Oxygen Tension and Oxygen Content

Oxygen is carried in the blood in two ways. A large portion (97.5%) is carried in combination with hemoglobin inside red blood cells, and a small portion (2.5%) is carried in the dissolved state in plasma. Therefore the patient’s arterial oxygen content (CaO₂)—the total amount of oxygen (in milliliters) carried per deciliter of blood—will be determined primarily by the patient’s total hemoglobin concentration and the oxy-hemoglobin saturation plus the dissolved oxygen.

Arterial oxygen content cannot be determined from the PaO₂, which is the partial pressure of oxygen. At sea level, the total pressure of gases in the atmosphere and in the blood must always equal 760 torr. Room air contains 21% oxygen, approximately 79% nitrogen, and a small quantity of inert gases. Therefore the PaO₂ of room air is 21% of 760 torr, or approximately 160   mm   Hg, and the partial pressure of nitrogen in room air is 79% of 760   mm   Hg, or 600   mm   Hg.

In the alveolus at sea level, the total pressure exerted by all gases will still equal 760   mm Hg, but these gases ultimately include both water and CO₂. Water vapor pressure of air that is 100% humidified is 47   mm   Hg, so the partial pressure of O₂ in the airways when the patient breathes room air is approximately 150   mm   Hg (0.21  ×  [760  −  47] mm Hg). Alveolar gas also contains CO₂ with a normal PaCO₂ of 40   mm   Hg, so the alveolar oxygen tension or partial pressure of oxygen in the alveoli (PAO₂) is approximately 110   mm   Hg. When blood passes through the capillary adjacent to the alveolus, CO₂ diffuses from the blood through the alveolar-capillary membrane and into the alveolus, and oxygen diffuses from the alveolus into the blood.

The total pressure of all gases in the blood also totals 760   mm   Hg at sea level. The partial pressure of O₂ is approximately 110   mm   Hg, and the partial pressure of CO₂ is approximately 40   mm   Hg. These numbers reflect the partial pressure of gases (including oxygen) dissolved in the blood.

Approximately 0.003   mL of oxygen is dissolved per deciliter of blood for every mm Hg partial pressure of oxygen present in the blood. For example, if the PaO₂ is 100   mm   Hg, 0.3   mL of oxygen is dissolved per deciliter of blood. This dissolved oxygen reflects only a tiny fraction of the oxygen carried in the blood, but this is the number reflected by the PaO₂.

Oxygen is carried most efficiently when it is bound to hemoglobin and each gram of hemoglobin is able to carry 1.34   mL oxygen. The total oxygen content is determined by multiplying the hemoglobin (in g/dL) by 1.34   mL O₂/g of saturated hemoglobin and then multiplying that number by the actual hemoglobin saturation. The small amount of oxygen carried in the dissolved form is then added to the amount of O₂ carried by hemoglobin. The normal arterial O₂ content is approximately 18 to 20   mL O₂ per dL blood (Box 9-2).²⁷¹

To emphasize the difference between PaO₂ and arterial O₂ content, consider the effects of varying hemoglobin concentration in three patients. If the patients all breathe room air, as noted previously, the PaO₂ of all patients will equal approximately 110   mm   Hg, regardless of hemoglobin concentration. If the three patients have normal lungs, their hemoglobin will be fully saturated (99%), so their total arterial oxygen content will differ according to their hemoglobin concentration. If the first patient has no hemoglobin at all (concentration of 0   g/dL), the patient’s PaO₂ is still 110   mm   Hg, but the patient’s arterial oxygen content is 0.33   mL/dL (equal to the amount of dissolved oxygen, or 0.003  ×  PaO₂). This example is not realistic, but it makes the point that the PaO₂ is not the same as O₂ content. Consider a second patient with a hemoglobin concentration of 8   g/dL; the second patient’s PaO₂ is 110   mm   Hg, with a total arterial oxygen content of approximately 11   mL O₂ per dL blood (slightly more than half normal). The third patient has a hemoglobin concentration of 15   g/dL; this patient’s PaO₂ is 110   mm Hg, and the patient’s arterial oxygen content is approximately 20   mL O₂ per dL blood (normal). Although all three patients have exactly the same PaO₂ and oxygen saturation, the second patient must almost double cardiac output to maintain the same oxygen delivery as the third patient (DO₂  =  CO  ×  CaO₂). These examples illustrate the importance of evaluating hemoglobin concentration, PaO₂, and arterial oxygen saturation when interpreting blood gas results. Additional patient examples are included in Box 9-3.

The Oxyhemoglobin Dissociation Curve

The relationship between the PaO₂ and the hemoglobin saturation is expressed by the oxyhemoglobin dissociation curve, as shown in Fig. 9-6, with the PaO₂ on the horizontal axis and the hemoglobin saturation on the vertical axis. The curve is not linear but S-shaped, with a large plateau at the higher levels of PaO₂. There are several important things to note about the oxyhemoglobin dissociation curve. As noted, the curve flattens when the PaO₂ exceeds 80 to 100   mm   Hg; this means that although the PaO₂ continues to rise beyond 100   mm   Hg, the hemoglobin cannot become more saturated than 100%, and it cannot carry any more oxygen. Any additional rise in the PaO₂ will result only in increases in the amount of dissolved oxygen in the blood, which contributes only 0.003   mL O₂ per mm   Hg rise in PaO₂. Therefore a rise in PaO₂ from 100 to 700 torr does not mean that sevenfold more oxygen is carried in the blood; it is associated with an approximately 10% increase in oxygen content. Because the hemoglobin is fully saturated once the PaO₂ reaches 100   mm   Hg, there is usually no advantage to maintaining the patient’s PaO₂ any higher than this value.

Fig. 9-6 Oxyhemoglobin dissociation curve. The horizontal or flat segment of the curve at the top of the graph is sometimes called the arterial portion, or that part of the curve where oxygen is bound to hemoglobin. This portion of the curve is flat because partial pressure changes of oxygen between 60 and 100   mm   Hg do not significantly alter the percent saturation of hemoglobin with oxygen. The wide range of partial pressures of oxygen (PaO₂  =  60-100   mm Hg) represented by the flat part of the curve, allows adequate hemoglobin saturation at a variety of altitudes. For example, a PaO₂ of 100   mm   Hg at sea level results in a hemoglobin saturation with oxygen of 98%. The steep part of the oxyhemoglobin dissociation curve occurs after the PaO₂ drops below 60   mm   Hg and represents the rapid dissociation of oxygen from hemoglobin. During this phase, oxygen diffuses rapidly from the blood into tissue cells. Conditions associated with altered affinity of hemoglobin for O₂ are listed. P50 is the PaO₂ at which hemoglobin is 50% saturated, normally 26.6   mm   Hg. A lower-than-normal P50 represents increased affinity of hemoglobin for O₂, such as is present in conditions such as alkalosis, hypocarbia, hypothermia. The lower P50 means that the hemoglobin will be better saturated at lower PaO₂ (e.g., at normal pH, a 90% oxyhemoglobin saturation is associated with PaO₂ of approximately 60   mm   Hg; at an alkalotic pH, a 90% oxyhemoglobin saturation will be associated with a lower PaO₂, probably nearer 50   mm   Hg). The increased affinity means that the hemoglobin does not release O₂ to the tissues as readily. A higher P50 is seen with decreased hemoglobin affinity for O₂. With decreased affinity for O₂, the hemoglobin is less saturated at a given PaO₂, but will release the oxygen more readily to the tissues. Note that variation from normal is associated with decreased (low P50) or increased (high P50) availability of O₂ to tissues (dotted lines). The shaded area shows the entire oxyhemoglobin dissociation curve under the same circumstances. 2,3-DPG, 2,3-diphosphoglycerate present in higher quantities in children with cyanotic heart disease and in lower quantities in neonates with large amounts of fetal hemoglobin.

(From Lane EE, Walker JF: Clinical arterial blood gas analysis, St Louis, 1987, Mosby.)

As shown in Fig. 9-6, the slope of the oxyhemoglobin dissociation curve becomes extremely steep once the PaO₂ is less than 60   mm   Hg. Thus when the patient’s PaO₂ falls below 60   mm   Hg, even small additional decreases in the PaO₂ will be associated with a significant fall in the hemoglobin saturation and arterial oxygen content. Therefore the patient’s PaO₂ should be maintained above 60   mm   Hg, if possible.

The position of the oxyhemoglobin curve can be altered by several factors (Table 9-3). If the curve is shifted to the right, then hemoglobin has less affinity for oxygen (it is less well saturated) at any partial pressure of oxygen (PaO₂). Conversely, if the curve is shifted to the left, then hemoglobin has a higher affinity for oxygen (the hemoglobin is better saturated) at any given PaO₂.

Table 9-3 Shifts in Hemoglobin Dissociation Curve

Factors that shift the curve to the right include acidosis, hypercapnia, and hyperthermia. Under these conditions the oxyhemoglobin saturation and oxygen content is lower at any given PaO_2, but within the normal range the amount of oxygen released to tissues is enhanced, which is an adaptive response that makes oxygen more available in the tissue beds of patients who are likely to need it (e.g., those who are acidotic, hypercapnic, febrile).²⁷¹ Factors that shift the oxyhemoglobin dissociation curve to the left include alkalosis, hypocapnia, and hypothermia. Although these factors increase oxyhemoglobin saturation at any given PaO₂, oxygen will not be as readily released to the tissues,²⁷¹ because oxygen is more tightly bound to the hemoglobin molecule.

The hemoglobin dissociation curve for fetal hemoglobin is located to the left of the adult hemoglobin curve. Thus at a given PaO₂ and hematocrit, fetal blood contains more oxygen than adult blood. This higher affinity of fetal hemoglobin for oxygen provides adequate fetal arterial oxygen content and delivery, despite the relatively low PaO₂ in the placenta and fetal circulation. Fetal hemoglobin, however, releases oxygen less readily to the tissues than does adult hemoglobin. Fetal hemoglobin usually disappears within 4 to 6 weeks after birth and is replaced by adult hemoglobin.

Regulation of Carbon Dioxide Tension and Hydrogen Ion Concentration

Carbon dioxide is carried in the blood in several ways. Like oxygen, it can be dissolved in plasma or carried by hemoglobin. In addition, CO₂ can react with water to form carbonic acid (H₂CO₃), or it can combine with other proteins to form carbamino compounds.

Unlike oxygen, the relationship between PaCO₂ and the arterial CO₂ content is linear. Furthermore, PaCO₂ is directly proportional to the metabolic production of CO₂ and inversely proportional to alveolar ventilation. Thus an increase in alveolar ventilation will result in a decrease in PaCO₂. For example, if the patient’s PaCO₂ falls from 40 to 20   mm   Hg, the patient must have doubled alveolar ventilation. Similarly, if the PaCO₂ increases from 40 to 60   mm   Hg, alveolar ventilation must have decreased by 50%. If the PaCO₂ increases, then CO₂ combines with water to form H₂CO_3, and carbonic acid then dissociates into bicarbonate and hydrogen ion:

The net result of these reactions is a rise in hydrogen ion concentration and a fall in pH, or respiratory acidosis. If this condition persists for several hours, the kidney will respond with the excretion of more hydrogen ions and reabsorption of more bicarbonate. Renal compensation can restore the arterial pH to nearly normal levels (see discussion of renal disorders in Chapter 13).

Alveolar ventilation may either increase or decrease as compensation for primary metabolic disorders. When metabolic acidosis develops, excess hydrogen ions are present, resulting in the formation of more carbonic acid, which then dissociates to CO₂ and water. Total ventilation then increases (e.g., a patient with diabetic acidosis develops hyperpnea), so additional CO₂ is eliminated, and the CO₂ tension falls. The arterial pH will then increase toward normal levels, because hydrogen ions are eliminated as CO₂ is excreted by the lungs.

Alveolar ventilation will decrease when metabolic alkalosis is present. Carbon dioxide may be retained until the PaCO₂ is extremely high. Carbon dioxide will combine with water to form carbonic acid, which will dissociate to form hydrogen ions and bicarbonate ions. Hydrogen ions accumulate and the arterial pH decreases. An example of this compensation is a patient who develops hypokalemic, hypochloremic metabolic alkalosis and slows respirations; the PaCO₂ rises and the pH falls toward normal. Table 9-4 summarizes changes in the arterial pH, PaCO₂, and serum bicarbonate (HCO₃⁻) that occur with respiratory and metabolic acidosis and alkalosis.

Regulation of Respiration

Alveolar ventilation is controlled by both neural and chemical factors. Spontaneous respiration requires a rhythmic discharge from the respiratory center in the ventral portion of the brain. The chemical control of breathing is modulated at two respiratory centers: the CO₂ sensor and the O₂ sensor. The sensor for CO₂ is located in the brainstem and is influenced primarily by CO₂-related changes in the hydrogen ion concentration of the cerebrospinal fluid (CSF; see previous equation). Carbon dioxide diffuses freely from the blood into CSF, so an increase in PaCO₂ will quickly increase the hydrogen ion concentration in the CSF near these sensor cells. The electrical output of these chemosensitive cells results in an increase in ventilation that restores the PaCO₂ to normal levels.

The oxygen sensor consists of chemoreceptors located in the carotid and aortic bodies. These peripheral chemoreceptors detect changes in arterial oxygen tension and not oxygen content. A fall in PaO₂ below 50 to 60   mm   Hg results in a progressive increase in the electrical activity of the carotid body, which is transmitted to the respiratory centers in the brainstem and results in an increase in alveolar ventilation. The carotid body sensors are also responsive to acidosis and, to a lesser extent, hypotension.

Neural Control of Airway Caliber

The walls of the airways are lined with smooth muscle; constriction of this smooth muscle causes bronchoconstriction. Relaxation of the smooth muscle lining the airways will cause bronchodilation.

Airway smooth muscle is innervated by branches of the vagus nerve (cholinergic nerves) and to a lesser extent by branches of the sympathetic nervous system (adrenergic nerves). Acetylcholine and related compounds cause bronchoconstriction, whereas acetylcholine antagonists such as atropine cause bronchodilation. Adrenergic stimulation of smooth muscle by epinephrine and related compounds causes bronchodilation. Mucous glands in the lung also have a dual cholinergic and adrenergic innervation. Cholinergic stimulation increases mucus secretion, whereas adrenergic stimulation decreases it.

Etiology

Upper airway obstruction can occur anywhere in the extrathoracic areas. There are several developmental factors that increase the risk of upper airway obstruction in infants and young children. The larynx of the infant or child is more anterior and cephalad than the larynx of the adult. As a result, the sniffing position optimizes the airway opening during bag-mask ventilation or intubation of the infant or young child. Extreme extension of the neck can lead to obstruction of the airway.²⁴³

Upper airway obstruction in infants and children may be caused by conditions such as congenital or acquired anatomic abnormalities, acute infectious processes, or compression from other organ systems (Table 9-5). Additional potential causes of upper airway obstruction are listed as follows:

Pathophysiology

Airway obstruction decreases airway diameter and increases the resistance to air flow and work of breathing. The child often can compensate for a mild airway obstruction by increasing the work of breathing, allowing ventilation (air flow) to remain unchanged. When the airway obstruction becomes more severe, the child will no longer be able to compensate and will demonstrate significant increased work of breathing, decreased aeration (ventilation) with eventual hypercarbia, and respiratory failure. When severe, this condition can also lead to hypoxemia and tissue hypoxia.

Clinical Signs and Symptoms

Upper airway obstruction can often be identified from the clinical signs and symptoms. Older children with upper airway obstruction and a normal level of consciousness often assume the position that provides the most relief (i.e., the best air flow). Typically, these children are more comfortable sitting up and leaning forward; this is referred to as the tripod position. Signs of respiratory distress are often exacerbated in the supine position or by agitation.

The infant or child will exhibit stridor, a high-pitched sound during inspiration. This sound may be accompanied by a hoarse cough or cry. Inspiratory stridor, hoarseness, and drooling indicate the presence of significant acute upper airway obstruction, which is often associated with airway edema or airway compression. Stertor, or snoring, is often noted in children with upper airway obstruction secondary to adenotonsillar hypertrophy or a tongue that obstructs the posterior pharynx.

The child with mild to moderate airway obstruction may be restless and exhibit tachypnea. The child will often use accessory muscles of respiration, demonstrating nasal flaring and tracheal tugging (supraclavicular retractions). Breath sounds may be adequate, although they may be difficult to assess if the child has concomitant stridor or stertor. Tachycardia may also be noted as a nonspecific sign of distress. Oxygenation usually remains adequate until there is severe obstruction and decompensation. Signs of profound airway obstruction with respiratory failure include slowed respiratory rate, decreased aeration, altered level of consciousness, compromise in systemic perfusion, apnea or gasping, and bradycardia.

Regardless of the site of obstruction, the hallmark of airway obstruction is hypercarbia with a respiratory acidosis. The PaO₂ may initially be normal, although hypoxemia will develop when the patient’s condition deteriorates.

Management

Acute upper airway obstruction must be rapidly evaluated and treated. It can sometimes be anticipated and prevented or treated in young children by proper positioning of the head and neck into the sniffing position. Infants with acute respiratory distress who are breathing spontaneously are positioned in the upright or lateral (supported) position, especially after feedings. An infant seat can be used to keep the infant upright. Care must be taken to avoid flexion or hyperextension of the neck, because these positions can cause upper airway obstruction by tracheal compression.

For the older child the side-lying position is preferred immediately after surgery, because the tongue and other upper airway muscles may be hypotonic and occlude the upper airway if the patient is supine. Children with large tonsils or adenoids may manifest signs of airway obstruction, including snoring or stertor if they are allowed to sleep in the supine position.

As noted previously, toddlers and older children with upper airway obstruction often instinctively assume a posture that maximizes airway caliber. It is best to avoid manipulating the child’s position until personnel experienced in airway management are present. The young child may be most comfortable when held and supported upright by a parent.

Treatment includes administration of warmed, humidified oxygen by face mask, hood, tent, or blow-by tubing. Minimize noxious stimulation, because agitation can worsen airway obstruction. Inhaled racemic epinephrine is an accepted treatment for upper airway obstruction related to moderate-to-severe croup or postextubation edema. The mechanism of action is thought to be related to α-adrenergic constriction of precapillary arterioles, with resulting fluid reabsorption from the interstitial space and decreased laryngeal mucosal edema. These effects increase airway diameter and ease of gas flow. Doses may be given as often as every 20   minutes. Inhaled l-epinephrine is as effective as racemic epinephrine. These inhaled agents are to be used with caution in patients with tachycardia, arrhythmias, or underlying congenital heart disease, because the agents can potentiate tachycardia.²⁰¹

Inhalation treatment with a helium-oxygen mixture (heliox) provides a lower density gas compared with a nitrogen and oxygen mixture. Helium is an odorless, tasteless inert gas that can be substituted for nitrogen in inhaled gaseous mixtures.^94,167 The benefit of providing inhaled gas with a lower density is that it promotes laminar flow within the upper and lower airways. Laminar gas flow promotes the delivery of oxygen and inhaled medications through the areas of obstruction and facilitates drug deposition (Fig. 9-7). Effects of the helium and oxygen mixture are noted almost immediately; if it is effective, then the patient’s work of breathing decreases and aeration improves. If the child is verbal, gas delivery is confirmed if the child speaks in a high-pitched voice. A higher pitched cry may be noted during therapy in preverbal infants.

Fig. 9-7 Laminar versus turbulent flow. Schematic depiction of the spatial and velocity profiles of gas molecules within A, a laminar and B, a turbulent flow regimen. The velocity of the gas molecules is proportional to the length of arrows. During turbulent flow, there is chaotic molecular movement between lamina that results in ever greater pressure being required to achieve incremental flow. C, Note the alinear pressure-flow relationship with turbulent flow.

One limitation to the use of the helium-oxygen mixture is the need for supplementary oxygen. Generally, helium mixtures are delivered at 20% oxygen and 80% helium, 30% oxygen and 70% helium, or 40% oxygen and 60% helium. There is generally no benefit to heliox if the patient needs an FiO₂ greater than 0.4 (40% oxygen plus 60% helium), because the gas mixture will have a density similar to that of a standard nitrogen and oxygen mixture. Some children, however, will need less oxygen if the inhaled gas is able to traverse the areas of obstruction to reach the lower airways.

Administration of heliox during mechanical ventilation necessitates close monitoring of the child and the circuit, because the helium may interfere with the pneumotachometers and ventilator function. Because heliox improves flow through areas of airway obstruction, it can be used to treat disease processes that produce turbulent flow (e.g., asthma). It is often used until therapeutic medications take effect, or it can be used until resolution of the disease process.⁹⁴ Most institutions develop specific protocols for management of acute, life-threatening upper airway obstruction to support efficient care (Box 9-4).⁶

When airway obstruction is severe, elective (supportive) intubation is always preferable to emergency intubation (i.e., during resuscitation) of a child with impending respiratory failure. The decision to intubate is based on the patient’s clinical appearance. If the child demonstrates severe respiratory distress with significant work of breathing, then consider intubation. Signs of severe airway obstruction include mottling or cyanosis, decreased air movement, altered level of consciousness, stertor, stridor, and compromised systemic perfusion. Apnea or gasping or bradycardia are late signs of severe airway obstruction and should be prevented by timely intubation and respiratory support.

The pulse oximeter is generally not a useful tool in the detection of significant airway obstruction and the need for intubation, because hypoxemia is a late sign of deterioration. However, a downward trend or a sudden substantial decrease in oxyhemoglobin saturation can indicate deterioration, especially when the patient is breathing room air (FiO₂ = 0.21). Blood gas analysis or noninvasive CO₂ measurements should be evaluated if hypercarbia is suspected.

The severity and etiology of the upper airway obstruction will determine the treatment needed. Obstruction may be acute, as in cases of infection and tissue inflammation, or it may be chronic, such as with tonsillar and adenoidal hypertrophy. In both categories of airway obstruction, assessment of the effectiveness of gas exchange will help determine appropriate intervention. Some obstruction will resolve with repositioning and suctioning. Significant obstruction, however, may be treated with a nasal trumpet to provide airway stenting, noninvasive positive pressure ventilation, or tracheal intubation and ventilation. Relief of some causes of upper airway obstruction may need surgical intervention.

Etiology

Obstruction in the lower airways can result from airway plugging caused by inflammation with mucosal edema and increased production of thick secretions, or it can result from hyperreactivity of the bronchial smooth muscle that leads to bronchospasm. Some lower airway obstruction results from both causes. Although asthma is the most common cause of lower airways disease and obstruction in pediatric patients, the obstruction can result from other causes, including infections and chronic lung disease.⁹²

Pathophysiology

Airflow obstruction results from decreased airway caliber, which causes increased resistance to the flow of both inspired and expired gas. However, exhalation is predominantly affected. Mucus plugging within the small airways results in air trapping and hyperinflation of the lungs, causing the diaphragm to be flattened instead of a typical dome shape at rest⁹² (Fig. 9-8).

Fig. 9-8 Chest radiographs of a patient with hyperinflation. No infiltrates are noted. The right side is more radiolucent (darker) compared with the left. This is subtle and may be difficult to appreciate unless the chest radiograph is viewed from a distance. The right hemidiaphragm is normally higher than the left hemidiaphragm; they are at about the same level in this patient. These findings suggest hyperinflation of the right lung. The clinical history indicated that the child was jumping on a bed while eating a snack, when she began choking. Since that time, she has experienced respiratory difficulty. Further radiographs revealed bilateral air trapping. Bronchoscopy revealed bilateral bronchial peanut fragment foreign bodies. Impression: Right-sided hyperexpansion and air trapping, which may represent a bronchial foreign body.

Clinical Signs and Symptoms

Lower airway obstruction typically produces increased work of breathing, forced or prolonged exhalation, and expiratory wheezing. If the obstruction is severe, verbal children will be unable to speak in complete sentences; they may speak in monosyllables because they need to interrupt speech to breathe. In addition, patients may demonstrate:

Management

A variety of pharmacologic agents is available for management of lower airways obstruction. These medications will be discussed in more detail in the sections on status asthmaticus and bronchiolitis. In addition to pharmacologic agents, heliox can be used to manage lower airway obstruction. Refer to additional information on heliox in the Upper Airway Obstruction section. Heliox may have additional therapeutic effects, because it may attenuate lung inflammation and reduce mechanical and oxidative stress in the management of acute lung injury.¹⁶⁹ Assisted ventilation, either noninvasive or invasive, is needed in some patients (see section, Status Asthmaticus later in this chapter).

Etiology

The etiology of apnea in the preterm infant may be multifactorial, with delayed maturation of cardiorespiratory control a likely factor. Infants and children with apnea must be evaluated for a variety of abnormalities (Box 9-5). Apnea in older children may be chronic, as when related to an underlying neurologic condition (e.g., brain tumor, hydrocephalus), or it may be acute as in conditions such as toxic ingestions or traumatic brain injury.

Obstructive apnea is seen in children with structural or mechanical upper airway obstruction (e.g., from adenotonsillar hypertrophy) during sleep. Clinical symptoms are exacerbated with sleep, because the tone in upper airway muscles is reduced in the sleep state. Reduced tone can result in prolapse of structures such as the tongue into the airway, leading to worsening of mechanical obstruction.

Mixed obstructive apnea is frequently documented in children with obstructive apnea syndromes. In these cases, respiratory pauses (central apnea) are present but are rarely physiologically significant. It is presumed that dysfunction in medullary respiratory centers explains both the lack of airway tone associated with obstructed breaths and the absence of effort that defines central apnea.

Management

The management of apnea is determined by the etiology. Patients with central apnea may need to be intubated and mechanically ventilated if it is severe (e.g., respiratory syncytial virus [RSV]-associated apnea, drug overdose, trauma, stroke, hypoxic-ischemic brain injury). Apnea of prematurity generally will resolve by the time the infant reaches 40 weeks postconceptual age. Cardiac and apnea monitoring are indicated for these patients. Some children may need home apnea monitoring.

Treatment includes management of the etiology of the apnea (e.g., underlying cardiac disease, anatomic abnormalities) when possible. If the etiology is not treatable, such as in premature infants, symptom control is the goal. This treatment can include tactile stimulation during events, administration of low-flow oxygen, methylxanthines (e.g., caffeine), or nasal continuous positive airway pressure (CPAP). In older infants and children, a complete evaluation will be needed to identify the etiology of the apnea.

In obstructive sleep apnea (OSA), management focuses on relieving the obstruction. Polysomnography can be used to quantify the respiratory distress index and document the severity of OSA. Surgical management (i.e., tonsillectomy, adenoidectomy, or both) is often needed for moderate to severe OSA. Nonsurgical management includes positive pressure ventilation, using either CPAP or bilevel positive airway pressure. Patients with severe obstruction may not achieve cure with surgical intervention alone and may need noninvasive positive pressure support after surgical intervention. Commonly, obese children with OSA will achieve improvement in their respiratory distress index and quality of life postoperatively, but OSA does not resolve completely in the majority. In these cases, chronic noninvasive ventilation support may be needed.¹⁶⁰

If airway obstruction is not resolved and becomes chronic, the chronic alveolar hypoxia can, over time, produce pulmonary hypertension and cor pulmonale (right-sided heart failure caused by pulmonary hypertension). A 12-lead electrocardiogram (ECG) and echocardiogram (Echo) may be indicated to determine whether cor pulmonale is present in children with longstanding OSA. A follow-up polysomnogram is generally indicated 4 to 6 weeks postoperatively or after implementation of noninvasive ventilation to ensure adequate control of obstructive disease. Long-term complications of OSA include cor pulmonale, systemic hypertension, behavioral disturbances, poor school performance, daytime somnolence, and enuresis.

Etiology

True hypoventilation is uncommon. When it occurs, it is most likely to result from central nervous system dysfunction.⁷⁹ The condition can be challenging to detect unless the patient is already being monitored or the condition is associated with additional clinical findings such as upper airway obstruction. The differential diagnosis for hypoventilation includes central nervous system injury, use of narcotic or anesthetic agents, neuromuscular disorders, infant botulism, and congenital central hypoventilation syndrome (Ondine’s curse).

Head trauma—especially when it is associated with ischemia, an intracranial mass, or infection—can decrease the brainstem response to chemoreceptor stimulation (i.e., hypercarbia or hypoxia). Pharmacologic agents and metabolic toxins can lead to similar clinical findings. In particular, opioid medications decrease the respiratory drive, leading to hypoventilation. This effect may be desirable when using this class of medication to facilitate mechanical ventilation, but it may be a hindrance when working toward extubation or when opioids are administered to children who are not intubated.⁸⁰

Hypoventilation can also be caused by significant muscle weakness. In these clinical situations, the child initiates a breath, but the muscles are so weak that the child is unable to generate adequate tidal volume to achieve CO₂ removal.

Clinical Manifestations

When hypoventilation is present, the rise in PaCO₂ approximately equals the fall in PaO₂, so oxyhemoglobin saturation (via pulse oximetry) will fall. Hypercarbia secondary to hypoventilation often produces nonspecific findings. If hypercarbia is severe, somnolence may be noted. Mild hypercapnia is often not associated with any clinical findings, so it is difficult to diagnose in the absence of other findings. Children with reduced respiratory effort associated with hypercarbia and hypoxemia need central nervous system evaluation.⁸⁰

Management

For acute hypoventilation, invasive or noninvasive mechanical ventilatory support is indicated to restore ventilation. Central respiratory stimulants have been successful primarily in neonates, after the child’s condition is stabilized. A reversal agent (naloxone) can be administered in cases of pharmacologically induced apnea (i.e., opioids), which can result in increased respiratory effort and temporary reversal of apnea. However, patients need close monitoring for recurrence of bradypnea and apnea, because the duration of action of the narcotic is longer than that of the naloxone. In chronic disease, diaphragm pacing has been provided in an attempt to avoid long-term mechanical ventilation; however, this practice is not widespread.

Etiology

Malacia can be primary or secondary. Primary tracheomalacia occurs when the trachea is unusually collapsible from incomplete hardening of the tracheal cartilage. Secondary malacia occurs in association with conditions that compress the trachea (Table 9-6).

Table 9-6 Classification of Tracheomalacia

Adapted from McNamara VM, Crabbe DCG: Traceomalacia, Paediatric Resp Rev 5:147, 2004.

Pathophysiology

Collapse of the extrathoracic airway (e.g., trachea) during inspiration causes narrowing of the airway lumen, resulting in inspiratory airflow obstruction. This effect can lead to severe respiratory distress and is exaggerated by increased respiratory effort or agitation, particularly during feeding, crying, and coughing, or by the presence of an intercurrent illness.^65,152

Clinical Signs and Symptoms

Severity of symptoms will be affected by the length, location and severity of the malacia. Most infants with malacia will present with stridor. Stridor and obstruction are exacerbated by agitation and increased respiratory effort, and lessened during sleep and restful breathing. Persistent wheezing with irreversible airway obstruction is another frequent presenting sign. Additional potential symptoms include cough, noisy breathing, hoarseness, dyspnea, and inspiratory retractions.

Management

In cases of primary tracheomalacia, gradual improvement occurs as the tracheal lumen increases in diameter with anatomic growth and firming of supporting cartilage. Most infants demonstrate improvement by 6 to 12 months of age, and signs and symptoms will resolve in most children by 2 years of age.

Symptoms may be alleviated by positioning. Prone positioning will allow gravity to contribute to enlarging or opening of the airway lumen. Conversely, supine positioning can lead to decreased airway lumen diameter and airway collapse.⁶⁵ Positioning with the head of the bed elevated may prevent episodes of gastroesophageal reflux, decreasing the risk for gastric contents irritating airways and further compromising airway diameter. Irritating an already collapsing airway can exacerbate symptoms. In addition, proton pump inhibitors, histamine blockers, and prokinetic agents are used often to reduce the effects of gastroesophageal reflux.²⁶⁷

Fortunately most cases of malacia are mild. In cases of moderate to severe malacia, conservative measures may not be adequate. Parents should be taught basic life support techniques. These children may also need cardiorespiratory monitoring, oxygen, and noninvasive PPV in the home.¹⁵²

Surgical options for severe tracheomalacia include aortopexy and segmental tracheal resection. The goal of aortopexy is to suspend the aorta in a ventral position to prevent tracheal collapse. Through either a thoracotomy or median sternotomy, the aortic root is exposed and the thymus is resected or retracted.²⁶⁷ Sutures are placed in the pericardial tissue over the aortic root and in the adventitia of the aortic arch and are tied to the underside of the sternum. As the aorta is pulled forward (i.e., toward the sternum), the front wall of the trachea is also pulled forward by fibrous attachments between the aorta and trachea. Intraoperative bronchoscopy can be used to visualize the trachea and to ensure adequate suspension and reduction of the tracheal compression.^152,267 There are few complications associated with aortopexy surgery. Recurrence (incidence is approximately 10% to 25%) may necessitate additional surgery in some patients. Other less common complications include phrenic nerve palsy, pneumonia, chylopericardium, and wound infections.²⁶⁷

If aortopexy does not successfully improve the diameter of the tracheal lumen, another option is to resect the region of malacia. This procedure may cure the malacia, but candidacy for it can be limited by the length of the segment involved, because long segments of malacia cannot be resected.¹⁵²

Additional treatment strategies include placing indwelling endotracheal or endobronchial stents to stabilize the collapsing airway. Expandable metallic airway stents have been used in adults since the 1980s to palliate airway strictures caused by malignancy. Expandable metallic coronary artery stents have been used in children, although experience is limited. In the short term, stents are highly effective in treating malacia. However, because indwelling airway stents do not epithelialize in the same way as endovascular stents, airway stents promote formation of granulation tissue that can contribute to recurrent airway obstruction and bleeding. There is also a risk that the stent may erode into neighboring vessels, causing catastrophic hemorrhage. Newer biodegradable stents are under development.¹⁵²

Etiology

Vocal cord paralysis may be idiopathic, or it may be associated with surgical procedures or related to a neurologic disorder, birth trauma, or brachial plexus injury. Cardiac procedures such as ligation of a patent ductus arteriosus or manipulation or repair of the aortic arch have been associated with vocal cord dysfunction. The recurrent laryngeal nerve loops around the aortic arch on the left and the subclavian artery on the right before it travels superiorly and enters the larynx. Surgery near these areas can result in manipulation of the nerve, producing vocal cord dysfunction.²⁵⁰

Neurologic conditions associated with vocal cord paralysis include midbrain/brainstem dysgenesis, Arnold-Chiari malformation, congenital hydrocephalus, neurofibromatosis, and global hypotonia.^58,162 Neurosurgical procedures near the brainstem also can result in vocal cord paralysis.

Uncommonly, vocal cord injury can be caused by physical trauma during endotracheal intubation. Postoperatively, all children who undergo these surgical procedures need to be monitored for clinical signs of vocal cord paresis.

Clinical Manifestations

Common clinical signs and symptoms include stridor, weak cry or voice, hoarseness, and swallowing dysfunction. In cases of bilateral paresis or paralysis, the stridor is more severe; in fact, children with bilateral paresis will have more significant clinical findings in general.⁵⁸ Swallowing dysfunction associated with vocal cord paralysis can lead to aspiration of saliva or food, placing the child at risk for aspiration pneumonitis.²⁵⁰

The diagnosis of vocal cord paralysis can be established using either direct bronchoscopy in the operating room or through dynamic assessment of the larynx using flexible fiberoptic laryngoscopy (generally performed at the bedside) to evaluate the motion of the vocal cords. Ultrasonography of the larynx is a useful adjunctive diagnostic technique.⁵⁸ The condition is confirmed when the there is no motion or abnormal motion of one or both of the vocal cords.²⁵⁰

Management

Spontaneous recovery can occur within approximately 6 months in some children. Intervention of any sort is needed only if the vocal cord injury results in problems with gas exchange or if the child is aspirating food or formula.

Some children will need only thickened foods and positioning with the head of the bed elevated during feeding. In addition, they will need close observation for signs of aspiration. Other children will need alternative enteral nutrition delivery (e.g., gastric tube) to bypass the paretic area. Speech therapy evaluation is crucial to determine the safest method for feeding.²⁵⁰ Rarely, a tracheostomy is needed to relieve airway obstruction associated with vocal cord paresis and to protect the lungs from soiling.¹²⁷

For children with unilateral vocal cord paresis, surgical intervention is an option, using a CO₂ laser to bring the paralyzed cord into a more medial position (i.e., medialization); this facilitates adduction of the paretic cord with the functional cord. Another method of medialization of the paralyzed vocal cord is to inject it with silicone elastomers. Injection with Teflon (DuPont, Wilmington, DE) is no longer used because it has been associated with granuloma development.⁶⁹

Etiology

Respiratory failure is defined as exchange of O₂ and CO₂ that is insufficient to meet the metabolic demands of the body; this results in hypoxemia, hypercarbia, or both. Virtually any critically ill or injured child is at risk for respiratory failure. Respiratory failure results from hypoventilation, ventilation or perfusion () mismatch, diffusion abnormalities, and intrapulmonary shunting.^9,82,243

Pathophysiology

Respiratory failure can be caused by failure of any component of the respiratory system, including central nervous system control of ventilation, airways, the chest wall, respiratory muscles, or lung tissue including the alveolar-capillary membrane (Box 9-6).

Box 9-6 Major Components of the Respiratory System and Potential Contribution to Respiratory Failure

• Brain or central nervous system control of breathing

Immaturity

Depressed because of narcotics, barbiturates, or anesthetics

Impaired in central nervous system disease, insult, or injury

• Airways

Bronchospasm

Airway obstruction caused by inflammation, edema, or mucus with significant increase in resistance to air flow and work of breathing

Airway musculature incompletely developed, so airways are compliant and may be compressed

Airway may be compressed by abnormal vascular or other anatomy

Artificial airway occlusion or displacement

• Chest wall

Extremely compliant in young children, so it may collapse during episodes of respiratory distress, resulting in further compromise in efficiency of respiratory function

Excessive inspiratory pressure and volume can be provided inadvertently during positive pressure ventilation.

• Respiratory muscles

If any respiratory muscles lack tone, power, or coordination, the upper or lower airway patency may be compromised, reducing inspiratory effort.

Diaphragm fatigue or paralysis: Intercostal muscles may be incapable of generating effective tidal volume during early childhood.

Phrenic nerve injury

• Lung tissue

Cardiogenic or noncardiogenic pulmonary edema

Surfactant inactivation

Parenchymal lung diseases

Anatomic abnormalities can result in lung restriction or compliance problems.

• Alveolar-pulmonary capillary interface (diffusion surface)

Pulmonary edema

Pulmonary hypertension syndromes

Pulmonary emboli

• Excessive positive pressure

Respiratory failure and hypoxemia result from: hypoventilation, low (O₂ responsive), (shunt, not O₂ responsive), diffusion disturbances, decreased PaO₂ (decreased SaO₂), and high altitude.⁹

The diagnosis of respiratory failure is based on both clinical and physiologic criteria. For example, oxygen criteria alone can be misleading in a child with cyanotic heart disease who is hypoxemic while breathing room air (i.e., intracardiac shunt). Physiologic criteria include hypoxemia while breathing room air and hypercarbia with acidosis. Oxygen therapy may result in a normalization of the PaO₂ in a patient with respiratory failure.²⁶⁰ The response to oxygen in a patient with lung disease is determined by the percent of alveoli represented by intrapulmonary shunting. If greater than 40% of the lung units are involved in the shunt, positive pressure ventilation and lung recruitment will be needed before oxygen therapy will increase the PaO₂.

Respiratory failure may be present despite oxygen therapy. Hypoxemia can result in inadequate tissue oxygenation and development of lactic acidosis. Cardiac output and pulmonary blood flow increase initially in response to hypoxemia. In addition, the hemoglobin affinity for oxygen is decreased (the oxyhemoglobin dissociation curve shifts to the right; see Fig. 9-6) so that oxygen is released more easily to the tissues.⁶⁴ These compensatory mechanisms will help maintain adequate oxygen delivery. With progressive hypoxemia, cardiac output falls and alveolar hypoxia may produce inadequate oxygen delivery.

Clinical Signs and Symptoms of Respiratory Failure

The clinical and physiologic indicators of respiratory failure in children are listed in Box 9-7. These indicators include hypoxemia despite oxygen therapy and hypercarbia with acidosis. The child’s baseline oxygenation and respiratory function must also be considered (Box 9-8).

Box 9-7 Clinical and Physiologic Indicators of Respiratory Failure

• Depressed level of consciousness

• Increased respiratory rate and effort, including retractions or grunting, decreased chest wall movement

• Absent or significantly decreased breath sounds

• Cardiovascular signs of distress, including tachycardia, peripheral vasoconstriction, mottled color, and pulsus paradoxus

• Signs of diaphragm muscle fatigue:

Paradoxic movement of diaphragm

Respiratory alternans

Apnea

• Late signs: apnea or gasping, agonal respirations, bradycardia, or hypotension

• Cyanosis and hypoxemia despite supplementary oxygen therapy (e.g., PaO₂  <  75   mm   Hg despite FiO₂ of 1.00)*

• Hypercarbia (PaCO₂ >  50-75   mm   Hg)^†, especially with acute acidosis

• Rising alveolar-arterial oxygen difference (normal, <  25   mm   Hg) or decreasing PaO₂/FiO₂ ratio

^* In the absence of intracardiac right-to-left shunt lesion.

^† In the absence of chronic lung disease and metabolic alkalosis.

The alveolar-arterial oxygen difference or gradient (A-a DO₂) is an objective calculation used to assess the initial severity and the evolution of lung injury. It is calculated as follows. A patient breathes a known concentration of oxygen for 15 to 20   min, and then an arterial blood sample is obtained. The inspired oxygen tension (PiO₂) is calculated by multiplying the fractional inspired oxygen concentration (FiO₂) by the difference between the barometric pressure and the water vapor pressure at body temperature (the water vapor pressure at body temperature is 47   mm   Hg). The alveolar oxygen tension (PaO₂) is equal to the PiO₂ minus the PaCO₂ as shown on the next page:

where R = Respiratory exchange quotient, which can be estimated as 1.

Note: If not at sea level, substitute barometric pressure for 760.

The A-a DO₂ is the difference between the calculated PAO₂ and the PaO₂ and is calculated as follows:

where normal is <  25 to 50   mm   Hg.

The difference between PiO₂ and the child’s arterial oxygen tension increases when perfusion of nonventilated alveoli occurs; this is called an intrapulmonary shunt. The severity of intrapulmonary shunting is estimated using a shunt graph (Fig. 9-9). The PaO₂/FiO₂ (P/F) ratio is more commonly used in clinical practice to estimate the degree of intrapulmonary shunting (e.g., P/F <200 is consistent with ARDS).

Fig. 9-9 Relationship between inspired O₂ concentration and arterial O₂ tension with changing severity of intrapulmonary shunting. By comparing the patient’s FiO₂ to the PaO₂, the percentage of nonfunctioning but perfused alveoli (i.e., the shunt) can be determined. Note that once the intrapulmonary shunt nears 50%, increasing the inspired O₂ concentration will produce little improvement in PaO₂ at this point, treatment must improve alveolar ventilation and the ventilation-perfusion ratio through the use of positive end-expiratory pressure. Changes in cardiac output and O₂ uptake can influence the position of the shunt curves.

(From West JB: Pulmonary pathophysiology: the essentials, ed 2, Baltimore, 1980, Williams and Wilkins.)

Management

The child with respiratory distress and evolving respiratory failure needs continuous monitoring of general appearance and responsiveness, pulse oximetry, and heart rate. The child needs to be kept as comfortable as possible. Position the child for maximal comfort to provide optimal oxygenation, and frequently evaluate the child’s airway, oxygenation, ventilation, and perfusion.

If the child’s airway is obstructed or if the child appears unable to maintain a patent airway, perform intubation immediately (see section, Intubation below). The goal of therapy for respiratory failure is to maximize O₂ delivery by increasing arterial oxygen content and supporting cardiac output. In addition, reduce oxygen demand by treating fever and pain. Avoid cold stress in young infants through the use of warming devices. A frightened child may be comforted by the presence of the parents. Minimize intrusive examinations and treatments. Monitor fluid intake and output carefully, because excessive fluid administration can contribute to pulmonary interstitial edema (from capillary leak) and worsening of respiratory failure.

Bag-Mask Ventilation

This method of ventilation uses a hand-ventilating bag joined to an oxygen source and a mask. A bag-mask system must be present at every bedside in the critical care unit. Because virtually any patient is at risk for developing respiratory failure, bedside nurses must be prepared to offer support of ventilation whenever necessary. Every healthcare provider must learn good bag-mask ventilation technique. The novice can begin skill acquisition by assisting during the suctioning of an intubated patient. It is important to provide effective ventilation without generating high peak inspiratory pressures, and it is also important to synchronize delivered breaths with the patient’s spontaneous ventilatory efforts.

To provide effective bag-mask ventilation, use a self-inflating bag and select a mask to fit properly over the child’s nose and mouth. Extend the child’s neck slightly, unless cervical spinal injury is suspected in a trauma victim, and lift the jaw. Create a seal between the patient’s face and the mask by grasping the mask between the thumb and index fingers of the nondominant hand while lifting the child’s lower jaw against the mask using the third, fourth, and fifth fingers; this creates the E-C clamp depicted in Fig. 9-10.

Fig. 9-10 Single rescuer bag-mask ventilation (E-C clamp) technique (“ventilating a baby is as ‘E-C’ as 1-2-3”). A, Hand displaying E-C shape. B, The E is formed with the ring, small, and index fingers. The C is formed with the index finger and thumb. C, The E fingers rest on the bony ridge of the jaw. D, The C fingers are positioned to hold the mask. E, Proper E-C clamp for assisted ventilation.

(Developed by the New York City EMS project and NYC*EMS! Adapted from the Center for Pediatric Emergency Medicine: Teaching resource for instructors in prehospital pediatrics, ed 2. Available at http://cpem.med.nyu.edu/teaching-materials/tripp-bls. (Modified from Foltin GL, et al: Teaching resource for instructors in prehospital pediatrics, New York, 1998, Center for Pediatric Emergency Medicine, Maternal Child Health Bureau, Emergency Medical Services for Children Grant.)

During bag-mask ventilation, the rescuer compresses the bag in synchrony with, or slightly faster than, the child’s spontaneous respiratory efforts. Inspiratory volume is administered to produce a visible chest rise. Bag-mask ventilation is effective if the chest expands equally and adequately bilaterally and if equal breath sounds can be auscultated over both sides of the chest during each breath. In addition, if bag-mask ventilation is effective, the child’s oxyhemoglobin saturation (SaO₂) will rise or remain adequate, and the heart rate will be appropriate for age and clinical condition. Ineffective ventilation produces inadequate breath sounds bilaterally, and the chest fails to rise during ventilation. If the SaO₂ is low or falling and heart rate is decreased, bag-mask ventilation is inadequate.

Bag-mask ventilation can result in the entry of air into the esophagus, producing gastric distension; this can be harmful because the child could vomit and aspirate gastric contents, and gastric dilation can impair diaphragm excursion. If the child is unconscious with no cough or gag reflex, a second person can apply light pressure at the cricoid cartilage during bag-mask ventilation; this will displace the trachea posteriorly and obstruct the esophagus, reducing or preventing further air entry into the esophagus. If this maneuver fails or if gastric distension is significant, insert a nasogastric tube to decompress the stomach (remove it before an intubation attempt).

If prolonged bag-mask ventilation is needed, an endotracheal tube (advanced airway) will be inserted, enabling delivery of mechanical ventilatory support with less potential inflation of the stomach. The endotracheal tube will permit suctioning and application of PEEP to improve oxygenation.

Intubation

The decision to intubate is primarily a clinical decision, based on assessment of gas exchange and respiratory effort. Indications for intubation in the critically ill child include respiratory arrest or apnea, inability to maintain an effective airway (as a result of a depressed level of consciousness), obstructed airway, or edema with stridor, and/or severe hypoxemia or progressive hypercarbia. Intubation will be needed for the child who has multisystem failure or increased intracranial pressure (Box 9-9).

Box 9-9 Indications for Intubation and Mechanical Ventilation

• Respiratory arrest, gasping, or agonal respirations

• Excessive work of breathing

• Respiratory muscle fatigue

• Upper airway obstruction (anatomic or functional) or potential obstruction (e.g., facial trauma, inhalation injuries)

• Actual or potential decrease in airway protective reflexes (i.e., cough, gag)

• Shock (especially septic shock)

• Anticipated need for mechanical ventilation support (e.g., impending acute respiratory failure, chest trauma, shock, increased intracranial pressure, neuromuscular disease)

• Hypoxemia despite supplementary oxygen (PaO₂  <  60   mm   Hg with FiO₂  >  0.6) in the absence of cyanotic congenital heart disease

• Inadequate ventilation (PaCO₂  >  60   mm   Hg acutely or unresponsive to other interventions)

• Need for airway and ventilation control for deep sedation or patient transport

• Emergency drug administration

• Altered mental status

• Glasgow Coma Scale score less than 8 (see Chapter 11, Table 11-6)

• Increased intracranial pressure (see Chapter 11)

Whenever possible, accomplish intubation on an elective basis (i.e., discuss it during morning and afternoon rounds and plan elective intubation) in anticipation of further deterioration in respiratory function. If nursing and medical assessment and care are skilled, respiratory arrests rarely occur in the hospital, because respiratory deterioration is recognized and appropriate support is provided to prevent the arrest.

Selection of Tube Type

In the past, all children 8 years of age and younger were intubated with uncuffed endotracheal tubes, because the cricoid cartilage (the narrowest point of the airway) creates a natural seal around the tube. There was concern that use of a cuffed tube could create inflammation and injury to this area, although it is now clear that both cuffed and uncuffed tubes may be used safely in children, provided cuff pressure is monitored and kept at 20 to 25   cm H₂O. The use of cuffed ETTs may be preferred over uncuffed tubes in children with decreased lung compliance or in those who have a large air leak when an uncuffed tube is used. When using cuffed endotracheal tubes, the cuff must be a low-pressure, high-volume cuff to reduce the risk of pressure injury to the tissues. Monitor and maintain cuff pressure at 20 to 25   cm H₂O pressure (or per manufacturer’s specifications).^122a,171

Selection of Tube Size

When the child is critically ill and is at risk for respiratory failure, intubation equipment should be readily available in a cart at the bedside. Proper ETT size is estimated most accurately from the child’s length, and the use of the color-coded Broselow Resuscitation Tape (Vital Signs, Armstrong Medical, Lincolnshire, IL) facilitates determination of proper tube size.¹³⁹ If the tape is not available, the uncuffed endotracheal tube size can be estimated roughly from the child’s age according to the following formula (accurate in children 1-10 years old)^122a:

The cuffed endotracheal tube can be estimated by the child’s age using the following formula^122a:

The diameter of the ETT is approximately the diameter of the child’s small finger. A reference table also can be used to estimate the proper tube size (Table 9-8).

Tube size is evaluated after placement. A tube can be too large yet still pass easily through the child’s vocal cords, because the narrowest portion of the child’s larynx is below the vocal cords at the level of the cricoid cartilage. Once the tube is placed, use a ventilation bag with pressure manometer to provide inspiration to a known pressure. If the tube size is appropriate, a small air leak will be detectable when the inspiratory pressure reaches approximately 25   cm H₂O. If a leak develops at lower pressures, the tube is probably too small, and a large air leak may develop during positive pressure ventilation. If the tube is too large, a leak will not be detectable despite inspiratory pressure exceeding 25   cm H₂O. The use of an excessively large tube can result in laryngeal or mucosal injury or necrosis or subglottic stenosis.

Insertion of the Tube

Before the intubation attempt, assemble all necessary equipment at the bedside (Box 9-10). Monitor the child’s heart rate continuously and make certain the heart rate (QRS tone) is audible.

Box 9-10 Intubation Equipment

• Bag, mask, and oxygen source, cardiac monitor with audible QRS tone

• Endotracheal tube: estimated size for body length and age (see Table 9-8) plus tubes sized 0.5   mm larger and 0.5   mm smaller

• Laryngeal mask airways in a variety of sizes (if available)

• Laryngoscope blade and handle (and extra bulbs and batteries)

Infants: 0-1 straight blade

Small children: 1 straight blade

Children (12-22   kg): 2 straight or curved blade

Large children (24-30   kg): 2-3 straight or curved blade

Adolescents (32-34   kg): 3 straight or curved blade

• Stylet

Children 3-17   kg: 6 French

Children >  17   kg: 14 French

• Exhaled CO₂ detector, capnography

• Suction equipment: wall or portable suction

• Appropriate catheter to pass easily through endotracheal tube (usually the next French size above twice the ETT size (in millimeters) will pass readily into any ETT  >  3.0   mm)

• Tonsillar suction or 12-14 French suction catheter

• Nasogastric tube

• Tape, liquid adhesive applicators, water-soluble lubricant

• Gloves and goggles

• Neuromuscular blocking agents, sedatives, analgesics, lidocaine

• Magill forceps for nasotracheal intubation

ETT, Endotracheal tube.

Table 9-8 Endotracheal and Tracheostomy Tube Sizes

Oxygen is administered before and between any intubation attempts to ensure that the child is well oxygenated. If a short-acting nondepolarizing or depolarizing neuromuscular blocking agent is administered to facilitate intubation, then atropine may be administered to prevent bradycardia (refer to section, Nursing Care of the Child during Mechanical Ventilation and Chapter 5). Routine administration of atropine before intubation attempts is discouraged, however, because it might prevent or minimize hypoxemic-induced bradycardia and delay the recognition of hypoxemia during intubation.

Intubation of the critically ill child should be attempted only by persons skilled in airway management. The intubation clinician is assisted by one or more team members. Proper positioning before the attempt is essential. Typically, infants and toddlers (without suspected cervical spine trauma) are placed on a flat surface with the chin lifted into a sniffing position. It may be necessary to place the torso on a small pad to achieve proper alignment. Children older than 2 years (without cervical spine trauma) are generally placed with the head on a small pillow, and the chin is lifted into a sniffing position. The child is appropriately positioned for intubation if the opening of the ear canal is above or just level with the front of the shoulder when viewed from the side.

One team member holds the ETT (prepared with a stylet if requested) and may provide bag-mask ventilation using 100% oxygen before and after any intubation attempt. That team member may also provide cricoid pressure if requested during the intubation attempt. One team member is responsible for monitoring patient color and heart rate during the intubation attempt and must advise the intubating clinician if the child’s heart rate or appearance deteriorates, so that the attempt can be interrupted and hand ventilation can be provided if the child’s condition worsens. A respiratory therapist is an important member of the team during this phase of intubation.

It may be necessary to insert a stylet into the tube to pass the tube through the vocal cords. If a stylet is used, insert it only up to the final 1   cm of the tube and bend the proximal end of the stylet over the universal adaptor at the proximal end of the tube, so that the stylet cannot be inadvertently advanced beyond the tip of the tube. It is important to prevent the stylet from extending beyond the end of the tube, because it can perforate the airway. The decision to use a stylet during intubation is made by the intubating clinician. Be prepared to apply pressure to the cricoid cartilage to facilitate intubation.

During intubation, the following materials must be available within reach of the intubating clinician: suction tubing (joined to a suction canister, set to provide approximately −  90   cm H₂O suction), a tonsillar suction device, a large suction catheter (used to suction the pharynx, if needed), a suction catheter of appropriate size for suctioning the ETT, liquid adhesive applicator, and tape (torn into strips appropriate for taping the tube), or device to secure the tube.

Suction devices are often needed to remove secretions, vomitus, or blood from the pharynx so that the intubating clinician can visualize the vocal chords. Once the tube is in place, the suction control is set to provide approximately −  60 to −  150   cm H₂O suction, based on the age of the child (Table 9-9).

Table 9-9 Typical Maximum Negative Pressure for Pediatric Airway Suctioning Based on Age

Age	Typical Negative Pressure (cm H2O)
Infant	60-80
Child	80-120
Older child	120-150

Orotracheal intubation is typically performed in the critical care unit. It can be achieved rapidly and is associated with few complications. Nasotracheal intubation may be performed if it is difficult to secure the oral tube (e.g., the child has mouth or facial burns or injuries). Nasotracheal intubation has been associated with development of sinusitis, so when it is performed it will be necessary to monitor the patient closely for evidence of sinus infection.

If orotracheal intubation is performed, the laryngoscope blade is inserted into the hypopharynx to control the tongue and lift the lower jaw and tongue upward, so that the vocal cords may be visualized. It may be necessary to suction the area above the vocal cords, with a tonsillar suction or a large suction catheter, to visualize the cords.

If nasotracheal intubation is performed, the tube is lubricated, gently inserted nasally, and advanced until the tip of the tube is visualized in the back of the pharynx. The laryngoscope blade is then used to visualize the cords, and McGill forceps are used to advance the tube from the pharynx through the vocal cords.

Rapid Sequence Intubation

The critically ill or injured infant or child who needs intubation may have a full stomach. In such a child, the goal is to safely insert an airway, without stimulating vomiting. For a patient who needs urgent intubation, rapid sequence intubation (RSI) may be performed (Box 9-11 shows the indications for RSI). RSI is defined as nearly simultaneous delivery of oxygenation, sedation, and neuromuscular blockade for the purpose of intubation.²⁰⁹ The goal is to provide near immediate intubating conditions.²⁸⁴

Box 9-11 Rapid Sequence Intubation

Indications

• Full stomach or oral intake within the past 4-6   h

• Pharyngeal or upper gastrointestinal bleeding

• Ileus or intestinal obstruction (includes acute onset of illness)

• Tense abdominal distension

• Pregnancy