The respiratory system is responsible for the gas exchange of carbon dioxide and oxygen. Inadequate oxygenation results in hypoxemia. Inadequate ventilation results in hypercarbia. 

During respiration, oxygen breathed in from the air diffuses across the capillary bed surrounding the air sacs in the lungs (alveoli). Oxygen travels to the pulmonary vein, where it mixes with blood and binds to hemoglobin in the red blood cells. Deoxygenated blood travels back from the tissues toward the pulmonary artery. Carbon dioxide gas in the blood diffuses from the pulmonary artery into the alveoli and is exhaled from the body.

Respiratory problems arise from any alterations in the process of oxygenation and ventilation described above. Pathology interrupting respiration may involve the lung parenchyma itself or be attributable to a central nervous system issue. The respiratory system can also be compromised by the deterioration of muscles for breathing, such as in muscular dystrophy or other conditions that cause muscle fatigue.

Infants and children have a higher oxygen demand than adults. Consequently, pediatric patients are more prone to tissue hypoxia and hypoxemia in the presence of inadequate alveolar ventilation or apnea than adults. Infants consume oxygen at a rate of 6–8 mL/kg/min as compared to 3–4 mL/kg/min in adults.

Hypoxemia and Hypoxia

Hypoxemia is an abnormally low level of oxygen in arterial blood and is most often caused by respiratory disorders or obstruction. Hypoxia is an inadequate oxygen supply at the tissue level. Hypoxemia does not necessarily lead to tissue hypoxia. Tissue hypoxia can occur even if a patient is not hypoxemic. 

Hypoxemia is present when arterial oxygen saturation is reduced (< 94%). Lower measurements may be considered normal if the patient is at a higher altitude or has other medical conditions such as cyanotic heart disease. 

The body adjusts naturally to hypoxemia. Tachycardia is an early response to hypoxemia as the body endeavors to increase cardiac output. Chronic hypoxemia increases cardiac output and hemoglobin production. An increase in hemoglobin production elevates the oxygen-carrying capacity of the blood. 

The table below describes the primary mechanisms of hypoxemia:

Mechanisms of Hypoxemia

Mechanisms of Hypoxemia

Tissue hypoxia occurs when there is low tissue perfusion (such as low cardiac output) or anemia (low RBCs), resulting in reduced oxygen-carrying capacity of the blood. Causes of hypoxia can include pulmonary disease, congenital heart disease, airway obstruction, or sepsis. Hypoxia will often lead to hyperventilation. 

Children with tissue hypoxia respond with hyperventilation. Tachypnea and an increased depth of respiration may be observed in the child who is hyperventilating to compensate for tissue hypoxia. Hyperventilation increases alveolar ventilation, decreases PaCO₂, and increases the alveolar oxygen pressure. When available, the team should utilize capnography to monitor PaCO₂ noninvasively. 

Early signs of tissue hypoxia include:

• Tachypnea
• Nasal flaring 
• Retractions
• Tachycardia
• Skin changes (pallor, mottling, and cyanosis)
• Agitation, anxiety, or irritability

As tissue hypoxia progresses, the following are late signs worrisome for progression to cardiopulmonary failure:

• Bradypnea
• Head-bobbing, seesaw respirations, grunting
• Bradycardia
• Skin changes
• Decreased level of consciousness

Hypercarbia

Hypercarbia is the presence of a higher than normal carbon dioxide concentration in arterial blood (PaCO₂). Untreated hypercarbia leads to an increase in PaCO₂ and worsening respiratory acidosis.

Airway obstruction and lung tissue disease compromise ventilation and may cause hypercarbia. A compromise in the respiratory drive, as with narcotic overdose or a CNS lesion, may result in hypercarbia. Diseases such as muscular dystrophy that cause respiratory muscles to fail also cause hypercarbia. 

Signs and symptoms of inadequate ventilation are nonspecific and may include tachypnea, an abnormal respiratory rate for age, nasal flaring, retractions, and changes in the level of consciousness. The patient may be agitated and anxious initially, but as the hypercarbia worsens, the level of consciousness declines, and the child may become unresponsive.  

Pediatric patients with hypercarbia may initially present with tachypnea as the body attempts to eliminate carbon dioxide. Over time, the patient may fatigue and develop bradypnea. Central nervous system disorders hinder compensatory tachypnea. The child with underlying muscle disease lacks the reserve to sustain compensatory tachypnea for very long and will progress quickly to respiratory failure. 

Many of the symptoms of hypercarbia mimic those of hypoxemia. If a patient presents with these symptoms despite oxygen supplementation, then the PALS provider should suspect inadequate ventilation, hypercarbia, and respiratory acidosis.

Blood gas analysis is the gold standard for diagnosing hypercarbia. Pulse oximeters are not an acceptable tool for assessing hypercarbia. SpO₂ levels do not begin to decline until hypercarbia is very severe and the patient is on the verge of cardiopulmonary failure. 

Exhaled carbon dioxide detectors may detect hypercarbia even without an advanced airway in place. However, ETCO₂ values do not always reflect arterial carbon dioxide. They correlate most closely with the PaCO₂ when there is adequate cardiac output, a patent airway, and no increase in dead space from air trapping (such as in the case of patients with asthma). A child on the verge of cardiopulmonary collapse may have a very low ETCO₂ due to poor cardiac output.

Airway Resistance

An increase in airway resistance leads to increased breathing effort. Medical conditions such as edema, bronchoconstriction, mediastinal masses, mucus, and secretions decrease the airway diameter and increase airway resistance. Airway resistance in the nasal and nasopharyngeal passages can contribute to total airway resistance and is more apparent in infants. Interventions such as bronchodilators, steroids, and suctioning reduce airway resistance. Lung volumes increase once airway resistance decreases.

Airway resistance is determined by several factors.

Under normal conditions, airflow during respiration is laminar, and a low driving pressure is sufficient to move air through the airways into the lungs. When airway resistance is increased, airflow becomes turbulent. Turbulent airflow causes a tenfold increase in resistance. Consequently, a much higher driving pressure is required to move air through the airways into the lungs. 

Crying and agitation further increase resistance to airflow, causing a significant increase in the child’s work of breathing. Therefore, the PALS provider must strive to keep the already compromised child as calm as possible.

Lung Compliance

As air enters and exits the lungs secondary to driving pressures, there is a corresponding volume change within the lungs. The ability of the lungs to conform to these pressure changes is known as lung compliance. High lung compliance means the lungs are easily inflatable, while low lung compliance indicates the lungs are stiff and difficult to inflate. 

When lung compliance is low, more effort is needed to inflate them. The diaphragm must exert more force. The work of breathing involved produces retractions in pediatric patients. Seesaw breathing may be present if a patient has low lung compliance along with weak respiratory muscles. 

During seesaw breathing, there is simultaneous retraction of the chest wall and expansion of the abdomen. Seesaw breathing may be seen in patients with neuromuscular disorders but is also present in the child whose muscles are fatiguing after a prolonged period of respiratory distress. Seesaw breathing signifies the child is closer to respiratory failure. 

Positive pressure ventilation is one of the crucial interventions for a patient with poor lung compliance who is at or near respiratory failure. Positive-pressure ventilation may be provided via invasive or noninvasive mechanical ventilation.

Pneumonia causes decreased lung compliance due to fluid build-up.

Driving Pressures of Respiration

The respiratory muscles dictate the driving pressures of airflow. They are responsible for creating negative intrathoracic pressure so that intrathoracic volume can increase. When the thorax has a lower pressure than atmospheric pressure, air is pulled in.

The diaphragm and the intercostal muscles are the primary muscles of respiration. Accessory muscles of respiration in the abdomen and neck are not usually needed during normal ventilation, but when there is increased airway resistance or reduced lung compliance, the accessory muscles begin to assist respiration. 

When the inspiratory muscles relax, the lungs and chest naturally recoil and create positive intrathoracic pressure, resulting in exhalation. When there is an increase in airflow resistance in the lower airways, the accessory muscles assist in expelling air out of the lungs.

The diaphragm is the major driving force of respiration and is usually dome-shaped. Lung hyperinflation (e.g., in asthma) flattens the shape of the diaphragm, causing inefficient diaphragmatic contractions. Likewise, high intra-abdominal pressure and significant abdominal distention also cause a decrease in diaphragmatic wall motion.

CNS Control in Respiration

The brainstem, central and peripheral chemoreceptors, and voluntary effort control respirations. The brainstem controls autonomic functions of breathing while the cerebral cortex produces voluntary control. Breath-holding, panting, and sighing are examples of voluntary control of breathing. 

Medical conditions that impair the respiratory drive include CNS infections, traumatic brain injuries, and drug overdose. Hypoventilation and apnea result when the respiratory drive is impaired.

Central chemoreceptors control breathing by responding to changes in hydrogen ion concentrations in the cerebrospinal fluid. The PaCO₂ influences the hydrogen ion concentration in the cerebrospinal fluid. 

Peripheral chemoreceptors are located in areas outside the CNS, such as in the carotid body. Some peripheral chemoreceptors control breathing by responding to changes in PaO₂. Other peripheral chemoreceptors are sensitive to changes in PaCO₂.