Respiratory Process

Respiratory values

The various terms used to describe lung excursion (movement) during quiet and maximal respiration are shown in figure 1:

The tidal volume (500ml) multiplied by the respiratory rate (14 breaths/min) is the minute volume (7,000ml/min). Not all of the tidal volume takes part in respiratory exchange, as this process does not start until the air or gas reaches the respiratory bronchioles (division 17 of the respiratory tree). Above this level the airways are solely for conducting, their volume being known as the anatomical dead-space. The volume of the anatomical dead-space is approximately 2ml/kg or 150ml in an adult, roughly a third of the tidal volume. The part of the tidal volume which does take part in respiratory exchange multiplied by the respiratory rate is known as the alveolar ventilation (approximately 5,000ml/min).

Functional residual capacity (FRC) is the volume of air in the lungs at the end of a normal expiration. The point at which this occurs (and hence the FRC value) is determined by a balance between the inward elastic forces of the lung and the outward forces of the respiratory cage (mostly due to muscle tone). FRC falls with lying supine, obesity, pregnancy and anaesthesia, though not with age. The FRC is of particularly importance to anaesthetists because:

• During apnoea it is the reservoir to supply oxygen to the blood
• As it falls the distribution of ventilation within the lungs changes leading to mismatching with pulmonary blood flow
• If it falls below a certain volume (the closing capacity), airway closure occurs leading to shunt (see later - Ventilation/perfusion/shunt)

Resistance / compliance

In the absence of respiratory effort, the lung will come to lie at the point of the FRC. To move from this position and generate respiratory movement, two aspects need to be considered which oppose lung expansion and airflow and therefore need to be overcome by respiratory muscle activity. These are the airway resistance and the compliance of the lung and chest wall.

Resistance of the airways describes the obstruction to airflow provided by the conducting airways, resulting largely from the larger airways (down to division 6-7), plus a contribution from tissue resistance resulting produced by friction as tissues of the lung slide over each other during respiration. An increase in resistance resulting from airway narrowing such as bronchospasm leads to obstructive airways disease.

Teaching Point In obstructive airways disease, it might be expected that airflow could be improved by greater respiratory effort (increasing the pressure gradient) to overcome the increase in airways resistance. Whilst this is normally true for inspiration, it is not necessarily the case during expiration, as the increase in intrapleural pressure may act to compress airways proximal to the alveoli, leading to further obstruction with no increase in expiratory flow and air-trapping distally. This is shown in figure 2 and demonstrates why expiration is usually the major problem during an asthmatic attack.

Compliance denotes distensibility (stretchiness), and in a clinical setting refers to the lung and chest wall combined, being defined as the volume change per unit pressure change. When compliance is low, the lungs are stiffer and more effort is required to inflate the alveoli. Conditions that worsen compliance, such as pulmonary fibrosis, produce restrictive lung disease.

Compliance also varies within the lung according to the degree of inflation, as shown in figure 4. Poor compliance is seen at low volumes (because of difficulty with initial lung inflation) and at high volumes (because of the limit of chest wall expansion), with best compliance in the mid-expansion range.

Work of breathing

Of the two barriers to respiration, airway resistance and lung compliance, it is only the first of these, which requires actual work to be done to overcome it. Airway resistance to flow is present during both inspiration and expiration and the energy required to overcome it, which represents the actual work of breathing, is dissipated as heat.

Although energy is required to overcome compliance in expanding the lung, it does not contribute to the actual work of breathing as it is not dissipated but converted to potential energy in the distended elastic tissues. Some of this stored energy is used to do the work of breathing produced by airways resistance during expiration.

The work of breathing is best displayed on a pressure-volume curve of one respiratory cycle (figure 5) which shows the different pathways for inspiration and expiration, known as hysteresis. The total work of breathing of the cycle is the area contained in the loop.

Diffusion

The alveoli provide an enormous surface area for gas exchange with pulmonary blood (between 50-100m²) with a thin membrane across which gases must diffuse. The solubility of oxygen is such that its diffusion across the normal alveolar-capillary membrane is an efficient and rapid process. Under resting conditions pulmonary capillary blood is in contact with the alveolus for about 0.75 second in total and is fully equilibrated with alveolar oxygen after only about a third of the way along this course. If lung disease is present which impairs diffusion there is therefore still usually sufficient time for full equilibration of oxygen when at rest. During exercise, however, the pulmonary blood flow is quicker, shortening the time available for gas exchange, and so those with lung disease are unable to oxygenate the pulmonary blood fully and thus have a limited ability to exercise.

For carbon dioxide, which diffuses across the alveolar-capillary membrane 20 times faster than oxygen, the above factors are less liable to compromise transfer from blood to alveoli.

Ventilation / perfusion / shunt

In an ideal situation the ventilation delivered to an area of lung would be just sufficient to provide full exchange of oxygen and carbon dioxide with the blood perfusing that area. In the normal setting, whilst neither ventilation (V) nor perfusion (Q) is distributed evenly throughout the lung, their matching is fairly good, with the bases receiving substantially more of both than the apices (figure 6).

For perfusion, the distribution throughout the lung is largely due to the effects of gravity. Therefore in the upright position this means that the perfusion pressure at the base of the lung is equal to the mean pulmonary artery pressure (15mmHg or 20cmH2O) plus the hydrostatic pressure between the main pulmonary artery and lung base (approximately 15cmH2O). At the apices the hydrostatic pressure difference is subtracted from the pulmonary artery pressure with the result that the perfusion pressure is very low, and may at times even fall below the pressure in the alveoli leading to vessel compression and intermittent cessation of blood flow.

The distribution of ventilation across the lung is related to the position of each area on the compliance curve at the start of a normal tidal inspiration (the point of the FRC). Because the bases are on a more favourable part of the compliance curve than the apices, they gain more volume change from the pressure change applied and thus receive a greater degree of ventilation. Although the inequality between bases and apices is less marked for ventilation than for perfusion, overall there is still good V/Q matching and efficient oxygenation of blood passing through the lungs.

Disturbance of this distribution can lead to V/Q mismatching (figure 7). For an area of low V/Q ratio the blood flowing through it will be incompletely oxygenated, leading to a reduction in the oxygen level in arterial blood (hypoxaemia). Providing some ventilation is occurring in an area of low V/Q, the hypoxaemia can normally be corrected by increasing the FiO2, which restores the alveolar oxygen delivery to a level sufficient to oxygenate the blood fully.

V/Q mismatch occurs very commonly during anaesthesia because the FRC falls leading to a change in the position of the lung on the compliance curve. The apices, therefore, move to the most favourable part of the curve whilst the bases are located on a less favourable part at the bottom of the curve.

At the extremes of V/Q mismatch, an area of lung receiving no perfusion will have a V/Q ratio of (infinity) and is referred to as alveolar dead-space, which together with the anatomical dead-space makes up the physiological dead-space. Ventilating the dead space is, in effect, wasted ventilation, but unavoidable.

In contrast an area of lung receiving no ventilation, owing to airway closure or blockage, its V/Q ratio will be zero and the area is designated as shunt. Blood will emerge from an area of shunt with a PO2 unchanged from the venous level (5.3kPa or 40mmHg) and produce marked arterial hypoxaemia. This hypoxaemia cannot be corrected by increasing the FiO2, even to 1.0, as the area of shunt receives no ventilation at all. The well-ventilated parts of the lung cannot compensate for the area of shunt because Hb is fully saturated at a normal PO2 . Increasing the PO2 of this blood will not increase the oxygen content substantially (see Oxygen Carriage later).

In the case of shunt, therefore, adequate oxygenation can only be re-established by restoring ventilation to these areas using measures such as physiotherapy, PEEP or CPAP, which clear blocked airways and reinflate areas of collapsed lung. Because closing capacity (CC) increases progressively with age, and is also higher in neonates, these patients are at particular risk during anaesthesia as the FRC may fall below CC and airway closure result.

Surfactant

Any liquid surface exhibits surface tension, a tendency for the molecules on the surface to pull together. This why, when water lies on a surface, it forms rounded droplets. If the surface tension is reduced, such as by adding a small amount of soap, the droplets collapse and the water becomes a thin film.

When a liquid surface is spherical, it acts to generate a pressure within the sphere according to Laplace's law:

The film of liquid lining the alveoli exhibits surface tension in such a manner to increase the pressure in the alveoli, with a greater rise in small alveoli than in large ones. Surfactant is a substance secreted by type II alveolar epithelial cells, which lowers the surface tension of this respiratory surface liquid markedly. Mainly consisting of a phospholipid (dipalmitoyl lecithin), its physiological benefits are:

• an increase (improvement) in overall lung compliance
• a reduction in the tendency for small alveoli to empty into large ones, leading to collapse
• a reduction in the fluid leak from pulmonary capillaries into the alveoli, as the surface tension forces act to increase the hydrostatic pressure gradient from capillary to alveolus 

(Continued ...)

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