When we left off in Part I, the SARS CoV 2 virus had hijacked Type 2 pneumocytes, the surfactant producing cells of the lungs, and made the cells produce more and more virus, eventually destroying the lung cells. As these cells are destroyed, the virus releases a number of chemicals which trigger the body’s immune system to investigate. These chemicals, whose names we do not need to worry about, begin a cascade of changes within the infected body.
Two of those changes will have a dramatic effect on the course of the Covid-19 disease process. The first change is known as vasodilation, which basically means the blood vessels expand. Think of taking a piece of material from an old pair of pantyhose. Leave it in its normal state and it is basically a solid piece of material. But if you were to stretch the material strongly, you would begin to see that the solid material now looks much more like a piece of mesh with a matrix of small openings. This is what happens with the capillaries and other vessels in the lung as well. Just as with the pantyhose, the walls of the vessels expand and we get something called “increased capillary permeability,” which simply means that plasma begins leaking out of the vessels. It leaks out into the area around the blood vessels and into the alveoli as well.
As the fluid leaks into the alveoli and gathers around them, the small breathing sacs begin to get squeezed. In addition, because the cells which create surfactant have been destroyed, the alveoli begin to have trouble holding themselves open. At the same time, the debris from the lung cells destroyed by the virus begin to fill the inside of the cells. Between the fluid building up, the squeezing and collapse of the alveoli, and the debris cluttering the lung cells, it becomes almost impossible for the cells to exchange oxygen and carbon dioxide. This leads to an increased “work of breathing” and a biological state known as hypoxemia, basically an abnormally low level of oxygen in the bloodstream.
At the same time, the body sensing the destruction of the lung cells begins to mount a response with the immune system. Very quickly, the immune system figures out it has no natural antibodies to this virus and instead mounts a brute force attack by rushing soldier cells called neutrophils into the lungs. Lacking specific antibodies which could target the virus alone, the neutrophils release chemicals which are capable of disrupting or destroying a wide number of cells, including the healthy lung tissue. This leads to more and more damaged alveoli, between the virus and the immune response. As the damaged cells begin to fill more and more alveoli with fluid and debris, something called consolidation, larger sections of the lung become incapable of gas exchange adding to the hypoxemia and work of breathing. This leads to shortness of breath and as the body tries to clear the lungs, a wet cough begin as the body tries to eject the fluid and debris built up in the lungs.
Outside the lungs, those chemicals released in the lungs have reached the brain, specifically a region known as the hypothalamus, which for our needs can be thought of as the body’s thermostat. This leads to development of a fever, as the body raises its temperature trying to use heat to kill the invader. By the way, most of us know that average body core temperature is 98.6° F. But fever is a different matter. For medical purposes, any temperature equal to or greater than 100.4° F is considered “fever.”
As the assault on the lungs continues, oxygen levels continue to drop. With oxygen essential for function of all the major organs, the brain acts to compensate for the low oxygen levels by triggering the nervous system to increase heart rate, medically known as tachycardia, and increasing breathing rate, in medical terms called tachypnea. In the majority of cases, things will level off here with the only other major symptom being wracking body aches caused by inflammation as the body sends white blood cells throughout the body to fight the disease process.
In those who have compromised immune systems and contributing factors such as high blood pressure, heart disease, lung disease, diabetes, and kidney disease, things can continue to worsen. As more and more alveoli are attacked by the virus and fill with fluid and debris, we see larger areas of consolidation, what is more commonly known as pneumonia. This is still not a fatal condition, as many will survive Covid-19 pneumonia just as they do from common pneumonia. When consolidation reaches a point where the person can no longer pull in enough oxygen on their own to support their major organ systems, they develop a Acute Respiratory Distress Syndrome, or ARDS. It is ARDS which can lead to a need for ventilator support.
If we get enough inflammation in the lungs, we can see the inflammatory response spread to other parts of the body, leading to septicemia, basically a full blown infection of the body, also called septic shock. As in the lungs, we see both vasodilation and capillary permeability spread from the lungs to the whole body, dumping large amounts of fluids from the blood vessels into the surrounding tissue. This reduces blood volume causing hypotension or low blood pressure and decreased blood flow to major organs, which can lead to organ failure. It is this cascade of failing organs that leads to death from Covid-19
In Part 3, we will look at what one can expect if they get the disease, whether self-isolating at home or ending up in the hospital.