Respiratory physiology 1 Lecture Notes

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General introduction:

* There are two types of respiration; internal (cellular) respiration and external respiration

Internal respiration: refers to intracellular metabolic processes occurring within mitochondria, which produce energy by using O2 and producing CO2

External respiration: refers to the steps of gas exchange between external environment and cells mediated by blood transport, and has 4 steps:

A/ Ventilation; movement of air in and out through lungs, to provide alveoli with O2 and takes CO2 away from them to out side

B/ O2 and CO2 exchange between air and of alveoli and pulmonary blood capillaries surrounding alveoli by the process of passive simple diffusion (from high to low)

C/ blood transport O2 and CO2 between lungs and tissue cells

D/ O2 and CO2 are exchanged blood and cells

Functions of respiratory system:

Regarding respiration, it provides ventilation and gas exchange between alveoli and pulmonary capillaries

Non-respirator functions:

Water and heat loss, it participates in acid base balance (through excreting CO2 which reduce acidity), for speeches, modification of some substances that pass through lungs (like angiotensin I), enhance venous return (when chest expand and contract it helps in venous pumping)

Anatomical considerations:

1) Air enter through nose or mouth then pass to pharynx (which is the passage for air and food) then to larynx (for air passage only and also serves for vocation , then to trachea which will branch near lungs to main left and right bronchi, each bronchus then progressively branch to many tree like bronchioles all these mentioned pathways are called air way conducting system (which serves only for conduction of air between atmosphere and air sacs (alveoli) and there is no gas exchange through them) then these bronchioles end in terminal bronchioles which end in alveoli(air sacs) that are grape cluster like structure where the gas exchange occur here

2) Lungs lie in the thoracic gage, they are surrounded by two layers of pleural membrane, these two layers form a thin space between them filled with lubricant fluid (pleural fluid), these two layers of pleura the inner one attached to lungs and the outer one attached to the chest wall (so the pleural membranes lie between lungs and chest wall)

3) When thoracic gage expand (by inspiratory muscle contractions) it will pull lungs from all directions to expand, so that lung will full fill the new size, and that will cause air to enter to alveoli, while when the thoracic gage contract (by means will be mentioned later) it will compress lungs and force air to get out

4) Inspiratory muscles:

a) External intercostals muscles, when they contract they pull ribs to outside and up and by this increasing anteroposterior diameter and bilateral diameter, in other word increasing thoracic gage diameter

b) Diaphragm, when it contracts it will be flattened so that it will pull the bases of the lungs down ward forcing them to increase vertical diameter and by this air will enter

* There is also inspiratory muscles called accessory muscles they are sternocleidomastoid muscle and some muscles originating from the cervical vertebrae and insert on first rib called scaleni muscles (single: scalenus)

These two muscles help in elevating ribs up and out ward so that increasing the horizontal diameter of thorax

Important note: during normal quiet breathing we don’t need these accessory muscles to act all what we need is the diaphragm, they are acting when we need large volume of air to enter like in exercise and disease states

5) Expiratory muscles: before mentioning them you have to realize important thing that is expiration during normal quiet breathing is a passive process i.e. doesn’t need for muscle contraction, and that’s due to the fact that lungs are elastic tissue (contain elastic fibers) means that if you stretched lungs by expansion it will return to it’s original size spontaneously after respiratory muscles relax, this feature is called lung recoiling, chest wall and muscles also has this feature but not like the lungs

* Expiratory muscles are:

a) Internal intercostals muscles; when they contract they pull the ribs in ward and down ward so that decreasing the horizontal diameter

b) Abdominal muscles; when they contract they push abdominal viscera and diaphragm to up making diaphragm more dome shape and decreasing the vertical diameter

Note: we use expiratory muscles when we need active forceful expiration like exercise or disease states, while in normal conditions all what we need is lung and chest wall elasticity for passive expiration

Mechanics of breathing (inspiration and expiration):

Physical facts:

1) When you expand any container, which contain air you will reduce the pressure inside it

2) Air passes from high to low pressure

3) Atmospheric pressure is 760 mm hg

4) Intra alveolar pressure is the pressure of air inside alveoli, alveoli are communicated with out side, so, when intra alveolar pressure increase above 760 mm hg because of compression on lungs air then flow to out side and vise versa

5) Pleural pressure which is the pressure inside pleural space is below atmospheric (it is 756 mm hg), and it will never be equal with atmospheric what ever is the state of the respiratory cycle, it may decrease further to reach 754 mm hg during inspiration

Note: some times we refer to intra pleural pressure as negative pressure in comparison to atmospheric pressure

Q. What is the wisdom of this intra pleural pressure to be less than atmospheric?

A. It acts to suspend lungs to outward so that acting against normal tendency of the lungs to collapse (by the feature of elasticity and surface tension which will be mentioned later)

Note: pleural space is a separated space that means it has no communication with atmosphere, and if it communicate for any reason like in disease state the pressure inside it will equilibrate with atmosphere and resulting in loss of the normal force that act against lung collapse (a clinical condition called pneumothorax)

Transmural pressure: it means the pressure difference between intraalveolar pressure and intrapleural pressure. The first one is equilibrated with atmospheric (760 mm hg) and the second one is 756 mm hg this pressure difference tend to pull lungs outward, the more pressure difference the more tendency to expand lungs that’s what happen in inspiration, and less pressure difference make lungs tend to collapse and that’s what happen in expiration

Back to mechanics:

* Before starting discussion, you have to know that when all respiratory muscles relaxed before inspiration, the intraalveolar pressure is equal to atmospheric 760 mm hg

1) When the inspiratory muscles contract mainly diaphragm and to some what intercostals muscles during normal breathing, they will increase the thoracic gage size so that will pull the pleural sac making the intraplueral pressure to fall to 754 mm hg i.e. further more away from atmospheric pressure and that’s mean increased Transmural pressure which will lead to lung expansion

2) Lung expansion will lead to decrease intraalveolar pressure less than atmospheric pressure about 659 mmhg and this will lead air to flow to inside from high to low pressure

3) If we need forceful inspiration (more air entry), we can use then accessory inspiratory muscles

4) When the inspiratory muscles relax in the end of inspiration, by this, the force which expanded the lungs will disappear, so, the lungs and chest wall tend to resume their original size by the force of the elasticity that make compression on lungs which result in increased intraalveolar pressure up to 761 mmhg and air flow to outside and that’s is expiration

Elasticity of the lungs: when talked about the elasticity of the lung we have to know that this is due to presence of elastic tissue inside lungs and presence of Alveolar surface tension

Alveolar surface tension:

* First we have to know that a thin layer of water from inside lines alveoli and this layer is important in the process of gas exchange, and the dryness of alveoli will affect the process of gas exchange

Physical facts:

1- when water is present as a small bubble (i.e. referring to water lining the alveoli), the molecules of this water attract each other tending to be together and reducing the bubble size and this force of attraction increase when the bubble is smaller in size (i.e. when the alveolus is smaller) so they tend to collapse the alveolus, this force is called surface tension

2- when we apply above fact on the alveoli then we realize that this force tend to collapse alveoli and compressing air to pass to outside, that’s why this force participate with lung elastic tissue to bring the lungs to their originally size after their expansion in inspiration (when the inspiratory muscles relax and lung recoiling occur)

Pulmonary surfactant:

1- it is a mixture of lipid and protein

2- if there is only water lining the alveoli, the force of surface tension will be very great that it may collapse alveoli and lungs

3- surfactant function: it intersperses through molecules of water that are lining the alveoli and by this reducing the attraction force between molecules and thus, resulting in reduction of surface tension force

So, the functions of surfactant: a) reduce surface tension of alveoli and prevent them from collapse b) reduce effort or work that is needed for inspiratory muscles to expand the lungs

4- surfactant is released from type II alveolar cells (which are present as apart of alveolar epithelium)

5- deficiency of surfactant in newborn baby will lead to difficult inspiration because surface tension is so strong making alveoli collapsed a condition called as “ respiratory distress syndrome”, which may lead to death

Laplace’s law:

When the alveolus is small in diameter it has greater force or tendency for collapse than the larger size diameter alveolus and that’s because the collapsing force (collapsing pressure) will be greater when the diameter or radius of alveolus decrease, and this is represented in the following equation:

P = 2 T / R

Where:

P = collapsing pressure

T = surface tension

R = radius of alveolus

So, you can conclude that when (R) reduced, as in small alveoli, thus we predict that small alveoli has greater collapsing pressure and may collapse…….!!! But, this doesn’t occur because surfactant is present to reduce surface tension (T) Examples:

Let’s say we have two alveoli, the first is 4 unit in diameter and the second is 2 unit and we have surface tension for pure water about 8 unit,, what are the collapsing pressure for each

First one: P = 2 T / R = 2 X 8 / 4 = 4 ……………….. Large alveolus

Second one = 2 T / R = 2 X 8 / 2 = 8 ……………… small alveolus

But, with surfactant the surface tension (T) is reduced, and by this, reducing collapsing pressure

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Posted in Physiology, Respiratory

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