Respiration: control of ventilation

Abstract

Control of ventilation involves the basic cycle of inspiration and expiration and the chemoreceptor reflexes. The inspiration-expiration cycle is generated by the medulla, but it is smoothed by the combined actions of the pons and vagi. Inspiration is initiated by neurons that promote lung inflation via the intercostal and phrenic nerves; it is terminated by a combination of fatigue of these neurons and inhibitory actions from the pons, expiratory centre and increasing lung volume (via the vagus). As a result, expiration is initiated; this, in turn, is inhibited by fatigue of the expiratory neurons and by loss of inhibitory influences from the pons and the vagus as the lungs deflate. The physical work during respiration is against lung compliance and airway resistance. Too slow a frequency of very deep breaths would require excessive amounts of work against compliance forces; and rapid shallow breaths would greatly increase the work done against airway resistance. A balance between these extremes is achieved by the vagal afferents that help to terminate inspiration. Whole-body responses to gas changes indicate that rising carbon dioxide levels promote ventilation, a reflex that is increased by the simultaneous presence of acidaemia and, particularly, hypoxia (asphyxia). These reflex changes originate from peripheral chemoreceptors (aortic and carotid bodies) that monitor the oxygen, carbon dioxide and acid levels of the plasma, and from central chemoreceptors (floor of the IVth ventricle) that monitor the pH of the cerebrospinal fluid. Details of the integration between these reflexes and the basic inspiraton-expiration cycle remain to be elucidated.