For inspiration to occur, the pressure in the alveoli must be lower than the air pressure in the atmosphere; this is achieved by increasing the size (volume) of the lungs through the contraction of the muscles of inhalation – the diaphragm and the intercostal muscles (Marieb and Keller [111]). The diaphragm flattens and descends and the intercostal muscles lift the ribcage and sternum, causing the ribs to broaden outwards and increasing the diameter of the thoracic cavity, both from side to side and from front to back (Patton [155]). During normal inspiration, the pressure between the two pleural layers in the pleural cavity (intrapleural pressure) is always just lower than atmospheric pressure (756 mmHg at an atmospheric pressure of 760 mmHg) (Marieb and Hoehn [110]). As the volume of the lungs and pleural cavity increases, the intrapleural pressure drops to 754 mmHg (Marieb and Hoehn [110]). At the same time, the pressure within the lungs (alveolar or intrapulmonary pressure) drops from 760 mmHg to 758 mmHg, and so a pressure difference between the atmosphere and the alveoli is established and air flows into the lungs (Tortora and Derrickson [199]). The relationship between these pressures can be seen in Figure 14.27.

Expiration also occurs due to a pressure gradient but in the opposite direction, such that the pressure within the lungs is greater than the pressure of the atmosphere (Patton [155]). In normal gentle breathing, the process of expiration is largely passive, not involving any muscular contractions but resulting from elastic recoil of the chest wall and lungs (Tortora and Derrickson [199]).

Expiration begins when the inspiratory muscles relax, causing the diaphragm to move superiorly and the ribs to depress, which decreases the diameter of the thoracic cavity and returns it to its normal size (Marieb and Keller [111]). This results in a decrease in lung volume and compression of the alveoli, causing an increase in alveolar (intrapulmonary) pressure to 762 mmHg (Tortora and Derrickson [199]). This forces gases to flow out from the area of higher pressure in the lungs to the area of lower pressure in the atmosphere (Tortora and Derrickson [199]). A summary of the events that occur during inspiration and expiration can be seen in Figure 14.28.

The accessory muscles of inspiration further increase the volume of the thoracic cavity and, therefore, increase the volume of breathing. These muscles include the sternocleidomastoid muscles, which elevate the sternum, and the scalene muscles and the pectoralis minor muscles, which elevate the first to the fifth ribs (Tortora and Derrickson [199]). These muscles may be used during exercise or in situations where the individual is in respiratory distress (Marieb and Hoehn [110]).

The accessory muscles of expiration are used only during forceful breathing, such as when playing a wind instrument or during exercise (Tortora and Derrickson [199]). Contraction of the abdominal wall muscles, primarily the oblique and transversus muscles, increases intra‐abdominal pressure, forcing the abdominal organs upwards against the diaphragm, and also depresses the ribcage (Waugh and Grant [207]). The internal intercostal muscles also depress the ribcage and decrease thoracic volume, forcing air out of the lungs (Marieb and Hoehn [110]).

Within the medulla are two clusters of neurones that are critically important in the co‐ordination of the respiratory system: the dorsal respiratory group (DRG) and the ventral respiratory group (VRG) (Marieb and Hoehn [110]).

The DRG contains neurones that generate impulses; they stimulate the diaphragm and the external intercostal muscles to contract, via the phrenic and intercostal nerves, and contraction of these muscles leads to inspiration. Generation of the impulses is then paused, allowing the diaphragm and intercostal muscles to relax, leading to passive expiration (Marieb and Hoehn [110]). The VRG contains neurones that act as ‘pacemakers’ and control the rhythm of breathing (Marieb and Hoehn [110]). It is also from the VRG that active or forceful breathing is controlled (Tortora and Derrickson [199]).

The DRG co‐ordinates input from the peripheral baroreceptors (or stretch receptors) and chemoreceptors and relays this to the VRG to alter respiratory rate as required (Marieb and Hoehn [110]). Baroreceptors monitor the stretch of the bronchi and bronchioles during overinflation of the lungs (Tortora and Derrickson [199]). Chemoreceptors monitor the arterial blood for changes in the partial pressure of carbon dioxide (PaCO₂) and pH, but also, to a lesser extent, the partial pressure of oxygen (PaO₂) (Patton [155]). For more information on the chemical factors that affect respiration, see Chapter c12: Respiratory care, CPR and blood transfusion.

Additionally, pontine respiratory centres relay impulses to the VRG to modify breathing rhythms so that there is a smooth transition from inspiration to expiration and so that breathing can be modified to allow for speech, exercise and sleep (Marieb and Hoehn [110]).

Although oxygen is essential for every cell in the body, the body's need to rid itself of carbon dioxide is the most influential stimulus to respiration in a healthy person (Marieb and Hoehn [110]). Arterial PaCO₂ is closely monitored and acceptable levels maintained by a sensitive homeostatic mechanism mediated mainly by the effect that increased carbon dioxide levels have on the central chemoreceptors of the brainstem (Tortora and Derrickson [199]). Carbon dioxide passes easily from the blood into the cerebrospinal fluid, where it forms carbonic acid, releasing hydrogen ions (H⁺) (Marieb and Keller [111]). This increase of H⁺ causes the pH to drop, stimulating the central chemoreceptors in the brainstem to increase the rate and depth of breathing and so increase the amount of carbon dioxide exhaled (Marieb and Hoehn [110]). Similarly, should a metabolic acidosis or acidaemia (low pH) exist (such as a build‐up of lactic acid), a change in respiration will ensue in an attempt to compensate for this (Marieb and Hoehn [110]). See Figure 14.29 for negative feedback mechanisms by which changes in PaCO₂ and blood pH regulate ventilation. Abnormally low PaCO₂ levels cause inhibition of respiration, with breathing becoming slow and shallow, and periods of apnoea may occur until arterial PaCO₂ rises again and stimulates respiration (Marieb and Hoehn [110]).

The peripheral chemoreceptors, found in the aortic arch and carotid arteries, are responsible for sensing the arterial PaO₂ (Marieb and Hoehn [109]). Normally, decreasing levels of oxygen only affect respiratory rate by causing the peripheral chemoreceptors to have an increased sensitivity to carbon dioxide (Marieb and Hoehn [110]). A normal arterial PaO₂, regardless of age, should be greater than 10.6 kPa (80 mmHg); a significant drop will cause the central receptors to become suppressed and at the same time the peripheral receptors will stimulate the respiratory centres to increase ventilation even if PaCO₂ is normal (Marieb and Hoehn [110]).

There are a number of receptors in the lungs that respond to a variety of irritants (Marieb and Keller [111]). Accumulated mucus or inhaled debris stimulates receptors in the bronchioles that cause reflex constriction of those air passages (Tortora and Derrickson [199]). When these receptors are stimulated in the bronchi or trachea, a cough is initiated, whereas when they are stimulated in the nasal cavity, a sneeze is triggered (Marieb and Hoehn [110]). These irritant receptors have a protective mechanism to prevent obstruction or aspiration of food or liquids (Patton [155]). There are also stretch receptors present in the conducting passages and the visceral pleura that are stimulated when the lungs inflate; these then signal the respiratory centres to end inspiration (Marieb and Hoehn [110]). These receptors are thought to act more as a protective response to prevent excessive stretching of the lungs than as a normal regulatory mechanism (Marieb and Hoehn [110]).

Respiration can also be altered in the higher cortical centres in response to factors such as strong emotions, pain and alteration of temperature (Tortora and Derrickson [199]). The cerebral motor cortex yields a degree of voluntary control over breathing; however, this can be overridden by the other mechanisms (Patton [155]).

Some of the mechanisms through which breathing is controlled are summarized in Figure 14.30.