4.2 Lower Airway, Lung Tissue Disease & Disordered Control
Key Takeaways
- Lower-airway obstruction (asthma, bronchiolitis) features prolonged expiration and wheeze; a silent chest after severe obstruction is a danger sign of near-failure, not improvement.
- Status asthmaticus management prioritizes oxygen, repeated bronchodilators (and systemic steroids in practice), and early assisted ventilation if effort becomes inadequate—avoid delaying support for perfect diagnostics.
- Lung tissue disease (pneumonia, pulmonary edema) impairs oxygenation through alveolar filling or collapse; oxygen, treat the cause (antibiotics, cardiogenic support), and ventilatory support as needed.
- Disordered control of breathing (raised ICP, overdose, neuromuscular weakness) presents with inadequate rate or depth without primary lung noise—open airway, assist ventilation, reverse reversible causes.
- PALS respiratory categories are management maps: same ABC priorities, different cause-specific therapies after oxygenation and ventilation are addressed.
Four Respiratory Problem Types in PALS
After you identify distress or failure (Chapter 3), PALS asks you to classify the type of respiratory problem so interventions match pathophysiology. The four categories used throughout provider materials are:
- Upper-airway obstruction (Section 4.1)
- Lower-airway obstruction
- Lung tissue disease
- Disordered control of breathing
All four can produce respiratory failure. What differs is the physical exam pattern and the cause-specific therapy layered onto universal ABC support (open airway, oxygen, assist ventilation when rate or effort is inadequate).
Quick pattern recognition
| Category | Classic findings | First cause-specific tools (after ABCs) |
|---|---|---|
| Upper obstruction | Inspiratory stridor | Calm care, nebulized epi (croup), FBAO relief, IM epi (anaphylaxis) |
| Lower obstruction | Prolonged expiration, wheeze | Oxygen, bronchodilators, steroids (asthma), supportive care (bronchiolitis) |
| Lung tissue disease | Crackles, grunting, hypoxemia out of proportion | Oxygen, antibiotics (pneumonia), treat heart failure/edema, PEEP/support as needed |
| Disordered control | Irregular/slow/shallow effort, little lung noise | Airway + assisted ventilation; reverse opioid, lower ICP, support neuromuscular failure |
Exam stems almost always include enough history and auscultation findings to place the child in one primary category. When mixed disease is present, stabilize gas exchange first, then treat all active causes.
Lower-Airway Obstruction: Asthma and Status Asthmaticus
Asthma is reversible lower-airway obstruction from bronchospasm, mucosal edema, and mucus plugging. Children present with cough, dyspnea, accessory-muscle use, and expiratory wheeze with a prolonged expiratory phase. Tachypnea and tachycardia are common. Pulse oximetry may be relatively preserved early because the child is still hyperventilating—do not use a single SpO2 reading as the only severity metric.
Severity and danger signs
- Mild–moderate: Wheeze, increased work of breathing, still speaks in phrases or short sentences, interactive.
- Severe: Marked retractions, inability to speak, agitation, significant hypoxia, peak flow (if obtained) severely reduced.
- Critical / near-failure: Silent chest (little air movement, so little wheeze), extreme fatigue, decreasing respiratory effort, rising lethargy, cyanosis, or bradycardia. A silent chest is not reassuring—it means airflow is critically reduced.
Status asthmaticus refers to a severe asthma exacerbation that does not respond promptly to initial bronchodilator therapy and requires continuous aggressive treatment. On PALS testing, treat the physiology: severe lower-airway obstruction with high risk of respiratory failure.
Management priorities
- Oxygen to correct hypoxemia; continuous monitoring of SpO2, work of breathing, and mentation.
- Inhaled β-agonist bronchodilators (albuterol/salbutamol) frequently or continuously as protocol allows; ipratropium is often added in severe exacerbations in clinical pathways.
- Systemic corticosteroids early for significant exacerbations (onset is not immediate, but delay worsens course).
- Adjuncts used in refractory severe disease in real practice (magnesium sulfate, etc.) may appear in advanced vignettes—know that they are adjuncts after oxygen and first-line bronchodilators.
- If the child progresses to inadequate rate or effort, begin bag-mask ventilation with oxygen. Allow adequate expiratory time; overly rapid ventilation can worsen air trapping and hemodynamics.
- Advanced airway and mechanical ventilation are high-risk in asthma (air trapping, barotrauma, hypotension)—use when failure is present, with experienced operators and careful rates/volumes.
Exam traps in asthma
- Interpreting a quieting chest and decreasing wheeze as improvement when the child is becoming lethargic.
- Withholding assisted ventilation because "we are still giving nebs." Nebulizers continue, but ventilation comes first when effort fails.
- Confusing asthma with croup because both can cause noisy breathing—phase of the respiratory cycle and quality of the sound distinguish them.
Bronchiolitis
Bronchiolitis is a viral lower-airway disease of infants (commonly RSV) with inflammation and mucus in small airways. Presentation includes rhinorrhea, cough, tachypnea, retractions, wheeze or crackles, and feeding difficulty. Hypoxemia is common.
PALS-relevant management points
- Supportive care is the mainstay: oxygen for hypoxemia, nasal suctioning for obstruction from secretions, hydration, and monitoring for apnea (especially young infants).
- Routine repeated bronchodilators are not as central as in asthma; some infants may get a trial, but do not treat bronchiolitis identically to status asthmaticus on every stem.
- Watch for apnea and fatigue → respiratory failure requiring assisted ventilation.
- High-flow nasal cannula and other noninvasive supports are common in clinical practice; exam focus remains recognition of failure and need for bag-mask or advanced support when effort is inadequate.
Differentiate bronchiolitis from asthma by age (young infants), viral prodrome with prominent congestion, and less dramatic response to β-agonists.
Lung Tissue Disease: Pneumonia and Pulmonary Edema
Lung tissue disease involves alveolar or interstitial pathology that impairs gas exchange—classically pneumonia (infection with consolidation) and pulmonary edema (fluid-filled alveoli from cardiogenic or noncardiogenic causes).
Clinical pattern
- Tachypnea, retractions, grunting (auto-PEEP to stent alveoli).
- Crackles, decreased breath sounds over consolidated areas, or diffuse wet sounds in edema.
- Hypoxemia that may be disproportionate to the degree of audible wheeze (this is not primarily bronchospasm).
- Fever and focal findings support pneumonia; gallop, hepatomegaly, or known heart disease support cardiogenic edema.
Management priorities
- Oxygen — often needs higher FiO2; titrate to adequate SpO2 while avoiding unnecessary hyperoxia once stable (post-arrest targets are detailed later; in acute hypoxemic failure, correct dangerous hypoxia first).
- Support ventilation if hypercarbia or fatigue develops—noninvasive support or bag-mask/advanced airway per severity.
- Pneumonia: antibiotics per likely pathogens and local protocols; fluid resuscitation if septic shock coexists (shock chapters).
- Cardiogenic pulmonary edema: oxygen, careful fluid strategy (avoid large indiscriminate boluses), and cardiogenic-shock therapies—do not treat pure cardiogenic edema like hypovolemic shock with repeated large boluses without reassessment.
- Treat fever, pain, and work of breathing contributors; suction and positioning as adjuncts.
On written items, the key is recognizing that oxygenation failure from lung tissue disease still starts with airway and oxygen, then cause-directed therapy—not endless bronchodilators when the exam clearly describes crackles and fever without wheeze-dominant disease.
Disordered Control of Breathing
Disordered control of breathing means the respiratory pump or central drive is failing even though the airways and lung parenchyma may be relatively clear. Common PALS contexts:
| Cause | Clues | Priority after open airway |
|---|---|---|
| Raised intracranial pressure | Trauma, ventriculoperitoneal shunt failure, Cushing pattern, unequal pupils, posturing | Careful airway, assisted ventilation; avoid hypoxia/hypercarbia; emergent neurosurgical pathway; do not use routine aggressive hyperventilation as a prolonged strategy except brief temporizing for herniation per advanced protocols |
| Drug overdose / toxins (e.g., opioids) | Miosis, track marks, known ingestion, very slow rate | Assist ventilation; naloxone for opioid when indicated; support ABCs first |
| Neuromuscular disease (e.g., Guillain-Barré, botulism, myasthenia crisis) | Weakness, poor cough, progressive shallow breathing | Elective early ventilatory support before crash; do not wait for full arrest |
| Central apnea / immature control (young infants, post-ictal, severe metabolic disease) | Irregular or absent effort with relatively quiet lungs | Bag-mask; treat cause (glucose, temperature, seizure control) |
What you will hear (or not hear)
Breath sounds may be clear or only diminished from low tidal volume. The problem is rate and depth, not stridor or wheeze. Mental status is often depressed. Pulse oximetry may fall late if the child was on oxygen; CO2 rises as minute ventilation falls.
Universal management sequence
- Open and protect the airway (position, OPA/NPA if no gag and indicated).
- Assist ventilation with bag-mask and oxygen to produce visible chest rise at an appropriate rate.
- Reverse what is reversible (naloxone for opioids, glucose for hypoglycemia contributing to depression, stop seizures).
- Plan definitive airway if prolonged ventilatory support is needed or protective reflexes are lost.
- Treat raised ICP and primary neurologic emergencies with parallel specialist care—never withhold ventilation while "only" managing imaging logistics.
Clinical scenario (synthesis)
Scenario A — Asthma failure: A 7-year-old with known asthma arrives with severe retractions and loud wheeze. After continuous bronchodilators the child becomes drowsy; wheeze nearly disappears and SpO2 falls. This is progression to respiratory failure with a silent chest. Priorities: open airway, bag-mask with oxygen (allowing exhalation time), continue medical therapy, prepare advanced support.
Scenario B — Pneumonia: A 2-year-old with fever, focal crackles, grunting, and SpO2 88% on room air has lung tissue disease. Oxygen, monitoring, antibiotics, and escalation if effort fails—not FBAO thrusts and not first-line IM epinephrine without allergic features.
Scenario C — Opioid: An adolescent is unresponsive with respiratory rate 4/min and pinpoint pupils after suspected overdose. Lungs are clear. This is disordered control: bag-mask ventilation immediately, then naloxone as indicated, while supporting circulation.
Section 4.3 converts these failure pathways into concrete bag-mask and advanced-airway performance standards during spontaneous circulation and during CPR.
A child with status asthmaticus was retracting vigorously with loud expiratory wheezes. Now the child is lethargic, respiratory effort is weak, and almost no wheeze is heard. SpO2 is falling. What is the best interpretation?
Which presentation best fits disordered control of breathing rather than primary lower-airway obstruction?
A febrile toddler has focal crackles, grunting, SpO2 89% on room air, and no significant wheeze. After oxygen is started, what cause-specific priority best matches lung tissue disease from pneumonia?