Respiratory Physiology

• Structure and function

• Respiratory Mechanics
• Ventilation and Lung Volumes
• Diffusion
• Blood flow and Metabolism
• Ventialtion Perfusion Relationship

CONTENTS
Structure and Function

•The conducting zone begins at the mouth

and continues until the 16th generation -
transports gas - no gas exchange.

•The respiratory zone continues from the

17th until the 23rd generation and is the
region where gas exchange occurs.
ACINUS DEAD SPACE
• Anatomical dead space - 150 ml
• Alveolar region - 2.5 to 3.0 ml
• Gas movement from alveoli to blood occurs by
diffusion
• Diameter of capillary is 7 to 10 microns
• Thickness of capillary wall - 0.3 microns
• Surface area - 50 to 100 sq.m
Clinical points

• The ETT in an adult should lie 1-2cm superior to the

carina

• On an X-ray the carina is the point at which the

trachea can be seen dividing into the right and left
bronchi – around T4

• Right major bronchus divides from the trachea at an

acute angle prone to endobronchial intubation
• The right upper lobe bronchus arises only a few centimeters from
the carina therefore for one lung ventilation a left sided double
lumen tube is favoured to avoid the risks of right upper lobe collapse
with a right sided double lumen tube
RESPIRATORY MECHANICS

Inspiratory muscles
• Diaphragm – very powerful, has the ability to
contact 10cm in forced inspiration
• External intercostals – pull the ribs up and
forwards
• Accessory inspiratory muscles – scalene
muscles (elevate first 2 ribs) and sternomastoids
(raise the sternum)
• Muscles of neck and head (seen in small babies
in respiratory distress)
Expiratory muscles
• Expiration is usually passive and relies on the
elastic recoil of the lungs and the chest wall.
Under anaesthesia or extreme exercise expiration
may become active due to the activation of
abdominal muscles. Muscles have their use in
forced expiration.
• Abdominal wall muscles – rectus abdominus,
internal and external oblique
• Internal intercostal muscles – pull ribs down and
inwards
 WORK OF BREATHING
• Work=force x distance, Force=pressure x area,
Distance=volume/area
• So WORK = PRESSURE x VOLUME
• If R or C increases, P increases ,Work of breathing
increases
• The metabolic cost of the work of breathing at rest is only
1-3% of the total O2 consumption , and increases up to
50% in pulmonary disease
• Expiration is passive using potential energy that has been
saved during inspiration (awake)
Compliance

• Compliance is defined as the volume change per unit

pressure change and is usually expressed in mls/cmH2O

• Reciprocal of elastane

• Compliance = ΔV/ΔP

• If during the measurement process no gas flow occurs at

each set volume then this is static compliance.

• If gas flow continues throughout measurement then this

is dynamic compliance.
• Includes chest wall compliance and lung compliance
• Compliance (ability of lung to distend) depends upon
the volume of the lung. Compliance is lowest at
extremes of FRC. It implies that expanded lung and
completely deflated lung has lower capacity to distend
to a given pressure
• Depends on lung volume and surface tension of the
alveoli
• Chest wall compliance depends on posture, obesity,
cartilage ossification, scarring of the chest wall
RESISTANCE

•Resistance is generally defined as flow per unit

resistance

•Respiratory resistance is defines as the ratio of

pressure gradient across the membrane to flow
• In anesthetized person with diffuse obstructive
airway disease resulting from the accumulation of
secretions, elastic and airway resistive component
of respiratory work would increase

• For a constant minute volume , both deep , slow

(elastic resistance ) & shallow , rapid (airway
resistance ) breathing will increase work of
breathing
• Clinical points
• Patients using their accessory muscles may indicate increased work
of breathing
• PEEP can help to maintain the lungs at FRC
• If used correctly CPAP can reduce the work of breathing by increasing
FRC
LUNG VOLUMES

• FRC: the volume of gas in lung at end of normal

expiration

• At FRC , There is no air flow & alveolar pressure =

ambient pressure

• Expansive chest wall elastic forces are exactly

balanced by retractive lung tissue elastic forces

• ERV: is part of FRC, the volume of gas that can be

consciously exhaled
• RV: the minimum volume that remains after ERV

• VC: ERV + IC

• IC : VT+ IRV

• TLC: VC+ RV
• Volumes that can be measured by simple spirometry
are VT , VC , IC , IRV ,ERV .

• TLC ,FRC & RV cannot be measured by spirometry

• How to measure TLC ,FRC & RV :

• Nitrogen wash out
• Total body plethysmography

• Disparity between FRC in 2&3 is used to detect large

nonventilating airtrapped blebs
Functional Residual capacity

• FRC = ERV + RV

• The FRC is the balance between the tendency of the

chest wall to spring outwards and the tendency of the
lung to collapse. FRC is not the same volume all the
time; it can be disrupted by many factors.

• Changes by minute to minute basis

• FRC affects oxygenation

• FRC is the main oxygen store in the body and can

be easily and quickly enriched with oxygen

• FRC will change due to a large number of factors

Factors decreasing FRC
• Age
• Posture – supine position
• Anaesthesia – muscle relaxants
• Surgery - Laparoscopic
• Pulmonary fibrosis
• Pulmonary oedema
• Obesity
• Abdominal Swelling
• Reduced muscle tone – Reduced diaphragm tone will
reduce pull away from the lungs
• Pregnancy – Increased abdominal pressure
• Factors increasing FRC
• Increasing height of patient
• Erect position – diaphragm and abdominal
organs less able to encroach upon bases of the
lungs
• Emphysema – decreased elastic recoil of lung
therefore less tendency of lung to collapse
• Asthma – air trapping
Closing capacity (CC)

• This is the volume at which the small airways close

during expiration.
• Under normal circumstances the FRC is always greater
than the CC
• Closing capacity increases with age. Typically closing
capacity is equal to FRC at the age of 66 in the erect
position or 44 in the supine position
• 15- 20% of vital capacity
• Inc with age due to loss of parenchymal support and an
increase in RV
• CC slowly changes overtime
Clinical points

• The FRC is reduced by anaesthesia and therefore

hypoxia is common in a patient with a decrease in FRC.
The application of PEEP enables the FRC to remain
greater then CC and improves oxygenation

• PEEP maintains the lungs on the steep part of the

compliance curve which lessens collapse at the bases of
the lungs.

• Preoxygenation should take place for 3-5 minutes or 4

vital capacity breaths
• Preoxygenation is essential in patients likely to
have a decreased FRC e.g. pregnant, obese

• Adequacy of preoxygenation can be assessed by

monitoring end tidal oxygen – aim for ETO2 >
90%
VENTILATION

• Total ventilation (MV) = VT x RR ( 500 x 14 =

7000ml)

• With each tidal volume about a third the total amount

of gas flowing into the airway and lung does not
participate in gas exchange. This is the Dead space.
• Anatomical dead space
• Physiological dead space

• Approximately 1/3 of VT is dead space - 150ml

• Alveolar ventilation is hence (VT-VD) x RR ({500 -

150} x 14 = 4900ml)
• Anatomical dead space is about 150mls in an
average adult and is measured by Fowlers
method

• Physiological dead space is measured using the

Bohr equation

• Minimise dead space by using the correct sized

equipment e.g breathing circuits Consider the
application of PEEP to prevent atelectasis and
V/Q mismatch
Factors Affecting Anatomical Dead Space

• Body Size - VD Anat with increasing body size- in ml ~

lean body weight in lb, or ~ 2.2 ml/kg

• Age - VD Anat with increasing age (?VD/VT)

• Lung Volume - VD Anat with increasing volume~ 20

ml/l increase in lung volume from FRC

• Posture - VD Anat with supine posture ® supine ~ 101

ml sitting ~ 147 ml (Fowler)
• Hypoxia- bronchoconstriction ® -VDAnat
• Drugs and Anaesthetic Gases - bronchodilatation ®and
increases VDAnat
• Lung Disease - emphysema ® VD Anat- loss or excision
of lung VD

• Endotracheal Intubation - VDAnat ~ 50%- but there is

the additional volume of the circuit
• Position of the Jaw & Neck - increases with jaw
protrusion in non-intubatedsubjects
Factors Affecting Alveolar Dead Space

• Age - ↑ V Alv with increasing age

• Pulmonary Arterial Pressure - a decrease in PA pressure (eg. hypotension)

decreases perfusion to the upper parts ofthelung → ↑zone1 & ↑V Alv D

• Posture V Alv increases in the upright and lateral positions due to

exaggeration of
hydrostatic differences → ↑ zone 1 this is theoretical, no data is available
(Nunn)

• IPPV increases V Alv due to exaggeration of hydrostatic failure of perfusion

D
also decreases total pulmonary blood flow
• Oxygen - hypoxic vasoconstriction V Alv D

• Lung Disease

i. ARDS microemboli & ventilation of non-vascular air spaces

ii. IPPV & lateral posture gross V/Q mismatch

Diffusion
Fick’s Law
Graham's Law: relative rates of diffusion are inversely proportional to the
square root of the gas molecular weight

Thus, lighter gases diffuse faster in gaseous media than heavier gases

lighter molecules for given energy have faster velocities

Henry's Law: the amount of a gas which dissolves in unit volume of a liquid,
at a given temperature, is directly proportional tothe partial pressure of the
gas in the equilibrium phase
Diffusion and Perfusion
limitations
CO - Diffusion Limited
• Binds tightly with haemoglobin - not available to mix in
blood

• Partial pressure in blood does not rise

• Solely dependant on membrane properties for

transport

• Hence Diffusion Limited

• Used to measure diffusing capacity of Membrane

N20 - Perfusion Limited

• Does not bind with haemoglobin - Soluble in blood

• Partial pressure in blood rises in blood very soon

resisting further transport

• Attains a saturation point following which transport

does not increase except for increase in blood volume

• Hence Perfusion limited

O2 - Diffusion/Perfusion
Limited
• Binds tightly with haemoglobin - also soluble in blood

• PP at the beginning of the capillary is 40 - venous

saturation

• Partial pressure in blood rises slowly and reaches a

threshold point - Hence Perfusion limited

• Becomes diffusion limited when membrane thickness

is increased (eg. RLD)
Oxygen Uptake in
Pulmonary Capillary
Rest and exercise
• Normally time taken by RBC to transverse the alveolar
capillary is 0.75s

• Saturation with oxygen occours when RBC has crossed

1/3rd of the distance - 0.25s at rest

• However during exercise the time taken to traverse the

alveolar capillary is reduced to 1/3rd - 0.25s

• Hence even though the rate of flow increases oxygenation

is not affected - except in pathological membranes,
Decreased oxygen PPs and decreased blood flow
Diffusion Capacity and
DLCO
• Diffusing Capacity (DC)

Def'n: the rate of gas transfer / partial pressure difference

for the gas

• CO is solely diffusion limited and hence used to measure

diffusion properties of lung

• Measured by single breath method

• 25ml/min/mmHg
Reaction with Hb and
diffusion
Blood Flow and Metabolism
Alveolar vessels
• Present in the walls of the alveoli

• Patency depends on the the pressure difference inside

and around the vessel called Transmural pressure

• Pressure around is alveolar and sometimes

atmospheric when alveoli are open in inspiration with
open glottis

• When pressure around increases vessels collapse

Extra Alveolar vessels

• Present in between alveoli

• Are pulled open when lung parenchyma expands

• Pressure around is very less compared to alveolar

vessels
Measurement of Pulmonary
Blood Flow

• Ficks Principle

• Indicator Dilultion

• ThermoDilution

• Total Body Plethysmograph

Lung Zones
• Zone 1 : Alveolar > Arterial > venous

• Does not occur normally as vessels are squashed and

no flow occurs

• Occurs in condition which cause decreased arterial

flow as in severe hemorrhage

• or on conditions causing increased alveolar pressure

as in PPV
• Zone 2 : arterial > alveolar > venous

• Arterial alveolar pressure differnce determines flow

rather than arteriovenous difference

• Flow is high at the beginning of the capillary but is

reduced towards the end because venous end is
compressed by higher alveoli pressures

• Called starling resistor or waterfall effect

• Zone 3 : arterial > venous > Alveolar

• Flow determined by artery venous difference

• Increased transmural pressures and hence increased

blood flow

• Recruitment also plays a role in blood flow through this

zone
• Zone 4 : Extra alveolar vessels
 Pulmonary circulation – Alveolar Perfusion Q

ZONE-I: Only exist if Ppa very low in

hypovolemia / PA in PEEP

ZONE-II: Perfusion α Ppa-PA

arterial-alveolar gradient

ZONE-III: Perfusion α Ppa-Ppv

arterial-venous gradient

ZONE-IV: Perfusion α Ppa-Pist

arterial-interstitial gradient
 Ventilation Perfusion Relationships
• The V/Q ratio is the crucial factor in determining alveolar and,
therefore, pulmonary capillary PO2 and PCO2,

• Alveolar PO2 is determined by the rate at which O2 is supplied

to the alveolus by ventilation, relative to its rate of removal by
pulmonary capillary blood flow

• Alveolar PCO2 is determined by the rate at which CO2 is

supplied to the alveolus by pulmonary capillary blood flow,
relative to its rate of removal by ventilation
• Normal alveolar ventilation(VA)=4lit/min

• Normal total perfusion=5lit/min.

• V/Q=0.8
• At the base of lung .Blood Flow > Ventilation.
V/Q=0.63 because ventilation is proportionally low.
S/O Shunted Blood

• At the top of lung. Blood Flow <Ventilation V/Q=3.3

because here perfusion is about nil - Dead space
ventilation

• Ventilation and perfusion are both missing

S/O Silent Unit
Ventilation

• Ventilation is unevenly distributed in the lungs.

• Rt lung more ventilated than Lt lung [53% & 47%]

• Due to gravitational influence on intra plural pr [decreased

1cm/H2O per 3cm decrease in lung height] lower zones
better ventilated
Ventilation
-6
Due to gravitational
influence on intra plural pr
[decreased 1cm/H2O per
3cm decrease in lung -3
height] lower zones better
ventilated
-1

Intra pleural pr
Ventilation pattern - VA
•Pleural pressure [Ppl] increased
towards lower zone
•Constricted alveoli in lower
zones & distended alveoli in upper
zones
•More compliant alveoli towards
lower zone
•Ventilation: distributed more
towards lower zone
Ventilation Perfusion ratio VA/Q
•Ventilation & Perfusion both are
distributed more towards lower zone. VA/Q

•Ventilation[VA] less increased

t0wards l0wer zone than Perfusion[Q]
Q

•Perfusion more increased towards

VA
Lower zone than Ventilation

•Ventilation Perfusion ratio VA/Q:

Less towards lower zone
 VENTILATION PERFUSION
RATIO

V V V

Q Q Q

Wasted Wasted
Normal
ventilation Perfusion
V&Q
V=normal V=o
V/Q=1
Q=0 Q= normal
IDEAL
V/Q=∞ V/Q=0
ALVEOLI
DEAD SPACE SHUNT
 Ventlation Perfusion ratio VA/Q
• The overall V/Q = 0.8 [ ven=4lpm, per=5lpm]
• Ranges between 0.3 and 3.0
• Upper zone –nondependent area has higher ≥ 1
• Lowe zone – dependent area has lower ≤ 1
• VP ratio indicates overall respiratory functional status of lung
• V/Q = 0 means ,no ventilation-called SHUNT
• V/Q = ∞ means ,no perfusion – called DEAD SPACE
 V

V/Q<1

Q
Means – Wasted perfusion
Shunt – 1. Absolute Shunt : Anatomical shunts – V/Q = 0
2. Relative shunt : under ventilated lungs –V/Q ≤ 1
Shunt estimated as Venous Admixture
Venous Admixture expressed as a fraction of total cardiac
output Qs/Qt
Qs = CcO2-CaO2
Qt CcO2-CvO2
Normal shunt- Physiologic shunt < 5%
•SHUNTS have different effects on arterial PCO2 (PaCO2 ) than on arterial PO2 (PaO2 ).
• Blood passing through under ventilated alveoli tends to retain its CO2 and does not
take up enough O2.
•Blood traversing over ventilated alveoli gives off an excessive amount of CO2, but
cannot take up increased amount of O2 because of the shape of the oxygen-hemoglobin
(oxy-Hb) dissociation curve.
• Hence, a lung with uneven V̇P relationships can eliminate CO2 from the over ventilated
alveoli to compensate for the under ventilated alveoli.
• Thus, with Shunt, PACO2 -to-PaCO2 gradients are small, and PAO2 -to-PaO2 gradients
are usually large.
•PAO2 is directly related to FIO2 in normal patients.
•PAO2 and FIO2 also correspond to PaO2 when there is little to no shunt.
•With no S/T, a linear increase in FIO2 results in a linear increase in PaO2.
•As the shunt is increased, the S/T lines relating FIO2 to PaO2 become
progressively flatter. With a shunt of 50% of QT, an increase in FIO2
results in almost no increase in PaO2 .
•The solution to the problem of hypoxemia secondary to a large shunt is
not increasing the FIO2 , but rather causing a reduction in the shunt
(fiberoptic bronchoscopy, PEEP, patient positioning, antibiotics,
suctioning, diuretics).
•PAO2 is directly related to FIO2 in normal patients.
•PAO2 and FIO2 also correspond to PaO2 when there is little to no shunt.
•With no S/T, a linear increase in FIO2 results in a linear increase in PaO2.
•As the shunt is increased, the S/T lines relating FIO2 to PaO2 become
progressively flatter. With a shunt of 50% of QT, an increase in FIO2
results in almost no increase in PaO2 .
•The solution to the problem of hypoxemia secondary to a large shunt is
not increasing the FIO2 , but rather causing a reduction in the shunt
(fiberoptic bronchoscopy, PEEP, patient positioning, antibiotics,
suctioning, diuretics).
HPV

• When hypoxic segments are small (<30%), HPV had little effect on PaO2,

because shunt was small.

• When most lung is hypoxic no significant normoxic region is seen to divert flow.

• When the lung is partially hypoxic (30-70%) as in OLV, large difference between

PaO2 to be expected with normal HPV and in its absence.HPV brings the PaO2

from dangerously lowlevels to acceptable levels.

 Molecular mechanism

Redox theory.
•Pulmonary vascular smooth muscle cells(pvsmc) and
type 1 cells of the carotidbody.
•Hypoxia causes inhibition of outward potassium
current. Thus causing membrane depol. and calcium
entry through voltage gatedcalcium channels
•The induction and maintenance of generalanesthesia
results in.,
• Decrease in resting lung volume hence FRC and the
compliance of the lung and chest wall reduces.
•These changes leads to atelectasis in the dependant area
of the lung.
•Pulmn shunting and perfusion of low V/Q regions
increases.
• HPV reduces blood flow to both atelectasis and the low
V/Q regions.
•Hence reducing the effects of the abnormalitiesduring the
gas exchange.
•The general view is that the inhalational agents inhibit HPV
and intravenous agents do not.
•The studies done on the same, none are withconsistent
results.
•But it is evident from these studies that both inhalational and
intravenous agents inhibit, but inhibition is less in
intravenous agents than inhalation
•It is Observed that ketamine- no reduction in FRC(adults),
impaired O2 exchange(children).
•Thiopentone- (sheep, dogs) not assoc with dec FRC,
atelectasis or abnormal oxygen exchange.
Inhibition:
•Trauma
•vasodialator drugs(nitroprusside, nitroglycerin, nitric
•oxide, isoprenaline).
•Vasoconstrictors: which constrict the pulmn
vasculature (noradr, dopamine, histamine) reduces
the effectiveness of HPV.
•Indirect inhibitors: mitral stenosis, volumeoverload,
hypothermia, thromboembolism, large hypoxic lung
segment.
• Potentiator: Almitrine a respiratory stimulant drug.

• Found to improve PaO2 in patients with COPD and to

have this effect in the absence of ventilatory
stimulation.

• It is tested in combination with nitric oxide to be used in

OLV.