart function: coronary artery disease, valvular heart disease, heart failure, and cardiac arrhythmias. I will now describe coronary artery disease and show how real numbers can mean debility.
Even though the heart pumps blood throughout the body, it must also supply adequate blood flow to itself so it can do its job. After all, the part of the heart that does the pumping is muscle, called the myocardium. As the blood flows out of the left ventricle, through the aortic valve, the coronary arteries turn back over the surface of the heart. These epicardial vessels supply blood to the myocardium.
The laws of nature demand that the coronary arteries be wide enough to accommodate enough blood flow so the heart can do what it needs to do. As noted previously, at rest, the amount of blood the heart pumps is about 5 L/min. To meet the metabolic needs of the myocardium when the body is at rest the coronary arteries receive about 250 mL/min of this cardiac output. The harder the body works, the harder the myocardium must work, and consequently, the more blood must flow through the coronary arteries to provide enough oxygen and nutrients to meet its metabolic needs.
With increasing activity, from walking slowly and rising to the maximum required for survival, cardiac output must increase to about 25 L/min. This increase in output is controlled by the autonomic nervous system, which stimulates the heart to pump harder, and faster by way of its sympathetic division. However, with maximum activity levels it is also the sympathetic division that relaxes the muscles surrounding the coronary arteries to more than quadruple the blood flowing through them to over 1,000 mL/min.
Just as a clogged fuel line can reduce the flow of gas and compromise engine function, resulting in loss of power to a car, so too, diminished coronary blood flow to any part of the myocardium can compromise the cardiac output, resulting in loss of power to the body. In other words, real numbers have real consequences. If our earliest ancestors could not provide more than 1,000 mL/min of blood flow to the myocardium, they never could have survived to reproduce. How do we know this? We know it from coronary artery disease.
The commonest heart condition in developed countries, and what most people think of when they hear someone has heart trouble, is coronary artery disease. The underlying condition that causes coronary artery disease is called atherosclerosis, commonly referred to as hardening of the arteries. Coronary atherosclerosis is the formation of hard and thick plaques, mainly consisting of fat, along the inner surface (endothelium) of the coronary arteries. These plaques not only cause narrowing and obstruction of blood flow, but can also activate the clotting mechanism within the blood.
The gradual or sudden disruption of a plaque from the endothelial surface and the release of chemicals by the blood cells attached to it can result in the formation of a thrombus (clot). This can further reduce blood flow to the heart muscle, which can lead to severe oxygen deprivation causing myocardial ischemia. If the ischemic injury is sufficient to cause irreversible cell damage, then myocardial tissue death takes place and is called amyocardial infarction, commonly referred to as a heart attack.
As I've already stated, the laws of nature demand that the coronary arteries be wide enough to accommodate enough blood flow so the heart can do what it needs to do. When a person with coronary artery disease performs an activity in which the oxygen demands of the heart exceeds what the coronary blood flow can provide, then ischemia of the myocardium takes place.
Just as pain is experienced from overworking poorly conditioned skeletal muscles, the body usually feels pain when the heart suffers from myocardial ischemia as well. This is called angina pectoris and usually manifests as a severe, tight, squeezing, and constricting pain under the middle of the breast bone (sternum). The pain may radiate across the chest, to either or both sides of the neck, shoulders, down either or both arms, and to the back and upper abdomen as well. It is not unusual for it to be accompanied by shortness of breath, sweating, nausea, fluttering of the heart, and dizziness.
If the activity that provoked the heart and brought on this warning pain is stopped immediately, often the angina will settle without any permanent myocardial damage taking place. However, clinical experience tells us that a person who has limited coronary blood flow is restricted from performing activities that our ancient ancestors would have had to be able to do to survive. In other words, coronary artery disease with its effect on functional capacity allows us to see that certain parameters regarding blood vessel diameter and the coronary blood flow must have been met to allow for survival.
Common sense dictates that to explain how our earliest ancestors came into being and were able to win the battle for survival requires much more than just pointing out how their DNA made their cardiovascular system and all of their other organs and tissues. As we've seen, the mere presence of coronary arteries does not fully explain how the heart muscle is able to receive the blood flow it needs to function adequately and provide for the metabolic needs of the body. What also has to be explained is the simultaneous development of how the body has the knowledge and ability to control its coronary blood flow and cardiac output to meet its different metabolic needs to survive.
However, coronary artery disease is just one of four common conditions that compromise the heart's function and cause debility. Next time we'll look at how the heart valves work.
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