The alveoli of the lung are essentially hollow spheres. Surface tension acting at the curved internal surface tends to cause the sphere to decrease in size. The surface tension within the alveoli would make the lungs extremely difficult to distend were it not for the presence of surfactant. The type II cells within the alveolus secrete an insoluble lipoprotein largely consisting of dipalmitoyl lecithin, which forms a thin monomolecular layer at the air-fluid interface. Surfactant reduces surface tension so that alveoli remain stable.
Fluid surfaces covered with surfactant exhibit a phenomenon known as hysteresis; that is, the surface-tension-lowering effect of the surfactant can be improved by a transient increase in the size of the surface area of the alveoli. During quiet breathing, small areas of the lung undergo collapse, but it is possible to re-expand these rapidly by a deep breath; hence the importance of sighs or deep breaths as a feature of normal breathing. Failure of such a mechanism - which can occur, for example, in patients with fractured ribs - gives rise to patchy basal lung collapse. Surfactant levels may be reduced in a number of diseases that cause damage to the lung (e.g. pneumonia). Lack of surfactant plays a central role in the respiratory distress syndrome of the newborn. Severe reduction in perfusion of the lung causes impairment of surfactant activity and may well account for the characteristic areas of collapse associated with pulmonary embolism.
Showing posts with label Physiology of respiratory system. Show all posts
Showing posts with label Physiology of respiratory system. Show all posts
The airways of the lungs
From the trachea to the periphery, the airways become smaller in size (although greater in number). The cross-sectional area available for airflow increases as the total number of airways increases. The flow of air is greatest 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 (0.1-0.2 kPa/L in a normal tracheobronchial tree), steadily increasing from the small to the large airways.
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 obstructive pulmonary disease (COPD) the small airways are narrowed and this can be partially compensated by breathing at a larger lung volume.
Control of airway tone
Bronchomotor tone is maintained by vagal efferent nerves and, even in a normal subject, is reduced by atropine or β-adrenoceptor agonists. Adrenoceptors on the surface of bronchial muscles respond to circulating catecholamines; there is no direct sympathetic innervation. Airway tone shows a circadian rhythm, which is greatest at 04.00 and lowest in the mid-afternoon. Tone can be increased transiently by inhaled stimuli acting on epithelial nerve endings, which trigger reflex bronchoconstriction via the vagus. These stimuli include cigarette smoke, solvents, inert dust and cold air; airway responsiveness to these increases following respiratory tract infections even in healthy subjects. In asthma, the airways are very irritable and as the circadian rhythm remains the same, asthmatic symptoms are usually worse in the early morning.
Airflow
Movement of air through the airways results from a difference between the pressure in the alveoli and the atmospheric pressure; alveolar pressure is positive in expiration and negative in inspiration. During quiet breathing the pleural pressure is sub-atmospheric throughout the breathing cycle. With vigorous expiratory efforts (e.g. cough), the central airways are compressed by positive pleural pressures exceeding 10 kPa, but 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 pleural pressure (PPL) plus the elastic recoil pressure (PEL) of the lung.
When there is no airflow (i.e. during 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(Fig. 14.7a).
In forced expiration, as mentioned above, the driving pressure raises both the alveolar pressure and the intrapleural pressure. Between the alveolus and the mouth, there is a point (C in Fig. 14.7b) where the airway pressure equals the intrapleural pressure, and the airway collapses. However, this collapse 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 collapse'.
The elastic recoil pressure of the lungs decreases with decreasing lung volume and the 'collapse point' moves upstream (i.e. towards the smaller airways - see Fig. 14.7c). Where there is pathological loss of recoil pressure (as in chronic obstructive pulmonary disease, COPD), the 'collapse point' starts even further upstream and causes expiratory flow limitation. The measurement of the forced expiratory volume in 1 second (FEV1) is a useful clinical index of this phenomenon. To compensate, these patients often 'purse their lips' in order to increase airway pressure so that their peripheral airways do not collapse. 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.
The relationship between maximal flow rates on expiration and inspiration is demonstrated by the maximal flow-volume (MFV) loops. Figure 14.8a shows this in a normal subject.
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 obstructive pulmonary disease (COPD) the small airways are narrowed and this can be partially compensated by breathing at a larger lung volume.
Control of airway tone
Bronchomotor tone is maintained by vagal efferent nerves and, even in a normal subject, is reduced by atropine or β-adrenoceptor agonists. Adrenoceptors on the surface of bronchial muscles respond to circulating catecholamines; there is no direct sympathetic innervation. Airway tone shows a circadian rhythm, which is greatest at 04.00 and lowest in the mid-afternoon. Tone can be increased transiently by inhaled stimuli acting on epithelial nerve endings, which trigger reflex bronchoconstriction via the vagus. These stimuli include cigarette smoke, solvents, inert dust and cold air; airway responsiveness to these increases following respiratory tract infections even in healthy subjects. In asthma, the airways are very irritable and as the circadian rhythm remains the same, asthmatic symptoms are usually worse in the early morning.
Airflow
Movement of air through the airways results from a difference between the pressure in the alveoli and the atmospheric pressure; alveolar pressure is positive in expiration and negative in inspiration. During quiet breathing the pleural pressure is sub-atmospheric throughout the breathing cycle. With vigorous expiratory efforts (e.g. cough), the central airways are compressed by positive pleural pressures exceeding 10 kPa, but 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 pleural pressure (PPL) plus the elastic recoil pressure (PEL) of the lung.
When there is no airflow (i.e. during 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(Fig. 14.7a).
In forced expiration, as mentioned above, the driving pressure raises both the alveolar pressure and the intrapleural pressure. Between the alveolus and the mouth, there is a point (C in Fig. 14.7b) where the airway pressure equals the intrapleural pressure, and the airway collapses. However, this collapse 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 collapse'.
The elastic recoil pressure of the lungs decreases with decreasing lung volume and the 'collapse point' moves upstream (i.e. towards the smaller airways - see Fig. 14.7c). Where there is pathological loss of recoil pressure (as in chronic obstructive pulmonary disease, COPD), the 'collapse point' starts even further upstream and causes expiratory flow limitation. The measurement of the forced expiratory volume in 1 second (FEV1) is a useful clinical index of this phenomenon. To compensate, these patients often 'purse their lips' in order to increase airway pressure so that their peripheral airways do not collapse. 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.
Flow-volume loops |
In subjects with healthy lungs, effects of flow limitation will not be apparent, since maximal flow rates are rarely achieved even during vigorous exercise. However, in patients with severe COPD, limitation of expiratory flow occurs even during tidal breathing at rest (see Fig. 14.8b). To increase ventilation these patients have to breathe at higher lung volumes and allow more time for expiration which both reduce the tendency for airway collapse. To compensate they increase flow rates during inspiration, where there is relatively less flow limitation.
The measure of the volume that can be forced in from the residual volume in 1 second (FIV1) will always be greater than that which can be forced out from TLC in 1 second (FEV1). Thus, the ratio of FEV1 to FIV1 is below 1. The only exception to this occurs when there is significant obstruction to the airways outside the thorax, such as with 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 FEV1 to FIV1 becomes greater than 1. This phenomenon, and the characteristic flow-volume loop, is used to diagnose extrathoracic airways obstruction (Fig. 14.8c).
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 flow is seen (Fig. 14.8d).
Ventilation and perfusion relationships
For efficient gas exchange there must be a match between ventilation of the alveoli ([Vdot]A) and their perfusion ([Qdot]). There is a wide variation in the [Vdot]A/[Qdot] ratio throughout both normal and diseased lung. In the normal lung the extreme relationships between alveolar ventilation and perfusion are:
- ventilation with reduced perfusion (physiological deadspace)
- perfusion with reduced ventilation (physiological shunting).
An increased physiological shunt results in arterial hypoxaemia. The effects of an increased physiological deadspace can usually be overcome by a compensatory increase in the ventilation of normally perfused alveoli. In advanced disease this compensation cannot occur, leading to increased alveolar and arterial Pco2, together with hypoxaemia which cannot be compensated by increasing ventilation.
Hypoxaemia occurs more readily than hypercapnia because of the different ways in which oxygen and carbon dioxide are carried in the blood. Carbon dioxide can be considered to be in simple solution in the plasma, the volume carried being proportional to the partial pressure. Oxygen is carried in chemical combination with haemoglobin in the red blood cells, and the relationship between the volume carried and the partial pressure is not linear (see Fig. 15.5, p. 960). Alveolar hyperventilation reduces the alveolar Pco2 and diffusion leads to a proportional fall in the carbon dioxide content of the blood. However, as the haemoglobin is already saturated with oxygen, there is no significant increase in the blood oxygen content as a result of increasing the alveolar Po2 through hyperventilation. The hypoxaemia of even a small amount of physiological shunting cannot therefore be compensated for by hyperventilation.
In individuals who have mild disease of the lung causing slight [Vdot]A/[Qdot] mismatch, the Pao2 and Paco2 may still be normal. Increasing the requirements for gas exchange by exercise will widen the [Vdot]A/[Qdot] mismatch and the Pao2 will fall. [Vdot]A/[Qdot] mismatch is by far the most common cause of arterial hypoxaemia.
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Breathing
Lung ventilation can be considered in two parts:
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 healthy individuals at rest, inspiration is almost entirely due to contraction of the diaphragm. Respiratory muscles are similar to other skeletal muscles but are less prone to fatigue. However, muscle fatigue contributes to respiratory failure in patients with severe chronic airflow limitation. Muscle weakness can also result from primary neurological and muscle disorders.
Expiration follows passively as a result of gradual relaxation 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; thus, 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 (L/kPa). 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 air in the lung is known as the functional residual capacity (FRC).
Diseases that 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-Barré syndrome), injury to the phrenic nerves, and myasthenia gravis.
The control of respiration
Coordinated respiratory movements result from rhythmical discharges arising in an anatomically ill-defined group of interconnected neurones in the reticular substance of the brainstem, known as the respiratory centre. Motor discharges from the respiratory centre travel via the phrenic and intercostal nerves to the respiratory musculature.
- 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 healthy individuals at rest, inspiration is almost entirely due to contraction of the diaphragm. Respiratory muscles are similar to other skeletal muscles but are less prone to fatigue. However, muscle fatigue contributes to respiratory failure in patients with severe chronic airflow limitation. Muscle weakness can also result from primary neurological and muscle disorders.
Expiration follows passively as a result of gradual relaxation 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; thus, 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 (L/kPa). 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 air in the lung is known as the functional residual capacity (FRC).
Diseases that 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-Barré syndrome), injury to the phrenic nerves, and myasthenia gravis.
The control of respiration
Coordinated respiratory movements result from rhythmical discharges arising in an anatomically ill-defined group of interconnected neurones in the reticular substance of the brainstem, 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 L/min carries 11 mmol/min (250 mL/min) of oxygen from the lungs to the tissues.
- Ventilation at about 6 L/min carries 9 mmol/min (200 mL/min) of carbon dioxide out of the body.
- The normal pressure of oxygen in arterial blood (Pao2) is between 11 and 13 kPa (83 and 98 mmHg).
- The normal pressure of carbon dioxide in arterial blood (Paco2) is 4.8-6.0 kPa (36-45 mmHg).
Breathlessness on physical exertion is normal and not considered a symptom unless the level of exertion is very light, such as when walking slowly. Recent surveys of healthy western populations reveal that over 20% of the general population report themselves as breathless on relatively minor exertion. 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:
- Changes in lung volume. These are sensed by receptors in thoracic wall muscles signalling changes in their length.
- Tension developed by contracting muscles. This is sensed by Golgi tendon organs.
- Central perception of the sense of effort.
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The nose
The major functions of nasal breathing are:
- to heat and moisten the air
- to remove particulate matter
About 10 000 L of air are inhaled daily. The relatively low flow rates and turbulence of inspired air are ideal for particle deposition, and few particles greater than 10 microns pass through the nose. Deposited particles are removed from the nasal mucosa within 15 minutes, compared with 60-120 days from the alveolus. Nasal secretion contains many protective proteins in the form of IgA antibodies, lysozyme 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, intercellular adhesion molecule 1 (ICAM-1), shared by neutrophils and eosinophils. Many noxious gases, such as SO2, are almost completely removed by nasal breathing.
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