Breathing of 100% O2 just for a few minutes before and during commencement of anesthesia, increases the safety margin in the event of difficult intubation of the airway with prolonged apnea. However there turned out to be a price for it.
Have a nice day
Respiratory function and importance to anesthesia final
Respiratory function and
importance to anesthesia
The principal function of the lungs is to allow gas exchange
between blood and inspired air.
1) Aerobic respiration
Nearly all human cells derive energy aerobically (i.e. by using
Carbohydrates, fats and proteins are metabolized to two carbon
fragments (acetyl-CoA) that enter the citric acid cycle within
Acetycl-CoA is metabolized to CO2- energy is derived and stored
in nicotinamide adenine dinucleotide (NDA), flavin adenine
dinucleotide (FAD), and guanosine triphosphate (GTP).
Energy is subsequently transferred to adenosine triphosphate
(ATP) through a process called oxidative phosphorylation.
2) Anaerobic respiration
In the absence of O-2, ATP can be produced only from the
conversion of glucose to pyruvate to lactic acid.
When O2 tension is restored to normal, lactate is reconverted to
pyruvate and aerobic metabolism is resumed.
Effects of anesthesia on Cell metabolism
General anesthesia typically reduces both oxygen consumption
and CO2 production by about 15%.
The greater reductions are in cerebral and cardiac O 2
MUSCLES OF RESPIRATION
I) Inspiratory muscles
A) During normal breathing
Contraction of diaphragm cause base of thoracic cavity to
descent 1.5 to 7 cm in deep inspiration.
Responsible for 75% of the change in intrathoracic volume
during quiet inspiration.
2) External intercostals muscles
B) During forced inspiration
Also other accessory muscles like sternocleidomastoid, scalene and
pectoralis major muscle play role.
II) Expiratory muscles
A) During normal breathing – Expiration is passive process occur
due to elastic recoil of lung.
B) During forced expiration - abdominal muscles and internal
intercostals muscle play role.
Mechanism of ventilation
The movement of lungs are determined by impedance of the
respiratory system which can be divided into the –
1) Elastic resistance of tissue and gas liquid interface
It governs lung volume and the associated pressure under static
2) Non elastic resistance to gas flow
It relates to frictional resistance to airflow and tissue deformation.
1) Elastic resistance
The lung and the chest wall are elastic structure. In between lung
and chest wall, a thin layer of fluid is present by which lung slide
easily on the chest wall but resist being pulled away from it.
Due to elastic recoil of the chest wall, chest wall has a tendency to
expand outward and lungs has tendency to collapse due to elastic
recoil of lung.
At the end of quiet expiration, the elastic recoil of the chest wall is
just balanced by the elastic recoil of lung.
If the chest wall is opened, the lung collapse and if the lung lose
their elasticity, the chest wall expands and become borrow shaped.
The recoil property of chest wall due to structure component that
resist deformation and probably include chest wall muscle tone. The
elastic recoil of the lung is due to their high content of elastin fibre
and the surface tension forces acting at the airfluid interface in
Surface tension forces
Surface tension forces tend to reduce the area of interface and
favour alveolar collapse.
According to Laplace law
So alveolar collapse is directly proportional to surface tension but
inversely proportional to alveolar size. Collapse is more likely
when surface tension increases or alveolar size decrease.
The surface tension of the alveoli is reduced by the surfactant
which is secreted by type II pneumocyte .
Ability of surfactant to lower surface tension is directly
proportional to its concentration with in alveolus.
In smaller alveoli
↓ ↓ surface tension
In larger alveoli
Surfactant are less
Relative ↑ in
Prevent overdistens of alveoli
Compliance of respiratory system
Elastic recoil is usually measured in terms of compliance which is
defined as the change in volume divided by change in
Compliance of lung =
Change in lung volume
Change in transpulmonary pressure
Transpulmonary pressure – The pressure needed to keep the
lung inflated at a certain volume, i.e pleural minus alveolar
pressure ,is known as transpulmonary pressure.
Normal lung compliance is 0.2-0.3L/cm of H2O (2-3 L/k Pa)
Pressure volume relationships of lung
• It is typical of an elastic structure.
pleural pressure is lower in upper regions.
• Regional transpulmonary pressure is thus higher for apical lung units than for basal ones in an
• The consequences will be that lower lung regions expand more for a given increase in
transpulmonary pressure than the upper units do.
• Thus ventilation goes preferably to the lower lung regions.
Compliance is critically dependent on the lung volume at which it is
Change in pressure volume curve in different disease
Fibrotic lung disease
Granulomatous diseases like sarcoidosis
Interstitial and alveolar edema
Emphysema (loss of elastic tissue)
Examples of pressure volume curves of the lung in health and lung disease. The much
flatter slope of the curve in fibrotic lung disease which reflects a considerable increase in
pressure variation and respiratory work. Parallel shift in the pressure volume curve of an
asthmatic and bronchitic patient, which shows that compliance need not change in these
diseases, although lung volume may have increased. Finally note the sleep slope of the
curve of an emphysematous patient. This indicates loss of elastic tissue and might even
suggest reduced respiratory work.
Compliance of chest wall
Compliance of chest wall =
Change in chest volume
Change in transthoracic pressure
* Transthoracic pressure equals atmospheric pressure minus
Normal value 0.2 L/cm H2O
Compliance of chest wall reduce : Obesity
Condition causing generalized edema
Joint disorder like amkylosing spondylitis.
These are important parameter in respiratory physiology and
clinical practice. Lung capacities are clinically useful measurement
that represent a combination of two or more volumes.
Average adult value
Tidal volume (V-T)
Volume of air that is expired and
inspired during normal breath
Inspiratory reserve volume (IRV)
Maximum additional volume that
can be inspired above tidal volume
Expiratory reserve volume (ERV) Maximum volume that can be
expired below tidal volume
Residual volume (RV)
Volume remaining after maximal
Total lung capacity (TLC)
RV+ERV+VT + IRV
Diagram showing respiratory excursions during normal breathing and
during maximal inspiration and maximal expiration
Functional residual capacity (ERV+RV)
FRC determined by the balance between the inward elastic recoil
of the lungs, and the outward recoil of the thoracic cage.
FRC decreases with paralysis and anaesthesia.
Other factor effect the FRC:
o Body size (increases of about 32-51 ml/cm of height)
o Gender (10% less in women of same height)
o Posture (supine posture decreases FRC by 0.5-1.0 litre in an
o Lung pathology.
Measuring FRC – 3 main approaches
1) Nitrogen washout
2) Helium wash-in
3) Body plethysmography
Closing volume (CV)
Small airway lacking cartilaginous support depend on radial
traction caused by the elastic recoil of surrounding tissue to
keep them open.
The volume above RV at which airways begin to close
during expiration is called closing volume.
Closing capacity (CC)
Sum of RV and closing volume is called closing capacity.
Airway closure is normal physiological phenomenon and is the
effect of increasing pleural pressure during expiration.
When pleural pressure became “positive”, it will exceed the
pressure inside the airway which is just or nearly atmospheric
at a low flow rate.
Higher pressure outside than inside will comprises the airway
and may close it.
There is a vertical pleural pressure gradient with a difference of approximately 7.5cm H 2O between the
upper most and lowermost regions, Causes a transpulmonary pressure gradient with higher pressure inside
the airway and alveolus in the upper part and higher pressure outside the alveolus and airway in the lower
part, This results in closure of the airways in lower part.
In young subjects airway closure may not occurs until they
have expired to RV.
With increasing age of 65 to 70 years, airway closure may
occurs above FRC.
This means that in elderly subjects, dependent regions are
intermittently closed during the breath, it is the major
explanation of why arterial oxygenation decreases with age.
In supine position FRC is reduced where as CC is not affected
by body position, so closure of airways may occur above FRC
even in young subjects.
In 70 years old subjects, in supine position, the airways may be
continuously closed if CC exceeds FRC plus VT.
Airway closure occurs at higher lung volumes in patients with
i. Obstructive lung disease
ii. Secretions, edema of the airway wall
iii. Increase bronchial muscle tone.
Vital capacity (VC)
It is the maximal volume of air which can be expelled from
lungs by forcefull effort following a maximal inspiration in
addition to body habits.
VC is also dependent on respiratory muscle strength, and
chest lung compliance.
Normal VC is ~60-70ml/kg.
II) Non elastic resistance
Normal total airway resistance is about 0.5-2cm H2O
Resistance is mainly contributed by medium sized bronchi.
Resistance in larger airway is low because of their larger
diameter, whereas resistance is smaller airway is also low
because of their large total cross sectional area.
The most important cause of increased airway resistance include
bronchospasm, secretions and mucosal oedema as well as volume
related and flow related airway collapse.
A) Volume related airway collapse
At low volume airway resistance become inversely proportional
to lung volume.
Increasing lung volume upto normal with positive end expiratory
pressure (PEEP) can reduce airway resistance.
B) Flow related airway collapse
During forced exhalation, reversal of normal transmural airway
pressure can cause collapse of these airway (dynamic airway
This is because of if generation of a positive pleual pressure
and if large pressure drop across intrathoracic airway.
The point along the airway where dynamic compression occurs
is called the equal pressure point. This equal pressure point
move towards smaller airway as lung volume decreases.
Emphysema and asthma predisposes patient to dynamic airway
compression. Emphsema destroys the elastic tissues that
normally support smller airway.
Forced vital capacity
Measuring vital capacity as an exhalation that is as hard and as
rapid as possible provides important information about airway
The ratio of the forced expiratory volume is 1s (FEV1) to the
total forced vital capacity (FVC) is proportionate to the degree
of airway obstruction.
Normally, FEV1/FVC >80%
Forced mid expiratory flow (FEV25-75%) is effort independent
and a more reliable measurement of obstruction.
Work of breathing
Component that make up the work of breathing during quiet
inspiration are :I)
Non elastic work
Viscous resistance (7%)
Airway resistance (28%)
II) Elastic work (65%)
VENTILATION PERFUSION RELATIONSHIP
Ventilation is usually measured as the sum of all exhaled gas
volumes in 1 min (minute ventilation, or V). if VT is constant.
Minute ventilation = respiratory rate × tidal volume
For the average adult at rest, minute ventilation is about 5L/min.
Some of the inspiratory gas remain in the airway and not take part
in alveolar gas exchange,is known as Dead space,
Dead space may be –
Apparatus dead space
Anatomical dead space
Alveolar dead space
Anatomical dead space – related to the volume of conducing
Alveolar dead space – related to alveoli that are well ventilated
but poorly perfused.
Physiological dead space – sum of anatomical dead space and
alveolar dead space
In upright position – dead space is normally about 150ml for
most adult (~2ml/kg)
Dead space is approximately 30% of VT.
PACO2= alveolar CO2 tension.
PECO2= mixed expired CO2 tension.
Distribution of ventilation
Alveolar ventilation is unevently distributed in the lungs.
Right lung receives more ventilation than the left one (53%
versus 47%), and lower (dependent) areas of both lungs tend to
be better ventilated than do not the upper areas because of a
gravitationally induced gradient in intrapleural pressure.
Pleural pressure increase by 0.3cmH2O/cm vertical distance.
Because of a higher transpulmonary pressure, alveoli in upper
lung areas are near maximally inflated and relatively
noncompliant, and they undergo little expansion during
In contrast, the smaller alveoli in dependent areas have a lower
transpulmonary pressure, are more compliant, and undergo
greater expansion during inspiration.
Approximately 5L/min of blood flowing through the lungs,
only about 70-100mL at any one time is within the pulmonary
capillaries undergoing gas exchange.
Small increases in pulmonary blood volume normally occur
during cardiac systole and with each normal (spontaneous)
A shift in posture from supine to erect decreases pulmonary
blood volume (upto 27%).
Changes in systemic capacitance also influence pulmonary
blood volume: systemic venoconstriction shift blood from the
systemic to the pulmonary circulation, whereas vasodilation
causes a pulmonary to systemic redistribution.
Hypoxia is a powerful stimulus for pulmonary vasoconstriction.
Distribution of pulmonary perfusion
Pulmonary pressure increases down the lung by 1cm H2O/cm
This cause pressure difference between apex to base of 11 to
Vertical distribution of blood flow in the
Zone I :
Alveolar pressur > vascular pressure
Zone II :
Pulmonary arterial pressure >alveolar
pressure whcih in trun exceeds venous
Increase blood flow
Both arterial and venous pressure exceed
alveolar pressure, so perfusion pressure is
arterial minus venous pressure.
In the bottom of lung decrease in blood flow
because of increase in interstitial pressure
comprising extraalveolar vessels..
Causes of Hypoxemia and Hypercapnia
Shunting of deoxygenated blood past the lung
Diffusion impairment (grossly abnormal lungs)
Defined as ventilation that results in a PaCO2 above 45mmHg.
Present when minute ventilation is high if the metabolic demand
or dead space increases.
At rest, both ventilation and perfusion increase down the lung.
Perfusion increases more than ventilation.
The difference between upper most and lowermost 5cm
segment being 3 times for ventilation and 10 times for
V/Q ratio :
At apex = 5.0
At middle = 1.0
At bottom = 0.5
Shunting denotes the process whereby desaturated, mixed venous
blood from the right heart returns to the left heart without being
resaturated with O2 in the lungs.
The overall effect of shunting decrease (dilute) arterial O 2
content ; this type of shunt is referred to as right to left.
Intrapumonary shunts are often classified as absolute or relative.
Absolute shunt refers to anatomic shunts and lung units where
V/Q is zero. A relative shunt is an area of the lung with a low but
finite V/Q ratio.
In normal person, the amount of shunt is 2-3% (due to venous
blood flow from bronchi entering the pulmonary vein, as well as
coronary venous blood entering the left ventricle via thebesian
Pathological shunt –
o Obstructive lung disease
o Vascular disorders
TRANSPORT OF GASES
Most oxygen is carried in the blood as oxyhemoglobins.
Hb carrying about 1.39ml of O2 per gram of Hb.
The normal adult hemoglobin –oxygen dissociation curve
• Increase CO2 concentriction
• Increase temperature
• Increase 2-3 DPG (diphosphoglycerate) concentration
• Increase pH (acidosis)
• Decrease PO2
• Fetal blood
• Decrease pH (alkalosis)
• Decrease temperature
• Decrease 2-3 DPG
II) CO2 Transport
This is carried in three forms :• Dissolved
• As bicarbonate
• As carbamino compounds, especially carbamino haemoglobin
Respiratory function during anaesthesia
Lung volume and respiratory mechanics during
FRC is reduced by 0.8 to 1.01 by changing body position from
upright to supine, and there is another 0.4-0.5L decrease when
anesthesia has been induced.
End expiratory lung volume is thus reduced from approximately
3.5 to 2L, the latter being close or equal to RV.
Anesthesia per se causes a fall in FRC despite maintenance of
Compliance and resistance of the respiratory system
Resistance of the total respiratory system and the lungs during
anesthesia increase during both spontaneous breathing and
Atelectasis and airway closure during anesthesia
Atelectasis appears in approximately 90% of all patients, who
are anesthetized. It is seen during spontaneous breathing and
after muscle paralysis and whether intravenous or inhaled
anesthetics are used.
15-20% of the lung is regularly collapsed at the base of the lung
during uneventful anesthesia.
After thoracic surgery and cardiopulmonary bypass, more than
50% of the lung can be collapsed even several hours after surgery.
The amount of atelectasis decreases toward the apex, which is
There is a weak correlation between the size of the atelectasis and
body weight or body mass index (BMI).
Obese patients showing larger atelectasis areas than lean ones do.
The atelectasis is independent of age, with children and young
people showing as much atelectasis as elderly patients.
Patients with COPD showed less or even no atelectasis during the
45 minutes of anesthesia.
The mechanism that prevents the lung from collapse is not clear but
may be airway closure occurring before alveolar collapse takes
place, or it may be an altered balance between the chest wall and
the lung that counters a decrease in lung dimensions.
Cranial shift of the diaphragm
and a decrease in transverse
contribute to lowered functional
residual capacity (FRC) during
Decreased ventilated volume
(atelectasis and airway closure)
is a possible cause of reduced
Decreased airway dimensions
by the lowered FRC should
contribute to increased airway
Prevention of atelectasis during anesthesia
Several interventions can help prevent atelectasis or even reopen
The application of 10cm H2O PEEP has been tested in several
studies and will consistently reopen collapsed lung tissue.
The persistence of shunt may be explained by a redistribution of
blood flow toward more dependent parts of the lungs when
intrathoracic pressure is increased by PEEP.
Under such circumstances, any persisting aatelectasis in the
bottom of the lung receives a larger share of the pulmonary blood
flow than without PEEP.
Increased intrathoracic pressure will impede venous return and
decrease cardiac output. This results in a lower venous oxygen
tension for a given oxygen uptake and reduces arterial oxygen
Second the lung recollapses rapidly after discontinuation of
PEEP. Within 1 minute after cessation of PEEP the collapse is as
large as it was before the application of PEEP.
Maintenance of muscle tone
Use of an anesthetic that allows maintenance of respiratory
muscle tone will prevent atelectasis from forming.
Ketamine does not impair muscle tone and does not cause
Another technique used in an attempt to restore respiratory
muscle tone in pacing of the diaphragm by applying phrenic
nerve stimulation, which did reduce the atelectatic area.
The use of sigh maneuver or a double VT has been advocated to
reopen any collapsed lung tissue.
For complete reopening of all collapsed lung tissue,an inflation
pressure of 40cm H2o is required.such a large inflation
corresponds to a maximum spontaneous inspiration, called VC
Minimizing gas resorption
Ventilation of the lungs with pure oxygen after a VC maneuver
that had reopened previously collapsed lung tissue resulted in
rapid reappearance of the atelectasis.
If one the other hand, 40% O2 in nitrogen is used for ventilation
of the lungs, atelectasis reappears slowly and 40 minutes after the
Breathing of 100% O2 just for a few minutes before
and during commencement of anesthesia, increases
the safety margin in the event of difficult intubation
of the airway with prolonged apnea.
Avoidance of the preoxygenation procedure (ventilation with
30% O2) eliminated atelectasis formation during induction and
Preoxygenation can also be provided without producing
atelectasis if undertaken with continuously increased airway
pressure, as with continuous positive airway pressure (CPAP).
Postanesthetic oxygenation (100% O2) 10 minutes before
termination of anesthesia together with a VC maneuver at the end
This is most likely the effect of first reopening collapsed tissue
and then under the influence of 100% O2 derecruiting previously
opened lung tissue.
A VC maneuver followed a lower O2 concentration, 40% kept the
lung open after recruitment until the end of anesthesia.
Intermittent closure of airways can be expected to reduce the
ventilation of dependent lung regions.
Such lung regions may then become “low VA/Q” units if
perfusion is maintained or not reduced to the same extent as
Because anesthesia causes a reduction in FRC of 0.4-0.5L, it may
be anticipated that airway closure will become more prominent
in an anesthetized subjects.
A simple three compartment lung model can be constructed to
explain the impaired oxygenation during anesthesia.
Three compartment model
Upper part of the lung, the alveoli
and airways are open (Zone A).
Middle and lower parts of the lung,
the airways are intermittently closed
and impede ventilation (Zone B).
The bottom of lung, the alveoli have
collapsed (atelectasis, Zone C).
Distribution of ventilation and blood flow during
Distribution of ventilation
Ventilation was shown to be distributed mainly to the upper lung
regions, and there was a successive decrease down the lower half
of the lung.
PEEP increases dependent lung ventilation in anesthetized
subjects in the lateral position.
More even distribution between the upper and lower lung regions
have also been made in supine anesthetized humans after previous
inflation if the lungs, similar to PEEP.
Thus, restrotation of overall FRC toward or beyond the awake
level returns gas distribution toward the awake pattern.
Distribution of lung blood flow
PEEP causes a redistribution of blood flow toward dependent lung
Forcing blood volume downward to the dorsal side of the lungs
may increase fractional blood flow an atelectatic region.
Ventilation perfusion matching during anesthesia
Dead space, shunt,
Both CO2 elimination and oxygenation of blood are impaired in
patients during anesthesia.
The impended CO2 elimination can be attributed to increased
dead space ventilation.
Anatomic dead space is unchanged, indicating that the “alveolar”
dead space must have increased during anesthesia.
The impaired CO2 elimination is most easily corrected by
increasing the ventilation.
The impairment is arterial oxygenation during anesthesia is
generally considered to be more severe at higher ages, obesity
worsens the oxygenation of blood and smokers show more
impairment in gas exchange than nonsmokers do.
Effects of anesthetics on respiratory drive
Spontaneous ventilation is frequently reduced during anesthesia.
Thus inhaled anesthetics, as well as barbiturates for intravenous
use, reduce sensitivity to CO2.
Anesthesia also reduces the response to hypoxia. Attenuation of
the hypoxic response may be attributed to an effect on the carotid
Factors that influence respiratory function during
During spontaneous breathing, the lower, dependent portion of
the diaphragm moved the most, whereas with muscle paralysis,
the upper, nondependent part showed the largest displacement.
Increased oxygen fraction
When FIO2 was increased to 0.5 an increase in shunt of 3% to
4% was noticed.
Thus a certain dependence on FIO2 appears to exist, explained
by attenuation of the HPV response with increasing FIO2 or
further development of atelectasis and shunt in lung units with
Because FRC is dramatically reduced by the combined effect of
the supine position and anesthesia, it might be advantageous to
choose a more upright position in an anesthetized subject to
Arterial oxygenation is further impeded with increasing age of
There appears to be increasing VA/Q mismatch with age, with
enhanced perfusion of low VA/Q regions both in awake subjects
and when they are subsequently anesthetized.
Major cause of impaired gas exchange during anesthesia at ages
younger than 50 years is shunt, whereas at higher ages
Obesity worsens the oxygenation of blood.
A major explanation appears to be a markedly reduced FRC,
which promotes airway closure to a greater extent than in a
Pre-existing lung disease
Smokers and patients with lung disease have more severe
impairment of gas exchange in the awake state than healthy
subjects do and this difference also persists during anesthesia.
Ventilatory effects of regional anesthesia depend on the type
and extension of motor blockade.
With extensive blocks that include all the thoracic and lumbar
segments, inspiratory capacity is reduced by 20% and
expiratory reserve volume approaches zero. Diaphragmatic
function however, is often spared.