Why have we got smooth muscle around our bronchi (tubes in our lungs)?

I am a general practitioner who hits “retirement age” in 3 days. I do feel qualified to ask this question but not really to answer it. It has been bugging me my whole career, but I have realised most people never contemplate this backwater of physiology.

I always expected to ask someone in the know and get a clear answer. I asked professors of paediatrics, as these muscles seem to cause a lot of trouble in young people. Nothing. I moved on to professors of respiratory medicine, as a lot of their work relates to this biological machinery that can narrow our airways. They smiled, looked around quizzically and got on with their work. More recently I trapped a respiratory professor in a pleasant restaurant, but he was not really interested. He proposed that the muscles were embryonic vestiges of bowel muscle.

You may not be interested in my explanation either. But it is an important question. These muscles are in a critical location in our lungs. The inappropriate contraction of these muscles, called asthma, is a significant cause of death in adults. It tragically happened to one of my otherwise healthy young patients and has been a near miss on a number of occasions. During that huge thunderstorm in Melbourne a few years ago, these muscles went on a rampage. We have drugs to relax these muscles that are contained in a blue inhaler and used by many people around the world. We know a lot about these muscles and how they work.

“These smooth muscle cells have muscarinic M3 receptors on their membrane. The activation of these receptors by acetylcholine will activate an intracellular G protein, that in turn will activate the phospholipase C pathway, that will end in an increase of intracellular calcium concentrations and therefore contraction of the smooth muscle cell. The muscle contraction will cause the diameter of the bronchus to decrease, therefore increasing its resistance to airflow.”

https://en.wikipedia.org/wiki/Bronchoconstriction

Searching the internet, has provided no explanation. So, I will have a shot, excused by unrequited inquisitiveness and my age.

My only real experience of these muscles in action is wheeze, the symptom that is caused by their contraction. The noise is generated by the air we breath going through a narrow tube. If you take a deep breath with your mouth open you will hear a soft noise, if you do it again with your mouth shut, you will get a lot more noise in your nose. The same amount of air will make higher pitched noises as the tube narrows. When the tubes get narrow enough they start to hum and whistle and we can hear a “wheeze”.

Living in London for a decade, I noticed that children wheezed a lot. It was usually with a viral infection and was almost always worse at night. It seemed relatively harmless for most, but a few had difficulty. I treated them with the medications we had available, and noticed that most of them settled down as they got older.

I imagined that the viral infection was causing some swelling of the tubes and narrowing them somewhat. I could explain the wheezes disappearing as children got older because the tubes of their lungs were getting bigger. The deterioration at night, something that was particularly evident with croup, was not so easy to explain.

Traveling piqued my interest in this phenomenon. In 1981, I got off a train at Linkoping in Sweden at 1am in the morning and the temperature was minus 30 degrees. The hairs in my nostrils froze in a snap and I began to wheeze gently for the first time in my life. It didn’t last long as we walked knee deep in powder snow to our friend’s apartment. In the early 90s when we returned from London to live in Darwin our wheezy child stopped wheezing altogether. The air was cleaner and it was a lot warmer, especially at night.

Someone told me that the surface area of our lungs, as an adult, is the size of a tennis court. There is a tiny membrane between our blood, pulsing at 37 degrees, and the air we breathe. How do we possibly stay alive and not die of hypothermia? Especially in Sweden! The solution is that our body heats and moisturises the air between entering our nose and delivering the oxygen to our blood in the tiny sacks at the end of the muscular tubes of our lungs. When we breath hard, we bypass our nose, but we are generally exercising when we do this.

Could these muscles have a role to play in temperature regulation? It seemed quite possible. To warm air, it needs to be in contact with a surface, so the thinner a tube the more likely it is to warm during its passage. But the same amount of air passing through a thin tube would travel faster and have less time to warm. What if we didn’t need so much air? That is the case when we are not exercising, especially when we are asleep. Could this be useful when we are at rest, particularly when we are asleep?

The other effect of reducing the diameter of the tubes is to reduce the volume of the tubes. It is dramatic. If you halve the width of the tube, the amount of air being drawn in is a quarter. So for a small reduction, perhaps to 3/4 width, only half as much air would need to be drawn in through our nose to get the same amount of oxygen to our lungs. This sounds handy, less air, more efficient warming and same oxygen.

It seemed to explain why children get wheezier at night. I was told by my Swedish friends that all Swedish footballers wheeze for the first few minutes of the game in winter. Could this explain exercise induced asthma, where the airways constrict until the person is generating enough heat from exercise? Cold air is a well known trigger to wheeze. A person probably also has some swelling in the lining of the tubes when this happens; allergy or a viral infection. Clearly things go horribly wrong with this mechanism at times, causing severe asthma, but a lot of wheeze can be explained physiologically.

So what is my answer to what has become a rhetorical question?

The muscles around your bronchi protect you from excessive heat loss when you are not exercising, and particularly when you are asleep. You can get by at those times with a lot less air coming into your lungs, and so can conserve heat efficiently. You can survive and sleep in cold weather and cold nights without becoming hypothermic.

Now that sounds like evolution.

Whether or not you like the answer, you can start asking experts the question. I think you will be as bewildered as I am by their inability to answer. You should at least consider why that is so and what it says about our profession? No doubt some of you will search the internet. Please comment if you find the answer out there.

Who’s Training in Whose Training?

WP_20131128_16_12_56_ProI am not sure if everyone is aware of the potential professional crisis for specialist general practitioners if the Department of Health and Ageing decide who is providing training for general practice in 2016. That is the stated aim, presumably not with advice from experts in health care delivery.

The Department contributes public money to primary care and so can decide who has access to what rebates and other financial assistance. This is the case for all specialist training.  During the Howard government a shortage of trained specialist general practitioners developed due to a failed policy to limit health care spending by limiting numbers of doctors. The ensuing GP shortage in outer suburban, rural and remote areas led to the government opening the door for doctors to work in primary care without the qualifications from the RACGP or ACRRM.  These qualifications have been developed to distinguish specialist general practitioners; the FRACGP has never been granted without submitting for the Fellowship exam, or equivalent international qualification. If the value of the FRACGP is not recognised by the community, then value in training to achieve Fellowship is also depleted. This is the crux of the issue and has led to the profession being at a precipice.

We specialist general practitioners understand how to deliver evidence-based sustainable primary health care across the broad range of community settings found in Australia. It is our space, not one invented by governments. Innovations and responses in our profession are not determined in Canberra. We are proud professionals delivering high quality care despite the limits of Medicare. I have worked in the NT for over 20 years and understand the issues with workforce distribution; I am keen to work with anyone who wants to ensure that all Australians have adequate access to primary health care. However the proposed takeover of our training by the Department of Health is unacceptable.

Universities and other large providers will no doubt see this as an opportunity. We will see massive conflicts of interest paying dividends to various agencies to meet workforce needs, fill departmental coffers or bring money to other organisations. Our new registrars have been learning on dolls and out of textbooks for years, and it shows. They want to be able to do doctoring – not be doctors. We have more to do than ever to prepare our registrars for delivery of the services our patients’ need. We need to do better at it.

I have a 7 principle approach to success:

  • The College must determine if placements are suitable for learning specialist general practice
  • The College must determine if supervisors are suitable for training registrars seeking to become specialist general practitioners
  • Our Fellowship must be seen as the hallmark of quality primary care, the doctor with FRACGP as the go to professional to provide primary ongoing medical care and lead the primary care team
  • The College must robustly represent and support our Fellows, particularly our supervisors, and our Members who are working towards Fellowship
  • The College should work hard for all Members to gain Fellowship and all Fellows to improve their standard of practice
  • Doctors with Fellowship should be recognised and promoted as specialist general practitioners and be expected to deliver a higher standard of care
  • The College should be the custodian of knowledge relevant to our professional practice and pathways to providing new and improved services to our communities.

 

The RACGP needs to advocate strongly for our Fellows (especially our Supervisors) and Members seeking Fellowship while working closely with ACRRM and GPRA to ensure that our profession and quality primary health care thrive.

It is our training and those training with us should feel that we are supporting them in their endeavour.