Respiratory Physiology

By:
Dr Muhammad Arslan Qureshi
FCPS Anesthesia

1
 Lecture Outline
 Lung Volumes
 Mechanism of Breathing and Lung Mechanics
 Ventilation Perfusion Relationships
 Alveolar, Arterial and Venous gas tensions
 Transport of Respiratory Gases in Blood
 Control of breathing

2
 Mechanism of Breathing
Lung Volumes and capacities

3
 Mechanism of Breathing
Lung Volumes and capacities

4
 Lung Volumes and capacities

• FRC
It is volume at the end of passive expiration
ERV + RV= 2400ml
At FRC inward elastic recoil of lungs approximates the outward recoil of chest wall ,
thus it defines a point from which normal breathing takes place
Factors affecting FRC
FRC increases with FRC decreases with
• Increasing height •Decreased height
•Supine position
• Erect position (30% higher)
• Increased lung recoil
• Reduced lung recoil •Obesity
• Muscle paralysis
•Pregnancy
• Anesthesia
FRC does not change with
5
age
 Lung Volumes and capacities

Functions of FRC
• Oxygen store
• Buffer for maintaining a steady arterial PO2
• Partial inflation helps prevent atelectasis
• Minimize the work of breathing
• Minimize pulmonary vascular resistance
• Minimized V/Q mismatch 
- only if closing capacity is less than FRC
• Keep airway resistance low (but not minimal)
6
 Lung Volumes and capacities

• Closing Capacity
 Patency of smaller airways depends on
lung volume
 The vol. at which these airways begins
to collapse in dependent areas of lungs
is called closing capacity
 Normally it is well below FRC
 But it increases with age
 By 66 yrs CC >FRC in upright position so
airway closure occurs at expiration
worsening V/Q
  Rise in CC is seen in smokers,obesity,
early chronic bronchitis.
 Use of PEEP raises Po2 by increasing
FRC above CC
7
 Mechanics of breathing
• Inhalation(Active
process)-Air
moves in WHY??
o Gas moves from area of high
pressure to low pressure
o Remember Boyle’s Law
V∞1/P
o When lungs expand , lungs
volume increases, so pressure
inside decreases acc to boyle’s
law
o Air moves in from high atm
pressure to low alveolar
pressure
Ptranspulmonary =Palveolar -Pintrapleural
8
 Mechanics of breathing
Lung Volume
Inc. by one TV
i.e. FRC+TV

LUNG
Volume is at
FRC

Lung volume
returns to FRC

9
 Mechanics of breathing
• Exhaling (passive
process) – breathing
out
 Diaphragm and muscles relax
 Volume in lungs and chest
cavity decreases,
 so now pressure inside
increases
 Air moves out because
pressure inside is HIGHER
than OUTSIDE atmosphere
10
 Mechanics of breathing
Inspiratory muscles provide the force necessary to
overcome
a. elastic recoil of the lungs and chest wall (ELASTANCE)
b. frictional resistance/ non- elastic resistance

i. caused by deformation of lung tissue and thoracic cage

→ tissue resistance
ii. to air flow in the conducting airways
→ airway resistance

11
 Mechanics of breathing

Concept of

1.Compliance and
2.Elastance

12
 Compliance
• Ability of lungs to expand as
transpulmonary pressure changes
• It describes the
distensibility/strechability of lungs
• Change in volume divided by change
in distending pressure C=
∆V/∆P
• It is the slope of pressure-volume
curve
• Inversely related to
elastance(property of resisting
deformity)

13
 Compliance
• C=∆V/∆P
• Tidal volume 600ml
• Change in intrapleural pressure before
inspiration and after inspiration = -5-(-8)=3
• So C=600/3 C=200ml/cmH2O
• For every 1cmH2O change in pressure
200ml air will move in or out
• Inc compliance means more air will flow
for given ∆P
• Dec. compliance means less air will move
for given ∆P
• Total compliance is C(chest wall) + C(lungs)
• Expressed as 1/Ctotal = 1/Cw + 1/CL

14
 Compliance
Things which oppose inflation or effect compliance
1) Tissue elastic forces
2) Surface tension forces
3) Diseased state
4) Lung volume
The slope of the P-V curve is not constant across different lung volumes.
At high lung volume
--> Elastic fibers already stretched
--> Greater pressure is required to inflate lung
-> Reduced compliance
At very low volumes
--> Alveoli radius reduced
--> (according to Laplace's Law), pressure required to inflate alveoli is increased
--> Reduced compliance
Other factors affecting compliance via effect on lung volume Posture ,Restriction of chest
expansion 

15
 Compliance
TYPES
1.Static compliance
Compliance measured when there is NO gas flow into or out of the
lung.
Static C = Plateau pressure-PEEP ,
It reflects elastic resistance of the lung and chest wall
2.Dynamic compliance
Compliance measured when there is gas flow into or out of the lung
Dynamic C =peak airway pressure-PEEP ,
It reflects condition of airway ( non-elastic ) and elastic properties of chest
wall and lung.

Airway resistance is a critical factor in its measurement .  16

 Compliance
• LOW COMPLIANCE
o The volume change per unit pressure change is low.
o Less air will flow for given change in pressure.
o The lungs are stiff and are resistant to expansion, restrictive lung.  
o The patient has low lung volumes and low minute ventilation.
o Seen in pulmonary fibrosis, pul-edema, atelectasis, prolonged under ventilated
lung with low volume, pulmonary venous hypertension

Low Static Compliance Low Dynamic compliance

Atelectasis Bronchospasm
ARDS Kinking of ETT
Obesity Airway obstruction
Retained secretions
Fibrosis

17
 Compliance
• HIGH COMPLIANCE
• Volume change is large with change in
pressure
• More air will flow for given change in
pressure
• Tendency to collapse is decreased
• Exhalation is incomplete due to lack of
elastic recoil of lung, obstructive lung
defect.
• New higher FRC, Barrel shaped chest
reflecting this high volume
• Seen in
Emphysema
Aging Lung
During Asthmatic attack

18
 Elastance
• Elastance, also known as the elastic
resistance
Inc. Elastance
• is the reciprocal of compliance, i.e. the
pressure change that is required to
elicit a unit volume change.
• This is a measure of the resistance of a
system to expand.
• Elastance = 1/C= ∆P/∆V Inc. Power of muscle of inspiration
• Elastance is a measure of the work
that has to be exerted by the muscles
of inspiration to expand the lungs.

Inc. in work of breathing

19
 Elastance
• The elastance of the whole respiratory system depends on
1. the elastance of the chest wall and
2. that of the lungs
• Changes in the elastance (and therefore the compliance) of the chest wall are
uncommon.
• In contrast, the elastance of the lungs is affected by many respiratory diseases.
• Elastance of the lungs, which is governed by two main factors:

a) Elastic recoil forces of the lung tissue

b) Forces exerted by surface tension at the air-alveolar interface

20
 Elastance
1. Elastic Recoil Forces of the Lung Tissue
The elastin fibers forming the pulmonary interstitium resist stretching and
exhibit the property of returning to its original length, when stretched (in
accordance with the Hook’s Law).

1/4th to 1/3rd of the elastic resistance of the lungs.

Holds the responsibility of generating the recoil forces necessary to increase

the intra-alveolar pressure during expiration, which is a passive process

21
 Elastance
2. Forces Exerted by Surface Tension at
the Air-Alveolar Interface
Responsible of remaining 2/3rd or 3/4th of elastic resistance
Force which try to collapse alveoli(due to attractive forces lining alveoli) is surface tension
Laplace’s law
P= 2xST / R

 Large alveoli(large radii) low collapsing pressure easy to keep open

 small alveoli (small radii) high collapsing pressure difficult to keep open
 Surfactant decreases alveolar ST so decreases collapsing pressure
 Small Alveoli more conc. Surfactant decreases ST effectively prevent collapse.

22
 Elastance
Surfactant
……..Dipalmitoyl
phosphatidycholine
FUNCTIONS
a. Lowers ST forces in alveoli so
lowers lung recoil and increases
compliance
b. Lowers ST more in small alveoli
than in large due to conc.
Difference
c. Reduces capillary filtration forces
thus reduces tendency to develop
pulmonary edema

23
 Mechanics of breathing

Resistance To Breathing
1. Elastic Resistance ~ 65%

2. Non-elastic resistance ~ 35%

i. Airflow ~ 80%
ii. Viscous ~ 20%

24
 Mechanics of breathing
• NON-ELASTIC RESISTANCE
 Airflow
Driven by pressure difference between mouth and alveoli
Inversely proportional to airway resistance
Q=∆P/R
Raw = 8 x Length x viscosity
∏ x R4
Airway Resistance
It is the pressure that is required to overcome the resistance
to gas flow through the airways during respiration.
Normal value for a healthy adult ~ 0.5-1.5 cmH20/l/s 25
 Mechanics of breathing
• Turbulent Flow • Laminar flow
High flow rates, particularly through
branched or irregularly shaped tubes,  Below critical flows, gas proceeds
disrupt the orderly flow of laminar gas. through a straight tube as a series of
concentric cylinders that slide over
Turbulent flow usually presents with a one another
square front so fresh gas will not reach the
end of the tube until the amount of gas
entering the tube is almost equal to the
volume of the tube
 

26
 Mechanics of breathing
• Four conditions that will
change laminar flow to
turbulent flow are
1) high gas flows,
2) sharp angles within the tube,
3) branching in the tube,
4) change in the tube's
diameter.

• During turbulent flow,

resistance increases in
proportion to the flow rate.

27
 Mechanics of breathing
• Factors affecting airway resistance(NON-ELASTIC
RESISTANCE)

• Viscosity and Density of the gas mixture

• Length, and lumen radius of artificial and patient’s airways:

Airway resistance and lumen radius are exponentially related to the fourth power.
SO any small amount of bronchospasm, secretion accumulation, in the
endotracheal tube, water in the ventilator tubing, or other obstruction
considerably increases airway resistance

28
 Mechanics of breathing
• Flow rate: The higher the flow, the greater the amount of turbulence and
consequent increase in the airway resistance.

• Flow pattern: Laminar flow decreases whereas turbulent flow increases it.

• Lung Volume: In general, as lung volume increases, resistance decreases. This is due
to radial traction exerted on the airways.

• Bronchial Smooth Muscle Activity:

– The contraction and relaxations alters radius so does changes resistance
– The tone of bronchial smooth muscle is determined by autonomic input. Adrenergic
stimulation, mainly by nor epinephrine acting on β2 receptors and by nitric oxide,
causes bronchial smooth muscle relaxation.
Substances such as acetylcholine, histamine, and prostaglandin F2α cause bronchial
smooth muscle contraction.

29
 Mechanics of breathing

• Second component of NON-ELASTIC RESISTANCE

Pulmonary Tissue Viscous Resistance
• Due mainly to the movement of pleural layers between lobes,
and between the lungs and chest wall during inspiration &
expiration
• Accounts for < 20% of the total non-elastic resistance in health
• Increased in pulmonary fibrosis, carcinomatosis, etc., but
rarely to significant or limiting values.
• Measurements of thoracic cage viscous resistance, rib cage &
abdominal contents, is difficult

30
 Ventilation/Perfusion Relationships
• Ventilation
 Mv= RR x Tidal Volume
 Part of Vt not participating in alveolar gas exchange is dead
space Vd
 Dead space = Anatomic + Alveolar dead space
 Normally 150ml in adults or 2ml/kg
 Weight in pounds approximates to dead space in mL
 Alveolar Ventilation Va = RR x (Vt-Vd)
 Rt lung recieves more ventilation than left lung
 Lower areas are better ventilated than upper areas

31
 Ventilation/Perfusion Relationships
• Perfusion
It equals cardiac output
5L/min
Due to gravitational influence the
lower – dependent areas receive
more blood

Upper zone – nondependent areas

are less per fused

32
 Ventilation/Perfusion Relationships
Distribution of Pulmonary blood
flow
ZONE 1
• Obstruction of BF and creating dead
space
• Small in spontaneously breathing
individuals
• Enlarge during PPV
ZONE 2
BF dependent on difference of Pa and PA
ZONE 3
Blood flow independent of alv pressure
ZONE 4
• most dependent part
• Where atelectasis and pulmonary
edema occurs
33
 Ventilation/Perfusion Relationships
• V/Q Ratio
• V — the air that reaches the alveoli =4L/min
• Q — perfusion — the blood that reaches the alveoli via the
capillaries=5L/min
• So V/Q= 4/5 =0.8

SHUNT
DEAD SPACE
34
Ventilation/Perfusion Relationships

35
 Alveolar, Arterial and Venous gas tensions

Components of the Oxygen Transport System

•Mass Transport from Environment to Alveolar Space

•Diffusion from Alveolar Air to Blood in the Pulmonary Capillary

•Mass Transport from the Pulmonary to the Systemic Capillaries

• Diffusion of Oxygen from Capillary Blood to Metabolizing Cells and

Within the Cell to the Site of Consumption, the Mitochondria
Oxygen transport
 Alveolar, Arterial and Venous gas tensions

Atmospheric Oxygen Alveolar oxygen Tension

Inspired air is humidified
tension Humidified air reduced partial pressure of other gases
Dalton’s Law of Partial pressure So pressure of inspired gas is
PiO2 =( Patm - PH2O ) x FiO2
=( 760 – 47 ) x 0.21
P= Total Pressure x Fractional gas conc.
= 713 x 0.21
= 150mmHg
In Alveoli inspired gas is mixed with residual gas from
In air Patm =760mmHg previous breaths so final
O2 conc.= 21% (0.21)
PAO2 = PiO2 – PaCO2
So PO2 (in air) = 760 x0.21 RQ
= 159.6
PAO2 ={( Patm - PH2O ) x FiO2 } – PaCO2
≈ 160mmHG
RQ
Simple method is
Multiply FiO2 with 6 it will give alveolar gas
tension
 Alveolar, Arterial and Venous gas tensions

Alveolar oxygen Tension

PAO2 ={( Patm - PH2O ) x FiO2 } – PaCO2
RQ
PAO2 = 150 – 40/0.8 = 100 mmHg (RQ is
normally is around 0.8)
so Alveolar gas tension PAO2 is dependent on
1. Atmospheric pressure
2. FiO2
3. PaCO2

 High Altitude will decrease Atm pressure so

In hyperventilation PaCO2 suppose is 20mmHg
……… will decrease PAO2
 Increased FiO2 will also increase PAO2 PAO2 will be (assuming RQ is 1)
 PaCO2 will effect PAO2 = 150 -20 = 130mmHg
In Hypoventilation PaCO2 is 80mmHg
PAO2 will be (assuming RQ is 1)
= 150 – 80
Arterial Oxygen Tension and A-a gradient
• PaO2 Arterial oxygen tension is measured by ABGS
• Normally is 80-100mmHg

Alveolar oxygen tension is 100mmHg calculated by formula

PAO2 ={( Patm - PH2O ) x FiO2 } – PaCO2
RQ
So A-a Gradient is = PAO2 - PaO2
= 100 – 90 = 10 (5-10mmHg is normal)

• PaO2 = 120 – Age /3

 Arterial Oxygen Tension and A-a gradient
•Suppose A pt has
•PaO2 = 50 mmHg
•PCO2 = 50mmHg at
• FiO2 of 50% … Calculate A-a gradient??
A-a Gradient is = PAO2 - PaO2
First calculate PAO2
PAO2 ={( Patm - PH2O ) x FiO2 } – PaCO2
RQ
= { (760-47) x 0.5} – 50/0.8
= { 713x0.5} – 62.5
= 356.5- 62.5
PAO2 = 294
A-a Gradient thus = 294- 50
= 244 mmHg
This is more than normal , seen in
Right to left shunting
Increase areas of low V/Q
Diffusion defect
Low mixed venous oxygen tension
 Arterial Oxygen Tension and A-a
gradient
Mechanism of Hypoxemia (PaO2 <60mmHg)
Low Alv Oxygen tension Increased A- Gradient
Low inspired oxygen tension Rt to Lt shunt
Alveolar hypoventilation Increased areas of low V/Q
Diffusion hypoxia low mixed venous oxygen tension
Increase oxygen consumption
 Diffusion from Alveolar Air to Blood in
the Pulmonary Capillary
Fick law of diffusion
Vgas = A x D X ∆P
T
Two
•A= Surface Area ( ↓ in
structur emphysema,↑ in exercise)
•T= thickness ( ↑in fibrosis

al and other restrictive

diseases)

factors

Two •D = diffusion
constant/solubility(
constant/solubility( CO
CO22 is
is more
more

gas soluble so diffuses faster than O2)2)

•∆P = Pressure gradient for O22 = 100
– 40 = 60 for CO22 = 47 – 40 = 7

factors
Diffusion from Alveolar Air to Blood in
the Pulmonary Capillary
• Diffusion capacity DLO2
Vgas = A x D X ∆P
T
As it is not possible to measure area and thickness
so one can introduce diffusion capacity
Vgas = DLO2 x (PAO2 - Pc’o2 )
So DLO2 = oxygen uptake
PAO2 - Pc’o2
 Diffusion from Alveolar Air to Blood in
the Pulmonary Capillary
• Diffusion limited vs Perfusion limited gas exchange
 Transport of Oxygen in Blood
• Oxygen is carried in two forms
1) Dissolved form
2) Bound to Hb
 Transport of Oxygen in Blood
1) Dissolved form
Henry’s law
Gas Conc. In solution= @ x Partial pressure
Solubility coefficient @ for O2 = 0.003ml/dL/mmHg
So
Dissolved O2 = 0.003 x 100
= 0.3ml/dL (1.5 % of total oxygen in blood)
2) Bound to Hb
Each g of Hb carries 1.39 ml of O2
So 15 g at 100% saturation caries= 15 x1.39
= 20.85ml/dL (98% of total oxygen in blood)
 Transport of Oxygen in Blood
• Hemoglobin
 Transport of Oxygen in Blood
Each Hb molecule can bind 4 O2
molecules
Four Separate chemical reactions are
involved in binding of each four
molecules
Binding of first O2 molecule
increases the affinity for second and so
forth
 Transport of Oxygen in Blood
• Hb dissociation curve
• It is plot of percent saturation as
function of pO2
• It is S-shaped curve that has two parts
a) Upper flat part (plateau)
b) Lower steep part

 At pO2 of 100mmHg, Hb saturation

is100 %
 At pO2 of 60mmHg saturation is
90%
 At pO2 of 40mmHg saturation is
75%
 At pO2 of 26.6mmHg saturation is
50%
 This is P50
 Transport of Oxygen in Blood
Rt Shift
P50 is increased

Unloading facilitated

Affinity of Hb is decreased

Lt Shift
Increased affinity of Hb for oxygen

Unloading is difficult

P50 is decreased
Transport of oxygen from blood to cell
•  The blood entering the capillary surrender its oxygen because it is
surrounded by an immediate environment of lower PO2,( initially giving off
oxygen dissolved in plasma, and followed by release of oxygen bound to Hb).

• The principal force driving diffusion is the gradient in pO2 from blood
to the cells

• The oxygen dissociation characteristics of Hb facilitate the rapid and

efficient unloading of oxygen within the capillary.

• The O2ultimately diffuses from the microcirculation into the cells

and finally into the mitochondria.
 Oxygen Content
• It is amount of oxygen carried by 100ml of blood
• CaO2 = dissolved O2 + O2 carried by blood
= ( 0.003x pO2 ) + ( So2 xHb x1.31)
= (0.003 x100) + ( 0.97 x 15 x 1.31)
= 19.5ml/dL blood
• For venous blood
CvO2 = (0.003x 40) + (0.75 x 15 x 1.31)
= 14.8ml/dL blood

CaO2 – CvO2 = 19.5 -14.8 = 4.7ml/dL blood

 Oxygen Delivery and consumption
Do2 = Cao2 x QT
={ ( 0.003x pO2 ) + ( So2 xHb x1.31)} x Qt
= 20ml O2 /dL blood x 50 dl per blood/min
= 1000ml O2 / min

Oxygen content is dependent on PO2 and Hb, so decreased oxygen delivery can be due to
 Low pO2
 Low Hb
 Inadequate cardiac output

O2 Consumption = VO2 = QT x (CaO2 – CvO2)

= 50 x 4.7
= 235 ml/min
Extraction fraction for O2 = CaO2 – CvO2 / CaO2
= 5/20 = 0.25 or 25%
When O2 demands exceeds supply, extraction fraction exceeds 25 %
 If supply exceeds demand , extraction fraction falls below 25%
 Oxygen stores
• Oxygen consumption is 235ml/min
• Oxygen stored at FRC is most imp source of oxygen
• If Fio2 is 0.21, FRC 2300ml, then O2 content is
FiO2 x FRC= 480 ml
 So usually hypoxemia occurs at 90 sec
 When we preoxygenate with FiO2 of 100%
Then 1 x 2300
= 2300ml of oxygen content which is sufficient
for 4 to 5 min( Bcz 80 % of stored oxygen at FRC is usable )
 Carbon dioxide
CO2 is by product of aerobic metabolism
Mixed venous CO2 tension= 46mmHg
Alveolar CO2 tension
It represents balance B/w CO2 production and
alveolar ventilation
PACO2 = VCO2 / VA
Arterial CO2 tension is approximately equal
Alveolar CO2 tension
Transport of Carbon dioxide
 Control of breathing
Central Control of Chemoreceptors
breathing Type Location Stimuli that Inc
RR
 Medullary Respiratory Central Medulla ↓pH
centre ↑pCO2
I. Dorsal respiratory Peripheral Carotid and ↓pO2
group aortic bodies ↓pH
↑pCO2
II. Ventral Respiratory
group
 Apneustic Centre in
lower pons
 Pneumotaxic centre
 Cerebral cortex