Mechanics Of Breathing Flashcards
RECAP: what is Boyle’s Law?
Boyle’s Law (derived from the ideal gas law) describes the relationship between pressure (P), volume (V) and molar quantity (n, the number of gas molecules present).
P ∝ n/v
Describe the structural events that occur that allow inspiration and expiration to take place.
INSPIRATION:
The diaphragm and the external intercostal muscles contract (while the internal intercostal muscles relax), causing the thoracic cavity to expand (volume increases). This means that the alveolar pressure decreases (according to Boyle’s Law), and now the pressure in the atmosphere is higher than the pressure in the alveoli, so the air is sucked into the lungs.
EXPIRATION:
The diaphragm and the external intercostal muscles relax (while the internal intercostal muscles contract), causing the thoracic cavity to condense (volume decreases). This means that the alveolar pressure increases (according to Boyle’s Law), and not the pressure in the atmosphere is lower than the pressure in the alveoli, so the air is sucked out of the lungs.
Describe the structure of the pleural cavity (the pleural membranes) and how it generates its force.
The (inner) visceral pleura lines each lung, whereas the (outer) parietal pleura lines the thoracic cavity, surrounding the chest, diaphragm and mediastinum (which contains the heart). Between the two pleural is the sealed, fluid-filled pleural cavity.
As the tissues attached to each pleura recoil in opposite directions (ie. the lungs recoil inwards, the chest wall recoils outwards), the sealed cavity is stretched slightly. This decreases the pressure within the pleural cavity (‘intrapleural pressure’) below atmospheric pressure (‘negative pressure’).
Negative pressure acts to pull the two pleura together: the greater the level of negative intrapleural pressure, the greater the level of force acting to pull the pleura together.
Now, with the information on the pleural cavity, explain how inspiration and expiration take place.
As inspiration begins, contraction of respiratory muscles (eg. the diaphragm) generates sufficient force to pull the parietal pleura outwards. This stretched the pleural cavity, decreasing the intrapleural pressure. As the intrapleural pressure becomes more negative, the force pulling the two pleurae together increases. When this force becomes greater than the force generated by the elastic recoil of the lung, the visceral pleura will be pulled outward, expanding the lung.
During (passive) expiration, relaxation of respiratory muscles that were previously contracted during inspiration occurs, reducing the outward force acting on the parietal pleura. This reduces the degree to which the cavity is stretched, increasing intrapleural pressure. When the increased (less negative) intrapleural pressure no longer generates sufficient force to overcome the elastic recoil of the lung, the visceral pleura will be pulled inwards (along with the pleural cavity and parietal pleura), decreasing the lung volume.
Alternatively, during a forced expiration, contraction of other respiratory muscles (such as abdominals and internal intercostals) acts to provide further inward force on the parietal pleura, compressing the pleural cavity (further increasing the intrapleural pressire), forcing an increased and more rapid decline in lung volume.
What is pneumothorax, and what are its consequences?
Intrapleural pressure is naturally sub-atmospheric due to the opposing recoil of the chest wall and lungs, and is required to generate expansion of the lungs during inspiration. However, if either of the pleural membranes is pierced (for eg. due to trauma, a wound or a cancerous growth), the pressure gradient between the pleural cavity and the atmosphere (or lungs, depending on the injury) will cause air to enter the pleural space. This is known as a pneumothorax.
Entry of air results in the loss of negative pressure (the intrapleural pressure increases until it equals atmospheric pressure) and expansion of the pleural cavity (at the expense of lung volume). Both of these factors then act to reduce intrapleural pressure changes during inspiration, preventing the lungs from expanding properly as the chest wall moves outwards.
As the parietal and visceral pleurae are no longer being pulled together by negative intrapleural pressure, they recoil in opposite directions, causing particular regions of the lungs to collapse depending on the site and extent of the injury.
Alveoli are lined with fluid. What is the purpose of this?
Alveoli are lined with fluid to enable efficient gas exchange. The water-air interface formed by the fluid lining on the wall of the alveolar airspace essentially creates a bubble. Within the bubble, surface tension arises due to the hydrogen bonds between water molecules combining to exert an overall collapsing force toward the centre of the bubble.
Bubbles generate inward collapsing pressure due to surface tension produced by the attractive forces that exist between water molecules. Unless sufficient force is generated to resist this collapsing pressure, the bubble will collapse/fail to inflate.
The role of pulmonary surfactant is to lower the surface tension at the air/liquid interface within the alveoli of the lungs.
How can Laplace’s Law help us calculate the alveolar pressure?
The collapsing force produced at the water-fluid interface generates pressure. The amount within a specific bubble can be calculated by the Law of Laplace, which describes the relationship between collapsing pressure (P), the radius of the bubble (r) and surface tension (T, which varies depending on the nature of the fluid).
P = 2T/r
Therefore, if T remains constant:
P ∝ 1/r
What is a problem with naturally differently sized alveoli?
Pressure gradients would be created between differently sized alveoli, resulting in smaller alveoli emptying into larger ones.
This would make inflation of the lungs extremely difficult.
How do we overcome the problem of differently-sized alveoli?
The problem is overcome by pulmonary surfactant, which reduces alveolar surface tension. It is secreted by Type II pneumocytes.
It acts to equalise pressure and volume across varying alveoli. As alveoli expand, the concentration of surfactant molecules decreases, increasing the surface tension. With this, larger alveoli tend to collapse into smaller ones, helping the consistent inflation of the lungs.
Describe Neonatal Respiratory Distress Syndrome (NRDS) and ways to treat it.
Neonatal respiratory distress syndrome (NRDS) is a condition that occurs in infants born prematurely, and who develop and produce insufficient levels of pulmonary surfactant (surfactant production occurs at 24-28 weeks). This deficiency results in respiratory failure due to alveoli collapsing, increasing the level of lung compliance, and the increased level of respiratory effort required. The increased forces and pressures involved within the lung also damage the alveoli and innervating capillaries.
This leads to hypoxia, and eventually pulmonary vasoconstriction, endothelial damage, acidosis, pulmonary and cerebral haemorrhage, etc.
NRDS is treated either by supplementation of affected infants with artificial surfactant, and/or by administering glucocorticoids (which increase surfactant production) to mothers deemed to be at risk (eg. diabetics).
What are four ways in which lung function can be investigated?
1) LUNG VOLUMES: what total volume of air can an individual breathe in/out?
2) VENTILATION: what volume of fresh air reaches respiratory surfaces over a given time?
3) LUNG COMPLIANCE: how much force is required to overcome the recoil of the lungs?
4) AIR FLOW: at what rate can air be moved between the lungs and the atmosphere?
What does the total level of ventilation depend on?
It depends on the volume of air inspired and the frequency of breathing.
To find minute volume (mL), we multiply the tidal volume by the frequency of breaths.
Describe how alveolar air has a mixture of ‘fresh’ and ‘stale’ air, and how we would calculate the volume of ‘fresh’ air reaching respiratory surfaces.
Total ventilation doesn’t perfectly reflect the volume of air reaching respiratory surfaces, as some of the fresh air is required to occupy the dead-space, since the volume of the respiratory system is greater than zero (ie. not collapsed) at the end of expiration.
Therefore, the alveoli (where gas exchange takes place) is a mixture of ‘fresh’ and ‘stale’ air.
This means that if we want to calculate the volume of air reaching respiratory surfaces (alveolar ventilation), we need to take into account the volume of the anatomical dead-space. This is typically around 150ml in adults.
How do we calculate alveolar ventilation?
Va = (Vt - Vd) x f
Va is alveolar minute volume, Vt is tidal volume, Vd is dead-space volume and f is frequency.
Vt - Vd represents the volume of fresh air entering the alveoli in each breath.
What is lung compliance? What is static and dynamic compliance?
The relationship between intrapleural pressure and lung volume changes is termed lung compliance, and essentially describe the degree of force required to expand the lungs.
Compliance (Cl) = ΔVolume/ ΔPressure
Static compliance is the measurement taken whilst there is no airflow. Dynamic compliance is the measurements taken during the movement of air.
