BASIC SCIENCE
Lung ventilation and the
physiology of breathing
Anna Barrow
Jaideep J Pandit
Abstract
This article summarizes the anatomical features of the lungs, airway
and thorax pertinent to the physiology of breathing and discusses
chemoreceptor detection mechanisms, brainstem centres and relays
involved in the control of breathing. We will discuss lung mechanics
including spirometry, lung compliance, airway resistance and the
role of surfactant and consider how these can be affected by disease
states. It is recommended to revise principles of arterial blood gas
analysis in addition to this article.
Keywords Airway resistance; breathing; control of breathing;
compliance; dead space; flow volume loops; perfusion; spirometry;
surfactant; VA/VQ mismatching; ventilation
Anatomy of the lungs, airways and thoracic cage
Airways
The upper respiratory tract begins at the nose and runs down to
the nasopharynx, oropharynx and the larynx. The function the
conducting airways is to filter, warm and humidify inspired
gases.
The lower respiratory tract begins with the trachea at the level
of C6 and extends to T4 where it bifurcates into the right and left
main bronchi, lobar bronchi, segmental bronchi and terminal
and respiratory bronchioles leading to the alveolar ducts and
sacs. The respiratory bronchioles, alveolar ducts and sacs are the
sites of gas exchange.
Lungs and pleura
The right lung is divided into upper, middle and lower lobes by
the oblique and horizontal fissures. The left lung is divided into
upper and lower lobes by the oblique fissure. The lungs are
separated from the thoracic cage by two thin layers: the visceral
pleura that invests the lung and, in continuity with it, parietal
pleura, which abuts the chest wall, diaphragm, mediastinum and
pericardium. The pleura are lubricated with pleural fluid and the
space between them is normally very small. The intercostal
nerves innervate the parietal pleura but the visceral pleura has
no sensory supply. The arterial supply of the main bronchi as far
as the terminal bronchioles is the bronchial arteries. The respi-
ratory bronchioles alveolar ducts and sacs are supplied by the
pulmonary veins.
Anna Barrow MBBS MA MRCP FRCA is an ST4 in Anaesthesia at Oxford
University Hospitals, Oxford, UK. Conflict of interest: none.
Jaideep J Pandit MA BMBCH DPhil FRCA FFPMRCA is a Consultant
Anaesthetist at Oxford University Hospitals, Oxford, UK and
Professor and Fellow, St John’s College, Oxford, UK. Conflict of
interest: none.
SURGERY 35:5
Ciliated columnar epithelium lines the airways as far as the
respiratory bronchioles. Goblet cells secrete mucus, which pro-
vides a physical defence mechanism through the mucociliary
escalator. Squamous epithelium lines the alveolar ducts and sacs.
Type 1 pneumocytes are thin walled and form the site of gas
exchange. The type 2 pneumocytes are important for two rea-
sons: surfactant secretion, which reduces surface tension, and
secondly they are stem cells thus can divide to repair areas of
damaged lung tissue.
Thoracic cage
The thoracic cage is formed by the sternum, ribs, thoracic
vertebrae and the diaphragm inferiorly. Of the twelve pairs of
ribs, the first seven pairs articulate via costal cartilages with the
sternum. Rib pairs eight, nine and ten articulate with the
cartilage superiorly and the last two pairs ribs are ‘floating’ ribs.
Intercostal spaces lie between the ribs and contain muscles,
arteries, veins and nerves. The intercostal muscles are arranged
such that the external intercostals run downwards and anteri-
orly, the internal intercostals downwards and posteriorly and
the innermost intercostal layer is incomplete. The intercostal
arteries, veins and nerves run on the underside of the rib,
protected in a groove.
The diaphragm
The diaphragm divides the thorax and the abdomen. It com-
prises peripheral muscular areas: the left and right crus that
arise from the upper two and three lumbar vertebrae, respec-
tively. The costal part of the diaphragm attaches to ribs seven to
twelve and their costal cartilages. The sternal part arises from
the xiphisternum. The central part is tendinous and forms the
medial and lateral arcuate ligaments which are condensations
of the fascia investing quadratus lumborum and psoas major.
The phrenic nerve (C3, 4, 5) supplies motor function of the
diaphragm. The sensory supply is from lower intercostal nerves
peripherally and from the phrenic nerve centrally. Openings in
the diaphragm exist for the inferior vena cava and right phrenic
nerve at T8; the oesophagus, left gastric artery and vein and the
vagus nerves at T10; and the aorta, thoracic duct and azygous
vein at T12.
Respiratory muscles
In order to generate a negative pressure gradient for inspiration,
inspiratory muscles act to increase the volume of the thoracic
cage. The diaphragm is the main inspiratory muscle during quiet
breathing. When it contracts, it descends by approximately 2 cm;
however, during exercise it can descend by 7 cm. This increases
the vertical dimensions of the thoracic cavity. Contraction of the
inspiratory muscles pulls the ribs upwards and outwards,
increasing the anterioreposterior diameter of the thorax. During
inspiration the action of the innermost intercostals prevents the
in-drawing of the intercostal space. As the diaphragm contracts
during inspiration, it increases the intra-abdominal pressure and
abdomen and chest wall both move outwards during normal
inspiration. The anteroposterior diameter of the chest is also
increased by the action of the scalene muscles that raise the
upper two ribs and move the sternum anteriorly. The sloping
lower ribs rise in a bucket handle fashion which increases the
transverse diameter of the thorax.
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 BASIC SCIENCE

When work of breathing is increased, accessory muscles
become important: the sternocleidomastoids, serratus anterior
and pectoralis major (when the arms are fixed) assist chest
expansion.
Expiration occurs largely by passive recoil of the chest wall
and lungs during quiet breathing. During exercise, expiration is
augmented by the action of rectus abdominis and the internal
and external obliques, which assist the recoil of the diaphragm
by raising intra-abdominal pressure.
Diaphragmatic paralysis leads to paradoxical movement (see-
sawing) of the chest and abdominal walls, as the diaphragm is
drawn up into the chest with negative intrathoracic pressure
during inspiration.
Dead space
The conducting airways, above the terminal bronchioles, do not
take part in gas exchange. They form the anatomical dead space
and the volume of this (Vd) is approximately 150 ml.
Alveolar dead space is formed by alveoli that do not take part
in gas exchange: for example due to reduced or absent perfusion
in pulmonary embolism, or shunting of blood from areas of
pneumonia.
The sum of anatomical and alveolar dead space is the physi-
ological dead space (i.e. the volume of gas that has not taken part
in gas exchange). Measurement of these proportions of the tidal
volume can be achieved using the Bohr method, details of which
are beyond the scope of this article.
The respiratory cycle
Intrapleural pressure
During inspiration, expansion of the chest wall increases the
pressure gradient between the intrapleural space and the alveoli
as the lungs are stretched. This creates a negative pressure
gradient from the mouth and nose to the alveoli which draws in
air. During quiet breathing, alveolar pressure rises towards
the end of inspiration, whereas intrapleural pressure remains
negative for the duration of the respiratory cycle. During forced
inspiration, in obstructed breathing, the intrapleural pressure may
reach
80 cmH2O (normal <
10 cmH2O). During forced expi-
ration, the both intrapleural pressure and alveolar pressure rise.
Intrapleural pressure may reach þ80 cmH2O in healthy in-
dividuals. Due to the lung’s elastic recoil, the pressure within the
alveolus exceeds that within the pleura. When airflow stops, at
end inspiration, and end expiration, the alveolar pressure is 0.
Lung volumes
The volume inhaled and exhaled during a ‘normal breath’ is
known as the tidal volume (TV) and is approximately 500 ml.
After a normal tidal breath, the volume further inspired with
additional effort, would be the inspiratory reserve volume (IRV).
Similarly, the volume which could be further exhaled at the end
of a normal tidal breath is the expiratory reserve volume (ERV).
Maximal inspiration and expiration to the expiratory and inspi-
ratory reserve volumes would give the vital capacity (VC). The
volume remaining in the lungs after maximal expiration is the
residual volume (RV). Functional residual capacity (FRC) is the
sum of the inspiratory reserve volume and the residual volume.
FRC is the volume left in the lungs at the end of a normal breath
and it is determined by the elastic properties of the lungs and the
chest wall. At FRC, outward recoil of the chest wall and inward
recoil of the lungs are exactly balanced. Thus, in lung fibrosis,
where the lungs are stiff with increased recoil, FRC will occur at a
smaller volume. Conversely in emphysema where there is
destruction of lung parenchyma and loss of elastic recoil, FRC
occurs at a larger volume. FRC can also be increased due to air
trapping and application of positive end-expiratory pressure
(PEEP). Total lung capacity (TLC) is equal to the residual volume
plus the vital capacity (Figure 1).
Lung mechanics
During inspiration, work must be done to overcome impedance
from the lungs and chest wall, mainly due to frictional forces:

Spirometry trace

Inspiratory
reserve
IRV volume
Inspiratory
capacity (IRV)
VC (IC) Vital
capacity Tidal Total lung
TV (VC) volume capacity
(TV) (TLC)
Expiratory
reserve
ERV Functional
volume
FRC (ERV) residual
capacity
Residual (FRC)
RV volume RV
(RV)

Figure 1 Lung volumes during tidal breathing, forced inspiration and forced expiration. Capacities are the sum of two or more lung volumes.
Residual volume and functional residual capacity cannot be directly measured by spirometry and are calculated by helium dilution or body
plethysmography.

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 BASIC SCIENCE
airway resistance and elastic resistance of the stretching lung and
chest wall.
Compliance is the change in unit volume per change in unit
pressure. The difference in alveolar and intrapleural pressure is
the distending pressure. Lung compliance is assessed by either
static pressure volume curve or dynamic continuous pressure
volume loops. Intrapleural pressure is measured indirectly via
oesophageal pressure. Alveolar pressure equals atmospheric
pressure when there is no airflow. A subject takes an inspiration
with a series of breath hold points at which measurements are
plotted, transmural pressure is the same as intrapleural pressure
at these static points. The steepest part of the curve lies just
above the FRC and is where there is the greatest change in vol-
ume for a given pressure change. In other words, the point at
which the lung is most compliant and this lies within the normal
tidal breath volume, making tidal breathing efficient. As the
curve approaches total lung capacity, it flattens out. The differ-
ence in shape of the expiratory and inspiratory curves is known
as hysteresis and is due to elastic energy stored in extensile
tissue.
Normal lung compliance is approximately 1.5 litres/kPa.
Compliance is reduced by fibrotic lung diseases and increased in
emphysema.
Dynamic lung compliance is measured continuously and
correlates well with static compliance curves except in disease
states which produce regions of stiffer lung that fills less easily
during inspiration. The area of the loop is a measure of work
done in overcoming airway resistance (Figure 2).
Surface tension
Surface tension opposes the forces expanding the lung during
inspiration. Attraction of molecules for each other within a
sphere opposes expansion. This is described by Laplace’s law for
Lung compliance: volume–pressure curves for
static compliance
Volume–pressure curves
Volume
I [BTPS]
TLC
Total compliance
1 ml/Pa
[P – P ] = Wall pressure
3 [Palv – PB ] = Mouth pressure
VC
Thoracic compliance
2 ml/Pa Lung compliance FRC
2 ml/Pa
[Palv – Pit ] = Lung pressure
0 b2 adrenergic receptors that cause relaxation when stimulated by
RV
Static
–50 0 50 mm Hg transmural
–6.7 kPa 6.7 kPa pressures
Healthy person: 1/1 = ½ + ½
FRC, Functional residual capacity; RV, residual volume; TLC,
total lung capacity; VC, vital capacity.
Figure 2
SURGERY 35:5
pressure within a bubble when there is air on both sides, creating
two fluid air interfaces.
P ¼ 4T=R
The law predicts that a smaller bubble will have a higher pres-
sure within it and that when two bubbles are connected, the
smaller bubble will empty into the larger bubble since this is the
downhill pressure gradient.
Alveoli are not spherical and are lined by surfactant that acts
to reduce surface tension. Surfactant is produced by type 2
pneumocytes. The main lipid component is dipalmitoylphos-
phatidylcholine (DPPC). The hydrophilic phospholipids lie in the
alveolar fluid and the hydrophobic portion aligns to face alveolar
gas. As an alveolus shrinks, surfactant molecules come into
closer contact with each other and their concentration increases,
polar regions become closer together and thus repel each other
more strongly, reducing the tendency to collapse. Neighbouring
alveoli interact by shrinking in different directions, which exerts
opposing forces thus improving stability.
Flow volume loops
Early expiration can be augmented by effort; however, expiration
becomes effort independent due to dynamic compression of air-
ways. At the beginning of expiration, intrapleural pressure is
negative and airways are splinted open by transmural pressure.
In a forced expiration, expiratory muscle contraction raises the
intrapleural pressure and this compresses airways causing
collapse until distal pressure builds up and reopen the airway.
Peak expiratory flow curves demonstrate this.
Inspiratory airflow is effort dependent (Figure 3).
Airway resistance
Laminar flow predominates in larger airways.
The HagendPoiseuille equation describes factors affecting
airflow.
Most of the airway resistance is contributed by the nose,
pharynx and larger airways. In wider airways and at branch
points, airflow becomes turbulent and energy is dissipated as
eddies form. The likelihood of turbulent flow increases in exer-
cise. Reynold’s number predicts the likelihood of turbulent
airflow.
Density of fluid is important in determining contributes to
turbulent airflow and viscosity is important in laminar flow.
Peripheral airways contribute little to the overall airway
resistance unless severely affected by disease.
Airway resistance is determined by bronchial smooth muscle
tone that is determined by the parasympathetic nervous supply
(acetylcholine and type 3 muscarinic receptors). It also contains
circulating adrenaline or salbutamol. Non-adrenergic non-
cholinergic (NANC) receptors also innervate the lungs, acting via
substance P, neurokinins, nitric oxide and vasoactive intestinal
peptide. The sympathetic nervous system has little effect on the
lungs in humans. Airway stretch receptor activation inhibits
bronchoconstriction and carbon dioxide is known to be a bron-
chodilator. Pollutants, irritants, chemicals from mast cell
degranulation such as histamine increase bronchomotor tone.
Mucosal oedema, mucus hypersecretion and airway plugging
229 Ó 2017 Published by Elsevier Ltd.
 BASIC SCIENCE

Typical flow volume loops

a Normal b Emphysema
Flow Flow
(litres/second) (litres/second)
Expiratory
flow

TLC RV (litres) TLC RV (litres)

Inspiratory
flow
VC

c Unilateral main-stem bronchial obstruction d Fixed UAO

Flow Flow
(litres/second) (litres/second)

TLC RV (litres) TLC RV (litres)

e Variable extrathoracic UAO f Variable intrathoracic UAO

Flow Flow
(litres/second) (litres/second)

TLC RV (litres) TLC RV (litres)

g Restrictive parenchymal lung disease h Neuromuscular weakness

Flow Flow
(litres/second) (litres/second)

TLC RV (litres) TLC RV (litres)

Figure 3 (a) Normal trace. Inspiration runs along the lower half of the graph and expiration along the upper half, starting at total lung capacity. (beh)
Typical traces in disease states. RV, respiratory volume; TLC, total lung capacity; UAO, upper airway obstruction.

also increase airway resistance in asthma. Chronic mucosal hy-
pertrophy in chronic obstructive pulmonary disease (COPD)
similarly increases airway resistance as do tumours and foreign
bodies.
Assessment of airway resistance
Airway resistance in healthy lungs is approximately 0.2 kPa/
litre/second.
Forced expiratory volume in 1 second, forced vital capacity
and peak expiratory flow can be used to assess airway resistance
(Figure 4).
Ventilation perfusion relationships
In health, alveolar ventilation and pulmonary blood flow are
approximately equal (5 litres/minute), and for optimal gas ex-
change need to be well matched. Local ventilationeperfusion
ratios (VA/VQ) should be close to 1. Mismatching creates
shunting in areas that are perfused but not ventilated (e.g. due to
consolidation). A right to left shunt has a VA/VQ ratio ¼ 0.
Conversely, a VA/VQ ratio greater than 1 occurs in an area that is
ventilated but not perfused (e.g. due to pulmonary embolism),
and this leads to an increase in alveolar dead space.

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 BASIC SCIENCE

<2 kPa) gives the ideal pO2 and increases are usually due to VA/
Forced expiratory volume (FEV1) and forced vital VQ mismatch.
capacity (FVC) ratios Regional ventilation and perfusion can be visualized by
FEV1/FVC ratio inhalation and injection of radioisotopes.
FVC
Control of breathing
Normal lungs Control of ventilation is mediated via central and peripheral
FEV1 chemoreceptor inputs, plus input from other sources including
Restrictive lung receptors, muscle and joint receptors and higher brain
Volume exhaled

diseases FVC
centres. These inputs are relayed to the brainstem where they
converge in a complex arrangement to form a central pattern
generator that consists of diffuse groups of neurones with indi-
FEV1 vidual roles, which interplay to create multiple respiratory pat-
Obstructive
terns in response to differing physiological demands.
diseases
Central chemoreceptors are a diffuse collection of neurones in
FEV1 the ventrolateral medulla, sensitive to pH changes in the cere-
brospinal spinal fluid (CSF) that correspond to changes in arterial
pCO2. Their responses are relatively slow, in the region of
20 seconds, since time is required for CO2 to diffuse across the
1 second
bloodebrain barrier separating arterial blood from CSF. CSF is
Time (seconds)
impermeable to charged molecules such as Hþ; however, CO2 is
Figure 4 The upper line shows a normal trace. The normal ratio of
able to diffuse freely and via the action of carbonic anhydrase,
FEV1 to FVC is usually greater than 80%. The lower trace represents produces an indirect decrease in CSF pH:
obstructive lung disease and demonstrates a much reduced FEV1.
FEV1/FVC is usually lower in obstructive lung disease (typically <70%), CO2 þ H2O 4 H2CO3 4 Hþ þ HCO3

however, FVC may be normal (although it takes much longer to exhale
that volume). In restrictive lung diseases, FVC is reduced but there is The protein content of CSF is much lower than that of blood, thus
no obstruction to expiration so although FEV1 is reduced in absolute changes in pH are less well buffered and small variations in
terms, the FEV1/FVC ratio will be normal. FVC, Forced vital capacity; arterial pCO2 produce augmented changes in CSF pH. The
FEV1, forced expiratory volume at 1 second.
decrease in CSF pH causes an increase in ventilation. Central
chemoreceptors account for the majority of the response to
hypercarbia (approximately 80%).
Gravity exerts a hydrostatic pressure on all vessels greatest
Peripheral chemoreceptors are of two types. Carotid bodies
when a subject is upright. Vessels at the bases of the lungs are
lie at the bifurcation of the common carotid artery and are the
more distended and so there is higher blood flow. Higher up the
most important. They are innervated by the carotid sinus nerve
lung, diastolic pressures may fall below alveolar pressure and
that relays to the glossopharyngeal nerve. The carotid bodies
flow becomes determined by the difference between arterial and
are made up of type 1 cells (glomus cells) and type 2 (sheath
alveolar pressure. At the apices, alveolar pressure exceeds arte-
cells). The glomus cells are the sites of chemo detection and
rial pressure and flow becomes intermittent. Intrapleural pres-
respond to increased pCO2, increased Hþ or decreased pO2 by
sure is less negative at the base than the apex, therefore at FRC
increasing the rate of signal relay in the carotid sinus nerve.
apical alveoli are proportionally more expanded than those at the
This is thought to occur by means of inhibition of Kþ channels
bases and have less capacity to increase their volume further.
depolarization, calcium entry and release of dense neuro-
Thus ventilation at the bases is greater than at the apices. In
transmitter granules.
healthy lungs, a degree of mismatching has little effect as the
Aortic bodies are relatively unimportant in humans. They lie
areas of the lungs with low VA/VQ ratios are still well ventilated
around the aortic arch and are innervated by the vagus nerve.
enough to achieve almost full saturation with oxygen. Hypoxic
J (juxtapulmonary) receptors on alveolar and bronchial walls,
pulmonary vasoconstriction reduces VA/VQ mismatch by
near to capillaries, are irritant receptors that have unmyelinated
causing vasoconstriction of areas with high PaCO2, diverting
afferents in the vagus nerve. Stimulation causes apnoea or
blood to better ventilated areas.
tachypnoea with small volume breaths, cardiovascular depres-
Higher degrees of mismatching can occur in diseases such as
sant effects and laryngeal constriction. Stimulation of lung re-
COPD, pneumonia, and pulmonary oedema, where there is
ceptors in bronchial smooth muscle (slowly adapting receptors)
reduced ventilation and regions of low VA/VQ ratios occur. In
causes shorter and shallower inspiratory efforts. They are also,
pulmonary embolism, where there is loss or reduction of lung
via the vagus nerve, involved in the HeringdBreuer reflex
perfusion despite undisrupted ventilation, high VA/VQ ratios
whereby lung inflation inhibits inspiration. Conversely, the
occur.
deflation reflex activates inspiratory muscles as the lung deflates.
The effect of VA/VQ mismatch may be seen on arterial blood
During normal breathing, these reflexes are relatively silent but
gases, however compensation may occur. Arterial hypoxia due
become more important with larger tidal volumes during exer-
to VA/VQ mismatch can be improved by increasing the inspired
cise. They are also more active in neonates, where a compliant
oxygen content, in contrast to the hypoxia due to a shunt.
chest wall risks over inflation.
Calculation of the alveolarearterial (Aea) gradient (normally

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 BASIC SCIENCE
Golgi tendon organs, muscle spindles and joint receptors
in respiratory muscles (but not the diaphragm) and in non-
respiratory muscles also have an input and can stimulate
breathing during exercise.
Pain receptor stimulation usually leads to a short apnoea
followed by hyperpnoea. Laryngeal receptors and trigeminal
nerve afferent stimulation causes apnoea or laryngospasm. Car-
diovascular receptors are also involved: stimulation of arterial
baroreceptors by increased blood pressure depresses ventilation,
whereas hypotension has the opposite effect.
These multiple receptor inputs are integrated in the medulla
and pons by a complicated array of neuronal groups that inter-
link to form a central pattern generator. The neuronal groups can
be loosely divided into inspiratory and expiratory in nature,
though their interactions are complex.
The medulla contains the dorsal respiratory group (DRG) in
the nucleus tractus solitarius. This receives input from central
and peripheral chemoreceptors and the vagus nerve and is
involved in inspiration. The ventral respiratory group (VRG)
comprises caudal expiratory and rostral inspiratory areas as well
as the Botzinger and pre-Botzinger complexes. The pre-Botzinger
complex probably contains pacemaker neurones; however, the
role of these is likely limited and only represents a reaction to
hypoxia when they generate gasping breaths. Descending output
from the medullary centres regulates activity of respiratory
muscles.
A pneumotaxic centre lies in the nucleus parabrachialis and
the KollikerdFuse nucleus in the pons. This receives inputs
from the VRG, lung receptors via the vagus and DRG and acts
to modulate respiratory patterns. It causes switching off of
inspiration as inflation occurs. An apneustic centre may exist
in the pons involved in prolonged inspiration with short
expirations.
Higher centres also exert a descending input. Emotion and
temperature affect respiratory pattern via the hypothalamus.
Voluntary control is exerted from the cortex via the pyramidal
tracts that bypass the pneumotaxic and medullary centres. Le-
sions of the brain causing damage above the level of the pons
leave eupnoea but voluntary control is lost.
The site of generation of the respiratory rhythm is contro-
versial. It probably involves the VRG, DRG and pneumotaxic and
apneustic centres, though some sources believe it involves the
VRG and pre-Botzinger complex. Reciprocal inhibition (switch-
ing on and off) is more likely than pacemaker neurone activity.
An array of respiratory rhythms can be generated by differential
activation of the different inspiratory and expiratory centres to
allow adaptation to differing physiological and pathological
situations.
Artificial ventilation
Artificial ventilation can be divided into invasive (requiring an
endotracheal tube) and non-invasive respiratory.
Invasive mechanical ventilation can be negative pressure or
positive pressure ventilation. Intermittent negative pressure
ventilation was used to support patients suffering from
poliomyelitis in the early part of the 20th century and
required an ‘iron lung’, which created an intermittent negative
SURGERY 35:5
pressure. Similar effects are produced by cuirass ventilators
but these are only suitable for augmentation of spontaneous
breathing.
Controlled mechanical ventilation or intermittent positive
pressure ventilation (IPPV) evolved in the 1950s. This involves a
non-physiological situation where air is driven into the airways
and lungs by positive pressure and expiration is usually passive.
Developments in ventilator technology have allowed sophisti-
cated patterns of ventilation to be developed. This allows syn-
chronization with patients able to generate spontaneous breaths,
with mandatory breaths to ensure adequate minute volume
(synchronized intermittent mandatory ventilation, SIMV).
Numerous modifications and variations have been developed;
however, for most patients in an intensive care setting, experi-
ence and research has shown that best results with fewest
complications are achieved by:
 avoiding muscle paralysis and performing ‘sedation holds’
to encourage spontaneous ventilation
 aiming for low tidal volumes to reduce volutrauma
 limiting peak pressures to reduce barotrauma
 addition of PEEP to reduce areas of collapse and atelectasis
and the resultant trauma of airways being forced open
(atelactrauma).
Complications of invasive ventilation
Immediate:
 cardiovascular compromise (raised intrathoracic pressure
reduces venous return and cardiac output)
 aspiration
 pneumothorax
Early:
 acute respiratory distress syndrome
 ventilator associated pneumonia
 increase in critical illness neuromyopathy
Late:
 need for prolonged weaning, rehabilitation and support
 need for tracheostomy and associated complications
 tracheal stenosis
 tracheomalacia.
Non-invasive ventilation avoids the use of tracheal intubation
or tracheostomy. The patient must be able to generate their own
respiratory efforts and therefore it is not suitable in certain
groups such as those with a decreased conscious level and un-
able to protect their airway, active vomiting and non-compliant
patients. It may be delivered using a tight-fitting nasal mask,
facemask or a hood. Continuous positive airway pressure (CPAP)
is the application of a positive pressure, usually in the region of 5
e10 cmH2O throughout the respiratory cycle, which acts to
prevent airway collapse, recruit collapsed alveoli and thereby
reduces VA/VQ mismatch and improves compliance. It may also
help in pulmonary oedema by increasing the transmural pres-
sure, reducing fluid exudation from capillaries into the alveolus.
By increasing FRC, the patient moves onto the steeper part of the
pressureevolume curve, which improves compliance and re-
duces the work of breathing. This is useful in obstructive sleep
apnoea.
Bilevel positive airway pressure is a modification of CPAP
whereby a higher level of positive pressure during inspiration
232 Ó 2017 Published by Elsevier Ltd.
 BASIC SCIENCE
and lower level during expiration are used to aid expiration and
reduce over distension.
Non-invasive intermittent positive pressure ventilation
(NIPPV) is IPPV delivered by nasal or facemask. The patient
needs to synchronize their breathing with the ventilator. Uses
include neuromuscular diseases leading to chronic respiratory
failure and COPD, since it avoids the need for intubation and
resultant complications in a patient who would be difficult to
wean from a ventilator. It has been shown to improve survival.
Summary
The physiology underlying breathing and the mechanisms con-
trolling it are complex and not yet fully elucidated. New de-
velopments in respiratory critical care include extracorporeal
membrane oxygenation (ECMO) and extracorporeal carbon di-
oxide removal (ECCO2R) that extend the possibilities for respi-
ratory support from ventilation alone to provision of gas
exchange. Understanding the physiological principles underlying
lung mechanics, acidebase balance and adaptation to disease
SURGERY 35:5
states is important to be able to interpret investigations and
institute appropriate treatment. Revision of the principles of
blood gas interpretation is also recommended. A
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Ward J. Physiology of breathing I. Surgery 2005; 23.
Ward JPT, Ward J, Leach RM. The respiratory system at a glance. 3rd
edn. Wiley Blackwell, 2010.
Ward SA. Physiology of breathing I. Surgery 2004; 22.
Ward SA. Physiology of breathing II. Surgery 2004; 22.
West JB. Respiratory physiology the essentials. 9th edn. 2012. Lip-
incott, Williams and Wilkins, 2012.
233 Ó 2017 Published by Elsevier Ltd.