Physiology of the respiratory system Medical Assignment Help

The nose

The major functions of nasal breathing are:
• To heat and moisten the air
• To remove particulate matter
About 10 000 litres of particle-laden air are inhaled daily. Deposited particles are removed from the nasal mucosa within 15 min, compared with 60-120 days from the alveolus. The relatively low flow rates and turbulence of inspired air are ideal for particle deposition, and few particles greater than 10 /-lm pass through the nose. For this reason nasal secretion contains many protective proteins in the form of antibodies, lysozymes and interferon. In addition, the cilia of the nasal epithelium move the mucous gel layer rapidly back to the oropharynx where it is swallowed. Bacteria have little chance of settling in the nose. Mucociliary protection against viral infections is more difficult because viruses bind to receptors on epithelial cells. The majority of rhinoviruses bind to an adhesion molecule, intracellular adhesion molecule 1 (lCAM-l), a receptor shared by neutrophils and eosinophils. Many noxious gases, for example S02′ are almost completely removed by nasal breathing .


Lung ventilation can be considered in two parts:
• The mechanical process of inspiration and expiration
• The control of respiration to a level appropriate for the metabolic needs


Inspiration is an active process and results from the descent of the diaphragm and movement of the ribs upwards and outwards under the influence of the intercostal muscles. In resting healthy individuals, contraction of the diaphragm is responsible for most of inspiration. Respiratory muscles are similar to other skeletal muscles but are less prone to fatigue. However weakness may play a part in respiratory failure resulting from neurological and muscle disorders and possibly with severe chronic airflow limitation.
Expiration follows passively as a result of gradual lessening of contraction of the intercostal muscles, allowing the lungs to collapse under the influence of their own elastic forces.
Inspiration against increased resistance may require the use of the accessory muscles of ventilation, such as the sternomastoid and scalene muscles. Forced expiration is also accomplished with the aid of accessory muscles, chiefly those of the abdominal wall, which help to push up the diaphragm.
The lungs have an inherent elastic property that causes them to tend to collapse away from the thoracic wall, generating a negative pressure within the pleural space. The strength of this retractive force relates to the volume of the lung; for example, at higher lung volumes the lung is stretched more, and a greater negative intrapleural pressure is generated.
Lung compliance is a measure of the relationship between this retractive force and lung volume. It is defined as the change in lung volume brought about by unit change in transpulmonary (intrapleural) pressure and is measured in litres per kilopascal (litres kPa -I). At the end of a quiet expiration, the retractive force exerted by the lungs is balanced by the tendency of the thoracic wall to spring outwards. At this point respiratory muscles are resting and the volume of the lung is known as the functional residual capacity (FRC). Diseases that can affect the movement of the thoracic cage and diaphragm can have a profound effect on ventilation.  These include diseases of the thoracic spine such as ankylosing spondylitis and kyphoscoliosis, neuropathies (e.g. the Guillain-Barre syndrome), injury to the phrenic nerves, and myasthenia gravis.


Coordinated respiratory movements result from rhythmical discharges arising in an anatomically ill-defined group of interconnected neurones in the reticular substance of the brain stem known as the respiratory centre. Motor discharges from the respiratory centre travel via the phrenic and intercostal nerves to the respiratory musculature.
The pressures of oxygen and carbon dioxide in arterial blood are closely controlled. In a typical normal adult at rest:
• The pulmonary blood flow of 5 litres min -I carries 11 mmol min-I (250 ml min-I) of oxygen from the lungs to the tissues.
• Ventilation at about 6 litres min-I carries 9 mmol min-I (200 ml min-I) of carbon dioxide out of the body.
• The normal pressure of oxygen in arterial blood (Pa02) is between 11 and l3 kPa (83 and 98 mmHg).
• The normal pressure of carbon dioxide in arterial blood (PaC02) is 4.8-6.0 kPa (36-45 mmHg). Neurogenic and chemical factors are involved in the control of ventilation.

Neurogenic factors

Neural stimuli include:
• Consciously induced changes in rate and depth of breathing
• Impulses from limb receptors, as in exercise, which cause respiratory stimulation
• Impulses arising from pulmonary receptors sensitive to stretch and bronchial irritation
• Juxtapulmonary capillary receptors (J receptors) stimulated by pulmonary congestion
• Impulses arising from receptors in muscles and joints of the chest wall
Abnormal stimuli include:
• Lesions in the pons and midbrain, which give rise to central neurogenic hyperventilation or hypoventilation
• Medullary compression, which leads to respiratory depression

Chemical stimuli

These cause an increase in ventilation when they stimulate central or peripheral chemoreceptors.
1 Central
(a) Carbon dioxide. The strongest respiratory stimulant to breathing is a rise in Paco2 Sensitivity to this may be lost in chronic bronchitis, so that in these patients hypoxaemia is the chief stimulus to respiratory drive; treatment with oxygen may therefore reduce respiratory drive and produce a further rise in Paco2
(b) Hydrogen ion concentration of arterial blood. An increase in [H+] due to metabolic acidosis will increase ventilation with a fall in Pac02. In respiratory disease, [H+] and Pac02 rise together.
2 Peripheral. A reduced Pa02 stimulates peripheral chemoreceptors in the carotid and aortic bodies. This stimulus is not strong unless the Pa02 is below 8 kPa. These chemoreceptors also respond to increases in [H+] and Pac02
The respiratory centre is depressed by severe hypoxaemia and sedatives (e.g. opiates) and stimulated by large doses of aspirin or by pyrexia. In certain common conditions such as mild asthma, pulmonary embolism and pneumonia there is an increase in ventilation, leading to a reduction in the Pac02  These conditions probably cause this effect through stimulation of irritant receptors in the bronchioles and J receptors stimulated deep in the parenchyma of the lung. Anxiety or hysteria cause hyperventilation, and increased ventilation is also a prominent feature of metabolic acidosis.
Breathlessness on physical exertion is normal and not considered a symptom unless the level of exertion is very light, e.g. walking slowly. Although breathlessness is a very common symptom the sensory and neural mechanisms underlying it remain obscure. The sensation of breathlessness is derived from at least three sources:
1 Changes in lung volume are sensed by receptors in thoracic wall muscles signalling changes in their length.
2 The tension developed by contracting muscles can be sensed by Golgi tendon organs. The tension developed in normal muscle can be differentiated from that developed in muscles weakened by fatigue or disease.
3 Central perception of the sense of effort.

The airways of the lungs

From the trachea to the periphery, the airways become smaller in size (although greater in number). The crosssectional area available for airflow increases as the total number of airways increases. The flow of air is maximum in the trachea and slows progressively towards the periphery (as the velocity of airflow depends on the ratio of flow to cross-sectional area). In the terminal airways, gas flow occurs solely by diffusion. The resistance to airflow is very low-0.l-O.2 kPa litre-I in a normal tracheobronchial tree.
Airways expand as lung volume is increased and at full inspiration (total lung capacity, TLC) they are 30-40% larger in calibre than at full expiration (residual volume, RV). In chronic bronchitis and emphysema, which principally affect the smaller airways, the airway narrowing is partially overcome by breathing at a larger lung volume.

Control of airway tone

This is under the autonomic nervous system. Bronchomotor tone is maintained by vagal efferent nerves and, even in a normal subject, is reduced by atropine or {3- adrenoreceptor agonists. The many adrenoreceptors on the surface of bronchial muscles respond to circulating catecholamines, although sympathetic nerves do not directly innervate them. Airway tone shows a circadian rhythm, which is greatest at 04.00 and lowest in the midafternoon. Tone can be increased briefly by inhaled stimuli acting on epithelial receptors, which trigger reflex bronchoconstriction via the vagus.
These stimuli include cigarette smoke, inert dust, cold air; airway responsiveness to these increases following respiratory tract infections even in healthy subjects. In asthma, the characteristic increased airway responsiveness is an exaggeration of this normal response and, as the circadian rhythm remains the same, asthmatic symptoms are worst in the early morning.

Air flow

Movement of air through the airways results from a difference between the pressure in the alveoli and the atmospheric pressure; a positive alveolar pressure occurs in expiration and a negative pressure occurs in inspiration. During quiet breathing the subatmospheric pleural pressure throughout the breathing cycle slightly distends the airways. With vigorous expiratory efforts (e.g. cough), although the central airways are compressed by positive pleural pressures exceeding 10 kPa, the airways do not close completely because the driving pressure for expiratory flow (alveolar pressure) is also increased. Alveolar pressure PALV is equal to the elastic recoil pressure of the lung plus the pleural pressure PEL’ When there is no airflow (i.e. a pause in breathing) the tendency of the lungs to collapse (the positive recoil pressure) is exactly balanced by an equivalent negative pleural pressure. As air flows from the alveoli towards the mouth there is a gradual loss of pressure owing to flow resistance. In forced expiration, as mentioned above, the driving  pressure raises both the alveolar pressure and the intrapleural pressure. Between the alveolus and the mouth, a point will occur  where the airway pressure will equal the intrapleural pressure, and airway compression will occur. However, this compression of the airway is temporary, as the transient occlusion of the airway results in an increase in pressure behind it (i.e. upstream) and this raises the intra-airway pressure so that the airways open and flow is restored. The airways thus tend to vibrate at this point of ‘dynamic compression’. The elastic recoil pressure of the lungs decreases with  decreasing lung volume and the ‘collapse point’ moves upstream (i.e. towards the smaller airways). Where there is pathological loss of recoil pressure (as in chronic bronchitis and emphysema), the ‘collapse point’ starts even further upstream and these patients are often seen to ‘purse their lips’ in order to increase airway pressure so that their peripheral airways do not collapse. The expiratory airflow limitation is the disordered physiology that underlies chronic airflow limitation. The measurement of the forced expiratory volume in 1 s (FEV,) is a useful clinical index of this phenomenon. On inspiration the intrapleural pressure is always less  than the intraluminal pressure within the intrathoracic airways, so there is no limitation to airflow with increasing  effort. Inspiratory flow is limited only by the power of the inspiratory muscles.

Diagrams showing the ventilatory forces during

Diagrams showing the ventilatory forces during

Flow-volume loops

The relationship between maximal flow rates on expiration and inspiration is demonstrated by the maximal flow-volume (MFV) loops. Figure 12.8a shows this in a normal subject.
In subjects with healthy lungs the clinical importance of flow limitation will not be apparent, since maximal flow rates are rarely achieved even during vigorous exercise. However, in patients with severe chronic bronchitis and emphysema, limitation of expiratory flow occurs even during tidal breathing at rest. To increase ventilation these patients have to breathe at higher lung volumes and also allow more time for expiration by increasing flow rates during inspiration, where there is proportionately much less flow limitation. This explains the clinical phenomenon of a prolonged expiratory time in patients with severe airflow limitation. The measurement of the volume that can be forced in from RV in 1 s (FIV,) will always be greater than that which can be forced out from TLC in 1 s (FEV,). Thus, the ratio of FEV, to FIV, is below 1. The only exception to this occurs when there is significant obstruction to the airways outside the thorax, e.g. a tumour mass in the upper part of the trachea. Under these circumstances expiratory airway narrowing is prevented by the tracheal resistance (a situation similar to pursing the lips) and expiratory airflow becomes more effort-dependent. During forced inspiration this same resistance causes such negative intraluminal pressure that the trachea is compressed by the surrounding atmospheric pressure. Inspiratory flow thus becomes less effort-dependent, and the ratio of FEV, to FlV, becomes greater than 1. This phenomenon, and the characteristic flow volume loop, is  used to diagnose extra thoracic airways obstruction.
When obstruction occurs in large airways within the thorax (lower end of trachea and main bronchi), expiratory flow is impaired more than inspiratory flow but a characteristic plateau to expiratory

and b) Maximal flowvolume loops, showing the relationship

and b) Maximal flowvolume
loops, showing the relationship

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