Breathing is triggered by the level of CO2 in the blood. Under normal conditions, and when breathing is functional, as soon as CO2 reaches an arterial pressure of 40mm Hg, the medullary sensor sends a message to the diaphragm causing it to contract and relax and initiate breathing.

The resultant rhythm produces a minute volume of 4-5 litres of air and this translates to approximately 8-10 breaths per minute. Functional breathing is gentle and can only exist when diaphragm and nose are used. The moment a patient uses the upper chest and breathes through their mouth, breathing becomes dysfunctional.

The brain is constantly polling the body for feedback regarding levels of various critical components. If the brain continues to receive the message that CO2 levels are consistently low, it will accept the situation and reset the medullary trigger to respond at the lower level. After all, it is concerned with survival as a first priority.

So, what happens then is that the brain accepts that 30mm or 33mm is the trigger level and will respond as soon as CO2 reaches this point. It is not difficult to determine the resultant pattern. Breathing is initiated earlier and becomes more frequent. This resulting hyperventilation then becomes the norm.

The fact that the breathing rate increases and causes mouth breathing to occur means that more air is exhaled with each breath and, as a consequence, more CO2 is dumped. This perpetuates the problem and the patient becomes a permanently dysfunctional breather.

Unfortunately, when this is the case, the patient is unaware of the situation and regards it as quite 'normal'. That is why this condition is referred to as "silent hyperventilation".