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Control Of Breathing


Control Of Breathing
Ventilation of the lungs provides O2  for the tissues and removes CO2. Breathing must therefore be closely matched to metabolism for adequate O2 delivery and to prevent a build-up of CO2. A central pattern generator located in the brain stem sets the basic rhythm and pattern of ventilation and controls the respiratory muscles. It is modulated by higher centres and feedback from sensors, including chemoreceptors, and lung mechanoreceptors (Fig. 29a). The neural networks are complex, as breathing must be coordinated with coughing, swallowing and speech, and are not fully understood.


Control Of Breathing

The brain stem and central pattern generator
The brain stem includes diffuse groups of respiratory neurones in the pons and medulla that act together as the central pattern generator (Fig. 29a); it is unclear whether there is a single pacemaker region. Some neurones only show activity during inspiration or expiration, and these exhibit reciprocal inhibition, i.e. inspiration inhibits expira- tion and vice versa. The medulla contains dorsal and ventral respira- tory groups that receive input from the chemoreceptors and lung receptors and drive the respiratory muscle motor neurones [inter- costals, phrenic (diaphragm), abdominal]. The medullary respiratory groups also provide ascending input to and receive descending input from the pneumotaxic centre in the pons, which is critical for normal breathing. The pneumotaxic centre receives input from the hypothala- mus and higher centres, coordinates medullary homeostatic functions with factors such as emotion and temperature, and affects the pattern of breathing. Voluntary control is mediated by cortical motor neurones in the pyramidal tract, which by-passes the respiratory neurones in the brainstem.

Chemoreception
Chemoreceptors detect arterial Pco2, Po2 and pH – Pco2 is the most important. Alveolar Pco2 (PAco2) is normally 5.3 kPa (40 mmHg), and PAo2 normally 13 kPa (100 mmHg). An increase in PAco2 causes ventilation to rise in an almost linear fashion (Fig. 29d). Increased acidity of the blood (e.g. lactic acidosis in severe exercise) causes the relationship between Pco2 and ventilation to shift to the left, and decreased acidity causes a shift to the right. Conversely, Po2 normally stimulates ventilation only when it falls below 8 kPa (60 mmHg) (Fig. 29e). However, when a fall in Po2 is accompanied by an in- crease in Pco2, the resultant increase in ventilation is greater than would be expected from the effects of either alone; there is thus a synergistic (more than additive) relationship between Po2 and Pco2 (Fig. 29e).
The central chemoreceptor comprises a collection of neurones near the ventrolateral surface of the medulla, close to the exit of the cranial nerves IX and X (Fig. 29b). It responds indirectly to blood Pco2, but does not respond to changes in Po2. Although CO2 can easily diffuse across the blood–brain barrier from the blood into the cerebrospinal fluid (CSF), H+ and HCO3 cannot. As a result, the pH of the CSF around the chemoreceptor is determined by the arterial Pco2 and CSF HCO −, according to the Henderson–Hasselbalch equation (Fig. 29b). A rise in blood Pco2 therefore makes the CSF more acid; this is detected by the chemoreceptor, which increases ventilation to blow off CO2. The central chemoreceptor is responsible for 80% of the response to CO2  in humans. Its response is delayed because CO2 has to diffuse across the blood–brain barrier. As the blood–brain barrier is impermeable to H+, the central chemoreceptor is not affected by blood pH.
The peripheral chemoreceptors are located in the carotid and aortic bodies (Fig. 29c). The carotid bodies are small distinct structures located at the bifurcation of the common carotid arteries, and are innervated by the carotid sinus nerve and thence the glossopharyngeal nerve. The carotid body is formed from glomus (type I) and sheath (type II) cells. Glomus cells are chemoreceptive, contain neurotrans-mission-rich dense granules and contact carotid sinus nerve axons. The aortic bodies are located on the aortic arch and are innervated by the vagus. They are similar to carotid bodies but functionally less important. Peripheral chemoreceptors respond to changes in Pco2, H+ and, importantly, Po2. They are responsible for 20% of the response to increased Pco2.

Lung  receptors
Various types of lung receptor provide feedback from the lungs to the respiratory centre. In addition, pain often causes brief apnoea (cessation of breathing) followed by rapid breathing, and mechanical or noxious stimulation of receptors in the trigeminal region and larynx causes apnoea or spasm of the larynx.
Stretch receptors. These are located in the bronchial walls. Stimulation (by stretch) causes short, shallow breaths, and delay of the next inspiratory cycle. They provide negative feedback to turn off inspiration. They are mostly slowly adapting (continue to fire with sustained stimulation) and are innervated by the vagus. They are largely responsible for the Hering–Breuer inspiratory reflex, in which lung inflation inhibits inspiration to prevent overinflation.
Juxtapulmonary (J) receptors. These are located on the alveolar and bronchial walls close to the capillaries. They cause depression of somatic and visceral activity by producing rapid shallow breathing or apnoea, a fall in heart rate and blood pressure, laryngeal constriction and relaxation of the skeletal muscles via spinal neurones. They are stimulated by increased alveolar wall fluid, oedema, microembolisms and inflammation. The afferent nerves are small unmyelinated (C-fibre) or myelinated nerves in the vagus.
Irritant receptors. These are located throughout the airways between epithelial cells. In the trachea they cause cough, and in the lower airways hyperpnoea (rapid breathing); stimulation also causes bronchial and laryngeal constriction. They are also responsible for the deep augmented breaths every 5–20 min at rest, reversing the slow collapse of the lungs that occurs in quiet breathing, and may be involved in the first deep gasps of the newborn. They are stimulated by irritant gases, smoke and dust, rapid large inflations and deflations, airway deformation, pulmonary congestion and inflammation. The afferent nerves are rapidly adapting myelinated fibres in the vagus.
Proprioceptors (position/length sensors). These are located in the Golgi tendon organs, muscle spindles and joints. They are important for matching increased load, and maintaining optimal tidal volume and frequency. They are stimulated by shortening and load in the respiratory muscles (but not the diaphragm). Afferents run to the spinal cord via the dorsal roots. It should be noted that input from non-respiratory muscles and joints can also stimulate breathing.