Respiratory failure in the paediatric population differs from the adult population by the presence of some discrete age-related groups of differentials, with specific focus on consequences of prematurity and congenital disease. There are also physiological and anatomical differences which predispose the children to respiratory failure. These can be summarised as "functional and structural immaturity", and describe a respiratory system which is poorly adapted to extrauterine life, reflecting the basic biological disadvantages of having a complex brain (as our maturation process necessarily takes much longer than that of a lamprey).

Previous SAQs discussing respiratory failure were heavy on the bronchiolitis:

  • Question 11 from the first paper of 2016 (all about bronchiolitis)
  • Question 7 from the second paper of 2011 (a list of differentials, risk factors, normal physiology... and bronchiolitis)
  • Question 6  from the first paper of 2009 (bronchiolitis)

So, it's all basically bronchiolitis and if you study bronchiolitis you're reasonably well set up for these sorts of questions. The only exception was Question 7 from the second paper of 2011, which was done reasonably well (pass rate 58%). The college wanted to know basic respiratory parameters (eg. resp rate) which would be normal for a given age group, as well as clinical features of respiratory distress, differential diagnosis of respiratory failure and factors which predispose neonates to this sort of collapse.  In this chapter, these and other generic respiratory failure issues will be discussed, whereas bronchiolitis seems important enough to deserve its own section.

Unfortunately, there does not seem to be any convenient single resource to answer SAQs like Question 7, and even Oh's manual (Chapter 105 by Tavey  Dorofaeff  and  Kevin  Plumpton) is somewhat uninformative. The most useful references for the answers below were from the  APLS handbook (I have the 4th edition) and the excellent article by Jürg Hammer ("Acute respiratory failure in children", 2013). Unfortunately it is not available as free full text.

Differential diagnosis of respiratory failure according to age group

This borrows heavily from the Oh's manual Blue Box number 105.1,  on page 1086 (7th ed). 

Category Neonates Young children
Vascular
  • Congenital heart defect
  • Vascular rings and slings
  • Pulmonary haemorrhage
  • Progression of congenital heart disease
  • Rheumatic fever
Infectious
  • Neonatal pneumonia
  • Bronchiolitis
  • Pneumonia
  • Croup
Neoplastic  
  • Intrathoracic solid tumours; lymphoma and neuroblastoma
Drug-induced  
  • Accidental ingestion of respiratory depressant, eg. opiate of some sort
Idiopathic
  • Transient tachypnoea of newborn
 
Congential
  • ARDS of prematurity
  • Congenital heart defect
  • Laryngo/tracheo/bronchomalacia
  • Pulmonary hypoplasia
  • Gastroschisis and omphalocele
  • Neuromuscular and skeletal disorders
  • Diaphragmatic hernia
  • Chronic neuromuscular conditions
Autoimmune  
  • Asthma
  • Anaphylaxis
Traumatic
  • Meconium aspiration syndrome
  • Diaphragmatic palsy (post cardiothoracic surgery)
  • Pneumothorax
  • Inhaled foreign body 
Metabolic
  • Metabolic acidosis
  • Decreased LOC due to some sort of metabolic coma 
 

Normal range of respiratory variables

The following table is from the Royal Children's Hospital In Melbourne, where it is available as a lanyard. If it's good enough to hang on their necks, its good enough for the CICM SAQs.

Age Weight (kg) Systolic BP (mmHg) HR (BPM) Resp rate 
Term 3.5 60-105 110-170 25-60
3 months 6 65-115 105-165 25-55
6 months 8 65-115 105-165 25-55
1 year 10 70-120 85-150 20-40
2 years 13 70-120 85-150 20-40
4 years 15 70-120 85-150 20-40
6 years 20 80-130 70-135 16-34
8 years 25 80-130 70-135 16-34
10 years 30 80-130 70-135 16-34
12 years 40 95-140 60-120 14-26
14 years 50 95-140 60-120 14-26
17+ 70 95-140 60-120 14-26

Clinical features of respiratory distress

Question 7 from the second paper of 2011 lists the following clinical signs:

  • Distortion of the chest wall (sternal and rib retraction, recession of intercostal, subcostal and suprasternal spaces) Accept alternative terminology
  • Pallor
  • Apnoea
  • Bradycardia
  • Lethargy, listlessness, decreased level of consciousness

To this, one might add:

  • Tachypnoea
  • Expiratory grunting
  • Nasal flaring
  • Cyanosis
  • Failure to feed

Factors which predispose infants to respiratory failure

This table was constructed mainly using Hammer's excellent review article, "Acute respiratory failure in children" (2013)

Airway anatomy
  • Upper and lower airways are more narrow and thus more easily obstructed by swelling or secretions.
  • The airways are also more compliant, which causes them to collapse more readily. For example with upper airway obstruction, the trachea will collapse with forceful inspiration.
  •  
  • In infants, end-expiratory volume is similar to closing volume and so they have small airway closure. 
  • Smaller lower airway diameter leads to increased susceptibility to distal airways disease. In adults bronchioles only contribute 20% of the total airway resistance, whereas in the infant they contribute up to 50%, which explains why that population is more susceptible to bronchiolitis (i.e. adults also get bronchiolitis all the time, but their bronchiolar disease is not clinically important)
Structural immaturity of the respiratory system
  • Chest wall is more compliant and this reduces the efficiency of breathing if there is increased effort. It is therefore more difficult to generate the negative intrathoracic pressure required to inspire sufficient tidal volumes in conditions where there is decreased lung compliance. Much energy is wasted by sucking in ribs rather than fresh air.
  • Expiratory failure: The infant chest wall has less elastic recoil, making it more susceptible to gas trapping in conditions where there is increased airway resistance. 
  • Collateral ventilation is poorly developed: in early neonatal life, no gas can pass through the under-developed  pores of Kohn and canals of Lambert. These appear by the 3rd-4th year of age.
  • Atelectasis is more likely to develop  because of poor collateral ventilation and higher risk of airway closure
  • The chest is structurally immature;  the ribs are short and horizontal, "bucket handle"  motion of the ribs is minimal and therefore tidal volume is dependent upon the downward displacement of abdominal contents by the diaphragm. The diaphragm is a weak strap-like muscle and any abdominal distension will cause respiratory compromise.
  • The respiratory muscles are inefficient, and therefore are fatigued rapidly. The diaphragm has too few Type I muscle fibres, and is therefore poorly equipped to sustain high worloads. This improves in the first year of life.
  • There are fewer alveoli; this is called "incomplete alveloarisation". Alveolar number increase during early life by septal division. 
Perinatal events or congential catastrophes
  • There could be perinatal asphyxia, leading to respiratory muscle weakness
  • Perinatal pneumothorax may have developed.
  • Congential abnormalities may be present which promote respiratory failure. These may include craniofacial anomalies, cystic hygromae, thracheomalacia, diaphragm eventration, etc.
  • Alveolar surfactant may be deficient if the infant is significantly pre-term (eg. ARDS of prematurity)
Post-uterine gas transport 
  • Foetal hemoglobin is present up to 4th -6ths month of life; dissociation curve shifted to the left: less oxygen is delivered to the tissues because of fHb’s higher affinity for oxygen
Circulatory peculiarities
  • Pulmonary vasculature is muscular: pulmonary hypoxic vasoconstriction occurs more readily. This can led to duct reopening and right to left shunting.
Neurological immaturity
  • The chemoreceptor-mediated respiratory drive reflexes are not mature, which may lead to impaired respiratory drive and apnoea (Martin et al, 2002)
Metabolic peculiarities
  • The metabolic demand per unit of body mass is increased - a neonate's oxygen consumption is twice that of the adult.
Immature immune system and increased susceptibility ro respiratory infection
  • Infants haven’t yet acquired immunity to the infections which adults are immune to, and are therefore predisposed to respiratory infections from pathogens which would otherwise be trivial (Tregoning et al, 2010).
  • Prematurity, malnutrition, day care attendance, sibling order, lack of breast feeding - all of these play a role in impairing immunity. 

References

Hammer, Jürg. "Acute respiratory failure in children." Paediatric respiratory reviews 14.2 (2013): 64-69.

Tregoning, John S., and Jürgen Schwarze. "Respiratory viral infections in infants: causes, clinical symptoms, virology, and immunology." Clinical microbiology reviews 23.1 (2010): 74-98.

Hermansen, Christian L., and Kevin N. Lorah. "Respiratory distress in the newborn." Am Fam Physician 76.7 (2007): 987-94.

Martin, Richard J., Jalal M. Abu-Shaweesh, and Terry M. Baird. "Pathophysiologic mechanisms underlying apnea of prematurity." NeoReviews 3.4 (2002): e59-e65.