Respiratory failure (pediatrics): Clinical sciences

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Introduction 0:00–0:42

Respiratory failure occurs when the respiratory system cannot adequately oxygenate the blood, remove carbon dioxide from the blood, or both.
This life-threatening condition requires rapid recognition and management. Underlying causes of respiratory failure include pulmonary or airway disease, as well as conditions affecting the chest wall, muscles of respiration, and central or peripheral chemoreceptors.
Respiratory failure can be categorized as hypoxemic, hypercapnic, or a combination of the two. Now, if a pediatric patient presents with a chief concern suggesting respiratory failure, you should first perform an ABCDE assessment.

ABCDE assessment 0:42–1:24

These patients are typically unstable, so you’ll need to immediately stabilize their airway, breathing, and circulation.
Then, provide supplemental oxygen, and consider noninvasive positive pressure ventilation. If your patient has poor respiratory effort, you may need to perform endotracheal intubation and begin mechanical ventilation.
Next, obtain IV access, and put your patient on continuous vital sign monitoring, including respiratory rate, pulse oximetry, and cardiac monitoring.
Once you’ve provided acute management, obtain a focused history and physical exam, and order a chest X-ray and an arterial blood gas, or ABG for short.

Diagnosis 1:24–2:54

Verbal patients may describe shortness of breath, and their history may reveal cardiac or pulmonary disease, a neuromuscular disorder, recent illness, head trauma, or narcotic exposure.
On exam, most patients are tachypneic, with signs indicating increased work of breathing, such as nasal flaring, head bobbing, grunting, tracheal tugging, retractions, and accessory muscle use.
In other cases, patients may exhibit slow, shallow respirations, or even apnea. Your patient might appear somnolent or cyanotic, and pulse oximetry frequently reveals an oxygen saturation below 90 percent.
Depending on the underlying cause, the chest X-ray might demonstrate abnormal findings, such as a foreign body, pulmonary edema, or a focal consolidation.
Here’s our first clinical pearl! While many patients with acute respiratory failure initially present with tachypnea and clear signs of respiratory distress; over time, progressive respiratory muscle fatigue can result in less obvious signs, like shallow and ineffective breaths.
It’s crucial to recognize these later signs, since prompt intervention can prevent cardiopulmonary arrest. Now, at this point, you should suspect respiratory failure, but to confirm the diagnosis, you’ll need to assess the ABG findings.

Assess ABG 2:54–3:03

If the arterial partial pressure of oxygen, or PaO2, is less than 60 millimeters of mercury, your patient has hypoxemic respiratory failure.

Hypoxemic 3:03–5:13

This means that a failure of gas exchange within the lungs is causing hypoxemia. Most of the time, hypoxemic respiratory failure is caused by a mismatch in alveolar ventilation and perfusion, or a V/Q mismatch.
When alveoli are well-ventilated but poorly perfused, the ventilation-to-perfusion or V/Q ratio is high, and an absence of perfusion creates alveolar “dead space”.
Conversely, when alveoli are well-perfused but poorly ventilated, the V/Q ratio is low, and a complete absence of ventilation with normal perfusion is called an intrapulmonary shunt.
Finally, in some cases, hypoxemic respiratory failure is caused by impaired diffusion of oxygen across the alveolar-capillary membrane.
Some conditions that lead to hypoxemic respiratory failure include asthma or other causes of small airway obstruction, as well as interstitial edema or fibrosis, atelectasis, and pneumonia.
Here’s a high-yield fact! If you're not sure why your patient is hypoxemic, you can use the alveolar to arterial oxygen or A-a, gradient to narrow your differential.
To do this, subtract the arterial partial pressure of oxygen from the alveolar oxygen concentration. An elevated A-a gradient indicates that the primary problem lies within the alveolar-capillary unit, and oxygen isn’t being transferred effectively from the alveoli to the pulmonary capillaries.
V/Q mismatch, intrapulmonary shunting, and impaired diffusion all create an elevated A-a gradient. However, a normal A-a gradient means that the hypoxemia is caused by factors outside of the alveolar-capillary unit.
Examples of this include a low inspired oxygen concentration and alveolar hypoventilation. Now let’s switch gears and discuss cases in which the ABG reveals an arterial partial pressure of carbon dioxide, or PaCO2, above 50 millimeters of mercury.

Hypercapnic 5:13–7:16

This indicates that your patient has hypercapnic, or hypercarbic, respiratory failure; which is characterized by inadequate ventilation and carbon dioxide removal.
Patients with hypercapnic respiratory failure have decreased minute ventilation, which is the volume of air that enters and exits the lungs in a minute.
Because minute ventilation is the product of tidal volume and respiratory rate, decreased minute ventilation means that your patient’s breathing is too shallow, too slow, or a combination of both.
Hypercapnic respiratory failure is sometimes referred to as “pump failure”, which means that there’s a mechanical impairment within the respiratory system, and consequently, your patient either can’t or won’t breathe deep enough or fast enough to effectively eliminate CO2.
Pump failure can be caused by decreased central respiratory drive, as a result of narcotic exposure or traumatic brain injury; or by respiratory muscle weakness from neuromuscular disorders or acute conditions that cause progressive muscle fatigue.
Here’s another clinical pearl! Hypoxemic and hypercapnic respiratory failure don’t always occur in isolation; in fact, many disease processes cause physiologic changes that impair oxygenation and ventilation simultaneously.
In these cases, the ABG will demonstrate both decreased PaO2 and increased PaCO2. Patients that initially present with hypoxemic respiratory failure may eventually develop hypercapnia as their clinical status deteriorates.
For example, conditions associated with an increased V/Q ratio, such as pulmonary embolism, can cause hypoventilation as a result of dead space.
Now, once you identify respiratory failure, you need to provide immediate management! Patients with mild hypoxemic respiratory failure may improve with supplemental oxygen alone, which is minimally invasive and easily tolerated.

Management 7:16–10:15

Depending on the amount of support needed, you can choose from various delivery methods, such as a low- or high-flow nasal cannula or a non-rebreather mask.
Continuous positive airway pressure, or CPAP, provides a constant level of positive airway pressure throughout inspiration and expiration, which increases functional residual capacity, prevents small airway collapse, and improves alveolar aeration.
CPAP is most useful for treating hypoxemic respiratory failure, since it doesn’t provide inspiratory pressure and therefore does not improve tidal volume or minute ventilation significantly.
If your patient has hypercapnic respiratory failure, or if they have hypoxemic respiratory failure that requires more support, you can consider noninvasive positive pressure ventilation.
Biphasic positive airway pressure, or BiPAP, provides positive airway pressure during exhalation as well as additional positive pressure during inspiration, which decreases the work of breathing.
BiPAP can be used in both hypoxemic and hypercapnic respiratory failure, because it prevents alveolar collapse and enhances tidal volume, which increases alveolar ventilation.
Now, if your patient’s respiratory failure persists despite these interventions, you’ll need to perform endotracheal intubation and start mechanical ventilation.
Other indications for mechanical ventilation include an inability to protect the airway, altered mental status, severe hemodynamic instability, midfacial anomalies, and facial trauma.
Last, but not least, remember to identify and treat the underlying cause. One last clinical pearl!
Most cases of respiratory failure in children have an acute onset, but some conditions like cystic fibrosis can gradually lead to chronic respiratory failure.
To distinguish acute respiratory failure from chronic, look at the arterial pH from the ABG, and check a serum bicarbonate level.
Chronic, compensated respiratory failure is characterized by a normal or slightly decreased arterial pH, increased PaCO2, and an increased serum bicarbonate level.
This indicates that the kidneys have had time to reabsorb bicarbonate and restore the acid-base balance. On the other hand, patients with acute respiratory failure typically have uncompensated respiratory acidosis, with a decreased arterial pH, increased PaCO2, and normal serum bicarbonate level.
Alright, as a quick recap…Pediatric patients with respiratory failure are typically unstable and require acute management.

Review 10:15–10:50

An ABG can be used to differentiate hypoxemic respiratory failure from hypercapnic respiratory failure; and findings from the history, physical exam, and chest X-ray can be used to identify the underlying cause.
To improve oxygenation and ventilation, provide supplemental oxygen, noninvasive positive pressure ventilation, or endotracheal intubation with mechanical ventilation.
Finally, be sure to treat any