Long have I laboured in ignorance of the music that you make.
Yesterday night I sat down and thought about you, attempting to ponder over your intricacies as a lover would their love. Then I suddenly realised that you are just as simple as my love, the heart, to understand. Like the vascular system, you too have tubes, and fluid dynamics that obey laws of relationships between pressure, volume, velocity, wavelength, and frequency. Just like the heart, you are a musical instrument which obeys the same laws that govern a Classical orchestra.
Bronchial breath sounds
You can simply be thought of in terms of a series of pipes (trachea, bronchi), branching like a tree into smaller and smaller (mini bronchi known as bronchioles) in cross sectional area / radius. When air enters this instrument by breathing in, it reverberates through the bronchi, creating the bronchial component of the breath sound. This would theoretically result in a long inspiratory sound as one breathes in, a pause of variable length, and long expiratory sound as one breathes out, with no gap in between them as the air reverberates (bronchial breathing).
The air that enters the larger airways are at a high pressure, low velocity, but as they progress to smaller airways, they are at low pressure, high velocity. Low velocity sounds are low frequency. High velocity sounds are high frequency. Thus the air travelling through the bronchi sounds deeper than the air travelling through the bronchioles. This accounts for the rise in pitch that is heard when you take a breath. Correspondingly, the sigh (lowering of pitch through the sound) of expiration is the product of the air being expelled from the most distant, narrowest passageways (bronchioles) through the larger passageways to the nose and mouth.
Vesicular breath sounds
Thinking about the breath sounds as a continuous rising pitch, then fall in pitch, does not account for the final component of your musical abilities - your alveoli, or tiny sacs at the end of those pipes. At the end of these pipes, there are small bags (alveoli, sing.=alveolus), which may collapse and expand depending on the air that enters them. As one breathes in, creating the inspiratory component, the air travels to the end of the air passageways, and the bags get inflated. When one breathes out, air leaves the lungs, starting with the alveoli. Imagine how suddenly, the pipes become encased with multiple deflated little sacs - almost like a porous sponge. This sponge acts to dampen the end part of the expiratory phase when you listen over the area with a stethoscope (vesicular breathing). Therefore, normal vesicular breathing through the pipes and bags has a long inspiratory phase, and shorter expiratory phase due to the muffling of the soft expiratory sounds at the end of expiration.
Crackles
Now, these bags may be surrounded by fluid (infection, oedema), or surrounded by a connective tissue wrapping (fibrosis), like little sweets in plastic wrappers. This makes for some interesting acoustics. When the bags are lined with fluid or surrounded by connective tissue wrappings, they tend to collapse. When air enters into the collapsed bags, they pop open. With infection, the fluid that lines the bags comes from the bags and the pipes themselves. In chronic bronchitis / COPD, the passageways that are closed off by obstructing fluid are the distal bronchi. As air passes into the ends of smaller bronchi, and terminal bronchioles, which are filled with fluid, the passageways snap open with a pop (early inspiratory crackles of COPD). Although this has not been suggested in the books that I've read, the way I see it, it is the sound of the pipes opening up that is heard, rather than the sound of the alveoli. This would account for the fact that the early inspiratory crackles of COPD are often less than 4 pops (fewer bronchi:alveoli) and occur early on in inspiration (air passes through the bronchial passageways first to get to the alveoli). Although I can't logically explain the reason why, the fewer 'pop' sounds correspond to their lower frequency (coarse quality). In contrast, when the fluid fills the alveoli/bags, rather than the bronchioles/pipes, as with pulmonary oedema, what one hears is the sound of the alveoli snapping open against the surface tension of the fluid filled bags, creating a higher pitched sound like bubbles popping (medium quality). This occurs later than the opening pop sounds of COPD crackles (late inspiratory). The more alveoli: bronchioles accounts for the fact that the medium late inspiratory crackles of pulmonary oedema are more pops compared with bronchioles (4-9). With bags popping open against fibrosis, imagine the rustle of sweet wrappers as they are opened. The crackles produced are >10 pops (estimates are from Talley's) and also occur in late inspiratory crackles. Once again, increased number of pop sounds corresponds with the higher frequency, i.e. fine quality of their sound (and are therefore described as fine late inspiratory crackles of interstitial fibrosis). As you know, the human ear hears higher frequency better, so although they are described as fine, high pitched sounds sound louder (and harsher) compared the lower-pitched coarse crackles.
| Variables | Pneumonia(n = 37) | CHF(n = 5) | IPF(n = 13) |
|---|---|---|---|
| Inspiratory crackles | |||
| Crackles per breath | 9 ± 5 | 13 ± 06 | 24 ± 17 |
| Crackle frequency or pitch, Hz | 316 ± 71 | 326 ± 43 | 441 ± 80 |
| Expiratory crackles | |||
| Crackles per breath | 6 ± 4 | 6 ± 2 | 8 ± 5 |
| Crackle frequency or pitch, Hz | 289 ± 79 | 303 ± 55 | 421 ± 78 |
Taken from Chest. 2009;135(1):156-164. doi:10.1378/chest.07-1562
Wheezes
The lumen of these pipes can become clogged with mucus (as with asthma or chronic bronchitis), thus becoming smaller in cross sectional area, or may obstruct complete such that no air can pass through (in which case no sounds would be transmitted). When one breathes in, the pipes expand slightly due to their compliance. When one breathes out, they reduce in diameter slightly as well. According to Poiseuille's law, when the diameter of the lumen is smaller, the air will travel at a faster velocity (and correspondingly, produce a higher frequency, or pitch, of sound which is be more likely to be heard than lower frequency sounds which may be inaudible to the human ear). Additionally, when the fluid-lined lumen is dilated during inspiration, the surface tension of the fluid is higher than when the lumen is constricted, as it would be with expiration. When the fluid is at high tension, it is less likely to generate as much vibration. When the fluid is at a lower tension in expiration, as is the case in smaller diameter airways during expiration, an audible sound is more likely to be produced. The air rushing along the surface of the fluid creates a wave, generating a musical note, similar to the way a violin string would if it were plucked (wheeze). If that process were more severe, i.e. more fluid in the airways, the smaller the diameter of the airways, and the greater the potential of the fluid to vibrate at an audible level. That would result in the transmitted wheeze being heard earlier and earlier. Wheezes can even be heard during inspiration in severe blockage.
So how would I manage the stuff that plagues you? Get rid of the fluid, make the airways bigger, and address the thing that causes the fluid to appear in the first place. As for fibrosis, well, there's not much I can do but appreciate your contribution to the music.
Oh lungs, if only I had known sooner how sweetly simple, and how simply sweet your melodies are.
Your dedicated servant,
Xin
References
- Chest. 2009;135(1):156-164. doi:10.1378/chest.07-1562
- Talley's Clinical examination
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