Asthma is an Obstructive plumonary disease. Pulmonary disease are divided into two sub-categories: Obstructive and Restrictive.

The obstructive disease include:

Obstructive pulmonary disease where the patient either has 1-asthma, 2-emphysema, 3-Chronic Bronchitis, or 4-COPD (Emphysema + Chronic bronchitis).

In your case you have Asthma which means that the smooth muscle lining your bronchi are hypersentative and have increased tonality (they contract harder) and that causes a constriction of your airways. Now it is a good time to bring in a little bit of physics into this discussion.

You all know of Hagen-Poiseuille's equation of Resistance for a fluid named after Ludwig Hagen and Marie Poisuille which sates:

R = 8 η l / π r^4

where R is the resistance against flow of a fluid, η is the viscocity of the fluid in question, l is the length of the conduit through which the fluid moves, and r is the radius of the conduit.

Also lets us remember the equation of constant flow that states that:

A v = flow , where A is the area of the conduit ( A = πr^2) through which the fluid moves and "v" is the velocit of the motion.

Also recall that

flow = ∆P / R , where P is the pressure gradient, and R is resistance.

Ok so let us go back to the moment that you have your asthma attack (or in sever cases status Asthmaticus):

You are walking outside and you suddenly encounter an allergen that increases your muscle's reaction causing them to contract. As your bronchi muscles contract, they cause "Bronchoconstriction" which is basically the bronchus's radius "r" getting smaller due to increases size and tonality of your smooth muscle.

What does it mean when your bronchi (being the conduit of air here) decreases its cross sectional area (radius)?

You have based on Hagen-Poiseuille's equatino that as r goes down R goes up, but also remember that any increase in r would have a factor ^4 increase in R or resistance!

So let us make a sequence chart:

Patient encounter inhaled irritant or allergen ---> Allergic reaction to the allergen (antibiody; foreign object) increases mast cell activity --> mast cells release histamine, heparin and other agents ---> histamine causse inflamation and hypersensativity of smooth muscle and other bronchial tissue ---> bronchial radius decreases (r↓) ---> based on Hagen-Poiseuille's equation (R↑) or in other words resistance increases.

[for those with a bit more of physics background recall that upper airways are arranged in series and when you add resistors in series the total resistance is R = R1+ R2 + R3 + ... and so asthmatic patients have a much higher problem with bronchoconstriction than they do with lower respiratory airways like alveolar ducts or bronchioles because although the areas is much smaller for these airways and their "individual" resistances is very high, since they are all in parallel, as we know resistors put in parallel would have a total resistance of 1/R = 1/R1 + 1/R2 + ... which means that asthma is really a problem of upper airway constriction namely bronchi not lower respiratory zone]

So as an Obstructive disease asthma causes narrowing of your air way resulting in increased fluid (air) resistance.

But what causes the wheesing? why do asthmatic patients have an inflated chest? and why is it hard to breath out? Why do they cough? Why do they breathe really fast and shallow (hyperventillate)?

Well lets take these questions one at a time.

Why Wheesing on exhale?: It is defined as a noise heard upon auscultation (term used by physicans when the use the stetoscope to hear your lungs, or neck, or etc.). Remember our flow equation that said: A v = flow! since an asthmatic patient the air way constrict (r↓) so does areas (A↓). But we know that our body would try to compensate for flow to keep the flow constant so if we keep flow constant and A↓ so by logic v↑.

But now remeber the Reynold's number and the concept of laminar vs. turbulent flow. Physicas defines laminar flow as a kind of flow in which layers of fluid move past each other with the most central layer having the highest speed, whereas physics defines turbulent flow as one in which there is high speed "hurricane" like motions of the fluid molecules and it is not as orderly as laminar. To decide when a flow is laminar and when it is turbulent they created the Reynold number wihch is:

R.N. = ρ v D / η

where η is viscocity, ρ is density of fluid, D is diameter of the cross sectional area, and "v" is the velocity. Accordingly the bigger the R.N. the more "turbulent" a flow is.

So we know that r↓ ---> A↓ ---> v↑---->R.N.↑ ---> therefore you have that "wheesing" noise as fast "turbulent" air tries to escape out of your lungs.

[same phenomenon happens whe one passes gas. The high pressure of gas accumulating in the colon creates a pressure gradient P and according to the equation A v = flow. as A suddenly increases as one loosens up his anal sphincter, at the very beginning A is very small so v is very large so the gass flow is very turbulent hence the "loud noise" but as one relaxes the sphincter further the rate of increase of A decreases , so A becomes larger, v smaller and sound less turbulent and more "laminar." Although this might sound like an inappropriate comparision it does make sense! normal breathing does also produce a noise upon auscultation but it is more laminar in nature as opposed to asthmatic noise]
____________

Why do asthmatic patients have an inflated chest? Why is it harder to breathe out?

I have had patients who came in with no complaint other than feeling a bit full in their chest. Upron observing them in physical I saw that their chest is hyper inflated, and the radiograph showed the same thing. But why?

Well, respiration (breathing) has two stages: 1-inspiration (inhalation) , and 2-expiration (exhaling). Inhaling is an active process meaning that you have to expend energy to inhale air, since your diaphragm which is the muscle that seperates your chest from your belly must contract downward. As it does contract downward your chest's pressure (intrapleural pressure) decreases compared to the atmospheric pressure therefore inviting air into your chest. Air comes in and your lungs exchange gasses and when it is time to expire (exhale) the "elastic recoil" of your lungs would be sufficient by itself to expell air out as your diaphragm returns to its original positoin and pushes the air out. Expiration (exhalation) is therefore a passive process meaning it requies no energy (ATP).

But in an asthmatic patient we have to remember that there is a increase in R due to bronchoconstriction. So this means that patient has a harder time breathing in and out! why? remember the equation:

flow = ∆P / R

as R↑ ---> Flow↓ , therefore an asthmatic patient has to try "harder" to breathe in and out. But also remember that breathing in (inhalation) is an active process so although it is harder to do it will eventually happen so patient can breathe in but for breathing out, lungs NORMALLY only use their "elastic recoil" but in this case due to asthma the patient can not properly ventilate out the air resulting in a hyper-inflated lung!

[for those of you who have a physiological background or a cardiovascular background you can also realize that according to the ideal gas equation: P V = nRT, as lungs in asthmatic patients inflate (V↑) the pressure assuming nRT is constant would decrease (P↓). As pressure drops in the thoracic chest of these patients, the pressure on superior vena cava would decrease resulting on dilation of vein (venodilation) which would then cause a drope in venous return to heart and end-diastolic volume would decrease (EDV↓). According to Frank-Starling mechanism as EDV↓ ----> decreased inotropic contraction of cardiac smooth muscle ---> decrease stroke volume (SV↓) ---> decrased cardiac output (CO↓) ---> as cardiac output goes down so does pulse pressure (PP) since PP = (SV - mullerian run off) / Compliance of aorta ---> as Pulse pressure falls down (PP↓), central and peripheral baroreceptors would signal back via vagas and glossopharyngeal neves to Nucleus of Solitary trac (NTS) which would in turn de-activate Dorsal motor nucleus of vagas ----> increased Sympathetic flow to SA node of heart (SA activity ↑)---> creating a positive chronotropic effect resulting in tachycardia and increased heart beat in asthmatic patients!!]

_____________

Why do asthmatic patients cough?

For two reasons: one is their reaction to the allergen by the irritant receptors in the upper airway, and the other is due to activation of Rapid Adapting Strech Receptors (SARs) in the upper airway in reponse to increased smooth muscle contraction and bronchoconstriction.

_______________

Why do asthmatic patients hyperventillate?

This is a response to increased CO2 pressure (Pco2) in blood and also set forth by anxiety. As the concentration of CO2 in blood increaes due to asthma the patient breathes faster (Ventilation rate goes up) while the breathe depth (Tidal volume) decreaes resulting in shallow hyperventillative breaths. This reaction is to sensing the increased CO2 by peripheral and central chemoreceptors that sense the increase in CO2 and respond by forcing lungs into hyperventillation.

[Ok, but before I actually start to deal with the original posts message of "Rubbing his left side to help relieve asthma attack" let me add one more thing. In asthma or any obstructive pulmonary disease Compliance is increased! But what is compliance? In physics C or Compliance (sometimes called capacitance) is C = V/P where V is volume and P is pressure. This resembles a lot the actual capacitor equation of C = Q/ V where Q is charge and V is voltage but in this case in lungs we do not have charge and so voltage is in reality pressure gradient, and charge is the volume this pressure can handle. So in asthmatic patietns we already concluded that volume of the lung increases so V↑ ---> C↑ so the lung compliance goes up, but also remember that C = 1 / E where E is elastance or elastic recoil. So patients with asthma have increased compliance, and decreased elasticity of chest wall resulting in a hyperinflated chest]


________________________
__________________

To the original poster:

You mentioned tha you 1-lied down, 2-rubed your left chest area around second or third intercoastals , 3-and that helped your feel better.

I think (not sure since I can not physically examine you) that when you rubbed your chest on the left that somehow you affected the vagal branch or somhow induced an increased strech of aortic baroreceptors or maybe you increased a sympathetic nerve's activity resulting in bronchodilation.

Anyhow the best advice is TO SEE A DOCTOR and to keep up with your medication. Usually treatment is Albuterol (you might heard it as salbutamol sulfate or albuterol sulfate or etc as well) whic is basically a bronchodilator. You must also avoid cold weather (since cold weather increases viscocity of air increasing Resistance (R↑), avoid strenous exercise, avoid allergens or allergen-inducing environments.

I know how you must feel having seen people who have had asthma and I know what a burden it can be in your life. I admire your resillience and your positive attitude. At the end of the road in this tiring life, we all have only one thing to hang on to and that is hope. At least for me having failed in true love, or friendsihp the only corner of relief is science and my profession and you too should find one thing that rlaxes you and focus on it. I am sure you know best how to deal with it but rest assured I hear how you feel and wish you the best.

Ulrich Drude (MD)

[Do not treat my post as a medical advice. I am writing here only in my capacity as a poster. Any treatment optoins or choices should AND SHOULD ONLY be discussed with your personal physican IN PERSON. God bless]