Physiology Of The Developing Respiratory Pump

In early life the ventilatory response to loaded breathing is limited. Ventilatory failure can occur in newborns and infants due to immaturity of the chest wall and respiratory muscles, poor coupling between thoracic and abdominal movements, and upper airway dysfunction. Furthermore, infants spend a large proportion of time asleep, with full-term newborns spending more than 50% of their time in rapid eye movement (REM) sleep and premature infants an even higher proportion of time in REM (l).

At birth, the ribs extend almost at right angles from the vertebral column. As a result, the rib cage is more circular than in adults (2) and, consequently, lacks mechanical efficiency. In adults, the volume of the rib cage can be increased by elevating the ribs. In infants, the ribs are already elevated, and this may be one reason why motion of the rib cage during room air breathing contributes little to tidal volume (Vt) (3). The diaphragm appears flattened with a very wide angle of insertion on the rib cage, resulting in the absence of an area of apposition (4). The orientation of the ribs does not change substantially until the infant assumes the upright posture. Concurrently, there is progressive mineralization of the ribs. Between 1 and 2 years of age (3), rib cage contribution to tidal breathing reaches a value that approximates that reported in adolescents during non-REM (NREM) sleep (5). Changes in shape and structure with advancing postnatal age play a central role in stiffening the rib cage. A high chest wall compliance (Ccw) relative to lung compliance (Cl) is an inherent characteristic of the newborn mammal (6). In infants, outward recoil of the chest wall is very low. Consequently, the static passive balance of forces between the lung and the chest wall would dictate a very small functional residual capacity (FRC). There are compelling reasons to believe that dynamic end-expiratory lung volume in newborns and infants is substantially above the passively determined FRC. It has been shown that in newborns, in contrast to adults, expiration is terminated at substantial flow rates (7). In addition to foreshortened expiratory time, infants use postinspiratory activity of the diaphragm (8) and expiratory glottic narrowing to actively slow expiration (9). Dynamic elevation of end-expiratory lung volume above passive FRC persists until around the end of the first year of life (10).

With growth, there is a progressive increase in the bulk of respiratory muscles. There are also important changes in the fiber composition, fiber size, and oxidative capacity and contraction characteristics of the diaphragm (11). Mean cross-sectional area of all fiber types increases postnatally. Maximal pressures exerted by infants and even children are surprisingly high compared with adults (12-14). This is probably related to the small radius of curvature of the rib cage, diaphragm, and abdomen that, according to the Laplace relationship, converts small tensions into relatively high pressures (12). However, the inspiratory force reserve of respiratory muscles is reduced in infants with respect to adults because inspiratory pressure demand at rest is greater. High pressure demand in infants is due to high minute ventilation and to high weight-corrected metabolic rate (15-17).

Fatigability of neonatal respiratory muscles as compared with adult muscles remains a controversial issue. The paucity of fatigue-resistant Type 1 fibers, the high ^proportion of fatigue-susceptible Type IIc fibers, and low oxidative capacity of the neonatal diaphragm suggest that the muscle may be rela tively prone to fatigue. An in vivo study in rabbits found that diaphragmatic fatigue occurred more quickly in neonatal than adult animals (18). However, other in vitro and in vivo animal studies have shown the opposite (19).

Chest wall muscle contraction helps to stabilize the compliant infant rib cage, minimizing inward displacement of the rib cage by diaphragmatic contraction. However, when the stabilizing effect of intercostal muscles is inhibited, such as during REM sleep, paradoxic inward motion of the rib cage occurs during inspiration (20, 21). During REM sleep, the diaphragm dissipates a large fraction of its force in distorting the rib cage rather than effecting volume change. This increase in diaphragmatic work of breathing (22) represents a significant expenditure of calories, and may contribute to the development of diaphragmatic fatigue and ventilatory failure. Furthermore, acidosis and hypoxia, both of which increase muscle fatigabil-ity, are not uncommon in sick premature infants.

As in adults, upper airway muscles actively dilate and stiffen the airway during inspiration in infants and children. As cited above, laryngeal adduction is prominent during expiration in infants, effectively increasing the time constant for lung emptying. Upper airway muscles, except for the nasal and laryngeal abductors (alae nasi and posterior cricoarytenoid muscles), become atonic during REM sleep, predisposing the upper airway to collapse during inspiration and possibly resulting in decreased end-expiratory lung volume due to loss of laryngeal airflow braking. The sparing of active nasal and la-ryngeal dilation during inspiration in REM sleep presumably decreases the work of breathing by maintaining low airflow resistance in the upper airway. The negative pressure required to collapse the upper airway appears to be low in the neonate (23) (approximately —3 cm H2O), increasing in children to about —20 cm H2O (24) and returning to levels similar to those in early infancy with adulthood (25). Children and adults with obstructive sleep apnea exhibit airway collapse at pressures at or near 0 cm H2O, suggesting that they have a more compliant upper airway than do normal subjects (24, 25).

TESTS OF RESPIRATORY MUSCLE FUNCTION Equipment and Measurement Conditions

Maximal respiratory muscle pressures in infants and children are similar to those encountered in adults (see 26-28). The equipment used to measure respiratory muscle and chest wall function must be modified, however, to accommodate the smaller flow rate and Vt of infancy and childhood. The following equipment should be available: pressure transducers (flow, ± 2 cm H2O; esophageal pressure [Pes] and airway opening pressure [Pao], ± 50 cm H2O); transducer amplifiers; heated pneumotachographs (0-12 L/minute for neonates to 6 months, 0-30 L/ minute for 3 months to 2 years); esophageal balloons; catheters (8F, internal diameter of 2 mm or 6F, internal diameter of 1.6 mm); face masks; timed shutter with pressure port; and multichannel strip chart recorder or computer screen, central processing unit, analog-to-digital converter, and printer. Because Pes may not adequately represent pleural pressure in the presence of high Ccw, all esophageal balloon and catheter measurements in infants should be validated by an "occlusion test" (29, 30). Equipment dead space should not exceed 1.5 ml/kg body weight.

For respiratory inductive plethysmography in children, the following are required: rib cage (RC) and abdominal (AB)

bands of a size appropriate for the subject's chest wall; a source of oscillatory current; signal processing equipment necessary to produce voltage output proportional to changes in RC and AB cross-sectional area. Also required is appropriate recording equipment such as strip chart, oscilloscope, or analog-to-digital converter with computer screen, central processing unit, and printer; or Respicomp, Respitrace PT (Non-Invasive Monitoring Systems [Miami Beach, FL], with computer hardware and analysis software integrated into system). Calibration of the respiratory inductive plethysmograph equipment is needed to measure Vt (spirometer or pneumotachograph). Frequency-amplitude response of respiratory inductive plethysmography has been shown to be flat to 13 Hz (31). The equipment necessary for the measurement of surface electromyograms (EMGs) in infants and children is identical to that used in adults (see EMG Equipment in Section 3 of this Statement).

At less than 5-7 years of age, children are not able to co-operate with lung function testing. For lung function testing of infants, a sedative such as chloral hydrate is usually administered. Therefore, the laboratory should be quiet, dimly lit, and conducive to sleeping. Sedation should not be given to infants with known upper airway obstruction. Continuous pulse oximetry should be measured in all sedated infants. Supplemental oxygen administration may be required, resuscitation equipment should be available, and personnel should be trained in pediatric car-diopulmonary resuscitation. Infants should not be discharged from the pulmonary function laboratory until fully awake.

For most tests in infants, the supine position is the position for which normal standards are defined. The neck should be in a neutral or a slightly extended position. The infant should be in clinically determined quiet sleep.

For tests in older children requiring maximal efforts, such as maximal respiratory muscle strength assessment, the technicians should be experienced in working with young children and in striking the right balance between exhorting the child to give his/her best effort, and not frightening the child. Other measurement conditions are identical to those for adult pulmonary function laboratories.

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