Basic Principles:   Receive, Process and Export

The lung and airways have the important role of bringing fresh air from the environment to the alveoli,  to enable a gradient for the oxygen and carbon dioxide to be exchanged, to facilitate the uptake of and removal of the gases from the blood stream and to transport the carbon dioxide to the environment.

In keeping with the basic principles outlined in the introduction, it receives the oxygen, transports it to the airways, processes by creating a filter and exchange mechanism, and then exports the oxygen intot the blood.  It has a dual function in the it receives the carbon dioxide from the blood and then after assisting the the conversion of CO2 from a fluid envoronment to a gaseous environment, it moves the carbon dioxide to the environment.

Lung Movement : Basic Principles

The lung is often compared to a bellows system, meaning that with alternate expansion and contraction, air travels one way through a tube during expansion and expelled the other way when the mechanism recoils.

 

     Inspiration is an active process requiring muscle contraction and therefore energy, while expiration is a passive process of elastic recoil requiring no energy.   As noted, one of the unique features of the lung is its ability to act as a two-way transport system. No other tube in the body is asked to perform this dual function.  At first this seems like a simple demand on the system, but as you will see it is more complicated than a simple bellows system, and a fine balance exists between the complex forces of inspiration and the complex forces of expiration.  Biology has had to make some considerable adaptations in order for the dual function of the airways to coexist.

Lung Movement: 5 Layers  

There are five general functional layers to the bellows system.  They include the bony cage, the muscle layer, the pleural layer, the lung and the layer of surfactant.  The overall complex with bony, muscular, membranous, spongy elastic and chemical properties keep the air moving in and out efficiently.

      First Layer – Bone

     The bony cage of ribs sternum and spine create the outer protective layer with the sternum and spine being the relatively rigid components and the ribs being both protective and the more pliable component.  The ribs move up and out during inspiration pivoting on the sternum and spine like bucket handles (ribs) on the two fixed points of the bucket (sternum and spine)

Second Layer – Muscle

The second layer includes the diaphragm inferiorly, the intercostal muscles circumferentially,  the serratus anterior anterolaterally, scapular elevators posteriorly and erector spinae muscles posteriorly.  Superiorly the scalene and sternocleidomastoid muscles assist when necessary.  The abdominal muscles also play a role as accessory muscles of respiration since movement of the chest cavity has effect on the abdomen, and vice versa.  In fact, a principle to always keep in mind is that no cavity, system, organ or cell is an isolated island – they all in the end work in concert for the greater health of the whole.  John Donne, an English poet of the 17^th century, proposed that “no man is an island,” promoting the same concept of the interconnectedness of all.

     During inspiration the diaphragm moves down and intercostal muscle contraction causes outward chest vectors, resulting in chest cavity expansion.  As a result there is a decrease in intrathoracic pressure and air flow into the lungs.  When the muscles relax, the diaphragm flattens, the intercostals return to baseline position by passive and elastic recoil, and the chest moves inward, causing the chest volume to decrease. The intrathoracic pressure rises and becomes higher than the atmospheric pressure and therefore air will move outward from a position of high pressure to one of low pressure.

      Third Layer – Pleura

     The third layer is the double-layered pleura, with one component intimately attached to the chest wall, and the other layer intimately attached to the lung.  Between them there is a thin layer of fluid that binds the two layers together by capillary action.  The pleural surface constantly absorbs the fluid or gas that enters the space and a negative pressure of about 10mm Hg is maintained.  We have all experienced the power of the thin fluid layer of water between two clean smooth surfaces of glass which cannot be pulled apart because of the adhesive and cohesive capillary action.  Capillary action is the interaction between contacting surfaces of a liquid and a solid.  The cohesion and adhesion that result keep the outer chest cage of bone and muscle in intimate contact with the lungs, being pulled and pushed together in the harmonious dance of respiratory movement.

The adhesion and cohesion of the lung to the chest wall is a lifelong relationship of intimate contact, characterized by 10-15 in and out movements per minute at rest, and sometimes up to 20 – 40 breaths per minute during exercise.  The harmony and intimacy continue despite the rigorous jolts of life including violent sneezes, cough whoops, jumps to the basketball hoops and the likes of usual rough and tumble.   It is a simple but marvelous mechanism that keeps two structures bound together by such a simple but powerful physical principle.   When there is a large effusion or pneumothorax then the cohesive and adhesive mechanisms fail, and collapse of the lung ensues.

 

Fourth Layer  –  Lung

     The lung as a whole provides the next functional layer, but within the lung there is a combination of structures, each with different properties and needs.  For the sake of understanding we will consider it a single layer.  The relatively rigid upstream airways do not change much with the ins and outs of respiration, while the smaller airways and to greater extent the alveoli undergo significant change in size, expanding with inspiration and getting smaller with expiration.

The alveoli exhibit a surface tension which creates an environment for recoil during expiration and if held unchecked would undergo complete collapse.  The tendency for recoil is necessary and healthy, while the collapse is of course harmful.  The total collapse of the alveoli is prevented by the automatic rhythm of involuntary inspiration which reverses the process as well as the presence of surfactant (our fifth layer) which prevents the collapse.  In the absence of surfactant the pressure required to keep the alveoli open is 20-30mmHg.  Surfactant reduces this to about 3-5mmHg.

Fifth Layer – Surfactant

     Surfactant, the fifth and last layer, is a lipoprotein solution secreted by specialized cells of the alveolus.  It serves to reduce the surface tension and ease the force necessary to open the alveoli during inspiration.   In blowing up a balloon, we find that the most difficult part is when the radius of the balloon is small.  Thus the surface tension on the balloon is high when the radius is small.  As the radius increases the surface tension decreases and it becomes easier to blow up the balloon. Surfactant if it were present in the balloon would decrease the wall tension by an order of 15, to ease the energy and pressure necessary to inflate it. 

 

Lung Movement: Applied Physiology

  We will now review the 5 layers and apply our knowledge of the physiology and anatomy to the diagnostic and therapeutic world.     

First Layer – Bone

Fractured Ribs

     The fracture of two to three ribs in one place does not result in respiratory difficulty.  The pain that ensues can cause decreased respiratory excursion and consequent mild atelectasis.  Pain limiting respiratory motion is a very common clinical and radiological scenario, often seen in patients who have had abdominal or chest surgery.   

     Flail chest, on the other hand, is fortunately not common, but is an urgent clinical problem following extensive blunt traumatic chest injury.  Flail chest arises when three or more ribs are fractured both anteriorly and posteriorly, resulting in a loss of chest support.  Paradoxical chest movement results so that during inspiration the fractured ribs follow the movement of the lung rather than the chest wall from which they have become detached.  Thus during inspiration the isolated ribs and associated chest wall move inward instead of out, and during expiration they move out instead of inward.  This injury is usually seen as a consequence of severe trauma, and associated lung parenchymal injury is common. Clinical consequences are a combination of the loss mechanical efficiency and loss of parenchymal function. 

     The following case represents a controlled situation of paradoxical motion of the chest.   The patient was asked to take a deep breath in.  Can you work out what the problem is?

The following CT shows the same patient during inspiration.

The following CT shows the same patient during expiration.

Scoliosis

            The effects of scoliosis on respiratory function both before and after surgical correction have revealed that the degree of scoliosis did not correlate with the severity of respiratory difficulty, though there was improvement by about 10% of lung function following surgical correction.

 Second Layer – Muscle

The ring of muscle is the next layer

Paralysis

It is not uncommon to see paralysis of one hemidiaphragm without untoward effect.  However, when both components of the diaphragm fail, therapeutic intervention is urgent.  Diseases that affect the neural signal (polio, Guillain Barre, quadriplegic syndromes), transmission of the neural signal (myasthenia gravis), or disease of the muscle itself (tetanus, myopathy), can result in respiratory failure.  In the acute situation when respiratory compromise is severe the patient will require a ventilator.  The iron lung was developed to treat polio in 1927.  It was the first respirator and was developed by a Harvard researcher Philip Drinker.  He used an iron box and two vacuum cleaners to create a push and pull motion on the chest.

     Third Layer – Pleura

The next layer is the pleura which act as the intermediary between the chest wall and the lungs.

The pleural adhesion/cohesion mechanism is quite robust system, but like all mechanical systems under duress it can fail.  Pneumothorax is a well known failure of this system and is caused by air leaking from the lung, which intervenes in the bonding mechanism and separates the two pleural components.

Pneumothorax

 

  When a patient has a small pneumothorax we ask that the patient lie in bed with the affected lung on the down side (ipsilateral decubitus position) so that we limit the chest wall movement on that side and hence air movement into the lung.  If the pneumothorax is large the patient can become symptomatic and a life threatening event called tension pneumothorax can ensue.  In tension pneumothorax, air leaks into the pleural space on inspiration and is trapped on expiration.  The air subsequently accumulates untl the pressure is sufficiently high in the pleural space to cause compression of the venous structures in the chest.  The elevated venous pressure prevents venous return to the heart and cardiac output falls. Quick recognition of this entity and immediate decompression by a needle or a tube is life saving.

Pleural Effusion Problem with Layer 4

The following is also a problem with the pleural space – Can you work out what the problem is in the right chest? 

 Fourth Layer – Lung

Restrictive Lung Disease

The next layer is the lung.  Restrictive lung disease occurs when the interstitial tissue of the lung lose elasticity and is replaced by fibrotic tissue.   The patient has greater difficulty in expanding the lung and the recoil mechanism is also affected.

Fifth Layer – Surfactant
Hyaline Membrane Disease

The next layer is the surfactant.

Premature babies do not produce surfactant and therefore their tendency to collapse the alveoli during inspiration is increased.  Also, greater forces are necessary to inflate the alveoli.   Extensive atelectasis or lung collapse results in this condition and the baby may require a respirator to help keep the lungs open.  This disease is called hyaline membrane disease, or respiratory distress syndrome.

              A parallel disease in older patients is called ARDS, or adult respiratory distress syndrome.  It is characterized by diffuse alveolar damage (DAD), resulting in a relative lack of surfactant and consequent micro-atelectasis.  There are many causes of DAD including sepsis, multisystem trauma, smoke inhalation, near drowning, and narcotic overdose.  The absence of production of surfactant, in combination with the fluid accumulation in the alveoli, causes increase surface tension and more patient effort to expand the alveoli.  When this effort fails there is atelectasis that may require a respirator to keep the alveoli patent.

Gas Exchange: Basic Principles

While the function of air transport is the domain of the tracheobronchial tree, it is the function of the alveoli to act as a membrane for gas exchange to and from the atmosphere and the blood.  The principles of gas exchange across a membrane are also universal in the body. The movement of both oxygen and carbon dioxide is by diffusion.  Diffusion is the movement of the gases, fluids or chemicals from a higher level of concentration to a lower level. The partial pressure of the two gases is a measure of their concentrations.  The greater the difference in partial pressure the greater the rate of diffusion. Oxygen is carried mostly by a macromolecule of protein called hemoglobin while carbon dioxide is mostly carried in the form of bicarbonate in the serum. 

The membrane across which the gases have to move is between .3 – 1.0 micron thick and consists of two cell layers.  One layer is the epithelium of the alveolus and the second layer is the epithelium (called endothelium) of the capillary.

Fick’s law governs the movement of air across a membrane.  The net movement or diffusion rate of a gas across a fluid membrane is proportional to the difference in partial pressure, proportional to the area of the membrane and inversely proportional to the thickness of the membrane. The total membrane surface area of the alveoli is about 80-100 square meters and the thickness is less than a millionth of a meter, so it is a very effective gas exchange interface.

 At rest about 6-10 liters of air is moved through the tracheobronchial tree per minute. In this same minute about 600ccs of oxygen moves from the alveoli into the blood, while 600ccs of carbon dioxide moves across the membrane into the alveoli.  During exercise up to 100 liters of air can be moved through the airways per minute and about 3 liters of oxygen and 3 liters of carbon dioxide is moved across the membrane. 

Composition of Air

Dry air is composed of 21% oxygen, .04% carbon dioxide, 78% nitrogen and less than 1% of other gases such as argon and helium.  The amount of gas present can also be expressed in terms of its partial pressure.  At sea level the partial pressure of oxygen is 160mmhg (21% of 760mmHg) and carbon dioxide is .3mmhg in the atmosphere.  In the lung the partial pressure of carbon dioxide (pCO2) is relatively higher being 40mmHg and the PO2 is 104mmHg, while the PCO2 in the pulmonary arteriole is 45 and the PO2 is 40mmHg.

Changes in PO2

Changes in PCO2

 

 

Gas Exchange: Applied

The alveolar membrane can get affected by diseases processes that may accumulate fluid or pus within the alveoli causing a thickened membrane.  Interstitial fibrosis is a second cause of thickening of the respiratory membrane which will affect the efficiency and speed of gas exchange. 

In general we intuitively know that when we take a deep breath we are using our muscles to actively inspire. When we breathe out it is a relaxation of that mechanism caused by actual muscle relaxation and the elastic recoil of the layers of the chest.  We can of course breath out all the way until we have expired right to what we think is the last drop of air, and this takes effort and muscle contraction as well.  When you as a technologist have a patient for a routine CXR you ask your patient to “take a deep breath in, blow it all the way out and hold it….”  And you click your exposure.  You can readily see that there is still quite a lot of air left in the lung.  This is called the dead space of the lung, found in patients who are well and alive!   Read on and learn all about what happens to the lung volumes and capacities during that process.

Lung Volumes

In order to explain the process we will pretend that you are a lung function technologist for a moment.  You are going to test your patient’s lung volumes, capacities and velocities.  We want you to think and apply what you see on these graphs to your own situation when you are doing a CXR, and to imagine the differences between an inspiration CXR and expiration CXR.  We particularly want you to see the difference in volume of air between the inspiration film and the expiration film.

So we go back to our theoretical patient undergoing lung function tests and we place a mouthpiece over her mouth and attach the tubing on the other end to a recording device called a spirometer.  As our patient lies on the table breathing quietly under resting conditions we notice a simple rhythmic pattern on the spirogram.  This pattern is entirely involuntary caused by the production of a signal from center of respiration located in the brain that causes the diaphragm and other muscles to contract and  to expand the chest, and then as it switches off, the muscular relaxation and elastic recoil cause the chest to contract.

Tidal Volume

   We reset our spirometer to get our basal conditions set between the 3 and 4 liter mark so that we have room on the graph to see what happens with forced inspiratory effort and forced expiratory effort.

For those of you who require your patient to “breath hold” for MRI and CT, we are in fact asking them to stop this involuntary breathing pattern in order to prevent chest wall and lung movement that would otherwise cause motion artifact  on our images.

For our CXR we now ask our patient to take as deep a breath in as possible and we see a dramatic change on the graph.

Inspiratory Reserve Volume

When we ask your patient to take a deep breath in we have a similar experience but the change is reflected in a CXR is a larger chest volume by more than 3 liters.  The patient will muster their muscular forces to contract the diaphragm and intercostal muscles to enlarge the chest cavity and pull in air.  The lung in the healthy patient will now contain about 6.7 liters of air.  When our patients can take a deep breath and hold it in, the radiologists are better able to identify disease processes since the interface of air and the soft tissue of the disease is larger and therefore the disease is more easily seen.

For those of you who are ultrasound technologists you use the consequences “deep breath in” to bring the diaphragm and upper abdominal organs down, beyond the rib cage, in order to optimize your window  to the upper abdomen. 

Now as the patient reaches peak inspiration we tell her to breath out as completely and rapidly as possible, and our spirometer reading does the following;

Forced Expiration

     The difference between the end of basal expiration and complete expiration is called the expiratory reserve volume. (ERV)

     For the lung function technologist the speed with which the expiration is performed is a key issue in lung function, but for you the degree to which the patient can empty their lungs is key for a good expiration film.

     At the end of this complete expiration, there is still a volume of air left in the lungs and airways, and this is called the residual volume (RV), which is the air filled space that keeps everything open after a full expiration.  When we perform a CXR in expiration, we ask our patients to breathe in and then all the way out, and to hold it out, and we then expose our film.   The air you see in the lungs at the end of expiration is called the residual volume.    The lungs are at their smallest volume in end expiration and at this point contain about 1.5-1.7 liters in our patient.  In the normal adult the RV ranges between 1.0 and 2.4 liters.

 Residual volume

Lung Capacities

We now move on to our patient’s lung capacities, which represent a combination of the volumes we have spoken about.  What do you think inspiratory capacity is?  It is of course the combination of the basal inspiration which is our tidal volume of 500css combined with the inspiratory reserve volume (3.2liters) giving us a total of a 3.7 liters capacity for inspiration

Inspiratory Capacity

Functional Reserve Capacity (FRC).

The amount of air left in the lungs after a resting expiration includes the expiratory reserve volume and the residual volume is called the functional reserve capacity (FRC).

The vital capacity (VC) is defined as is the maximum volume of air expelled after a maximum inspiration.  For you, this is the difference in amount of air in the lungs between a CXR with maximum inspiration and a CXR with maximum expiration.   In this patient it is about 5 liters – a large difference in volume and a large difference in the appearance of the chest, sometimes making the difference as to whether a pneumothorax is seen or not seen.  Why is this so important?  A small pneumothorax itself may not have any functional significance meaning the patient has no untoward effect.  It does however reflect a leak, and a leak can get better or worse. In the situation in which it gets bigger it can cause a life threatening situation and so it is essential to make the diagnosis of even a small pneumothorax.  Using expiration technique for the clinical question of pneumothorax is essential. .

Vital Capacity (VC)

 

Total Lung Capacity

Total Lung Capacity

 

Ventilation and Perfusion