RESPIRATORY PHYSIOLOGY

Presented by Dr. Sonal Chandra

OVERVIEW

A. Functional Anatomy
B. Lung Volumes
C. Dead space
D. Respiratory mechanics
E. Hypoxic pulmonary circulation
F. West zones of lung
G. Ventilation/perfusion relationship
H. Shunts
I. Gas tensions
A FUNCTIONAL ANATOMY: RESPIRATORY ZONES

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A FUNCTIONAL ANATOMY

Knowledge of the bronchopulmonary segments is important for :

• Localizing lung pathology • Identifying lung regions during bronchoscopy
• Interpreting lung radiographs • Operating on the lung
B LUNG VOLUMES
B LUNG VOLUMES (1/2)

TIDAL VOLUME
Volume of air inspired or expired at each breath
TV = 6-8 ml/kg

FUNCTIONAL RESIDUAL CAPACITY

The volume of gas remaining in the lungs after a normal expiration
FRC=30 ml/kg

INSPIRATORY CAPACITY
The maximum volume of air that can be inspired after a normal expiration.

VITAL CAPACITY
Maximum volume of air that can be expired after a maximum inspiration
VC = 60 -70 ml/kg

INSPIRATORY RESERVE VOLUME

Maximum volume of air that can be inspired after a normal inspiration.
IRV=45 ml/kg
B LUNG VOLUMES (2/2)

TOTAL LUNG CAPACITY

The total volume of air contained in the lungs at maximum inspiration. ( Maximum
amount of air the lungs can hold)
TLC – 75-80ml/kg

EXPIRATORY RESERVE VOLUME

Maximum volume air that can be expired after a normal expiration.
ERV=15 ml/kg

RESIDUAL VOLUME
Volume of air remaining in lungs after a maximum expiration

All pulmonary volumes and capacities are about 20 to 25 percent less in

women than in men
B
FUNCTIONAL RESIDUAL CAPACITY
 Volume of air remaining in the lungs after a normal expiration (normal values range from 3300ml
for male to 2300ml for female)
 RV + ERV

Factors affecting FRC :

Increases with: Decreases with :

 ↑ height  Supine position
 Upright position  Obesity
 Age  Fibrosis
 Males > Females  Kyphoscoliosis, Pulmonary
 Emphysema  Fibrosis
 Asthma  Pregnancy
 Anesthesia
 Surgery - Laparoscopy
B
Functions of FRC
 Oxygen reserve
 Buffer to maintain a steady PaO2
 Prevent atelectasis
 By keeping lung volume above closing capacity

Preoxygenation/Denitrogenation

Normally, FRC = 2000 ml containing 21% O2

Total oxygen reserve=2000 x 0.2 = 400 ml

Total body O2 consumption ~ 250ml/min → just over 1 minute apnea.

With 100 % O2, Total oxygen reserve=2000 x 1 = 2000ml → Apnea time increased to 7-8 min
C
DEAD SPACE

The part of the tidal volume not participating in alveolar gas exchange is known as

dead space

Types of Dead Space :

 Anatomical dead space

 Alveolar dead space

 Physiological dead space

 Apparatus dead space

C
ANATOMICAL DEAD SPACE
 Fraction of the tidal volume that remains in the conducting airways i.e. from nostrils and

mouth down to respiratory bronchioles

 ~ 150 ml in most adults in upright position ( approx. 2ml/kg)

Factors affecting anatomical dead space :

Factor Effect

Size of the subject ↑ with body size

Age ↑
Posture
Upright ↑
Supine ↓
Position of neck and jaw
Neck extension ↑
Neck flexion ↓
Lung vol. at the end of inspiration 20ml ↑ for each L ↑ in lung volume

Artificial airway ↓

Drugs—anticholinergic ↑
C
ALVEOLAR DEAD SPACE

 The part of the inspired gas that passes through the anatomical dead space to mix
with gas at the alveolar level, but which does not take part in gas exchange (wasted
ventilation, high V/Q zones)
 Too small to be measured accurately in healthy subjects

Factors increasing alveolar dead space :

• Low cardiac output states
• Pulmonary hypotension → failure of perfusion of upper most parts of lung (West
zone 1)
• Pulmonary embolism
• Artificial ventilation in lateral position
C
PHYSIOLOGICAL DEAD SPACE
 That fraction of the tidal volume which is not available for gaseous exchange

 Includes both anatomical and alveolar dead space

Bohr equation : Measures physiological dead space

 PACO2 is alveolar CO2 tension

 PECO2 is mixed expired CO2 tension
C
Apparatus dead space

It is the volume contained in any anaesthetic apparatus between the patient

end and that point in the system where rebreathing of exhaled carbon
dioxide ceases to occur (FGF)

It is very important factor to be considered in anesthetizing newborns and

small children
D RESPIRATORY MECHANICS

For air to flow into the lungs, a pressure gradient must be developed to overcome:
a) Elastic resistance of lungs & chest wall to expansion
b) Non elastic resistance of lungs to airflow (Airway resistance)

ELASTIC RESISTANCE
 Force tending to return the lung to its original size after stretching.
 Elastic resistance governs the lung volume and associated pressures under static
conditions
 Elastance is reciprocal of compliance
 Chest has a tendency to expand outward due to structural components that resist
deformation & probably include chest wall muscle tone
 Lungs have a tendency to collapse due to high elastin content and surface tension
forces acting at the air-fluid interface in the alveoli
D
NON-ELASTIC RESISTANCE

 Airway Resistance = (Pressure Gradient / Rate of Airflow)

 Normal = 0.5 - 2 Cm H2O/L/sec
 Highest contribution - medium sized bronchi ( before 7th generation)
 Gas Flow In Lung:
 Laminar
 Turbulent

REYNOLD’S NUMBER
 Predicts flow = (linear velocity x diameter x gas density / gas viscosity)
 < 1000 = Laminar flow
 > 1500 = Turbulent flow
D
SURFACE TENSION

 Acts in the air-water interface lining the alveoli

 Tends to reduce the area of the interface → favour alveolar collapse

 Laplace equation :

 Pressure derived is that within the alveolus

 Collapse is thus more likely when surface tension increases or alveolar size
decreases

 Surfactant :
 lowers surface tension
 effect is directly proportional to its concentration within the alveolus
 As alveoli become smaller, the surfactant within becomes more concentrated, and
surface tension is more effectively reduced
 Conversely, when alveoli are overdistended, surfactant becomes less concentrated, and
surface tension increases
The net effect is to stabilize alveoli:
• Small alveoli are prevented from getting smaller, whereas
• Large alveoli are prevented from getting larger
COMPLIANCE
 Defined as change in volume per unit change in pressure.

 Measure of elastic recoil.

 Compliance = ∆V/∆P

Factors affecting compliance :

 Lung elastic recoil
 Lung volumes
 Disease state – obstructive/restrictive
Static compliance: measured when Dynamic compliance: measured

airflow has ceased as during breath when air flow is present

holding or during apnea in  Reflects airway + elastic resistance

 Decreased in :
anaesthesia
 Reflects elastic resistance of lung & 1. Bronchospasm
chest wall
2. Kinking of ETT
 Decreased in:
3. Airway obstruction
1. Atelectasis
2. ARDS
3. Tension pneumothorax
4. Obesity
5. Retained secretions
E PULMONARY CIRCULATION
Pulmonary artery pressure:
 Systolic 20-30 mmHg
 Diastolic 8-12 mmHg
 Mean 12-15 mmHg
 Contains 10% of total blood volume → may be altered upto 50%
 Low pressure system, easily distensible with low resistance to blood flow
 ↑ pulmonary blood volume: negative pressure breathing, supine position, systemic
vasoconstriction, overtransfusion, LVF
 ↓ pulmonary blood volume: IPPV, upright position, vasalva, haemorrhage, systemic
vasodilation
Pulmonary artery hypertension:
 Pulmonary artery systolic pressure > 30 mmHg
 Due to back pressure changes:
 ↑ PBF (left to right shunt)
 ↑ PVR
E Hypoxic pulmonary vasoconstriction

 Homeostatic mechanism
 Blood flow diverted away from poorly ventilated (hypoxic) areas to better ventilated
areas → V / Q ratio improved
 Stimulus is low alveolar oxygen tension ( hypoventilation or by breathing gas with a
low PO2)

 At high altitude → generalized pulmonary vasoconstriction → Pulmonary

hypertension and pulmonary oedema may develop
 Chronic lung disease with hypoxemia → HPV → slow progress of the disease →
remodelling & thickening of the pulmonary vascular wall → edema formation
prevented
E
INHIBITORS of HPV :
Inhalational anaesthetics
Drugs:
- Calcium channel blockers
- Beta agonists
- Alpha blockers
Direct inhibitors:
- Infection
- vasodilators – NTG / SNP
- Hypocarbia
- Respiratory & metabolic alkalosis
Indirect inhibitors:
- volume overload
- thrombo-embolism
- Hypothermia
- Inhaled NO – pulmonary vasodilation
E DISTRIBUTION OF PERFUSION

 Low pressure of the pulmonary circulation allow gravity to exert a significant

influence on blood flow.

 Pulmonary artery pressure increases by 1 cm H₂O/ cm distance down the lung

(hydrostatic pressure builds up).

 This causes a pressure difference in the pulmonary arterial vessels between the apex
and the base of 11 to 15 mmHg

 Blood flow in upright position: Base > Apex

 supine position: Base = Apex
 Posterior > anterior
F
WEST ZONES OF LUNG
F
Zone 1
• No blood flow
• Wasted ventilation → alveolar dead space
• Under normal conditions little or no zone 1
exists.

Becomes significant in conditions :

 Pa is greatly reduced-hypovolemic
shock
 PA is greatly increased during IPPV
with
 large VT ventilation
 high PEEP ventilation during
IPPV
F
Zone 2
 Blood flow begins
 Determine by Pa – PA
 “Waterfall Effect”
 Pa is The height of the upstream river
before reaching the dam.
 PA the height of the dam
 The rate of water flow over the dam is
equivalent to the difference b/w Pa – PA
 It does not matter how far below the
dam the height of the downstream river
bed, PV
 Also known as Starling resistor,
weir / sluice effect
F
Zone 3
 Capillary systems are thus
permanently open
 Blood flow is continuous
 Blood flow is governed by the
pulmonary arteriovenous pressure
difference

Hughes Zone 4 : Pa > Pist > Pv > PA

Blood flow decreases due to compression of vessels by ↑ interstitial pressure
G
V/Q MISMATCH
Situation where alveoli are either over or under perfused relative to their ventilation

Variations in the relationship b/w ventilation and perfusion have smaller effect on the
CO2 than on the uptake of O2
G
ALVEOLAR – ARTERIAL PO₂ DIFFERENCE (PAO₂ - PaO₂)

 Normally PAo₂ = 13.5 kPa and Pao₂ = 12.9 kPa

 PAo₂ - Pao₂ ranges from 0.7-3.3 kPa
 Increases with age(for every decade  by 0.1 kPa)

FACTORS responsible for increase :

 Increased partial pressure of oxygen in inspired gas
 Venous admixture
 LOW V/Q RATIO
 TRUE SHUNT
 Reduced partial pressure of O₂ in mixed venous blood (P ѵO₂)
H SHUNTS

Desaturated, mixed venous blood from the right heart returns to the left heart without
being re-saturated with O2 in the lungs.

Anatomical Shunt  True shunt

Physiological Shunt  normal degree of venous admixture due to true shunt and
blood which has passed through low V/Q ratio.

Pathological Shunt  not present is normal subject. CHD RL shunt.

Atelectatic Shunt  blood which has passed through collapsed zones of lung.
CLASSIFICATION OF CAUSES OF ‘’TRUE-SHUNT’’

Physiological Shunt Pathological Shunt

(NORMAL SHUNT) (ABNORMAL SHUNT)

Extra-Pulmonary Thebesian veins Congenital disease of heart or great

vessels with RIGHT TO LEFT
SHUNT.

Intra-Pulmonary Bronchial veins Atelectasis

Possibly some slight degree Pulmonary edema, Pulmonary
of atelectasis contusions,
Pulmonary hemorrhage
Pulmonary infections
(pneumonia, consolidation)
Pulmonary arteriovenous shunts,
Pulmonary neoplasms including
haemangioma
I ALVEOLAR GAS EQUATIONS

In alveoli, inspired gas is mixed with residual alveolar gas.

Alveolar oxygen tension (PAO2) = PIO2 – PaCO2/RQ

PAO2 alveolar partial pressure of oxygen

PiO2 inspired pressure of oxygen
PACO2 alveolar partial pressure of carbon dioxide (approximates with Paco2 due to rapid
diffusion of co2)

The RQ stands for respiratory quotient and is normally 0.8. It is determined by the amount
of CO2 produced/ oxygen consumed
 Pulmonary end capillary oxygen tension = PAO2 (for all practical purposes)
 Arterial oxygen tension (PaO2) = 10.5-13.3 kPa
 Alveolar-arterial partial pressure gradient = (A-a gradient)
= 1.5 kPa
Mixed venous oxygen tension (PvO2) = 5.3 kPa
 Obtained from pulmonary artery
 represents the overall balance between O2 consumption & delivery.
GAS TRANSPORT - OXYGEN

Oxygen is transported in the blood in 2 forms:

1. Dissolved in plasma

Henry's Law: the amount of a gas which dissolves in unit volume of a liquid, at a given
temperature, is directly proportional to the partial pressure of the gas in the equilibrium
phase.
Solubility coefficient for O₂ at 37°C = 0.0225 ml O2/ kPa
Therefore, at PO₂ 13.3 kPa- dissolved O₂ ~ 0.3 ml/100ml blood
2. Oxygen Carriage by Haemoglobin

 1 gm pure Hb combines with 1.34 ml O₂

 O2 content: dissolved + combined with Hb

 Arterial O2 content = (0.0225 x PO2) + (Hb x 1.34 x SaO2)

= (0.0225 x 13.3) + (15 x 1.34 x 1.0) = 20.4ml/dl

 Venous O2 content = (0.0225 x 5.3) + (15 x 1.34 x 0.75)

= 15.2ml/dl
Oxygen delivery/ flux = amount of O2 leaving LV/minute
= arterial O2 content X Cardiac Output
= 20ml/dl X 50dl/min
= 1000ml/min

Oxygen consumption = Cardiac Output X (arterial O2 content –

mixed
venous oxygen content)
= 50 dl/min X (20-15)
= 50 X 5 = 250 ml/min

Oxygen extraction ratio = (CaO2-CvO2)/CaO2

= (20-15)/20 = 25% (normally)
Oxygen cascade
OXYGEN DISSOCIATION CURVE

 Graph that shows the percent saturation of haemoglobin at various

partial pressures of oxygen.

 Sigmoid shaped curve

 Combination of 1st heme Hb molecule with O2↑ affinity of other heme

molecules
Measure of Hb affinity for O2 quantified by P50
which is the PO2 when Hb is 50% saturated, at pH = 7.4, T = 37°C
P50 = 3.5 kPa

Shift of curve to right : lowers O2 affinity → displaces O2 from haemoglobin,

and makes more O2 available to tissues
 Fall in blood pH due to
a. ↑ CO2
b. Presence of any acid in blood
 ↑ temp
 Inhalational anesthetics: Isoflurane shifts P50 to right by 0.3 mmHg
 ↑ conc of 2,3- DPG
 2,3-DPG is a by-product of glycolysis
 with chronic anaemia and may significantly affect the O2-carrying capacity of
blood transfusions
Shift of curve to left

 Carbon monoxide
- inhibits synthesis of 2,3 DPG
- Affinity of CO for Hb is 200 times than that of O2 .
 Fetal Hb - has greater affinity for O2
 Alkalosis
 Hypothermia
 ↓ 2,3 DPG
 Abnormal Hb:
- Hbs in sickle cell anemia has less affinity for oxygen than HbA, deoxygenated blood is
less soluble, crystallization & sickling occurs
- In methHb Fe2+→ Fe3+, cannot bind with O2
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