Most divers cannot understand why "asthma" is such a problem for divers nowadays, particularly as it is so easy to control and so few children and young adults with "asthma" suffer major problems. I would therefore like to provide an explanation. (Without the aid of diagrams this is difficult! My apologies).
Apologies also to scubadoc, although I havent yet read your link.
I have used parentheses because "asthma" is not really a diagnosis. It is a term used to describe certain, common, reversible variations of Chronic Obstructive Pulmonary Disease (COPD) all of which are characterised by shortness of breath and an expiratory wheeze during an attack. All forms of COPD carry the same risks to divers because the constant factor, as the name implies, is an obstruction to expiration, leading to the trapping of stale air within the lungs and a considerable reduction in gaseous exchange.
Not all forms of COPD have wheezing as a feature but to gain an understanding of the pathophysiology of an asthma attack it is helpful to understand the mechanics that generate the audible wheeze. If you inflate a toy balloon it often makes an amusing noise as it deflates. The noise is generated from vibration of the flexible rubber tubing as it rapidly opens and closes as the air passes through it. It is generally accepted that this flap-valve effect is due to the Venturi principle and the fact that when the air passes through the nozzle the STATIC pressure within it becomes less than the surrounding atmosphere causing the tube to collapse and close. Once closed, air movement stops, the internal static pressure subsequently increases to above that of the atmosphere and the nozzle again opens to allow air to escape once more. Once there is movement the Venturi effect again causes the internal pressure to drop and the nozzle closes again; - The nozzle vibrates noisily.
If the same balloon is re-inflated and a stiff tube (such as a peashooter) is inserted to support the full length of the nozzle no vibration occurs, very little noise is generated and, in fact, the balloon empties much more quickly. In life, the larger airways of the trachea and bronchi are similarly reinforced by cartilage rings which hold these larger airways open against the Venturi effect but the smaller airways conveying the air from the alveoli to the bronchi are not reinforced. In healthy lungs, these smaller airways remain open but in COPD, where there is obstruction to the flow of air (and static pressure) from the alveoli into these unsupported airways, they behave very much like the nozzle of the toy balloon, causing a reduction in flow and a noise we hear as wheezing. Clearly, the greater the expiratory effort made the greater becomes the intrathoracic pressure against the airways and the worse the obstruction becomes.
In asthma, whatever the trigger, inflammation and oedema of the bronchial walls and the secretion of mucus plugs cause the initial obstruction. In addition, the muscles in the airway walls contract. These all contribute to a considerable reduction in the diameter of the airway and Pascal's law confirms that laminar airflow is proportional to the fourth power of the diameter of the airway. So if airway diameter is reduced to 90% of normal, airflow is reduced to 65%; - Diameter to 75% flow to 30%. When airflow in not laminar, as with wheezing, the flow rate reduction is even greater and there is significant obstruction.
Usually an asthma attack is easy to treat. Inhaled steroids reduce the inflammation, while inhaled bronchodilators, such as Ventolin, rapidly reverse airway muscle spasm. Clearly a diver cannot use his inhalers underwater but, unfortunately, it is not as simple as that. All sufferers of COPD are at increased risk of burst lung - pneumothorax - where air is trapped within the chest cavity. There are two routes of air entry.
1) penetrating chest wounds or
2) torn airways within the lung.
The latter are a frequent feature of advanced COPD such as bullous emphysema, where the alveolar walls are considerably weakened by disease. (This is one more reason divers should not smoke!)
As with DCI, unless there is effective off-gassing any trapped air increases in volume (or relative pressure) as the diver ascents. Even a very mild degree of obstruction can cause some air to be trapped in parts of the lungs. With nowhere to go this air expands on ascent, inflating the alveolar sacs like a balloon which compresses adjacent normal lung tissue until, like a balloon, it bursts allowing air into the mediastinum or the pleural cavity. In the latter case the affected lung rapidly collapses and stops working completely.
The most dangerous form is a tension pneumothorax, most frequently seen in stabbing and gunshot wounds to the chest, the so-called sucking chest wound. Here the entry wound (external or internal) acts as a flap valve, allowing air in but not out. Each breath results in an inexorable increase in intrathoracic pressure with air pressing in turn against the affected lung, the unaffected lung and the mediastinum (the heart and great vessels). In time, the pressure within the chest may exceed central venous pressure, which is about 0.1 bar, completely stopping venous return to the heart with a potentially fatal cardiac arrest. These are the circumstances where a Cerebral Artery Gas Embolism CAGE is also likely to occur.
Theoretically at least, if a diver suffers a pneumothorax at 20 M, on surfacing the pressure within the chest cavity could exceed that of a car tyre! Quite clearly, a pneumothorax sustained even at moderate depth is potentially fatal and must be avoided at all costs. Hence the respect all doctors have for a declared history of "asthma" in diver recruits. Even if there are few diver deaths directly related to "asthma" I contend that any diver recruit with a history of "asthma", or indeed their parent, would be very wise to determine that individual's specific risk by consulting a chest physician with an adequate knowledge of diving physiology. I feel it would be reckless indeed for any parent to allow his teenage son to dive if his offspring formerly suffered from childhood asthma, even if currently asymptomatic, without formal testing and the recommendation of an appropriate specialist.
I think Mike is right "the choice is individual, and the "risks" have to accepted." and the Australinas are wrong to operate a blanket ban. However, in Britain, about 2,000 non-divers still die each year from asthma, the majority of whom are young adults whose disease was thought to be quiescent. A very sobering thought indeed.
Thankfully a tension pneumothorax is very easy to treat. All that is required is an escape route for the high-pressure gas trapped within the chest wall by the surgical creation of a penetrating wound that remains patent; - a chest drain. Army medics are taught needle thoracostomy (pleuroscentesis) and I firmly believe this life-saving procedure should also be taught to sport-diver medics as the diagnosis is usually obvious, it is very simple to perform and must be provided within seconds. The inevitable delays awaiting the emergency services are likely to be fatal and without it CPR is totally ineffective, even with 100% Oxygen.
I hope you find the above interesting.
What do you scuba docs think about my ideas on needle thoracostomy?
kind regards,
Paul T
