Work of Breathing = Pressure x Volume (WOB = P x V)
This is consistent with work as the law of physics defines it. The physical equation is as follows:
Work = Force x Distance (W = F x D)
Pressure is force per unit area (P = F/A). Thus the equation for force is the following:
Force = Pressure x Area (F = P x A)
After making the equivalent substitutions the physiologic equation for work is:
Work of Breathing = Pressure x Area x Distance (WOB = P x A x D)
The negative force (P x A) around and through the lungs which the breathing muscles generate during inhalation is the top number of the pressure equation. The volume of inhaled air that makes contact with the lungs is the bottom number of the equation. Since volume is three-dimensional it accounts for the distance over which the air force (P x A) moves.
In the normal state WOB applies only to inhalation. The reason is exhalation does not require the expenditure of energy. It is a passive process that results from the elastic recoil of the lungs and chest wall.
In certain disease states though, the mechanics of breathing during exhalation are abnormal. Lung and chest wall recoil are not sufficient to expel air. As a result, active use of the diaphragm and chest wall muscles is required to produce enough positive pressure to force air out of the lungs. The cost of this normally passive but now active process is extra work of breathing.
Factors that increase the work of breathing
There are five main factors that increase the work of breathing. They are:
- Lung and chest elasticity
- Airway resistance
- Rate of breathing
- Depth of breathing
Lung elasticity (lung elastance) relates to the tendency for the lungs to recoil inward back to their initial volume after airflow into them. There are two main factors that are responsible for this property. They are surface tension and elastin. The work required to overcome these forces that oppose inhalation is elastic work of breathing.
Surface tension is the inwardly directed forces at the boundary between the air and the small amounts of fluid normally present in alveoli. The forces are due to the mutual attraction of the water molecules. These forces favor collapse of the alveoli. But in the normal state alveoli don’t collapse because of the presence of surfactant. Surfactant is a substance the lungs produce which reduces surface tension at the air/water interface. Surface tension is responsible for most of the lungs’ elastance.
Elastin and chest wall recoil are responsible for less of the lung elasticity than surface tension in the normal state. Elastin is the main protein component of elastic fibers in lung tissue. In some disease states elastin and chest wall recoil play a greater role than in the healthy state.
Lung compliance is the reciprocal of elastance or 1 ÷ elastance. It is the ability of the lungs to expand and increase their volume as air is entering. That is to say, it is the ability of the lungs to resist recoil to their original dimensions as air is entering.
When compliance is less than normal lung expansion is more difficult. The lungs are stiff, so to speak. It thus takes more effort and greater use of the muscles of respiration to achieve the negative pressure to draw air into the lungs, in which case WOB is increased.
- decreased elastin in the lungs
- increased alveolar surface tension
- chest wall deformities
- pleural disease
- problems below the diaphragm – ascites, pregnancy, others
Airway resistance is the opposition to the flow of air through the lungs’ due to friction within the airways. It is inversely proportional to the size of the airways. The size of the airways is a function of the radius or diameter of their lumens. The greater the resistance to the flow of air, the more driving pressure it takes to breathe air in and out. The work performed under this condition is flow-resistive work of breathing.
When there is increased resistance to air flow from the lungs, expiration is no longer a passive process. The muscles of respiration have to work to force air from the lungs. The greater use of these muscles during inhalation and the use of them at all during exhalation amount to an increase in the work of breathing.
Different mechanisms can lead to a decrease in the size of lumens of airways. The most common one is bronchospasm – contraction of the smooth muscle in the walls of bronchi. This smooth muscle squeezing effect is mainly a feature of small airways but can occur in larger ones. Other means by which airway resistance increases are the following:
Some of the more common diseases or conditions associated with increased airway resistance are the following:
- Acute bronchitis
- A foreign body lodged in an airway
- Tumor tissue within or around an airway(s)
Increased airway resistance can increase the work of breathing during expiration or inspiration. When it affects both, the effect is greater on expiration. The reason is twofold.
- During breathing in the negative pressure within the lungs slightly inflates the airways. This increase in the lumen size lowers the increased airflow resistance to some degree.
- During active breathing out the positive pressure within the lungs causes compression of the airways. This results in a further increase in opposition to the outward flow of air.
Effect of respiratory rate and tidal volume on WOB
Respiratory rate and tidal volume are not independent factors that affect the work of breathing. They work together and have their effects through changes in lung compliance and flow resistance for a given level of activity or at rest.
The body makes adjustments in the depth and rate of breathing in order to keep minute ventilation constant. If a disorder reduces the tidal volume the respiratory rate increases to compensate and vice versa.
When breathing is slower and tidal volume is greater the lungs and chest wall are closer to their maximum degree of stretching. The resulting state of decreased lung compliance or increased lung elastance increases elastic WOB during inhalation. Airflow WOB is less in this state however, because airways resistance is less. The reason is the airways are more patent due to their supporting connective tissue holding them open when the lungs are more inflated.
When breathing is more rapid and the lung volumes are less, airways are less open. This state of increased airway resistance results in greater flow-resistive WOB during inhalation and exhalation. Because the lungs are less distended in this state elastic WOB is less though.
Minor factors that affect WOB
There are some other factors which can cause a minimal increase in the work of breathing. They are the following:
- Tissue resistance – frictional resistance from deformation of the lungs and chest wall at the end of a breath out
- Viscous resistance – airflow resistance from the thickness of the air (gas mixture)
- Airflow turbulence – random fluctuation in the pressures and velocities of local airflow; most common in large airways with high flow rates; also contributes to airflow resistance