Presenter-Dr.

Dhananjay
Moderator- Prof. L Deban Singh
RESPIRATORY PHYSIOLOGY
RESPIRATION

 External respiration- absorption of O2 and

removal of CO2 from the body as a whole.

 Internal respiration- utilization of O2 and

production of CO2 by the cells & gaseous
exchange between cells and blood.
RESPIRATORY SYSTEM

 Gas exchanging organ –Lungs.

 Ventilates the lung –Pump (chest wall,
respiratory muscles, areas in brain which
control respiration).
 The conducting airways
warm and humidify the
inspired air but are not a site
of gas exchange.

The combined
surface area of the The alveoli are composed
alveoli is of a single layer of
approximately that epithelial cells and are the
of a tennis court. site for gas exchange.
MECHANICS OF PULMONARY VENTILATION

 Inspiration- Active process- Diaphragm,

external intercostal muscles.
sternocleidomastoid, scaleni

 Expiration- Passive process- elastic recoil of lungs.

 Deep/Forceful expiration- Internal intercostal,
(active process) Ant. Abdominal muscles.
PRESSURES IN THE LUNGS AND CHEST

 Intra-alveolar pressure/Intrapulmonary pressure -the

pressure within the lungs.

 Intrapleural pressure is the pressure with in the pleural

cavity, ie between parietal pleura & visceral pleura
 Intrapleural pressure is always negative, less than
atmospheric pressure for whole life time.

 Transpulmonary pressure- difference between intra

alveolar & intra pleural pressure.
BOYLE’S LAW

 Changes in intrapulmonary pressure occur as a result

of changes in lung volume.
 Pressure of gas is inversely proportional to its volume.

 Increase in lung volume decreases intrapulmonary

pressure.
 Air goes in.

 Decrease in lung volume, raises intrapulmonary

pressure above atmosphere.
 Air goes out.
INSPIRATION

Diaphragmatic & ext intercostal contraction

increase in vertical & AP diameter

decrease in intra-thoracic and intra-pleural pressure (from -5 to -8 cm H2O)

decrease in intra-alveolar pressure (from 0 to -3)

 inflow of gas from atmosphere into the thoracic cavity.

 Ext intercostal bucket handle Ext intercostal  pump handle
movement Increase in Lateral movement  Increase in AP
diameter. diameter.
EXPIRATION

 Passive process under normal resting

conditions.
 50% energy expent during Insp stored as
potential energy.
 intra-pleural pressure returns to -5 cm
water and the original lung volume is restored
by the elastic recoil of the lung.
 Inspiration Expiration

0.5

During inspiration
Volume Change (L)
and expiration,
changes in 0

intrapleural -5 Intrapleural Pressure (cm H2O)

pressure alter
alveolar pressure, -8
which generates +0.5
a pressure Air Flow (L/sec)

0
gradient leading
to airflow and -0.5

volume changes. +1
Alveolar Pressure (cm H2O)

-1
ALVEOLI

 Polyhedral in shape and clustered like units of

honeycomb.
 ~ 300 million air sacs (alveoli).
 Large surface area (60–80 m2).
 Has Thick side ( 1-2 µm)- fluid & solute exchange.
Thin side (0.4 µm)- gas exchange.
 2 types of cells:
 Type I pneumocytes:
 Structural cells. Provides structural support. Prevents
entry of large molecules into alveoli.
 Not capable of cell division, not resistant to O2 toxicity.
 Type II pneumocytes:
 Largecells, numerous in number. Secrete surfactant.
Capable of cell division and resistant to O2 toxicity.
Dead Space
DEAD SPACE

 Volume of gas which doesn’t take part in

exchange.
 Physiological dead space=anatomical + alveolar
 Anatomical dead space is the space where there is
no exchange of gases in the conduction zone.
 Alveolar dead space arises from ventilation of
alveoli where there is little or no perfusion.eg.
1)zone1
2)pulmonary embolus
3)destroyed alveolar septa.
 VD /V T = 0.3 (2.2 ml/kg) approx. 150ml
 Clinical condition that modify anatomical dead space -
1) tracheal intubation
2) tracheostomy

 The most common causes of increased physiological dead space

are,
1) Decreased CO
2) Pulmonary embolism
3) ARDS
4) Therapeutic/supportive manipulation (IPPV, positive
airway pressure therapy).
Factor Effects

TABLE
Posture
Upright Increased
Supine Decreased

Position of airway
Neck extension Increased
Neck flexion Decreased

Age Increased

Artificial airway Decreased

Positive pressure ventilation Increased

Drugs like anticholinergics Increased

Pulmonary perfusion Increased

Pulmonary vascular disease Increased

PULMONARY VASCULATURE

 Blood supply to lungs

(i) Pulmonary artery-mixed venous blood
provides metabolic and O2 needs of alveolar
parenchyma beyond terminal bronchiole.
(ii) Bronchial artery- provides nourishment
from trachea down to terminal bronchioles and
also to pleura & hilar lymphnodes.
PHYSICAL PROPERTIES THAT AFFECT LUNG
FUNCTION
 Compliance

 Elasticity

 Surface tension
 Compliance(Distensibilty/strechability)
-defined as volume change per unit pressure
change.
- C= △V／ △P
-approximately 0.2L/cm H2O
RELATIONSHIP BETWEEN COMPLIANCE &
VOLUME
 Volume is directly proportional to compliance.
-bigger the volume, more the compliance
-Tall people, adults>children, M>F—more
compliance.
 Compliance is reduced:
 RLD- silicosis, ILD, TB
 Inflammation- pneumonia, pneumonitis.

 No change of compliance in Obst. Lung

diseases.
ELASTICITY

 Tendency of a substance to return to its initial

size after distension.
- lungs has high content of elastic proteins
- elastic tension increases during inspiration & decreases
during expiration.
 Elasticity is inversely proportional to
compliance– only true for elastic substances.
 Inelastic- both elasticity & compliance
decreases (TB fibrosis).
SURFACE TENSION (T)
 Force exerted by fluid in alveoli to resist
distension.
 There is very thin rim of fluid on the alveoli

Air-water interaction

surface tension
 Law of Laplace-pressure in alveoli is directly
proportional to T & inversely proportional to
radius of alveoli.
 P = 2T/r
Surfactant action is
maximum during expiration.
SURFACTANT

 Dipalmitoyl phosphatadyl choline.

 Secreted by Type II pneumocytes, amphipathic
molecule.
 Main function is to reduce surface tension.
 Surfactant molecules gets interpersed between water
molecules & reduces air-water interaction.
 Physiological significance
 It is beneficial to maintain alveolar volume (stability);
 It reduces interstitial fluid production, prevent pulmonary edema
& keeps alveoli always dry.
 It decreases inspiratory resistance, reduces inspiratory work &
help pulmonary ventilation & lung expansion.
 Production- starts at 18-20wks.
 Secretion/action- starts at 28wks.

 Maximum secretion occurs at 34-35wks.

 Glucocorticoids, thyroid hormones, prolactin,

estrogen & progesteron increases production.
NON-ELASTIC RESISTANCE TO GAS FLOW

 For air to flow into lungs pr. gradient must develop

to overcome non-elastic resistance
 R = 1/C (ΔP/ΔV)
AIRWAY RESISTANCE TO GAS FLOW- airflow pattern.
 Laminar flow- concentric cylinders of gas flowing at
different velocities, highest at the centre
 Turbulent flow- random movement of gas
molecules
 Critical velocity – velocity at which gas flow
becomes turbulent
 Re = 2rvd/n;
 Re> 1500  turbulent flow, Re<1000 less likely
 V- velocity of air flow
 r- radius
 n- viscosity of gas
 d- density of gas
 Re – Reynolds number
- more AR is seen in upper resp tract, most in
the nasal cavity.
WORK OF BREATHING
 Of the 2-barriers of respiration =
airway resistance & lung
compliance, only force used to
overcome airway resistance
contributes to work of breathing.
 Airway resistance is present both
during inspiration & expiration,
so energy is spent to overcome
this, which is released as heat.
 Approx. 3-5 % of total body
energy is used for work of
breathing.
LUNG VOLUME & CAPACITIES
CLOSING VOLUME

 Volume at which airways begin to close in dependent

areas of the lung. ST α CV
 Normally, CV<<FRC
 Closing capacity= CV + RV
PULMONARY & ALVEOLAR VENTILATION

 PV/ minute ventilation- air going in & out in 1m.

 PV=MV= TV x RR= 6 L/m.
 AV- air getting exchanged in lungs per min.
 AV=(TV-DS) x RR= 4.2 L/m.
 Increase in dead space decreases AV.
VENTILATION IS UNEVEN WITHIN THE LUNGS
 weight of lungs produces uneven inflation of alveoli.

-Lungs wt. make difft alveolar vol. at top & bottom of lungs (e.g. alveoli
at apex of lungs are at a larger volume (more -ve intrapleural pr.)
than those at the base (less –ve intrapleural pr.).

Alveoli also exhibit a changing compliance as vol. changes. Those at

base are ventilated more than those at apex of lung (compliance
regulation).

 Surfactant helps alveoli of different sizes remain inflated.

Surfactant can reduce surface tension which tries to make alveoli
smaller and keep alveolar pr. constant.
DISTRIBUTION OF VENTILATION

Gravity cause difference in vertical intra-pleural pr, which

in turn cause difference in alveolar vol, compliance and
ventilation

 Lungs has tendency to assume globular shape because

of gravity and visco-elastic nature, -ve pressure at
apex prevent collapse & alveoli are larger.

+ve pr. at base small & compressed alveoli

 Thus TV is preferentially distributed to dependent alveoli

because they expand more per unit change than non-
dependent alveoli.
VENTILATION - PERFUSION RATIO
 V/Q= AV/perfusion= 4.2/5= 0.8.
SHUNTS
 “Shunt” is a term used to describe a condition in which VA／Q is 0,
due to no ventilation.
 Anatomical shunts result from blood vessels that do not flow past
alveoli (arterial blood perfusing the bronchi goes directly into
pulmonary veins without passing through the lungs).
 Alveolar shunts result from alveoli that are not ventilated or are not
capable of exchanging gas.
 Perfusion of non-ventilated alveoli= True shunt.
 Physiological shunt is the sum of anatomical and alveolar shunts.
 Greater the magnitude of physiological shunt, lower will be Po2 and
higher Pco2 of arterial blood.
 Greater the magnitude of physiological shunt, greater will be alveolar-
arterial oxygen difference.
DIFFUSION OF GASES

 Rate is given by Fick’s law.

D= diffusion constant
A= area of the resp memb
S= solubility
T= thickness of memb
(0.5µm)
P1-P2 – Partial pressure
gradient
REGULATION OF RESPIRATION

Neuronal Chemical

Respiratory centres chemoreceptors

respiration correction
NEURONAL CONTROL
 Brain stem
-Medullary centre
(i) DRG- Inspiratory centre
(ii) VRG- Expiration

 Pneumotaxic center
 dorsally in N. parabrachialis of upper pons
 inhibits the duration of inspiration by turning off DRG ramp signal after start of
inspiration
 Ventral respiratory group of neurons
 located bilaterally in ventral aspect of medulla
 can + both inspiratory & expiratory muscles during increased ventilatory drive
 Apneustic center (lower pons)
 located in the middle & lower pons – activation of which sends impulses to
inspiratory DRG and sustain Inspiration
 Prebotzinger complex in medulla
 Pacemaker of respiration
 Discharges every 5-6 secs but its irregular

 Pons- makes respiration regular &smooth.

HIGHER RESPIRATORY CENTRE

 Midbrain – stimulation of RAS increase heart

rate and amplitude of ventilation.

 Cerebral Cortex—overrides automatic control of

the brain stem

 Hippocampus & Limbic system- emotions

(anger, rage) increases depth of ventilation.
 Herring-Breuer Inflation reflex
 stretch receptors located in wall of airways supplied by
vagus nerve.
 + when stretched at tidal volumes > 1500 ml
 inhibits the DRG- prevents excessive inspn.
 Irritant receptors-along airway epithethium
 +  sneezing & coughing & possibly airway constriction
 J reflex - in alveoli next to pulmonary caps
 + when pulmonary caps are engorged or pulmonary
edema. Pathological reflex.
 create a feeling of dyspnea
HEAD’S PARADOXICAL REFLEX

 1st respiratory reflex to appear.

 Inflation stimulates further inflation.

 Occurs during 1st breath of newborn.

 CHEMORECEPTORS

Central Peripheral

Ventral medulla Aortic & Carotid bodies

 Main drive for respn is co2.

 Secondary drive is hypoxia.
 Apnea point- paco2 at which respiration
stops=37mmhg.
CENTRAL CHEMORECEPTORS
 Situated in ventral surface of medulla near IX, X CN

 Most imp. receptors involved in minute by minute ventilation

 sensitive to pH, since BBB is impermeable to H+, medullary

chemoreceptors do not directly sense pH of blood. But, CO2 can diffuse
from blood into CSF where it is converted to H+ & HCO3-. H+ ions thus
formed stimulate medullary chemoreceptors.

 ↑ pH (+) ventilation, ↓ pH (–) ventilation

 Cerebral vasodilatation seen in ↑ PCO2 enhances diffusion of CO2 to

the CSF

 Indirectly sensitive to the PCO2 but not PO2 of blood

TRANSPORT OF GASES IN BLOOD
 Transport of O2- 5ml/dl is carried lungs-tissue
 Dissolved- 3%

 Hb bound- 97%

 Dissolved form important for maintaining partial pressure.

 Carbon Dioxide- 4 ml/dl from tissue-lungs

 Dissolved-7 to 10%

 Bound to hemoglobin (and other proteins)-20%

 Bicarbinate ion-70%- main transport form.

O2 transport CO2 transport

Bound to Hgb Dissolved

Dissolved bound to Hgb
HCO3-
 Oxygen binding to hemoglobin is influenced by pH, carbon
dioxide, 2,3-diphosphoglycerate (2,3-DPG) & temperature.

 Carbon monoxide decreases the blood’s oxygen content and

capacity.

 O2- Hb dissociation curve is sigmoid shape- because of co-

operative binding/relative affinity.
HAEMOGLOBIN-DISSOCIATION CURVE
Haldane’s
effect

Bohr’s
effect
Tissue
level
 P50 – Po2 at which Hb is half filled( 50%
saturated Hb)= 27mmhg.
 CO poisoning causes left shift of the curve
leading to no O2 release at tissues causing
severe hypoxia and death.
CO2 TRANSPORT
RESPIRATORY FUNCTION DURING
ANAESTHESIA
 Impair in Pulm Fn. Both in spontaneous or controlled
 Min FiO2 therefore given is 0.3 – 0.4
 Despite this mild to moderate hypoxemia persist in 85% - 90.

LUNG VOLUME
 FRC ↓ by 0.8 to 1 L d/t change in position, further ↓ by 0.4 –
0.5 L when anaesthetised by IV or inhalational agents.
 Average , 20 % ↓ FRC when awake due to –

1) loss of resp tone shifts the balance of elastic recoil

force of lung and chest wall to a lower FRC
2) cranial shift of the diaphragm
COMPLIANCE AND RESISTANCE

 Decrease
compliance – 95
to 60 ml/cm H2O
 Increase
resistance both
spont. and
controlled
 Merely reflects
decrease in FRC
ATELECETASIS & AIRWAY CLOSURE
 seen in 90% of anesthetised patients
 15%-20% collapse at the base of the lung
 Atelectasis decreases towards apex

PREVENTION OF ATELECTASIS

1. PEEP 10 cm H2O
 Atelectasis persist in most
 Not ideal due to
i) shunt not reduced proportionately due to redistribution toward dependant
parts ( Atelectatic part)
Also increase Intra thoracic pressure which impedes Venous return to Rt heart
decreasing CO
ii) lung collapses rapidly after discontinuation

2. Muscle tone
 Maintaining muscle tone prevents atelectasis
 Ketamine does not impair muscle tone
 Only anaesthetic that does not cause collapse
3. Recruitment maneuvers
 Sigh maneuver/double VT – Paw 20 cm H20 – minimal opening
 VC maneuver –Paw of 30 – 40 cm H2O maintained for 7 to 8 secs
30 cm H2O- opening of half of collapsed alveoli
40 cm H2O- all collapsed alveoli open

4. Minimising gas resolution

 Ventilation with 100% O2 after VC maneuver causes collapsing of
opened alveoli
 Ventilation to be done with moderate levels of FiO2 0.3 – 0.4.
Increase only when arterial Oxygenation is compromised
 Avoid preoxygenation with 100% O2.
 If at all CPAP + 100% O2

5. Post anaesthetic Oxygenation

 Giving 100% O2 10 mins before termination of anaesthesia with VC
maneuver did not prevent atelectasis formation
 VC maneuver followed by lower O2 conc ( 0.4) kept lung open after
recruitment until end of anaesthesia
DISTRIBUTION OF VENTILATION

 Redistribution of gas away from dependent to non-

dependent – ventn more in upper part decreasing down
lower half of the lung
 PEEP increases dependent lung ventn by opening collapsed
alveoli increasing FRC

DISTRIBUTION OF BLOOD FLOW

 Increase in perfusion from ventral to dorsal in supine
position
 Same as in awake subjects
 PEEP causes redistribution to other dependent lung regions
 Upper region – dead space like effect
HYPOXIC PULMONARY VASOCONSTRICTION (HPV)
 All inhaled anaesthetics (-) HPV

V/Q RELATIONSHIP
 CO2 elimination & Oxygenation impaired in pts under GA –
overcome by increase in ventilation.
 Increase in alveolar dead space
 Impairment in arterial oxygenation also seen, which will be
more with increasing age, obesity, smoker.
 Shunt increase from 5% to 10% Cardiac output

RESPIRATORY DRIVE
 Dose dependant decrease in ventilatory response to CO2.
FACTORS INFLUENCING RESPIRATORY
FUNCTION DURING ANAESTHESIA
1. Spontaneous breathing:- FRC decreases to same extent in
anesthesia whether spontaneous or with muscle paralysis.
 Spontaneous- cephalad shift of dependent diaphragm
 Muscle paralysis – shift of non dependent diaphragm
2. FiO2:- Increasing FiO2 increases shunt fraction because of
absorbtion of low V/Q regions in the lung
3. Position:-decrease in FRC by both positioning and under
anaesthesia
4. Age:-
 arterial oxygenation impede with increasing age

 Babies have more atelectasis than adults

5.OBESITY

 Decrease FRC -promotes airway closure.

 High FiO2 promotes atelectasis
 Shorter time until desaturation prevented by PEEP/CPAP during
induction of anaesthesia
 If shunt > 30%, increasing FiO2 does not improve oxygenation

6.PRE-EXISTING LUNG DISEASE

 Smokers and pts with lung disease – more severe impairment in
gas exchange in anaesthetised than awake
 Chronic bronchitis- absent or less atelectasis - minimal shunt but
impaired oxygenation due to considerable V/Q mismatch – large
perfusion to Low V/Q regions
 Obst disease have large regions of low V/Q converted to
resorption atelectasis
7. REGIONAL ANAESTHESIA

 Depend on type and extent of motor blockade

 Thoracic and lumbar blockade – IC ↓ by 20% and ERV 
zero
 Diaphragmatic function spared even when there is motor
blockade upto cervical segments
 Skillfully handled RA affects pulmonary gas exchange only
minimally
 Arterial oxygenation and CO2 elimination well maintained
during SAB and Epidural because of unchaging Closing
capacity and FRC
 DIFFERENCES IN PAEDIATRIC AGE GRP

 Trachea- short & narrow.

 Tongue- relatively large, tends to fall backwards under
anaesthesia
 Larynx- more ventral & higher up
 Epiglottis- large & U-shaped
 Compliance- low
 Thorax is more elastic than adults & offers little resistance to
over inflation
 NON-RESPIRATORY FUNCTIONS OF R.S.

 Filteration
 Warming & humidification

 Coughing, sneezing

 Alveolar macrophages

 Reservoir of blood

 Metabolic activity