Pediatric Respiratory Physiology

Introduction

“‘Children are not small adults,’ the most famous aphorism by Jean Jacques Rousseau, is a cornerstone for pediatricians: as a matter of fact, during childhood, all organs and systems undergo a continuous process of maturation and development with subsequent modifications not only in their dimensions but also in their structure, physiology, location, and neurological control. Somatic and functional development is particularly evident in the airways, as remarkable modifications occur from the nose to the alveoli, especially in the first 2 years of life. Later in life, differences between pediatric and adult airways are less noticeable, and by 6–8 years old, the pediatric respiratory system becomes very similar to that of an adult.” (Di Cicco et al)¹

• Significant differences in the anatomy and physiology of the respiratory system exist between infants, older children, and adults, which explain the increased vulnerability to perioperative respiratory adverse events.²
• Potential or current perioperative airway problems may be classified into those involving “normal,” “impaired normal” (previously normal but altered by trauma, infection, edema, etc.), or “known abnormal” (congenital abnormalities) airways.³
• Table 1 presents several anatomical and physiological characteristics of the pediatric airway, along with relevant anesthetic considerations.

Work of Breathing: Neonate vs. Older Children. vs Adults

Lower Airway Resistance

• Neonates have a smaller internal tracheal diameter, leading to increased airway resistance and predisposition to mucosal injury; this resistance decreases significantly during the first year of life (Neumann).
  • Airway resistance may be considered with Poiseuille’s Law, where resistance to flow (R) is inversely proportional to airway radius (r) to the fourth power:

(In this equation: η is the coefficient of viscosity of the air, L is the length of the airway, and V is the airflow volume)

• • This is particularly impactful in the context of subglottic edema, where even a small change in radius has a significant impact on resistance and flow.¹

Alveolar Considerations

• Neonates have fewer, larger alveoli.
• Interalveolar communicating pores and canals don’t develop until after the first several years of life and continue maturing into adolescence.
• Decreased surfactant production in specific neonatal populations (preterm, maternal gestational diabetes, perinatal asphyxia) leads to poor lung compliance, reduced lung volumes, widespread atelectasis, VQ mismatch, and hypoxia.

Respiratory Muscles and Chest Wall Compliance

• Pediatric ribs are more horizontally aligned, which reduces the efficiency of the intercostal muscles for respiration.
• The infant diaphragm, as well as other respiratory muscles, contains fewer type 1 muscle fibers (fatigue-resistant fibers). This, combined with inefficient accessory muscles due to underdevelopment and muscle angulation, increases the risk of fatigue and higher respiratory rates.¹
• Higher compliance of the pharynx, larynx, trachea, and bronchial tree also predisposes neonates to dynamic airway collapse as compared to older children.

Putting It All Together

• Neonates have high chest wall compliance (low chest wall muscle tone) and relatively low lung compliance (fewer alveoli), leading to:
  • Decreased functional residual capacity (FRC)
  • Increased risk of alveolar collapse
  • Terminal airway closure during normal tidal ventilation (closing volume higher than FRC)
  • Paradoxical inward movement of the chest wall in respiratory distress leading to decreased efficacy of diaphragmatic contraction
• By 2 years of age, increased alveoli lead to decreased airway resistance and increased lung compliance, while increased chest wall musculature and rib ossification lead to decreased chest wall compliance. Combined, this allows passive maintenance of FRC with aging.⁶
  Pediatric Circuit: Dead Space
• Normal dead space includes the anatomical dead space (conducting airways) and alveolar dead space (alveoli that are ventilated but not perfused). Physiologic dead space volume for spontaneous respiration is expressed as:

• In pediatric patients, particularly smaller patients, apparatus dead space significantly affects the Vd/Vt ratio.
  • Apparatus dead space is defined as portions of breathing that have bidirectional flow, including the endotracheal tube, flow sensors, and any other pieces on the patient side of the Y-piece.
  • This can impair carbon dioxide elimination, requiring increased minute ventilation to maintain normocapnia.
  • Minimizing apparatus dead space can have a significant impact on patient ventilation, particularly in reducing ventilator-induced lung injury by limiting tidal volume and ventilator cycles.
  • Apparatus dead space can be minimized by limiting the area where fresh gases mix with exhaled gas, such as by using a Y-piece with a septum in a circle system or a fresh gas inflow port in the elbow.⁷
  • Notably, preterm infants with respiratory distress syndrome and bronchopulmonary dysplasia (BPD) have increased dead space compared to term infants.⁸
• For more information, please see the OA Summaries: Pediatric Ventilation: Physiology Link and Pediatric Ventilation: Breathing Circuits Link.

Neonatal Apnea/Hypoxemia Physiology

Metabolism

• Minute ventilation (tidal volume x breaths/min) is determined by metabolic demand.
  • The basal metabolic rate for infants is 2-3 times higher than that of adults (7 mL/kg/min vs. 3-4 mL/kg/min), resulting in significantly less reserve and an increased risk of hypoxia and hypercapnia.⁴
  • Smaller children primarily increase their respiratory rate to compensate for increased metabolic demand due to anatomic constraints.
  • Lower FRC, combined with higher oxygen demands, leads to increased carbon dioxide production and respiratory acidosis, even during preoxygenation.
  • Rapid desaturation/ hypoxemia during induction or airway manipulation is common and often precedes serious adverse events.⁴
• Immature antioxidative systems also increase the risk of oxygen toxicity, including BPD and retinopathy of prematurity.

Respiratory Control

• The respiratory control system comprises brainstem centers, chemoreceptors, and baroreceptors, as well as voluntary cortical regulation.
• Neonates, particularly those born preterm, may have physiologic or pathologic apneic events and irregular breathing due to incomplete development of the respiratory control circuit.
  • Apneic events typically develop during the first days of life and may continue for several months.
  • Apneas of prematurity occur in virtually all neonates with a gestational age ≤ 28 weeks.
  • The American Academy of Sleep Medicine defines apnea as an event lasting 20 seconds or more, associated with an arousal from sleep, 3% or greater oxygen desaturation, or bradycardia (in infants less than 1 year old).⁹
  • These events may occur once or in series (periodic breathing).
• Postoperative apneas are increased in those with younger gestational age, history of recent apnea, history of methylxanthine use, or mechanical ventilation or oxygen support.

Hypoxia and Hypercarbia

• Infant respiratory rate and tidal volume do not respond the same to hypoxia and hypercarbia as in older children and adults. This response is further blunted by anesthetic agents.²
• During the first 2-3 weeks of life, neonates exhibit a biphasic response to hypoxia, initially characterized by hyperventilation, followed by a decrease in rate and an increased risk of apneas after ~1 minute.
  • Neonates older than 3 weeks will exhibit a sustained hyperventilatory response similar to that of older children and adults.²
• Additional causes of neonatal hypoxia include congenital heart disease, pulmonary disease (BPD, pulmonary hypertension), airway obstruction, and sepsis.

Neonatal Nasal Continuous Positive Airway Pressure (CPAP): Mechanism

• Neonates, particularly preterm, are at increased risk of atelectasis. Nasal CPAP is often used to maintain positive pressure, thereby keeping the alveoli open and decreasing the risk of respiratory failure.
• Humidified, high-flow nasal oxygenation systems have been shown to effectively prolong the time to desaturation in pediatric patients aged 0-10 years, although their effect on the rise in carbon dioxide has not yet been demonstrated in this population, unlike in adults.⁴
• It is unclear what pressure should be used, though the goal is to avoid extremes
  • Excessively high pressures may cause distension, impaired gas exchange, worsened respiratory, cardiovascular/ pulmonary function, and airway trauma leading to BPD.¹⁰
  • Low pressures may lead to ineffective gas exchange and fail to prevent atelectasis
• Advantages include non-invasive oxygen delivery, which can be used after extubation, a decreased risk of BPD, and the absence of pressure necrosis associated with a face mask.⁹
• Disadvantages include unclear parameters for use, duration-dependent nasal trauma, potential to deliver excessively high pressures, requirement of orogastric placement for decompression, and effectiveness may be compromised by crying or mouth breathing.⁹