- 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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