Final Words

We get the view from the head of the bed. So, that means we are the ones who intubate. Well, where I work we do not intubate. But we are the ones who assist with all intubations. So, when a COVID patient needs to be intubated, we are there at the head of the bed. 

COVID patients are generally with it all the way to intubation. So, we RTs get to see firsthand what a person does just prior to being intubated. In most cases, COVID patients are in the hospital for a while before being intubated. In other words, we try everything else. And then it gets to the point they need to be intubated. 

Perhaps the hardest part is the fact we get to know these patients. This was a year ago. And back then, COVID patients weren't allowed, visitors. So, when I entered his room, I would often sit in a chair and visit with him. And we talked. And we chummed. 

We spend quality time with them. We hear their stories about their kids or their spouses. We learn what their lives were like. We learn what they do for a living. We learn their dreams and aspirations. 

We became friends.

And then we are there as the disease that is ravaging through their lungs doesn't seem to be getting better. And so they need to be intubated. 

One guy was a very successful talker. He had a job that allowed him to talk. And he was a funny guy. And he was crying at the end. He was talking on the phone with his kids. It was a joint call. And he said, "I really want to live. I want to see my grandkids grow up. And if I die, I am going to come back and haunt all those who were responsible for my demise." And he looked at me, all teary-eyed, and said, "Except for John." And he smiled. 

Those were his last words. He passed away less than a week later. 

Another guy I met was a very big guy. But he was very nice. And he was humble. And he was tough. One nurse described him as a teddy bear. He had a very friendly disposition. And he went out with grace and dignity. By now patients were allowed to have visitors. So, his son was in the room. And he was chumming with his kids. He was telling stories of old, "Remember when we..." And it was neat to hear how peaceful this conversation went. You could tell that they were a close family. 

All the way to the end, he kept his head held high. Through the sound of his voice, and the actions of his demeanor, you couldn't tell he was sick and was going to be intubated. And that he was probably going to die. You could not tell these were the last words of a man. Except for the fact, he had a high flow nasal cannula in his nose and his respiratory rate was in the 40s. Other than that, he was just a normal guy enjoying time with his son. 

And then we were ready to intubate. The son said and dad said to each other, "I love you." And then it was just me and the intubation team and this nice man. And he looked up to me. He said, "It was real." 

And that was the last thing he said before being intubated. I hope they were not his last. He will remain in my prayers. I hope he makes it. He was a cool guy. 

So, it's humbling. 

What Is A Cytokine Storm?

Cytokines are small proteins. They allow cells to communicate with each other. When a virus enters a cell, that cell releases cytokines. And some of these cytokines are responsible for causing inflammation, while others travel through your blood system to recruit white blood cells to the area of invasion. And this creates even more aggressive inflammation of the invaded tissue.

Initially, this response is good. It is how cells and tissues kill invaders. It is how cells and tissues heal themselves. Although, when cytokine levels remain elevated, they start to do more harm than good. Cytokines, when left unchecked, become cytotoxic. This means that they start to damage the same tissues they are meant to protect.

So, COVID-19 tends to cause the over-production of cytokines procured by white blood cells. This is called a cytokine surge or cytokine storm. It is this storm that is responsible for the development of Acute Respiratory Distress Syndrome (ARDS). And this storm may continue even after patients even as these patients move into post-COVID status.

It also causes what is called endothelitis. This is a condition where the inside walls of blood vessels become inflamed. This causes vasoconstriction. This sets up an environment where your blood more easily clots (hypercoagulability). It also causes less blood to get to organs (hypoperfusion). And this means less blood gets to organs (Ischemia). And this is what leads to shock and death.

A cytokine storm can be caused by other diseases. Although, this seems to be more prevalent with COVID-19. 

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References. 

1. Jain, Uday, "Effect of COVID-19 On The Organs," Curius, August 2020, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7470660/, accessed 12/ 22/2021

Should Pregnant Women Get The COVID Vaccine?

We healthcare workers have cared for some pregnant women with COVID. A pediatrician informed me that we like to keep their oxygen saturation above 95%. This is due to concerns that anything less might cause fetal asphyxia. So this is what we have been doing. 

For most people with COVID, we want to keep their oxygen saturation 88 percent or higher. But with pregnant women, obviously, we are caring for two patients. So, this is the reason for the goal of higher minimal oxygen saturation. At the time of this writing, I am not sure if this is based on actual studies or if it is just a number that is made up. 

The goal though is to make sure the baby, along with the mother, is getting enough oxygen. And so, I had one such patient a doctor was thinking about incubating. And I said, "Well, she is getting 94% FiO2 from the high flow. And she is needing an NRB above that to maintain a sat of 95 percent. But, if we were just treating the patient, I don't think she would even need the high flow. In fact, her saturation was 95% on just an NRB before I set that up. And the estimated FiO2 with that is about 75%. So, I don't think she needs to be intubated based on the amount of oxygen she is currently on. But, you are the expert. I will do as you say."

I added the disclaimer at the end there as I do not have much experience taking care of pregnant women, let alone pregnant women with COVID. 

This brings up some questions. Does pregnancy act as a co-morbidity that increases a woman's risk for developing severe COVID-19? Does COVID-19 affect pregnant women worse than women of the same age who develop COVID-19 but are not pregnant? What impact does COVID-19 have on the fetus? More specifically, what impact does severe COVID-19 have on the fetus? 

And then we have the topic of vaccines. Many, if not most, of these patients, are unvaccinated. So, what is the percentage of pregnant women who are vaccinated? What percentage go unvaccinated? Is this number higher than for non-pregnant women of the same age? If fewer pregnant women are getting the vaccine compared to non-pregnant women, why is this? 

My theory is fear of what the vaccine might do to the unborn child cause pregnant women to think twice before getting the vaccine. Or perhaps this same fear resides in the medical community. 

I am wondering if it would bode better for the mom and child to just get the vaccine. Because fetal asphyxia can cause fetal neurological problems that the child would have to live with. It can and has caused fetal death 

So, this is just me thinking. I will investigate this further and report my findings. 

How does COVID affect your lungs

So, let's say you inhale the SARS-CoV-2 virus. This is the virus responsible for causing a disease now referred to as COVID-19. What happens to your lungs? Here's what to know. 

The virus travels down your airway. And it attaches to an airway cell. It enters the cell and starts to make changes inside the cell. Within several days, it turns the cell into a virus-making factory. Soon, there are so many viruses inside the cell that that cell bursts. This sends thousands of viruses into the surrounding airway cells. And, of course, those viruses enter those cells to turn them into virus-making factories. 

Your immune system plays a role here too. Airway cells that viruses attach to release chemicals. And these chemicals tell immune cells that there is an invader. So, immune cells release more chemicals that travel to the infected tissue. These chemicals are pro-inflammatory chemicals. They cause inflammation of your respiratory tract, including your nose and airways. And this is what causes your COVID symptoms.

Sometimes, viruses make it down into your alveoli. According to studies, about 14% of people who develop COVID develop severe COVID. And this happens when the virus causes inflammation of both your airways and your alveoli. Inside the alveoli, this inflammation causes the puss to fill the alveoli. And this is diagnosed as COVID pneumonia. When this happens, your oxygen levels may drop. this is because, while oxygen gets to your alveoli, it is unable to travel through them to your blood. (1)

According to another study, 40% of COVID patients develop ARDS. And about 20% of ARDS cases become severe. And these patients are most likely to require hospitalization and supplemental oxygen. And these patients are at the greatest risk for developing pulmonary fibrosis. Studies show that about one-third of those with severe COVID will develop pulmonary fibrosis. (2-3)

The exact mechanisms of how pulmonary fibrosis develops from COVID remains unknown. What is known is that the SARS-CoV-2 virus uses an angiotensin-2-converting enzyme (ACE2). This ultimately leads to "interstitial lung damage followed by parenchymal lesions." (3)

The most common cause is idiopathic. This means the method of development or cause of fibrosis is unknown. However, one common theory is the "cytokine storm" theory. (2) This theory postulates that 

the same inflammatory chemicals that cause inflammation damage cells. How does this happen? 

Usually, inflammatory cells are released when cells are damaged. This causes inflammation. This inflammation causes goblet cells to release extra mucus. And a combination of inflammation and mucus traps and kills viruses. This is how we get better. Of course, this inflammation also causes your symptoms, as noted above. 

Usually, the infection goes away, and the inflammation subsides. And the inflammatory chemicals subside. But, a prolonged infection, or one that seemingly lasts a long time, causes those inflammatory markers to stay elevated. This causes an abnormally elevated level of inflammatory chemicals, such as cytokines. And this is referred to as a cytokine storm. (2)

So, when inflammatory markers are high in number, they may be cytotoxic (harmful) to cells. They start to cause changes or damage to cells. And this damage causes scar tissue or fibrotic tissue that makes airways stiff. This is what may lead to pulmonary fibrosis secondary to a COVID-19 infection. (3)

This fibrosis develops in alveoli. Alveoli are mostly lined by type I pneumocytes. These are cells that are ideal for gas exchange. Scattered between these are type II pneumocytes. These are cells that secrete surfactant, the soap-like substance that reduces surface tension that makes your lungs expand more easily.  (4-6)

Type II pneumocytes are also involved in the repair of alveoli following certain disease conditions like pneumonia (i.e. COVID pneumonia). They are involved in alveolar tissue repair and regeneration. And, during disease states like pneumonia, type II alveolar hyperplasia may occur. And hyperplasia is when a cell is reproduced over and over.  When this happens with type II alveolar cells, It can cause an abnormal amount of type II alveolar cells. And this causes a thickening of alveolar walls. (5, 7

So, COVID pneumonia, or ARDS from COVID pneumonia, causes "diffuse alveolar damage and resultant type II pneumocyte hyperplasia." This hyperplasia is the result of an acute lung injury, such as what occurs with COVID pneumonia. And this causes alveolar walls to be abnormally thick and stiff. This is a change that may be described as scarred or fibrotic alveolar walls. This can reduce gas exchange and make it difficult to oxygenate, thereby reducing oxygen levels. (5, 7-9)

There are many cytokines involved in the cytokine storm responsible for severe COVID. Some cytokines involved are interleukins IL-1, IL-2, IL- 4, IL-7, IL-10, IL-12, IL-13, IL-17. Although, those most likely to require critical care admissions are those with elevated levels of IL-6, IL-2, IL-7, IL-10, GCSF, IP10, CCL2, MIP1A, and TNFα. (10)

Of these cytokines, two are noted to be most likely responsible for pulmonary fibrosis  They are called Interliekine 6 (IL6) and TNFα. Another substance that may play a role in the development of pulmonary fibrosis is a protein called VEGF. These are thought to be the leading agents in the cytokine storm in patients with severe COVID that lead to pulmonary fibrosis. (2, 10) 

I will delve into these further in a future post. So I will not describe them further here. That said, to help prevent or reduce the incidence of pulmonary fibrosis in patients with COVID-19, researchers are looking into medicines that will block the effects of these cytokines. (10)

Those who develop ARDS and severe COVID are the most likely to have a prolonged COVID illness.

And this may increase their risk of developing pulmonary fibrosis.  And the cytokines responsible for the "escalation of disease" and severe illness may be IL6 and TNFα. These cytokines may partly explain why 10 percent of those with severe COVID die. Further research may confirm or shoot this theory down. (10). 

In those who survive, this pulmonary fibrosis would then continue even as the patient recovers from COVID. This pulmonary fibrosis has no treatment. Therefore, it would be something these patients would have to deal with for the rest of their lives.  And this is an area where researchers are continuing to research. And the goal of this research is to find ways of presenting pulmonary fibrosis, or ways of treating it in those who do develop it. 

References. 

1. "What does COVID-19 do to your lungs," Web MD, https://www.webmd.com/lung/what-does-covid-do-to-your-lungs#2, accessed 12/5/2021
2. Rai, et al., "Post COVID pulmonary fibrosis: Is it a real threat?" Indian Journal of Tuberculosis," 2021, July, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7654356/, accessed 12/5/2021
3. Alhiyari, et al, "Post COVID-19 fibrosis, an emerging complication of SARS-CoV-2 infection," ID Cases -- Journals, 2020, December 31, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7785952/, accessed 12/5/2020
4. Brandt, Joseph P., Pujyitha Mandiga, "Histology: Alveolar Cells," NCBI, 2021, April 25, https://www.ncbi.nlm.nih.gov/books/NBK557542/, accessed 12/5/2021
5. "Type II Pneumocytes," Science Direct, 2013, "https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/type-ii-pneumocyte, accessed 12/5/2021
6.  "Pulmonary surfactant in newborn infants and children," https://breathe.ersjournals.com/content/9/6/476, accessed 12/5/2021
7. "Hyperplasia, My Pathology Report, https://www.mypathologyreport.ca/definition-hyperplasia/, accessed 12/5/2021
8. "Hyperplasia," Medline Plus, https://medlineplus.gov/ency/article/003441.htm, accessed 12/5/2021
9. Stanley, M. W., et al, "Hyperplasia of type II pneumocytes in acute lung injury. Cytologic findings of sequential bronchoalveolar lavage," American Journal of Clinical Pathology, 1992, May, https://pubmed.ncbi.nlm.nih.gov/1575213/, accessed 12/5/2021
10. Kovalchuck, et al., "Fighting the storm: could novel anti-TNFα and anti-IL-6 C. sativa cultivars tame cytokine storm in COVID-19?" NCBI, 2021, January 31, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7880317/, accessed 12/5/2021

Are Asthmatics At Increased Risk Of Getting COVID-19

Question. Am I more likely to get the COVID-19 Virus compared to non-asthmatics?

Answer. Probably not. There is no evidence suggesting asthmatics are at greater risk than non-asthmatics of getting the COVID-19 virus. Still, there are precautions you can do to lower your risk. 

Reference.

1. McCall, Rosie, "Does Coronovirus Affect Asthma? What Sufferers Need To Know About Covid-19," Newsweek, 2j020, March 18, https://www.newsweek.com/does-coronavirus-affect-asthma-what-sufferers-need-know-about-covid-19-1493022, accessed 3/31/20

Should I stop using nebulizers as to not spread COVID-19?

Your Question. Should I stop using my nebulizer so I don't spread the virus?

My humble answer You do not have to stop using nebulizers at home. Nebulizers do aerosolize medicine. They also aerosolize any germs you might have, including COVID-19. This is a concern in the hospital setting, as healthcare workers in the same room as the person getting the treatment have an increased risk of inhaling COVID-19 during and for an hour after a nebulizer breathing treatment. To reduce this risk, most hospitals are using inhalers instead. This is not an issue at your home. You should continue taking your medicine (including nebulized medicine) as you have been prescribed.

Is There A Shortage Of Asthma Inhalers

Your Question. Are their any shortages of asthma meds due to dr's using them on Coronavirus patients. Are we safe at this point from these meds being hoarded?

My Humble Answer. HI. Thanks for the question. At the present time, hospitals have cut down on the use of nebulizers for COVID-19 or suspected COVID-19 patients due to the threat of aerosolizing the virus. So the use of albuterol inhalers in the hospital setting has increased due to the COVID-19 outbreak. For this reason, some areas are seeing a shortage of albuterol inhalers. At the present time, I believe this is the only inhaler affected. Albuterol solution for nebulizers should still be available. Does this answer your question.