Physiology of Breathing

Diaphragm (Structure and Function)

The diaphragm arises from the embryologic pleuroperitoneal fold. Myoblasts migrate from cervical somites to the pleuroperitoneal fold where they arrange themselves into a sheet on a mesenchymal substrate that separates the peritoneum from the abdomen. Once fully formed, the diaphragm originates from bilateral tendinous crura attached to the spinal column and inserts as a costal tendon attached to the chest wall between the sixth and twelfth ribs. The dome of the diaphragm remains largely tendinous. This structure, a circular attachment to the thoracic wall, vertical muscle orientation adjacent to the thorax, and attachment to a flattened central tendinous dome (Figure 40-1), works like a piston during breathing to enlarge the thorax and displace abdominal contents downward.

Figure 40–1 The diaphragm is attached circumferentially to the thoracic wall. Its muscular portion extends onto the dome, where it is tendinous and flattened. When the muscle contracts, the dome descends like a piston, enlarging the thorax and displacing abdominal contents downward.

Approximately 50% of the diaphragm consists of type I fast twitch muscle fibers, which have high endurance and are resistant to fatigue. The remainder of the diaphragm is made up of type IIA and type IIB fibers, which have different properties.¹ Type IIA fibers are important in achieving high levels of minute ventilation quickly, have good endurance, and can contract rapidly, but are not able to sustain long-term power output. Type IIB fibers cannot sustain their force of contraction because they possess lower oxidative capacity and are more susceptible to fatigue. The greater the force of contraction required, the more motor units of the diaphragm are recruited. There appears to be little difference between the activity of costal muscles and crural muscles, either during normal breathing or in response to hypoxia and hypercapnia.

When a patient lies supine, the diaphragm rests against the inner surface of the rib cage. When the diaphragm contracts and its muscle fibers shorten, the whole diaphragm moves down, lowering pleural pressure and increasing intra-abdominal pressure. The increase in intra-abdominal pressure generated by descent of the diaphragm acts as a caval pump to enhance cardiac filling.² Because of its alignment against the lower ribs (zone of apposition), descent of the diaphragm also expands the caudal portion of the rib cage.

The muscle of the diaphragm extends from the costal insertion onto the dome of the diaphragm. When the diaphragm is “high,” it is loaded for greater force of contraction. When it is “low” or “flat,” it is unloaded and disadvantaged.

The diaphragm is the major inspiratory muscle of the neonate. It increases in thickness with age (as its muscle mass increases). It also becomes appositional to a longer segment of chest wall with growth, enhancing its effectiveness as an inspiratory piston.³ In the neonate, the muscular diaphragm has a greater angle from the vertical than that of the adult, which reduces its effectiveness as an air pump (Figure 40-2). This angle approaches zero with growth, increasing the diaphragm’s effectiveness with advancing age. The importance of this angle as an impediment to diaphragmatic effectiveness becomes exaggerated at total lung capacity, with air trapping, and when the abdomen is distended, all of which flatten and unload the diaphragmatic muscle (Figure 40-3).

Figure 40–2 The angle of the muscular diaphragm to the vertical is narrow in the older child (A) and adult than it is in the infant (B). This more horizontal traction on the dome may be disadvantageous when the muscle of the infant diaphragm contracts.

(Courtesy Women & Children’s Hospital of Buffalo, NY.)

Figure 40–3 The normal position of the diaphragm (A) allows it to stretch or “load” during expiration. In inspiration, its muscular attachment to the thorax pulls it vertically downward. Air trapping (B), abdominal distension, or other disorders that cause flattening of the diaphragm interfere with “loading” and with the direction of contraction.

(Courtesy Women & Children’s Hospital of Buffalo, NY.)

Intercostal Muscles

The rib cage is fixed to the spine and to the sternum. Thoracic volume is modified during breathing primarily by changing the angle of the anterior ribs to the horizontal. At rest, the ribs slope caudad from their spinal attachments. The rib cage tilts upward during inspiration. The intercostals muscles form three functional sheets. The outermost (external) sheet and the parasternal sheet act to displace the ribs cephalad as they shorten. This increases both the anteroposterior and lateral dimensions of the thorax. There is also a deep (internal) layer of intercostal muscle at right angles to the external sheet that acts to displace the ribs caudad when it contracts. Thus, the intercostals muscles play both inspiratory and expiratory roles in breathing by reshaping the thorax.

Accessory Muscles of Respiration

Though quiet expiration is largely passive, resulting mostly from elastic recoil of the lung, active expiration may be assisted by contraction of abdominal muscles (rectus abdominis, transverse abdominis, and the obliques). During quiet breathing, abdominal muscle tone elevates the diaphragm during expiration, increasing the zone of apposition and loading the diaphragm for greater inspiratory contractile efficiency.

Accessory muscles of inspiration include the scalenes, sternocleidomastoids, pectoralis minor, and erector spinae, all of which elevate the ribs during contraction. During quiet breathing, accessory muscles play a minor role, but during respiratory exertion, they may play a major role and may act to unload and unburden the diaphragm and intercostals. Even profoundly neurologically impaired children, who exhibit little volitional activity, can use accessory muscles of breathing when distressed. Children with dysfunction of the primary muscles of respiration may rely on their accessory muscles even at rest.

Integrated Control of Breathing

Control of breathing involves numerous afferent and efferent neural arcs, including volitional, sensory, and biochemical input and motor output to respiratory muscles, facial structures, and airway effectors. All of these signals are integrated, modulated, and emitted to effector organs by the brain. It is for this reason that brain death eliminates all breathing function.

The phrenic nerve arises from the cervical spinal cord (C3-C5) and migrates with the myoblasts to the pleuroperitoneal fold. Separate branches innervate the crural and costal regions of the diaphragm, and both regions include slow and fast twitch muscle fibers. These nerves secrete acetylcholine and transmission may be blocked by many drugs and toxins, including the clinically useful neuromuscular blocking agents. Phrenic motor neurons and muscle fibers continue to grow postnatally. The intercostal muscles are innervated by thoracic intercostals nerves.

The diaphragm and intercostal muscles work in unison, but also have individualized functions in breathing. When their functions are separately impaired, as in quadriplegia or diaphragm paralysis, abnormalities of gas exchange occur. DiMarco et al ⁴ showed that ventilation to basal lung regions is generally preserved when intercostal function alone is impaired, whereas, with isolated diaphragmatic paralysis, ventilation of more cephalad regions of the lung is relatively preserved. Costal and crural portions of the diaphragm are both responsive to hypercarbia and hypoxia.⁵

Neural Automatic Control of Breathing

The generation of respiratory patterns resides in the brainstem, in a respiratory complex consisting of the dorsal and ventral medullary and pontine respiratory groups.⁶ These three neural groups coordinate and control inspiration and expiration. They modulate input from chemoreceptors, mechanoreceptors, and lung stretch receptors. In this manner, they integrate blood gas stimuli, chest wall tension, and lung stretch signals to generate and modulate an oscillatory pattern of breathing.⁷

Innervation of the laryngeal muscles modulates airway dilation and constriction. Neurons in the hypoglossal nucleus, which is the motor nucleus for the tongue, provide breath-by-breath signals to protruder muscles of the tongue to enlarge the oral airway. The trigeminal motor nucleus also plays a role in tensing the tensor palate muscle of the nasopharynx, which helps to minimize airway resistance. The alae nasi muscles, controlled by the facial motor nucleus, can actively enlarge the nostrils to facilitate inflow of breath.

The ventral medullary group functions in sleep, anesthetized, and awake states, but how organization of activity differs in these distinct states is not known. Blood pressure is tied into excitatory or depressant respiratory activity. This is thought to occur in the rostral ventromedullary area. It is also suggested that this area mediates responses to carbon dioxide (through both tidal volume and rate control), and responses to resistive breathing.⁸ Lesions in the ventral medulla have been implicated in the etiology of sudden infant death syndrome and apneic episodes.⁹

Automatic control of breathing is so widely dispersed within the brainstem that it is no wonder that elements of respiratory cycling persist in many patients severely devastated by brain injury. Use of accessory muscles of respiration and motor components of respiratory distress may persist even when supratentorial function and most brainstem reflexes are absent. In the awake state, breathing patterns may be dominated by voluntary cortical activity that reaches the muscles of respiration by way of the corticospinal motor tract. Specific brain lesions may independently impair either automatic or spontaneous breathing controls.

Chemoregulation in the Physiology of Breathing

The aortic arch and the bifurcation of the common carotid artery house chemoreceptors that respond to both hypercapnia and hypoxemia. Changes in carbon dioxide are recognized by both central and peripheral chemoreceptors. The brainstem may distinguish acute from chronic hypercapnia by sensing the acid base status of the cerebrospinal fluid. Sustained hypoxia evokes a cascade of ventilatory, neurochemical, and metabolic responses. Responses in immature animals are characterized by earlier and more marked depression of ventilation than is found in fully mature animals. Ventilation during hypoxia incorporates a number of compensatory mechanisms (stimulation or depression) from multiple systems. The time course of these responses is developmentally regulated. When hypercapnia is combined with hypoxia, the ventilatory responses are exaggerated.

The predominant drive to breathe during hypoxia and hypercarbia is mediated by stimulation of chemoreceptors of the carotid and aortic bodies. Hypercapneic drive predominates under most circumstances, but hypoxic drive may persist and predominate if the response to carbon dioxide is blunted (as in chronic respiratory acidosis). These chemoreceptors then stimulate the respiratory center in the medulla to increase minute ventilation. In the absence of brainstem function, there is no respiratory response to either hypercarbia or hypoxia.

Breathing Failure

When challenged, muscle tension can be increased either by increasing the frequency of firing or by increasing the number of motor units being fired. At low muscle tension, the number of motor units participating in contraction may be increased before frequency is raised. Recruitment is used to increase work. To achieve an even greater increase in force, the frequency of firing of individual motor units may be raised, such that while the number of motor units is held constant the work of each motor unit is increased.

Working skeletal muscles rely on a continuous supply of oxygenated blood. Diaphragmatic function can be impaired if blood flow or oxygenation is reduced. Diaphragmatic muscle cannot operate at optimal length (force-length relationship) to generate the appropriate contraction (force-velocity relationship) if energy demand outstrips energy supply. The combination of suboptimal force-length and force velocity relationships causes rapid, shallow breathing, largely from dysfunction of Type II B fast-twitch glycolic fibers.

Respiratory muscle fatigue develops during exhaustive exercise. Prolonged malnutrition has also been shown to affect the diaphragm’s muscle structure and to impair its ability to generate force. On the other hand, it has been shown that respiratory muscle training can lessen the development of respiratory muscle fatigue.¹⁰ Training of the diaphragm can increase capillary density, myoglobin content, mitochondrial enzyme concentration, and the concentration of glycogen, but persistent mechanical ventilation (particularly during deep sedation or paralysis) decreases muscle strength by allowing disuse muscle atrophy.

In acute illness, breathing fails if respiratory muscle demand for blood flow, metabolic substrate, and oxygen delivery outstrips supply, just as it does in exhaustive exercise.¹¹ The point at which this occurs is influenced by many factors, including the energy cost of breathing, duration of contraction per breath, velocity of contraction, operational length of muscle fibers, energy supply, efficiency of muscles, and state of muscle training.¹² Respiration can also fail if control of breathing is impaired. In any event, breathing failure, if untreated, may cause respiratory arrest and death.

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