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 Physiology, Sheet 4, Dr.yanal 8\2\2012

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Majed Sharayha

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PostSubject: Physiology, Sheet 4, Dr.yanal 822012   Fri Feb 10, 2012 12:28 am

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Physiology lec #4 , Feb.8 .

A recall from feb.7 's lecture :
Encountering an increase in the airway resistance results in Hypoxia or inadequate oxygenation of the blood .
Airway resistance is a measure of how difficult the air is going tp pass through the airways ; which start by the openings of the nose or the mouth , passing through the pharynx , larynx , trachea .. etc , which are collectively known as the conducting zone " 1st 16 generations " .
The 4 home take messages were :
1. Airway resistance is usually small or negligible because we don't feel like facing resistance during ventilation, and the pressure difference or the driving force is very small , equals +1 mm Hg .
2. Airway resistance usually resides in the large airways because the total cross sectional area is small compared with bronchioles .
3. pathophysiologic conditions in airway resistance usually arise in the small airways , because of these significant factors :
a. They lack cartilaginous support . Unlike the trachea and major bronchi which are supported by C shaped cartilaginous rings , small airways are left with no support , surrounded by remnants of cartilage and smooth muscles. After generation 11 cartilage is absent .
b. contraction of smooth muscles found in the wall of small airways will cause broncho-constriction which decreases their lumen .
c. Goblet cells found in the respiratory epithelium secretes mucus , recall that mucus is simply water and protein , excessive mucus secretion leads to re-absorption of water by the respiratory epithelium leaving a solid plug that obstructs small airways whilst such a plug in the trachea won't cause it's obstruction .
d. Bronchiolitis or inflammation in the submucosal layer of respiratory epithelium will decrease the lumen by developing edema .
As a result of these factors if we face a 10-fold increase in airway resistance , 9 are in site of small airways and 1 are caused by large airways .
4. When facing increased airway resistance ,greater resistance is accompanied with expiration which is explained immediatly after taking these 3 notes in consideration :
* -4 is the intra-pleural pressure which surrounds the alveoli & the small airways " bronchioles '' .
* If the diameter of the small airways is decreased " let's say a mucus plug is blocking the bronchioles " , airway resistance would increase .
* Negative pressure is an opening pressure ,Positive pressure a closing pressure .
Inspiration :
- during inspiration intra-pleural pressure becomes -6 , more negative pressure surrounding small airways is an opening pressure which pulls the airways outwards increasing their lumen .

So the blockage of small airways is countered by the negative pressure that develops during inspiration .
- pressure in the 4 compartments in normal conditions at rest :
Atmospheric pressure = zero
Airways pressure = zero
Intra-pulmonary pressure " lung " = zero
Intra-Pleural pressure = -4
- The Intra-Pleural cavity is neither connected with the outside nor with the intra-pulmonary cavity " lung " .
- We cannot manipulate the atmospheric pressure in order to create a driving force that leads air inside the lungs .
- during inspiration : in order to create a -6 intra-pleural pressure, the intra-pulmonary pressure must become -1 . Which creates the required driving force and air is lead inside.
- The respiratory minute ventilation = flow = 6 liters .
Flow = ∆P/AWR
- in the presence of a plug AWR increases , flow must be kept constant , so ∆P increases to the same extent as AWR .
- increasing ∆P is achieved by either 2 methods only 1 of them is valid which is making the intra-pleural pressure more negative . the other method is to increase the atmospheric pressure to a more positive value which is not applicable .
- pressure values with the presence of a plug during respiration :
Atmospheric pressure = zero
Intra-pulmonary pressure " lung " = -10
Intra-Pleural pressure = -16
- pressure values in normal conditions during respiration :
Atmospheric pressure = zero
Intra-pulmonary pressure " lung " = -1
Intra-Pleural pressure = -6
So as a summary , facing increased AWR is countered by increasing the driving force which is achieved by increasing the intra-pleural pressure to a more negative value and pressure values are as follows :

Expiration :
- During expiration in order to push air out , the intra-pulmonary pressure must exceed the atmospheric pressure , which becomes normally +1 , and the intra-pleural pressure will fall from -6 to -4 .
- In the presence of a plug those values are not valid , because we need to push air against a higher AWR . the intra-pulmonary pressure might rise to +10 and the intra-pleural pressure might rise to -3- +3 , in accordance with the AWR .
- recall that positive pressure is a closing pressure or a compressing force , and a slight closure in the small airways will be during expiration a complete closure or an ''obstruction'' because of the raised positive pressure .
Notes :
1. positive or negative ∆P as a magnitude is the same driving force and signals indicate the direction inside or outside of the lungs .
2. an increase in ∆P will always be in accordance with the increase of AWR , that is to keep the flow constant and equals 1 unit " 1 unit = 6 liters " an increase in AWR by 2 units is followed by an increase in ∆P by 2 units .
3. inflating lungs means creating more negative pressure , compressing lungs means creating more positive pressure , which comes by default .
We Use our respiratory muscles to increase or decrease the intra-pleural surrounding pressure :
- Inspiratory muscles are the external intercostals that inflate the thorax .
- Expiratory muscles are the internal intercostals that lessen the thorax & the abdominal muscles that push the diaphragm upwards which reduces the vertical diameter of the thorax .
Summarizing our problem : every time we exhale against a plugged small airway we create more positive pressure which obstructs the airway completely ,there is no point of increasing the intra-pulmonary pressure to +20 because this will result in more obstruction .
- A person who experiences a plugged small airway has no problem in inspiration as discussed previously , but during expiration a problem arises , this problem is solved by making expiratory effort which is using the mentioned expiratory muscles to a certain point , if this point is crossed and the maximum expiratory effort is reached obstruction will happen .
- Example : intra-pulmonary pressure of +10 mm Hg is achieved by making expiratory effort , the small airway is slightly open , intra-pulmonary pressure of +12 mm Hg is achieved be exerting a maximum expiratory effort , the small airway is obstructed .
* Meaning that the maximum expiration is reached before exerting the maximal expiratory effort .
- Expiratory effort is a synonym for driving force .
- Apparently this scheme of expiration is ineffective , not practical and tiring . Here maneuvers that guarantee an open airway when exerting a maximum expiratory effort of +12 mm Hg are applied .
- then this person will have to expire through pursed lips to increase the intra-airway pressure and keep the airways permanently open .
- A plug in the small airways falls under the category of COPD's which are the Chronic Obstructive Pulmonary Diseases .
- Expiration through a narrowed area produces sound named wheezing which is audible without a stethoscope . If wheezing is produced during both expiration and inspiration then this indicates an advanced condition of obstruction " advanced obstruction " .
- Increased air way resistance by a way or another is manifested by 3 pathological conditions, Emphysema , Chronic Bronchitis , and ± bronchial asthma .
Emphysema literally means excess air in the lungs . too much entering that has got no exit , some sort of condition called barrel chest .

- the wall of the alveoli consists of proteins and a lipid bilayer which is a typical cell membrane , protected from proteases that digest proteins such as trypsin by trapping them into lysosomes .
- if trypsin is freed , it is going to digest proteins that make up the cell membrane and eventually will destroy the alveolar wall ending up with marked loss of alveolar walls .
- This infinite loss of alveolar walls greatly decreases the area available for diffusion and gas exchange , consequently blood oxygenation decreases and levels of carbon dioxide in the blood increase . Oxygen diffusion is affected 1st .
- a patient with decreased oxygen levels and increased carbon dioxide levels is said to have 90% damaged lungs .
- antitrypsin inhibits trypsin digestive actions , and antitrypsin is in turn inhibited by cigarette smoking , and to emphasize how big of a problem this is , the damage processed on the alveolar wall is irreversible , so quitting will not restore the damaged lung tissue but it will prevent additional tissue loss .
- any common disease e.g cold & flu do not cause irreversible damage .
- destruction of alveolar walls leads to destruction of capillary networks surrounding them .
- What is the penalty of destruction pulmonary capillary beds , other than decreased oxygenation and increased levels of carbon dioxide ?

* the pulmonary circulation begins by pumping blood from the right ventricle to the pulmonary artery/ trunk causing a mean pressure of 14 mm Hg , passing through the pulmonary capillaries and ending up with the right atrium .
The mean pressure is calculated as ⅔ the diastolic pressure 8 mm Hg and ⅓ the systolic pressure 25 mm Hg .
* During a cardiac cycle , the right ventricle faces an after load which is the pressure in the pulmonary artery , and from the right ventricle perspective this pressure is not a good guy because the right ventricle has to exceed the pulmonary artery pressure to pump blood successfully during each cardiac cycle .
- if the after load rises to a much higher value of 24 , 44 , 54 , 100 … etc , the right ventricle is going to dilate and suffer much more than the left ventricle due to it's decreased thickness 2-3 mm compared to the left ventricle 10-12 mm .
- As a conclusion , the right ventricle does not like the so called pulmonary hypertension which is increased pressure in the pulmonary artery .
- The pressure in the pulmonary capillaries is 7 mm hg , and in the pulmonary artery is 14 mm Hg , ∆P or the driving force is 7 mm Hg .
- flow = cardiac output = ∆P/ TPR
- ∆P = 7 and TPR = 7 , Q = 1 unit or 5 Liters .
- increased pulmonary vascular resistance must be followed by an increase in ∆P , so if the resistance increases to 17 , ∆P increases to 17 and so forth , only to keep the flow constant and equal to 1 unit or 5 liters .
- remember we are still talking about emphysema , emphysema as mentioned earlier has lead to destruction of pulmonary capillaries , so instead of having sufficient surface area , we ended up with few capillaries and small surface area .
- decreasing the surface area creates more pulmonary resistance , and consequently more ∆P , or after load imposed on the right ventricle , leading to right ventricular failure .
- Pulmonary diseases " emphysema , chronic bronchitis , fibrosis , obstruction , restriction or whatever " lead to Cor Pulmonale which is right ventricular hypertrophy & dilatation , ± right ventricular failure .
- ± sign preceding the right ventricular failure means that failure if not present ,is going to happen sooner or later .
* Summarizing effects of emphysema :
1. Increased airway resistance .
2. Decreased area available for exchange and diffusion .
3. Increased pulmonary vascular resistance .
4. Right ventricular hypertrophy and dilatation .
5. Pulmonary hypertension .
6. Heart failure or Cor Palmonale .
- Expiration is a passive process , achieved by the elastic recoil of elastic fibers found in the lung tissue , on the contrary inspiration is an active process that needs ATP .
- the elastic recoil passively brings the lung back to its functional residual capacity .
- destruction of those elastic fibers , leads to active expiration ! using the expiratory muscles .
- The lung is a compliant organ but either too much compliance or too little compliance is not a good thing .
- inflating the lung during inspiration is not a problem if the elastic fibers are destroyed but the lung faces a problem during expiration .
- the lung acquires more compliance during emphysema and as said before too much compliance prevents the lung from recoiling back to its initial state .
- too much compliance : problem in recoiling back to initial state .
- too little compliance : problem in inflating during inspiration " which is not the case in emphysema " .
- Emphysema is diagnosed by taking a biopsy " pathological diagnoses " and there are many types of emphysema e.g centrilobular , panlobular , or clinically through the X-ray .
Chronic Bronchitis
- Chronic Bronchitis is a continuous productive cuff '' mucus which has a greenish or yellowish texture '' for 3 months in 2 successive years " during cold months " .
- Chronic Bronchitis like emphysema is caused by smoking .
- smoking affects :
1. excessive mucus production .
2. cilliary paralysis in the respiratory epithelium found in the anatomic dead space .
3.inhibitis anti-trypsin e.g α-1 anitrypsin .
- Symptoms and effects of chronic bronchitis and emphysema usually occur simultaneously but the majority would be one of them . " chronic bronchitis and emphysema overlap " .

Asil Mahmood Marahle .
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Physiology, Sheet 4, Dr.yanal 8\2\2012
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