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Asthma – About Breathing

Asthma – About Breathing

Causes of asthmaTo summarize:

The normal work of breathing is the work needed to expand the respiratory system from its resting position, plus the work needed to overcome friction created by air moving against the airway walls. Overcoming both elastance (the reciprocal of capacitance) and resistance combines the efforts of the respiratory and expiatory muscles. And taking larger breaths and breathing faster both make the respiratory muscles work harder.

Higher resistance:

Because COPD permanently narrows the airways, the air flowing through them meets greater resistance—sometimes more than 25 times normal. So the respiratory muscles often have to work harder—especially during expiration—even under non-strenuous circumstances. Since resistance is affected by breathing speed as well as airway width, a problem with one can often be compensated for by changing the other. When moderate COPD has narrowed your airways, breathing out more slowly than normal does away with a lot of the added resistance. But this compensation eventually fails if airway obstruction continues to worsen.

Then airflow resistance continues increasing, and the compensatory time needed for breathing out becomes longer and longer. Simultaneously, the lungs are continuing to lose elasticity. Finally, the loss of elasticity becomes so widespread that elastic recoil is too weak to push air out of the lungs effectively. Then each expiration requires so much time—from the combined inroads of high resistance and low elastance—that it cannot be completed before the next inspiration must start. Air now remains trapped in the lungs.


The expiatory muscles jump in to help expiration, but this effort increases pressure around the airways, narrowing them further and trapping more air. The COPD lungs—which for some time have already been somewhat hyper-inflated at rest—now become grossly hyper-inflated.

Because such hyper-inflated lungs cannot return to their normal resting position, they interfere with the inspiratory muscles. The diaphragm—our main source of inspiratory power—can no longer contract effectively. Normally it is dome-shaped, pulling the dome down as it contracts. But hyper-inflated lungs press down on the dome to such a degree that the diaphragm is always in a contracted position. And the other inspiratory muscles can no longer return to their full—that is, optimal—resting length before contracting again.

The more any muscle approaches its optimal length between contractions, then the more it can contract, the stronger it is, and the more it can do. In advanced COPD, the inspiratory muscles have, in effect, been shortened. So the biggest breath they can help achieve is a lot smaller than it once was.


Working against increasingly greater airflow resistance and the stress of hyperinflation can eventually exhaust the respiratory muscles.

If this happens, respiration fails. And failure permits the amount of carbon dioxide in the blood to rise to potentially fatal levels.

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