Control of Ventilation

Emergence from an underwater world, in which the child relied on placental exchange of gases and nutrition, induces tremendous changes in the neonate’s physiology and anatomy. Some of these changes occur rapidly at birth; others proceed more slowly. These significant changes can complicate interpretation of the neonate’s problems. In particular, the assessment of the control of ventilation in the neonate may be difficult. Interventions used to obtain measurements, such as placement of a facemask or insertion of a laryngotracheal tube, may induce significant changes in ventilation. Measurements of ventilation to assess respiratory drive also depend on the assumption that the respiratory muscles are capable of converting this drive into work—which is not always the case in infants and neonates.

Muscle fibers have been found to fall into two categories. Type I fibers are slow twitch, highly oxidative, and fatigue resistant. Type II fibers are fast twitch and are easily fatigable. Newborns have a paucity of type I muscle fibers but develop them shortly after birth. The muscle fibers in the diaphragm of a preterm infant are composed of less than 10% of type I fibers. The muscle fibers of a full-term infant may be 30% type I fibers. The percentage of type I fibers increases to 55%, the expected adult level, during the first year of life. Preterm infants are more prone to respiratory fatigue; this predilection disappears as they reach maturity.

Other subtle differences in sleep patterns also affect control of ventilation. Preterm infants spend as much as 50% to 60% of their sleep state in the rapid eye movement (REM) state. During REM sleep, the intercostal muscles are inhibited, as are most of the other skeletal muscles. This places a greater burden on the diaphragmatic activity. Much of this activity may be wasted, because the chest wall can move paradoxically in the very young. This purposeless movement readily leads to hypoventilation, increased respiratory drive, and diaphragmatic fatigue.

Biochemical and reflex controls of ventilation are similar but incompletely developed in full-term neonates when compared with adults. Neonates have a higher basal metabolic rate than that in adults. This is reflected in higher ventilatory rates relative to body mass at any given partial pressure of carbon dioxide. Increases in ventilation are proportionately similar, however, in infants and adults with an increased partial pressure of carbon dioxide. This concordance in response is not seen in preterm infants. Their response to increases in partial pressure of carbon dioxide is blunted when compared with that in full-term infants and adults. Differences also are seen in the response to partial pressure of oxygen between premature infants and full-term infants and adults. The administration of 100% oxygen decreases ventilation in the very young, suggesting the existence of chemoreceptor activity not generally seen in adults.

Gestational age, postnatal age, body temperature, and sleep state modify the ventilatory response of newborns to hypoxia. Preterm and full-term infants less than a week old who are awake and euthermic usually demonstrate biphasic breathing patterns. They often experience tachypnea followed by hypoventilation. Hypothermic infants demonstrate a blunted response to hypoxia with respiratory depression, but they do not have the initial hyperpnea. The central effects of hypoxia on the respiratory center may cause depression of ventilation. Active peripheral chemoreceptors are unable to maintain a significant influence over this response. REM sleep also may decrease the response to hypoxia in these infants. Sleep states other than REM are associated with an increase in the ventilatory response to hypoxia. Arousal from sleep during hypoxia is not seen in newborns but develops during the first few weeks of life. In these slightly older infants, further maturation of the chemoreceptors increases their ventilatory drive to hypoxia. Of interest, a decreased response to hypercarbia associated with hypoxia also occurs in newborns but not in older infants and adults.

Reflexes arising from the lung and chest wall probably are more important in maintaining ventilation in newborns and in determining the respiratory tidal volume. Periodic breathing is common in preterm and full-term infants. These periods of alternating rapid ventilation followed by apnea may be common and can be considered normal. Periodic breathing is thought to result from dyscoordination of the feedback loops controlling ventilation. During the apneic part of periodic breathing, partial pressure of carbon dioxide may increase, but changes in heart rate do not. Generally, no serious physiologic consequences are seen. This response often ceases by the age of 6 years. Some preterm infants, however, may demonstrate serious and potentially life-threatening episodes of apnea. These episodes may last longer than 20 seconds and are accompanied by bradycardia. Apneic episodes may represent a failed response to hypoxia. Because these episodes are more commonly seen during REM sleep, ventilatory fatigue, as well as impaired chemoreceptor response to hypoxia, may be the cause. Usually, stimulation is all that is required to terminate the apneic event. Aminophylline treatment generally decreases the apneic episodes through central stimulation. Continuous positive airway pressure (CPAP) also may be helpful to decrease apneic episodes by modifying the lung and chest wall reflexes.

Laryngospasm

The primary function of the larynx is to protect the lungs from aspiration. Hence, the laryngeal adductor response is a very strong reflex. The robustness of the reflex has been shown to change with age and maturity in animal models. It is strong enough to be lethal in some instances. When laryngeal adduction is coupled with tachycardia, hypertension, and apnea, it is termed the laryngeal chemoreflex (LCR). The LCR can be induced by laryngeal exposure to acid, base, and pressure, but it is most sensitive to water and is ablated by saline. This may have implications for sudden infant death syndrome (SIDS). Evolving responses with age to hypoxia, hypercarbia, and the laryngeal stimulation that causes the LCR may explain the age pattern seen with SIDS. Deaths attributed to SIDS have dramatically decreased as a result of a change in the recommended sleep position of children—from prone to supine. Elimination of hypercarbia from rebreathing may be the mechanism behind the decrease in SIDS deaths. Hypercarbia is a known potentiator of the LCR. An increased awareness of and more aggressive stance toward the treatment of infant reflux also may have decreased a potential stimulus for the LCR. Decreased bolus size, increased feeding frequency, frequent burping, and positioning to discourage regurgitation have been helpful to decrease the incidence of reflux in infants and perhaps the incidence of apneic spells and infant breathing issues.

Lung Volumes

In proportion to body size, the total lung capacity, functional residual capacity, and tidal volume are roughly equivalent in adults and in infants. In the full-term infant the total lung volume is approximately 160 mL, with functional residual capacity at one half of this volume. Tidal volume is approximately 16 mL and dead space is approximately 5 mL. In comparison with adults, however, any increase in dead space is much more significant in infants, related to their small lung volumes. In contrast with static lung volumes, however, alveolar ventilation is proportionately much greater in newborns (100 to 150 mL/kg of body weight) than in adults (60 mL/kg of body weight). This higher alveolar ventilation in infants results in a higher alveolar–functional residual capacity ratio, 5 : 1, compared with 1.5 : 1 in adults. Consequently, the functional residual capacity is much less of a buffer in infants, so that changes in the concentration of inspired gases are much more rapidly reflected in alveolar and arterial levels. This explains why induction of anesthesia using inhalational techniques is easier in infants than in adults. Along with the higher metabolic rate for body weight seen in infants, this differnce also explains why the ventilatory reserve in infants is not as great as in adults. The time from apnea to oxygen desaturation is much shorter in infants than in adults. Accordingly, surgical maneuvers that require short apneic periods may pose more of a challenge in infants than in adults.

The total surface area of the air-tissue interface of the alveoli in infants is small (2.8 m²). When this relatively small gas exchange area is combined with the higher relative metabolic rate, infants have a reduced reserve capacity for gas exchange. This difference is of increased importance when congenital defects interfere with lung growth and development or if the lung parenchyma becomes damaged. The remaining healthy lung may not be adequate to sustain life.

Respiratory Rate

The most efficient respiratory rate for newborns has been calculated to be around 37 breaths per minute. This rate is close to that observed for average newborns. Full-term infants are similar to adults in requiring approximately 1% of their metabolic energy to maintain ventilation. The cost of breathing is then 0.5 mL/0.5 L of ventilation. In preterm infants, this nearly doubles to 0.9 mL/0.5 L of ventilation. The cost of respiration also dramatically increases if the lung parenchyma is diseased or damaged by processes other than prematurity. In either case, the result is higher caloric and nutritional demands. Respiratory rate can directly affect the infant’s ability to complete the suck-swallow-breathe cycle as well. If gas exchange is poor, ventilation rates may increase. This increase in respiratory rate may not allow adequate time for the suck-swallow portion of feeding. Caloric intake decreases precipitously as the infant chooses breathing over feeding. This vicious circle can eventuate in failure to thrive.

Ventilation-Perfusion Relationships

Ventilation and perfusion are imperfectly matched in the neonatal lungs. Some persistent anatomic shunts in the newborn circulatory system, as well as a relatively high closing volume in the lungs, cause this mismatch. The normal arterial oxygen tension in a newborn breathing room air is 50 mm Hg. This increases dramatically during the first 24 hours of life with changes in fetal circulation and maturation of lung parenchyma. It continues to change slowly during the ensuing months and years (Table 180-1).

Table 180-1 Arterial Oxygen Tension (PaO₂) in Healthy Infants and Children

Newborn Heart and Cardiac Output

The heart of a healthy neonate is much different from that of an adult. The thickness of the right ventricle exceeds that of the left, as seen by the normal right axis deviation on the neonatal electrocardiogram. Shortly after birth and with closure of the fetal circulation, the left ventricle enlarges disproportionately. By the age of 6 months, the adult right-left ventricular size ratio is established.

The newborn myocardium is significantly different from the adult myocardium as well. The newborn myocardium contains fewer contractile fibers and more connective tissue. Consequently, neonatal ventricles are less compliant at rest and generate less tension during contraction. The usual Starling curves of contractility for adult cardiovascular physiology do not hold true for the neonatal heart. Cardiac output is rate-dependent in the neonatal heart. Bradycardia invariably equates with reduced cardiac output. Because of the differences in compliance and contractility in the neonatal heart, the increased contractility necessary to maintain cardiac output during bradycardia is not possible. The low compliance of the relaxed ventricle limits the size of the stroke volume; therefore, increases in preload are not as important in neonatal physiology as is heart rate. This distinction is extremely important to recognize during surgical and anesthetic procedures, which may induce bradycardia. Autonomic innervation also is incomplete in the neonatal heart, with a relative lack of sympathetic elements. This relative underdevelopment may further compromise the ability of the less contractile neonatal myocardium to respond to stress.

Heart rate is crucially important in the very young. The normal range for the newborn is 100 to 170 beats per minute. The rhythm is regular. As the child grows, the heart rate decreases (Table 180-2). Sinus arrhythmia is common in children, but all other irregular rhythms should be considered abnormal. The average newborn systolic blood pressure is 60 mm Hg; the diastolic pressure is 35 mm Hg.

Table 180-2 Normal Heart Rate for Children by Age

Blood Volume

Intravascular blood volumes vary tremendously during the immediate postnatal period, related to the amount of blood transferred from the placenta to the child. “Stripping” the cord after birth or delays in clamping the umbilical cord may increase the blood volume by more than 20%, resulting in transient fluid overload and respiratory distress. Conversely, fetal hypoxia during labor causes vasoconstriction and a shift of blood to the placenta. Thus, fetal hypoxia may lead to hypovolemia after birth.

Stay updated, free articles. Join our Telegram channel

Join