Neonatal Respiratory Physiology

Okay, so this isn’t a particularly exciting title but stick with me. Some foundation year doctors have placements in NICU and understanding the basics of neonatal respiratory physiology is key to understanding mechanical ventilation. This is also super useful information for anyone working a paediatric job (particularly in winter) who may look after babies on non-invasive respiratory support.

This article will break down the definitions of terms used for lung mechanics and ventilation and will give you the basic knowledge necessary to understand mechanical ventilation. There will be a second article for explaining the basics of mechanical ventilation in neonates

Gas Exchange

The goal of ventilation is to allow for adequate gas exchange.

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Image sourced from Biorender [1]

For stable and steady gas exchange we need 5 things:

  1. Normal alveolar oxygen content
    • Ventilation is responsible for the alveolar oxygen content
    • Determined by oxygen content at the end of inspiration
    • The oxygen content at the end of inspiration is determined by the functional residual capacity and ventilation
  2. Normal alveolar perfusion
    • Determined by blood flow to the lungs
    • Can be affected by shock/ pulmonary hypertension / lung congestion (increased blood content of the lungs at the end of systole.)
  3. Normal pressure gradient of all gases
    • Inlcuding partial pressures of oxygen, nitrogen and carbon dioxide
    • For example, giving an unnecessarily high fraction of inspired oxygen causes washout of nitrogen and nitrogen is partly responsible for functional residual capacity maintenance so this can lead to lung collapse
  4. Normal alveolo-capillary diffusion
    • The diffusion between blood vessels and alveoli through the alveolocapillary membrane
  5. Normal lung mechanics and pulmonary haemodynamics
    • Normal inspiration and expiration
    • A normal ventilation perfusion (V:Q) ratio is around 0.8


Functional Residual Capacity (FRC) the volume of air left in the lungs at the end of expiration – around 25-35ml/kg in a term baby. Optimising FRC is the main step in lung recruitment. Increasing PEEP can increase the FRC to help improve gas exchange.

Expiratory reserve volume (ERV)– the volume when exhaling to maximum point until you can no longer exhale

Residual Volume (RV) the only volume remaining in the lung after exhalation to a maximum point is the residual volume and this is always maintained, even in severe collapse or pneumothorax.

FRC = ERV + RV (RV = 15ml/kg, ERV = 15ml/kg, FRC = 25-35 ml/kg)

Inspiratory reserve volume (IRV) when we inspire or breath in to the maximal point.

Tidal Volume amount of air that moves in or out of the lungs with each respiratory cycle

Total lung capacity (TLC) volume of air in the lungs upon the maximum effort of inspiration

TLC = IRV + tidal volume + ERV + RV

Vital capacity greatest volume of air that can be expelled from the lungs after taking the deepest possible breath

Vital capacity = TLC– RV

Resp 2

Image sourced from Quizlet: BPK lecture 24 (Respiratory Foundations II The Respiratory system: Mechanics of Breathing) [2] Please note the volumes are values for adults

Minute Ventilation = tidal volume X respiratory rate. Measurement of the amount of air that enters the lung per minute. Determines your ventilation and therefore C02 clearance

PEEP – peak end expiratory pressure- the positive pressure that will remain in the airways at the end of the respiratory cycle (at the end of exhalation).  Functions to recruit lung up to the FRC.

PIP – peak inspiratory pressure, highest level of pressure applied to the lungs during inspiration

Surfactant is produced by alveolar type 2 cells which appear at around 25 weeks gestation in the foetus, but surfactant production continues until full term so preterm infants have a deficiency. It reduces surface tension at the alveolar-air interface and contributes to the distensibility of alveoli. Lungs of preterm infants are deficient in surfactant and prone to collapse.

Surface Tension When there is a liquid gas interface, liquid molecules at the interface are strongly attracted to liquid molecules within the liquid mass which creates surface tension. Surface tension forces maintain the shape of a droplet. The lungs have a huge air-liquid interface, which is mostly the lining of the alveoli. The lung fluid lining contains surfactant which lowers the surface tension of lining fluid and makes alveoli stable against collapse. Surfactant reduces alveolar surface tension by interspersing itself between water molecules increasing compliance and reducing tendency of lungs to recoil inwards.

Compliance Pulmonary compliance is a measure of the ability of the lung to stretch and expand. Compliance is affected by elastin in connective tissue, and surface tension which is decreased by surfactant. Net compliance of the lung and chest wall allows lungs to achieve appropriate FRC.

Dynamic Compliance the compliance measured during breathing which involves a combination of lung compliance and airway resistance.

Static Compliance pulmonary compliance when there is no airflow. The change in lung volume by the change in pressure, in the absence of flow.

Volume Pressure Curves

Imagine blowing up a balloon. When you first start blowing up the balloon it takes more effort and more pressure to get minimal inflation, then once the balloon starts to inflate it takes much less pressure to inflate fully. This is similar to inflating alveoli. If FRC is not achieved with optimal PEEP on a ventilator or due to respiratory distress the alveoli will collapse, there will be atelectasis and it will be more difficult to re-inflate them. Once FRC is achieved with optimal PEEP the alveoli remain inflated and are much more compliant and easier to inflate with PIP.

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So you can see in this diagram of a volume pressure curve, in the zone of atelectasis (where pressure is < FRC) the curve is relatively flat so it takes more pressure to inflate the alveoli.

Once beyond the zone of atelectasis and into the inspiratory limb where pressure is equal to or greater than FRC it takes less pressure to increase the volume of the alveoli as the curve is steeper.

There is another plateau at the top of the curve represnting hyperinflation where the pressure is too high and the alveoli become overdistended and the volume does not increase as much with increases of pressure.

Image sourced from Obgyn Key [3]

We can also liken surfactant deficiency to blowing up a balloon. In the absence of surfactant, surface tension is increased, making it harder to inflate the alveoli, similar to inflating a balloon in the beginning. With surfactant and decreased surface tension, inflating the alveoli becomes much easier and requires less pressure as the lung is less “stiff”, like fully inflating a balloon once it is already slightly inflated. This is depicted in this pressure volume curve, where respiratory distress syndrome (RDS) represents a baby with surfactant deficiency and you can see they need a lot more pressure to inflate the alveoli and can only achieve a fraction of the inflation of a healthy term baby. Imagine blowing up a long thing balloon which is really stiff, that is like trying to inflate alveoli in a preterm baby

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Image sourced from The Pathophysiology of Respiratory Distress Syndrome in Neonates [4]

Oxygen-Haemoglobin Dissociation

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Oxygen-haemoglobin dissociation curve – the amount of oxygen bound to haemoglobin is determined by the partial pressure of oxygen in a relationship of oxygen-haemoglobin dissociation curve. Despite atmospheric 02 concentration changing frequently, haemoglobin buffering maintains a constant tissue partial pressure of oxygen. The curve is sigmoid shaped, there is low saturation of haemoglobin when oxygen levels are low as haemoglobin preferentially releases oxygen to hypoxic tissues. There is high saturation of haemoglobin when oxygen levels are high as haemoglobin is binding oxygen in oxygen rich tissues. Foetal Hb has a higher affinity for oxygen than adult Hb and therefore the curve is shifted to the left. Other factors that cause a left shift of the curve include decreased temperature, decreased 2-3DPG, increased pH, decreased C02. Factors that cause the curve to shift to the right, thereby increasing the affinity of Hb for 02 are decreased pH, increased C02, increased temperature and increased 2-3DPG

*It’s important to note that neonates have mostly foetal haemoglobin meaning less oxygen is needed to saturate Hb but release of oxygen to tissues is low. After a red cell transfusion they have some adult Hb which shifts the curve to the right and you then need a high partial pressure of oxygen to saturate well. Therefore in a ventilated preterm neonate who has had multiple transfusions, you might notice their Fi02 requirement increase following a transfusion

Image sourced from Bio ninja [5]

Hypoxaemia – Sp02 < 80% or Pa02 < 50 mmHg

Hypoxia – low oxygen delivery to tissues of < 18 ml/kg/min affected by hypoxaemia or low blood flow or low Hb. Normal oxygen delivery = 20-40 ml/kg/min. Oxygen delivery < 10 ml/kg/min causes lactic acidosis. Hypoxia occurs when oxygen delivery is insufficient to supply the demand set by the metabolic utilisation.

Physioxia when the oxygen delivery matches the oxygen demand of the tissues. The oxygen tension of physioxia varies from tissue to tissue. When oxygen demand increases the threshold oxygen delivery required to maintain physioxia increases.

Mechanisms of hypoxaemia

  • Hypoventilation
    • Increased alveolar carbon dioxide or decreased alveolar oxygen content
    • C02 is perfusion dependent and this means exchange and partial pressure of C02 depends on the volume of plasma inside the vessels passing through the pulmonary circulation as all C02 is dissolved in plasma
    • 02 is diffusion dependent which means it mainly depends on pressure gradients and the affinity of Hb to attract oxygen. Therefore, the pressure gradient is very important to maintain the passage of oxygen from alveoli to capillary.
    • Diffusion of oxygen from alveoli to the blood occurs swiftly in one cardiac cycle.
  • Limited diffusion through alveolocapillary membranes
    • For example in a baby with chronic lung disease (CLD) the alveolar membrane is thicker so oxygen diffusion takes longer. Therefore, in a baby with CLD, tachycardia can result in hypoxaemia.
  • Ventilation perfusion (V:Q) mismatch
    • If ventilation is compromised but perfusion to the lungs is normal this reduces the V:Q ratio and blood passes through the lungs but with very little oxygen exchange causing right to left intrapulmonary shunt. If there is a 50% right to left shunt, there is 50% of blood passing through the lungs with no alveolar gas exchange. This occurs with lung collapse, pneumonia, bronchopulmonary dysplasia, lung congestion and pneumothorax.
    • When ventilation is compromised and causing V:Q mismatch this generally means the FRC is reduced and the lung is de-recruited. Therefore you need to apply reasonable distending pressure to re-recruit lung. As the required Fi02 is reduced you can continue to increase pressure (in the form of PEEP) until the Fi02 requirement plateaus.
    • Increasing the perfusion to the lungs can have a similar effect to reducing the ventilation. This occurs with a large patent ductus arteriosus with left to right shunt and reduces the V:Q ratio – this is because blood congesting the lungs takes up space where air should be.
    • If there is normal ventilation but poor perfusion to the lungs the V:Q ratio is increased. So air is moving in and out of the lungs but it is not being exposed to blood for gas exchange (physiological dead space). Lung perfusion can be decreased by pulmonary hypertension, high pulmonary vascular resistance, massive pulmonary embolus (very rare in neonates), air embolism, shock with reduced blood flow and bronchopulmonary dysplasia with pulmonary hypertension. Or there may be pulmonary flow obstruction, e.g. in cyanotic heart disease such as tricuspid atresia or pulmonary atresia
    • Increasing ventilation gives a similar effect to reducing perfusion, for example if hyperinflating the lungs with a high PEEP, the lungs become distended with an increased FRC beyond physiological values and this limits blood flow and venous return to the heart, therefore reducing cardiac output and increasing the V:Q ratio.
    • Why prone? After only working in neonates for a short time you’ll notice neonatal nurses and doctors love to prone babies, but why? Well, a baby in a prone position can better equally inflate both lungs, overall compliance of the chest wall is better and the alveoli are better inflated. Blood is distributed more equally between the anterior and posterior portions of lung improving V:Q matching, whereas when a baby is supine there is good ventilation at the front but perfusion is not as good as blood pools posteriorly and so perfusion is good at the back but ventilation is not as good, leading to V:Q mismatch.
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Image sourced from The Airway Jedi [6]

Managing Hypoxaemia

  • Respiratory distress syndrome, transient tachypnoea of the newborn, bronchopulmonary dysplasia, and pneumonia increase the risk of hypoxaemia through affecting ventilation.
  • Severe lung disease or collapse directly cause hypoxaemia through decreasing the FRC and intrapulmonary right to left shutning.
    • We can reduce the risk of hypoxaemia by increasing PEEP to improve lung recruitment and reach FRC. Usually unresponsive to Fi02.
  • Pulmonary hypertension and large PDA with left to right shunting also increase risk of hypoxaemia, but in these cases the baby will have normal lungs resposnive to oxygen but not PEEP.
    • In babies with congested lungs and left to right intracrdiac shunting there is limited response to PEEP and oxygen. These babies can be managed with inhaled nitric oxide if very unwell, or medical management to close the PDA
  • Congenital cyanotic heart disease, and severe supra-systemic pulmonary hypertension cause ventricular dysfunction.
    • These babies require surgery for congenital heart disease, and if there is pulmonary hypertension they require pulmonary vasodilators + inotropes to increase the systemic blood pressure above the pulmonary.

Mechanisms of Hypoxia

  • Hypoxaemic hypoxia
    • Caused by insufficient oxygen supply or uptake, or inadequate haemoglobin saturation.
    • Alveoli are comprised of type 1 and type 2 cells. There is a capillary immediately adjacent to these cells with a unicellular layer of endothelial cells. This makes up the diffusion distance which oxygen and C02 have to travel. The thicker the membrane, the longer it takes for 02 to diffuse across, e.g. in case of oedematous cells or fibrosis of tissues.
    • Increasing heart rate (HR) can also reduce transit time for blood in the lungs and can lead to hypoxaemia in already compromised babies.
    • Intrapulmonary right to left shunt occurs due to collapse with normal perfusion and means there is venous blood that has not reached a gas exchange surface and this mixes with arterial blood that has achieved gas exchange when leaving the lungs (venous admixture)
    • Hypoxia causes pulmonary vasoconstriction which is mediated by redox of vascular potassium channels in smooth muscle cells in muscularised cells of arterioles leading up to an alveolar capillary unit. This reduces blood flow to areas of low oxygen tension by increasing low arteriolar tone. Blood then bypasses poorly ventilated areas and is preferentially sent to well ventilated areas. This can cause a V:Q mismatch if the whole lung is diseased and leads to pulmonary hypertension.
    • The relationship between the amount of supplemental oxygen given and the maximum oxygen saturation achieved by this is determined by V:Q matching and varies with the percentage shunt. Optimising PEEP eliminates atelectasis and reduces intrapulmonary shunting. In a V:Q scatter (a mix of well ventilated areas and poorly ventilated alveoli with shunting) the well aerated alveoli have high V:Q ratio so are on the flat part of the oxygen dissociation curve. Collapsed alveoli have a lower partial pressure of oxygen so are on the steep part of the curve and have low V:Q ratio (more perfusion than ventilation). Therefore an increase in oxygen associated with an increase in arterial partial pressure of oxygen is smaller than the reduction in oxygen content associated with a reduction in arterial partial pressure of oxygen of the same magnitude because the dissociation curve is steeper for low V:Q. Therefore in a V:Q mismatch, Pa02 drops exponentially compared to saturations.
    • If arterial partial pressure of oxygen increases when position is changed there is probably a V:Q mismatch as you have transiently rearranged V:Q. Can also trial increasing PEEP to recruit atelectatic areas.
    • Why do hypoxic babies become more hypoxic when crying? When there is severe V:Q mismatch crying can worsen this and increase the intrapulmonary right to left shunt. This is because crying increases airway resistance and reudces the inspiratory:expiratory ratio causing overdistension of the most compliant alveoli and worsening compliance of weak alveoli. Overdistension compresses capillaries and reducing blood flow. Weak alveoli with worse compliance also collapse.
  • Anaemic Hypoxia
    • 98.5% of oxygen is transported bound to Hb. Oxygenation of Hb also facilitates nitric oxide carriage on Hb and this vasodilates tissue capillary beds for 02 to be delivered.
    • 30% of C02 is bound to Hb – 10% as dissolved and 60% as bicarbonate
    • The oxygen dissociation curve is shifted to the left by increased pH, low pC02, low temp and this increases Hb affinity for 02.
    • The oxygen dissociation curve is shifted to the right by low pH, increased pC02, increased temp, and this decreases Hb affinity for 02.
    • Improving cardiac output and Hb improve oxygen delivery through decreasing the oxygen extraction ratio. This is because you are delivering more blood to tissues than they need. This increases venous saturation without changing arterial oxygen saturation and thereby we can optimise oxygen carrying capacity via transfusion, optimising cardiac output and intravascular volume.
  • Circulatory hypoxia
    • Red blood cells entering the capillary have increased partial pressure of 02 which they drop off as they travel along in tissues. If the diffusion distance is small then the increased Pa02 pushes 02 across the interstitial space towards cells and mitochondria. If there is a greater distance between tissue and capillary this makes it harder to deliver 02 and therefore more vascular tissues are easier to perfuse and are less at risk of tissue hypoxia
    • Interstitial oedema increases the distance between capillary and cell and therefore increases the distance for oxygen to diffuse.
    • If there is hypoxia and oedema then there is reduced arterial partial pressure of 02 and reduced oxygen gradient so it is harder for oxygen to diffuse to tissues, reducing oxygen delivery. Less oxygen is delivered and utilised and this increases the residual oxygen in venous blood.
  • Metabolic hypoxia
  • Oxygen extraction increases as delivery of oxygen falls
  • In normal circumstances you deliver much more oxygen than you use until oxygen delivery decreases to a certain point of maximal oxygen extraction. As oxygen delivery keeps decreasing, then utilisation of 02 becomes supply dependent and you develop a linear relationship between utilisation of oxygen and delivery of oxygen and this is no longer physioxia.
  • Once the utilisation of oxygen is supply dependent and there is not enough supply, tissue lactate rises.
  • Oxygen extraction increases based on tissue metabolism and need and on basis of delivery of oxygen. When delivery of oxygen is high, extraction is supply independent.
  • Metabolic hypoxia can be caused by reduced mixed venous oxygen due to reduced supply of oxygen and this is due to hypoxaemia, ischaemia or anaemia. When it is due to reduced supply of oxygen the critical point is normal (point at which utilisation of oxygen becomes supply dependent)
  • One last cause is high oxygen consumption causing reduced mixed venous 02 leading to a high critical point. This can be caused by high cardiac output in sepsis, uncoupled respiratory chain not producing ATP in hypermetabolic states
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Relationship between delivery, consumption and extraction of oxygen. (Costello JM, 2015) [7]

  • We can estimate tissue oxygen utilisation with Near infrared spectroscopy (NIRS) and use this to calculate an oxygen extraction ratio.

Basic Principles of Ventilation

You need to create a pressure gradient to move air in and out of the lungs. The lung cannot expand by itself, it can only move passively in response to external pressure.

There are two ways to get air into the lungs:

  • Create positive pressure at the airway opening to push air into the lung, (mechanical)
  • Create negative pressure within the lung so air flows (physiological)

Volume changes lead to pressure changes and pressure changes lead to flow of gases to equalise pressure.

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Boyles law states that pressure and volume are inversely related , e.g. the pressure of gas decreases as the volume of the container increases and as volume decreases the pressure increases. Therefore as the lung inflates with inspiration the volume increases and the pressure decreases and becomes negative compared to atmospheric pressure, so air flows into the lung.

In spontaneous breathing a volume change causes a pressure change and leads to gas flow.

In ventilation a pressure change leads to gas flow and leads to a volume change.

Image sourced from Socratic Q&A [8]

Functional residual capacity (FRC) is maintained by the elastic recoil of the lungs and thorax. The visceral pleura is attached to the lungs and pulled inwards, the parietal pleura Is attached to the ribs and pulled outwards and this creates negative pressure and a vacuum in the chest wall and prevents collapse.

Pneumothorax occurs as air in the pleural cavity counteracts negative pressure and the lung collapses and thoracic cavity expands and the negative pressure disappears. Negative pressure needs to be re-established for the lung to re-inflate.

Transmural pressure

Transmural pressure is the difference in pressure between the inside and outside of an elastic structure. (Pin-Pout). It is the same as the distending pressure / recoil pressure.

There are 3 important types of transmural pressure:

Transpulmonary pressure = Palv-Pple. This increases to inflate the lungs by increasing pressure inside the alveoli or decreasing pressure outside the lungs. This is the driving pressure for spontaneous breathing. This pressure increases as a baby fills their lungs during inspiration

Transrespiratory pressure= Palv-Patm

Transthoracic pressure = Pple-Patm. This represents the total pressure needed to expand and contract the lungs and the chest wall.

  • Alveolar Pressure (Palv)
  • Pleural Pressure (Pple).
    • The Pple is negative at rest and becomes more negative with inspiration as the chest wall expands.
  • Atmospheric Pressure (Patm)

To achieve adequate lung inflation and gas exchange we need to be able to achieve physiological transmural pressures which in turns helps us to achieve a good FRC. This is influenced by compliance.

Work of Breathing

Work of breathing can be calculated by the pressure difference across the respiratory system multiplied by the volume of air moved by it (DeltaP X DeltaV). This equates to the amount of energy required by the inspiratory muscle (the diaphragm) to expand the lungs by overcoming airway and tissue resistance. The energy required to overcome airway resistance is usually converted to heat and lost. Energy required to overcome elastic recoil is not lost and is recovered during expiration. But increased work of breathing can overwhelm small infants as they could overwhelm their metabolic energy requirements resulting in acidosis if acute and severe or results in stunted growth if chronic.

Compliance X resistance = time constant (which is normally 0.12s in healthy term infants). The time constant is the time needed for alveolar pressure to reach 63% of airway pressure. Babies need 3-5 time constants to complete inspiration and expiration.

In small babies with homogenous lung disease the time constant is very short because compliance and resistance are low.

In babies with CLD, meconium aspiration, pneumonia, resistance increases, the time constant is longer and you need a longer inspiratory time and expiratory time. If the inspiratory time is too short the pC02 will rise. If the expiratory time is too short you get air trapping and a rise in C02 as dead space increases and this can also then reduce cardiac output through significant lung distension.

The inspiratory time should be at least 3 X time constant.

There is a linear relationship between Fi02 and mean airway pressure. C02 elimination depends on alveolar ventilation which is determined by minute ventilation (minute ventilation= (tidal volume X respiratory rate) -dead space)

Cardiorespiratory dynamics

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Elastic fibres exist in lung tissues and the lung is continually expanding and recoiling due to elasticity and surface tension. The chest wall contains spiral shaped elastic fibres, these work to expand and recoil in the opposite direction to the lung – the lung recoils inwards like an elastic band that is stretched and then let go and the chest wall recoils outwards, like a spring that is compressed and then let go. The chest wall and the lung moving in opposite directions creates negative pressure between the pleura.

There is a continuous tendency of the lung to collapse and a continuous tendency for the chest wall to expand and these opposing forces maintain the functional residual capacity. This creates negative pressure inside the chest wall of -5 mmHg. Pressure inside the lung during expiration is equal to atmospheric pressure.

Image sourced from Netters Essential Physiology [9]

  • Compliance is a measure of distensibility of the respiratory system and increased compliance = a larger delivered volume per unit change in pressure. When the lungs expand very easily you need more volume to create the changes in pressure. Compliance = tidal volume / driving pressure. Normal values for a term infant is around 1.5-2 cmH20/kg
  • Resistance = change in pressure / flow. A normal value in a term infants is 30cmH20 / L / second. Resistance is a property of the lungs which resists airflow, calculated by the pressure difference divided by the flow caused by it. Airway resistance depends on flow rate, length of airways, diameter of airways, and viscosity of inhaled gas. Tissues resistance gives elastic recoil
  • Preterm infants have poor lung compliance as lung development has stopped in its early stages and they are deficient in surfactant, but chest wall compliance is increased as the chest wall is very pliable and weak.
    • Preterm infants have highly compliant chest walls and poorly compliant lungs. Lung collapse creates negative pressure (but not as much as in term infants as the chest wall follows). Once the lung expands, the chest wall expands, and less haemodynamic instability is expected with hyperinflation. Pneumothorax could happen early in life with mechanical ventilation but is unlikely in later life when there is CLD because the lung is stiff and pleura is tough.
    • Haemodynamics are less likely to be affected in preterm compared to term infants with healthy lungs as the chest wall is too compliant and the mediastinum is not compressed with lung expansion.
    • In a poorly compliant lung there is reduced lung volume and increased pressure. The lung is collapsed to residual volume, increasing lung pressure and reducing mediastinal pressure. If you apply pressure, e.g. in the form of CPAP, you overcome compliance and restore the lung to FRC. This expands lung volume and pushes on the mediastinum without compression.
  • Term infants have less compliant chest walls than preterm infants and may have reduced lung compliance in cases of meconium aspiration or RDS. This creates more negative pleural pressure as the lung is collapsed and the chest wall is more rigid. This increases left ventricular afterload as the left ventricle is contracting against a higher negative pressure.
    • In term infants, mediastinal contents are more easily compressed once mechanical ventilation is applied to the increased rigidity of the chest wall.
    • There is an increased incidence of pneumothorax in term infants with increased work of breathing due to increased negative pressure in the lung causing it to collapse against a rigid chest wall. This increases negative pressure and leads to pneumothorax if the lung is not appropriately recruited.
    • Term infants on mechanical ventilation are more likely to develop pneumothorax with poor lung compliance due to more negative pleural pressure during lung collapse. They also have an increased tendency to develop haemodynamic instability with lung overdistension as the lungs are being inflated up to a rigid chest wall and this compresses the mediastinal contents.
  • Monitor haemodynamics through heart rate, urine output and lactate and pulse pressure. If pulse pressure is < 15 this could be due to hyperinflation as pulse pressure is reflective of stroke volume and stroke volume is reduced by increasing mediastinal pressure. An echo may show reduced venous return and left ventricular filling in hyperinflation.


Well done on reaching the end of this article!

After reading this you should understand the basic lung mechanics in neonates which can then be applied to the principles of ventilation. When you’re ready there are two more articles to help build this knowledge, one on invasive ventilation and one on non-invasive

The most important points to take away from this article are:

  • Minute ventilation determines your C02 clearance (tidal volume X respiratory rate) e.g. if you have a ventilated baby with a high pC02 you can increase their tidal volume or respiratory rate to help C02 clearance.
  • Alveolar oxygen content at the end of inspiration is determined by your functional residual capacity and ventilation. e.g. if you have a ventilated baby not oxygenating well you could increase their PEEP to increase their FRC.
  • A normal lung compliance allows babies to achieve a good FRC and oxygenate well. It is affected by elasticity and surface tension (decreased by surfactant). Babies with chronic lung disease have reduced elasticity and therefore reduced compliance, whilst preterm babies have surfactant deficiency and therefore reduced compliance. These babies can be difficult to ventilate as they have stiff lungs and need higher pressures
  • Hypoxaemia is defined as Sp02 < 80% or Pa02 < 50 mmHg (6.66 kPa). It is caused by hypoventilation, underlying lung pathology e.g. CLD, and V:Q mismatch (congenital heart disease can cause V:Q mismatch)
  • Hypoxia is defined as oxygen delivery < 18ml/kg/min. Hypoxia occurs when oxygen delivery is insufficient to supply the demand set by the metabolic utilisation. Hypoxia can be caused by insufficient oxygen supply, V:Q mismatch, anaemia, poor circulation, ischaemia or sepsis.


  1. Biorender. (2023, December 20th). Alveolar Gas Exchange Template. Retrieved from Biorender:
  2. Miniato, A. (2023, December 18th). BPK 205 Lecture 24. Retrieved from Quizlet:
  3. Admin, P. (2024, January 16th). Setting the Ventilator in PICU. Retrieved from Obgyn Key:
  4. Holme N, C. P. (2012). The Pathophysiology of Respiratory Distress Syndrome in Neonates. Paediatrics and Child Health, 507-512.
  5. Bioninja. (2024, Jaunary 16th). Oxygen Dissociation Curve. Retrieved from BioNinja:
  6. Whitten, C. (2024, Jaunary 16th). Ventilation Perfusion Mismatch. Retrieved from The Airway Jedi:
  7. Costello JM, M. M. (2015). Critical Care for Paediatric Patients with Heart Failure. Cardiology in the Young, 74-86.
  8. Meave SF. (2024, January 16th). How Does Boyle’s Law Relate to Breathing? Retrieved from Socratic Q&A:
  9. S, M. (n.d.). Respiratory Physiology: The Mechanics of Breathing. In M. A. Mulroney SE, Netters Essential Physiology (pp. 163-178). Elsevier.

Written by Dr Bex Evans, Paediatric Registrar

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