RESPIRATORY PHYSIOLOGY

BY moderator
Dr Dhanesh Dr Chaithanya
Postgraduate SENIOR RESIDENT
Dept. of Anesthesia DEPT. OF ANAESTHESIA, DH BALLARI

1
 INTRODUCTION

Supplies the body with oxygen and disposes off carbon dioxide

Filters inspired air

Produces voice

Clears the body from excess water and heat

Control blood pH

2
 AIRWAY
Primary function is to
obtain oxygen for use
by body's cells &
eliminate carbon
dioxide that cells
produce

• Upper airway
• nose -------- > vocal cords
Nose---> distal alveolus
• Lower airways
• trachea ------- > alveoli
3
4
 Breathin
g
Breathing (pulmonary ventilation) consists of two cyclic
phases:

Inhalation, also called inspiration - draws gases into the

lungs.

Exhalation, also called expiration - forces gases out of

the lungs.
5
 Respiratory events

Pulmonary ventilation = exchange of gases between lungs and atmosphere

External respiration = exchange of gases between alveoli and pulmonary

capillaries

Internal respiration = exchange of gases between systemic capillaries and

tissue cells AKA cellular respiration

6
 MUSCLES OF RESPIRATION-DIAPHRAGM,
EXTERNAL INTERCOSTALS, SCALENE

 The major muscles of respiration include the

 diaphragm
 the external intercostals
 scalene
 Skeletal muscles
 provide the driving force for ventilation
 the force of contraction increases when they are stretched
and decreases when they shorten.
 The force of contraction of respiratory muscles increases at larger lung
volumes.
 The process of respiration or gas exchange begins with the act of
inspiration, which is initiated by contraction of the diaphragm.
7
PHASES OF PULMONARY
VENTILATION
• Inspiration, or inhalation - A very active process that
requires input of energy. The diaphragm contracts,
moving downward and flattening.
• Expiration, or exhalation - A passive process that takes
advantage of the recoil properties of elastic fiber. The
diaphragm relaxes. The elasticity of the lungs and the
thoracic cage allows them to return to their normal size
and shape.
• This two processes are happens when phrenic nerves
Stimulates.
8
 Inhalation

• Breathing in is called inhalation (inspiration)

• Each inhalation, the air pressure inside the lungs is equal to the air
pressure of the atmosphere, which is about 760 mmHg.
• Air to flow into the lungs, the pressure inside the alveoli
must become lower than the atmospheric pressure.
• This condition is achieved by increasing the size of the lungs.

9
 Exhalation

Breathing out or exhalation starts when the inspiratory muscles relax. As the diaphragm relaxes, its dome
moves superiorly owing to its elasticity. As the external intercostals relax, the ribs are depressed.
• The pressure in the lungs is greater than the pressure of the atmosphere.

• Normal exhalation during quiet breathing is a passive process. Instead, exhalation results from elastic
recoil of the chest wall and lungs, both of which have a natural tendency to spring back after they have
been stretched.
• Two inwardly directed forces contribute to elastic recoil:

a. The recoil of elastic fibers that were stretched during inhalation

b. The inward pull of surface tension due to the film of alveolar fluid.
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11
External respiration or pulmonary gas exchange

• It is the diffusion of O2 from air in the alveoli of the lungs to blood

in pulmonary capillaries and the diffusion of CO2 in the opposite

direction.

• External respiration in the lungs converts deoxygenated blood

(depleted of some O2) coming from the right side of the heart into
12
 Internal respiration

The left ventricle pumps oxygenated blood into the aorta

and through the systemic arteries to systemic
capillaries. The exchange of O2 and CO2 between systemic
capillaries and tissue cells is called internal respiration
or systemic gas exchange

13
 Lung mechanics- Compliance(CL)
 is a measure of the elastic properties of the lung.

 It is a measure of how easily the lung is distended.

 is defined as the change in lung volume resulting from a 1-cm H2O
change in the distending pressure of the lung.
 The units of compliance are mL (or L)/cm H2O.
 High lung compliance refers to a lung that is readily distended.
 Low lung compliance, or a "stiff" lung, is a lung that is not easily
distended.
14
 Airflow in
Airways
 There are two major patterns of gas flow in the airways-
laminar and turbulent flow.
 Laminar flow is parallel to the airway walls and is present at low

flow rates.
 As the flow rate increases and particularly as the airways divide, the

flow stream becomes unsteady and small swirls occur.

 At higher flow rates, the flow stream is disorganized and

turbulence occurs. French physician 15

16
 Airway Resistance

 Airflow resistance is the second major factor that determines rates of

airflow in the airways.
 Airflow resistance in the airways (Raw) differs in airways of different
size.
 In moving from the trachea toward the alveolus, individual airways become
smaller while the number of airway branches increases dramatically.
 Raw is equal to the sum of the resistance of each of these airways (i.e., Raw =
Rlarge + Rmedium + Rsmall).
 The major site of resistance along the bronchial tree is the
large bronchi.
 The smallest airways contribute very little to the overall total resistance of the bronchial
17
tree
In a normal lung, most of the resistance to airflow occurs in
the first eight airway generations
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Surface tension forces
• Surface tension forces tend to reduce the area of interface
and favour alveolar collapse.

According to Laplace law

2T 2×surface tension
Pressure = =
Radius
R

• 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. 19
• 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.

Surfactant are
  surface tension Prevent collapse
more concentrate

Surfactant are less Relative  in Prevent over-

concentrated surface tension distens of alveoli

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 II) Non elastic resistance
• Resistance in larger airway is low because of their diameter,and
resistance in smaller airway is also low
• Resistance is mainly contributed by medium sized bronchi because of
their large total cross sectional area.
• Normal total airway resistance is about 0.5-2cm H2O
• The most important cause of increased airway resistance include
bronchospasm, secretions and mucosal oedema as well as volume
related and flow related airway collapse

21
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.

22
23
B) Flow related airway collapse
•During forced exhalation, reversal of normal transmural airway pressure can
cause collapse of these airway (dynamic airway compression).
•This is because of 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 smaller airway.
24
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
transpulmonary pressure.
Change in lung volume
Compliance of lung =
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)

Compliance is critically dependent on the lung volume at which it

25
 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 upright subject.

 The consequences will be that lower lung regions expand more for a given
increase in transpulmonary pressure than the upper units do.
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 Thus ventilation goes preferably to the lower lung regions.
Change in pressure volume curve in different disease

Right shift : Left shift

1. Fibrotic lung disease •Emphysema (loss of elastic

2. Idiopathic fibrosis
tissue) Chronic
3. Alveolar proteinosis

4.Granulomatous diseases like bronchitis

sarcoidosis
5.Interstitial and alveolar edema •Asthma
27
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. 28
Compliance of chest wall
Change in chest volume
Compliance of chest wall =
Change in transthoracic pressure

* Transthoracic pressure equals atmospheric pressure

minus intrapleural pressure.
Normal value 0.2 L/cm H2O

Compliance of chest wall reduce :-

 Obesity
 Condition causing generalized edema
 Joint disorder like ankylosing spondylitis.
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 LUNG
VOLUMES
• Minute ventilation (MV): if RR is 12breaths/min, 500mL/breath = 6
liters/min. total lung capacity.
• TIDAL VOLUME (TV): Volume inspired or expired with each normal breath. = 500
ml
• INSPIRATORY RESERVE VOLUME (IRV): Maximum volume that can be inspired over the
tidal volume/normal breath.
• Used during exercise/exertion.= Male 3100 ml/ Female 1900 ml

• EXPIRATRY RESERVE VOLUME (ERV): Maximal volume that can be expired after the
expiration of a tidal volume/normal breath. = Male 1200 ml/ Female 700 ml
• RESIDUAL VOLUME (RV): Volume that remains in the lungs
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after a maximal expiration. Male 1200 ml/ Female 1100 ml
• Inspiratory capacity : sum of tidal volume & inspiratory reserve volume:
(IRV + TV)(3100+500ml=3600 ml in males, and 1900+500ml=2400 ml in
females).
• Functional residual capacity: sum of residual volume and expiratory reserve
volume, ERV + RV (1200 ml+1200=2400ml in males and 1100+700=1800 ml in
females).
• Vital capacity is the sum of inspiratory reserve volume, tidal volume, and
expiratory reserve volume, IRV + TV + ERV = IC + ERV (4800 ml in males and
3100 ml in females).
• Total lung capacity is the sum of vital capacity and residual volume IRV+ TV +
ERV + RV = IC + FRC (4800 ml +1200=6000 ml in males and 3100+1100=4200
31
32
 Measurement o f Lung Volumes
 RV and TLC can be measured in two ways:
 helium dilution
 body plethysmography.

 Both are used clinically and provide valuable information about lung
function and lung disease.

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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:
 Body size (increases of about 32-51 ml/cm of height)
 Gender (10% less in women of same height)
 Posture (supine posture decreases FRC by 0.5-1.0 litre in an adult)
 Lung pathology.

34
 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.

35
 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 compresses the airway

and may close it.
36
There is a vertical pleural pressure gradient with a difference of approximately 7.5cm H2O
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
37
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.

38
•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 still higher lung volumes in patients with
i. Obstructive lung disease
ii. Secretions, edema of the airway wall
iii.Increase bronchial muscle tone.
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 VITAL CAPACITY
•It is the maximal volume of air which can be expelled from lungs by
forceful 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. Measuring FRC – 3 main approaches:
1) Nitrogen washout
2) Helium wash-in
3) Body plethysmography
40
 Forced vital capacity

Measuring vital capacity as an exhalation that is as hard and as rapid as possible

provides important information about airway resistance.

 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. 41
 Work of breathing
Component that make up thework of breathingduring
quiet inspiration are :-
I) Non elastic work

a. Viscous resistance (7%)

b. Airway resistance (28%)

II) Elastic work (65%)

42
VENTILATION PERFUSION
RELATIONSHIP
Ventilation
Ventilation is usually measured as the sum of all exhaled
gas volumes in 1 min (minute ventilation, or V).

Minute ventilation = respiratory rate × tidal volume if VT is

constant
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 43
Anatomical dead space – related to the volume of conducing passage.

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.

VD PACO2- PECO2
= =
VT PACO2 0.3

PACO2= alveolar CO2 tension.

44
PECO2= mixed expired CO2 tension.
Factors effecting dead space

45
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

lung
upper areas are near maximally inflated and
noncompliant, relatively and they undergo little
inspiration. expansion during
 In contrast, the smaller alveoli in dependent areas have a lower
transpulmonary pressure, are more compliant, and undergo
greater expansion during inspiration.
46
 Pulmonary perfusion

 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) inspiration.
 A shift in posture from supine to erect decreases
pulmonary blood volume (upto 27%).
47
 Distribution of pulmonary perfusion
• Changes in systemic capacitance also influence pulmonary
blood volume: systemic venoconstriction shift blood from the
systemic to the pulmonary circulation, whereas vasodilation causes
a pulmonaryc to systemic redistribution.
• Hypoxia is a powerful stimulus for pulmonary vasoconstriction
Pulmonary pressure increases down the lung by 1cm H2O/cm
distance.
• This cause pressure difference between apex to base of 11 to
15mmHg.

48
 perfusion pressure is arterial minus venous
pressure.

Vertical distribution of blood flow in the lung

Zone I :
Alveolar pressur > vascular pressure
No perfusion
Zone II :
Pulmonary arterial pressure
pressure whcih >alveolartrun exceeds
in pressure. venous
Distance
Increase blood flow
Zone III:
Both arterial and venous pressure exceed
alveolar pressure,
Zone IV:
Blood flow In the bottom of lung decrease in blood flow
because of increase in interstitial pressure
comprising extraalveolar vessels..

49
Causes of Hypoxemia and Hypercapnia
 Hypoventilation
 Shunting of deoxygenated blood past the lung
 Ventilation/perfusion mismatched.
 Diffusion impairment (grossly abnormal
lungs)
Hypoventilation
 Defined as ventilation that results in a PaCO2 above 45mmHg.

 Present when minute ventilation is high if the metabolic demand

or dead space increases.

50
Ventilation/perfusion mismatched
 At rest, both ventilation and perfusion increase down the lung.
 Perfusion increases more than ventilation.
 The difference between upper most and lowermost 5cm
segment times for ventilation and 10 for
being 3 times
perfusion.
V/Q ratio :
At apex = 5.0
At middle = 1.0
At bottom =
0.5 51
Shunts
 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 O2

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.

52
 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
vein).
 Pathological shunt –
o Obstructive lung disease
o Vascular disorders
o Atelectasis
o Consodilation

53
TRANSPORT OF GASES

I)Oxygen transport

 Most oxygen is carried in the blood as oxyhemoglobins.

 Hb carrying about 1.39ml of O2 per gram of Hb.

54
55
Right shift
 Increase CO2 concentriction
 Increase temperature
 Increase 2-3 DPG (diphosphoglycerate) concentration
 decrease in pH (acidosis)
 Decrease PO2
 Anaemia
Left shift
 Fetal blood
 increase pH (alkalosis)
 Decrease temperature
 Decrease 2-3 DPG 56
57
II) CO 2

Transport

This is carried in three forms :-

 Dissolved
 As bicarbonate
 As carbamino compounds, especially carbamino haemoglobin

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59
Respiratory function during
anaesthesia
Lung and respiratory mechanics during
volume
anesthesia
Lung
 FRCvolume
is reduced by 0.8 to 1.0L 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
spontaneous breathing.

60
Compliance and resistance of the respiratory system
 Resistance of the total respiratory system and the lungs during
anesthesia increase during both spontaneous breathing
and mechanical ventilation.

Atelectasis and airway closure during anesthesia

Atelectasis
 Atelectasis appears in approximately 90% of all patients, who
are anesthetized. It is seen during spontaneous breathing
after muscle paralysis and whether intravenous or inhaled
and
anesthetics are used.
 15-20% of the lung is regularly collapsed at the base of the lung
during uneventful anesthesia.

61
 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 mostly spared.
 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.
62
• 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.

63
Cranial shift of the
and a decrease in
diaphragm
diameter of transverse
contribute to lowered
thefunctional
residual capacity (FRC)
thoraxduring
anesthesia.
Decreased ventilated volume
(atelectasis and airway closure)
is a possible cause of reduced
lung compliance.
Decreased airway dimensions
by the lowered FRC should
contribute to increased airway
resistance (Raw).
64
Prevention of atelectasis during anesthesia
• Several interventions can help prevent atelectasis or even reopen collapsed
tissue.
• 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 atelectasis in the bottom of the lung
receives a larger share of the pulmonary blood flow than without PEEP.
65
• 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 tension.

• 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.

66
 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
collapse.

 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.

67
Recruitment maneuvers
 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
maneuver

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
68
VC maneuver only 20% of the initial atelectasis had reappeared.
 Breathing of 100% O 2
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.

69
 Avoidance of the preoxygenation procedure (ventilation with
30% O2) eliminated atelectasis formation during induction and
subsequent anesthesia.
 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
of anesthesia.
 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. 70
Airway Closure
 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
 ventilation.
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.

71
Three compartment model
of the lung in an
anesthetized subject.
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).

72
ventilation and blood flow during anesthesia
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
subjects in the lateral position.
anesthetized
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.
73
Distribution of lung blood flow

PEEP causes a redistribution of blood flow toward dependent lung

regions.
Forcing blood volume downward to the dorsal side of the lungs may
increase fractional blood flow an atelectatic region.

74
Ventilation perfusion matching during anesthesia
Dead space, shunt, and ventilation perfusion
relationships
 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.
75
 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
body chemoreceptors.

76
Factors that influence respiratory function during
anesthesia
Spontaneous breathing
 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 77
• Body position : 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 preserve FRC

• Arterial oxygenation is further impeded with increasing age of the patient.

• 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 mismatch becomes increasingly important.
78
Obesity
 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
normal subject.

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.

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Regional 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.

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 Regulation of respiration
• Regulation of respiration control is the rate and depth of respiration
as per the physiologic demand. Control of respiration primarily
involves neurons in the reticular formation of the medulla and pons.
Because the medulla sets the respiratory rhythm. The purpose of
Regulation of respiration are

1. To maintain a constant O2 and CO2 level in blood

2. It adjust the O2 supply as per the metabolic demand of the
body.
3. It helps to regulate acid base balance or pH.

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• The size of the thorax is altered by the action of the respiratory muscles, which
contract as a result of nerve impulses transmitted to them from centers in the brain
and relax in the absence of nerve impulses. This impulses travels along the phrenic
and intercostal
nerves to excite the diaphragm and external intercostal muscles

• These nerve impulses are sent from clusters of neurons located bilaterally in the
medulla oblongata and pons of the brainstem.

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Mechanism of Regulation of respiration

• There are two major mechanisms

1. Nervous regulation of respiration
2. Chemical regulation of respiration

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 1. Nervous regulation of respiration

Respiratory Center
The respiratory centers are divided into four major groups, two
groups in the medulla and two in the pons.
The two groups in the medulla are
a. The dorsal respiratory group
b. The ventral respiratory group.
The two groups in the pons are the pneumotaxic center and the
apneustic center also known as the pontine respiratory group.

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• Respiratory centers can be divided into three areas on
the basis of their functions:
1. The medullary rhythmicity area in the medulla oblongata
2. The pneumotaxic area in the pons
3. The apneustic area, also in the pons

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 Medullary Rhythmicity Area
• The function of the medullary rhythmicity area is to
control the basic rhythm of respiration. It includes
two areas

a. Inspiratory medullary rhythmicity area or

inspiratory centre
b. Expiratory medullary rhythmicity area or expiratory
centre

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a. Inspiratory centre:
It establish the basic rhythm of breathing. When
its inspiratory neurons fire, a burst
impulses along the of
travels
intercostal nerves to excitephrenic
diaphragm
and
the and external
intercostal muscles.
b. Impulses
Expiratory centre:the expiratory area cause
from the internal intercostal and
contractionof
abdominal muscles, which decreases the size of
the thoracic cavity and causes forceful
exhalation.
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Pneumotaxic Area
• It transmits inhibitory impulses to the inspiratory area. The major
effect of these nerve impulses is to help turn off the inspiratory
area before the lungs become too full of air.

APNEUSTIC AREA

• This area sends stimulatory impulses to the inspiratory area that

activate it and prolong inhalation. The result is a long, deep
inhalation.

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2. Chemical regulation of respiration

• There are three important chemical

factors controlling respiration
1. Concentration of CO2 in blood
2. Concentration of H+ ions or pH
3. Concentration of oxygen In blood

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 Concentration of CO2 in
blood

• When CO2 concentration in blood increases,

it stimulates the chemoreceptors. There are
two group of chemoreceptors
1. Peripheral chemoreceptors – situated at the
carotid body and aortic body
2. Central chemoreceptors – situated at the
medulla oblongata

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 When CO2 concentration in blood increases

Stimulates the chemoreceptors

Transmission of sensory impulses to respiratory centers

Activation of respiratory centers

Increases the activities of respiration

(rate and Depth) Increase alveolar ventilation

Expulsion of CO2 and decreases the level of

CO2 in blood 93
 Concentration of H+ ions or pH

When Concentration of H+ ions increases, it stimulates the

peripheral chemoreceptors.
H+ ions diffuses with CO2 and form carbonic acid, to cross the blood
brain barrier then dissociates into H+ and HCO3. There by H+ ions
stimulates the central chemoreceptors then the respiratory centers,
resulting a reduction in the level of CO2 in blood. This will inturn decrease
concentration of H+ in blood or increase the pH in to normal.

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Concentration of oxygen In blood
When O2 concentration in blood decreases

Stimulates the peripheral chemoreceptors

Transmission of impulses to respiratory centers

Activation of respiratory centers

Increases the activities of respiration (rate and Depth)

Increase alveolar ventilation

Increases the uptake of O2

Thereby increases the level of O2 in blood 95

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 Normal Values
• Normal respiration: 12 – 16 breaths/min
• Normal Arterial blood gas values
– pH: 7.35 – 7.45
– Pa O2 : (80 to 100 mm Hg) and Sa O2 (95% to
98%)
– P CO2 : 35 – 45 mm Hg
– HCO3 : 22 – 27 mEq/L

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