Respiratory disease: Attention turns to the air pump

Abstract

T he respiratory muscles constitute the body’s air pump, a part of the respiratory system as critical for maintenance of life as is the heart. By and large physicians have taken the air pump for granted and have tended to ignore the possibility that it plays a role in clinical and physiologic manifestations of respiratory disease. Yet evidence accumulated in the last decade strongly suggests that air pump dysfunction in respiratory disease is partly responsible for limitation of physical exercise capacity and that it contributes to the pathogenesis of dyspnea and respiratory failure [l]. The functions of the respiratory muscles and air pump are prescribed by two mechanisms, central nervous system control and intrinsic muscular responses to external influences. This editorial focuses on the latter aspect. Space restrictions make it impossible to give credit to the many investigators whose work underlies this brief review. For detailed information on all facets of respiratory muscle physiology the reader is referred to the State-of-the-Art review by Derenne, Macklem and Roussos [2] and to the Proceedings of the International Symposium on the Diaphragm, held at the University of Virginia in 1978 [3]. The principal role of the respiratory muscles is to sustain breathing. The mechanics of the respiratory system are such that the energy required to breathe is derived almost entirely from contraction of the inspiratory muscles. The expiratory muscles often facilitate breathing by assisting with expiration or setting the position of the diaphragm prior to inspiration [4], but by far the greatest portion of ventilatory work is born by the inspiratory muscles, including the diaphragm, the inspiratory intercostals and the accessory inspiratory muscles. The inspiratory muscles, especially the diaphragm, are arranged around the thoracic cavity in such a way as to pull away from it. Goldman and his colleagues [4] have established that the diaphragm is primarily responsible for the act of inspiration, the inspiratory intercostal and accessory muscles playing a supporting role. At rest the adult rib cage is stable enough to resist collapse when diaphragmatic contraction produces a small negative intrathoracic pressure. At exercise or in obstructive disease of the airways, diaphragmatic contraction produces a larger negative intrathoracic pressure and the chest wall would collapse unless it were further stabilized by simultaneous contraction of the inspiratory intercostal and accessory muscles. This accounts for the well known use of these muscles in asthma, chronic bronchitis and emphysema. At times, the roles of airmover and fixator are reversed [5]. This happens when the excursion of the diaphragm is limited, as occurs normally in recumbent positions. It can also occur in diseases which limit or restrict diaphragmatic excursion, such as severe emphysema or obesity. The fixating function of inspiratory muscles is critical in the infant whose thorax is extremely compliant. Absence of the fixating function can have devastating consequences. In quadriplegics whose diaphragms are intact, air pump function is moderately impaired, but the inherent stability of the rib cage offsets loss of intercostal muscle function. In contrast, with bilateral diaphragmatic paralysis the function of the air pump is severely compromised because contraction of the other inspiratory muscles is largely dissipated in displacement of the flaccid diaphragm. The cardiac analogue is the ventricular aneurysm, in which the contractile energy of intact ventricular muscle is dissipated in distending the aneurysmal segment, with consequent reduction of stroke volume and cardiac output. The respiratory muscles, like the heart, exhibit a characteristic length-tension relationship. For skeletal muscle there is an optimum resting length from which the muscle produces maximum contractile tension. A departure from this length in either direction reduces contractile force despite maximum neural stimulation. For muscles which surround cavities and by their contraction generate pressures therein, it is more convenient to speak of the pressure-volume relationship which, for the heart, is known as the Frank-Starling law. In the heart, most alterations in the pressure-volume relation result from dilatation of the ventricle with elongation of the muscle fiber. The converse is true for the air pump. Inspiratory muscle force, expressed by