1. The document discusses the anatomy and physiology of the respiratory system including the structure of the lungs and airways, lung volumes and capacities, ventilation-perfusion ratios, and the control of breathing. 2. Key points covered are the tracheobronchial tree structure, functional airway division into conducting and respiratory zones, bronchopulmonary segments, factors affecting lung volumes such as tidal volume and vital capacity. 3. Concepts of dead space, alveolar ventilation, and the factors controlling respiration including the respiratory centers in the brainstem and response to changes in carbon dioxide and oxygen levels are summarized.

1. RESPIRATORY PHYSIOLOGY-1
LUNG VOLUMES, CAPACITIES, VENTILATION-
PERFUSION
MODERATOR : DR. NISHANT
PRESENTER : DR. DEEPTI

2. STRUCTURE AND FUNCTION OF THE RESPIRATORY TRACT
The nose, mouth and pharynx conduct air to the larynx, humidify and filter the air gases.
TRACHEOBRONCHIAL TREE
Adult trachea –
• 10 - 11 cm long
• Starts at the level of 6th cervical vertebra
• Ends by dividing into Rt. and Lt. main bronchi at the carina, level of T5
Trachea moves with respiration and with alterations in the position of the head :
• On deep inspiration carina decends by 2.5 cm.
• Extention of head and neck- ideal positon to maintain airway in anesthetised patient-increase the
length of trachea by 23-30 percent.

3. Rt. Main bronchus is wider, shorter (2.5 cm) and more vertical than Lt. main bronchus
•
• Unintentional endobronchial intubation or foreign body aspiration on Rt. Side
• Short length makes it difficult to occlude when required in thoracic anaesthesia
• Right upper lobe bronchus dives passes in an upward and lateral direction at ∼90 degrees to the right main bronchus for 1cm
before dividing into its three main divisions, facilitating aspiration of foreign bodies and fluid into the right upper lobe in the
supine patient.
Angles of the main bronchi- 25 degrees (Rt.), 45 degrees (Lt.)
In children < 3 yrs, the angles created by the Rt. and Lt. mainstem bronchi are almost equal ~ 55 degrees.

4. FUNCTIONAL AIRWAY DIVISION
• Dichotomously branching tubes, same generation
have identical dimensions
• Conducting zone- 1-16- allows basic gas
transport/ no gas exchange/ 10 % total airway
volume
• Respiratory zone- next 7 divisions/ gas exchange/
surface area 70 m²

5. Knowledge of the bronchopulmonary segments is important for :
• localizing lung pathology,
• interpreting lung radiographs,
• identifying lung regions during bronchoscopy
• operating on the lung.
10 8
BRONCHO-PULMONARY SEGMENTS

6. Common sites of lung abscess :
•Posterior segment of upper lobe + apical/superior segment of lower lobe
in supine
• Lateral portion of posterior segment of upper lobe in lateral
• when propped up in postop period → lower lobes
Surgery offers one the most favourable conditions for aspiration & Lung abscess as :
i. Inadequate cough reflex
ii. Prolonged immobilisation

7. LUNG VOLUME & CAPACITIES

8. LUNG VOLUMES
Tidal Volume(tv) :  Volume of gas that moves in and out of the lung during quite breathing.
6-8 ml/kg or 500 ml
Reduces with : Decreased lung compliance
Reduced respiratory muscle strength.
InspiratoryReserveVolume(irv): Maximum volume of gas that can be inhaled following normal inspiration
while at rest.
 45 ml/kg
 Male : 3000 ml & Female : 1900 ml

9. Expiratoryreserve volume (erv) :  Maximum volume of gas that can be exhaled following normal expiration
while at rest.
 15 ml/kg
 Male : 1100 ml & Female : 700 ml
Residual volume (rv) : Volume of gas that remain in lung after forced exhalation.
 15-20 ml/kg
 Male : 1200 ml & Female : 1100 ml
 Not measured by Spirometry

10. LUNG CAPACITIES
• VITALCAPACITY:  Maximum amount of gas that can be exhale after maximum inhalation.
 60-70 ml/kg
INSPIRATORY CAPACITY:  Maximum amount of gas that can be inhaled from the resting expiratory position
after normal expiration.
TOTALLUNGCAPACITY:  Is the lung volume at the end of a maximum inspiration.
 80 ml/kg
TLC= VC + RV
VC =IRV + TV + ERV
IC =IRV + TV

11. FUNCTIONAL RESIDUAL CAPACITY
• Amount of the air remaining in lung after normal expiration.
• It is the balance between tendency of the chest wall to spring outwards and the tendency of the lung to collapse
.
• FRC = RV + ERV
• 2500 ML or 30-40 ml/kg
• Contribute around 40% of total lung capacity .
• Factors decreasingFRC
- Ageing - Abdominal swelling ( ascites )
- Posture – supine position , Trendelenburg position - Reduced muscle tone
- Anaesthesia- muscle relaxants , sedation - Pregnancy
- Surgery – Laparoscopic surgery -Neuromuscular disease :
- pulmonary fibrosis myasthenia gravis
- Pulmonary oedema poliomyelitis
- obesity

12. • Factor increasingFRC:
- Increasing height of patient
- Erect position
- Emphysema : decreased elastic recoil of lung , therefore less tendency of lung
to collapse.
- Asthma : air trapping
- PEEP
Measurement of FRC is done by :
1. Helium dilution technique
2. Body Plethysmography
3. Nitrogen washout technique

13. SIGNIFICANCE OF FRC
• Help in gas exchange
• Dilute inhaled toxic gases
• Load on rt ventricle is reduced as collapsed lung increases the PVR
• Preoxygenation fills FRC with oxygen. It increases oxygen reserve from 500ml to 2400 ml ,
thus increases apenic time to 7-8 min
• Effects of Anaesthesia :
- FRC reduced by around 20% after induction , reduction may account to around 50% in
obese patients.
-Mechanism of reduced FRC :
1. Loss of inspiratory muscle tone causing loss of outward recoil
of
chest wall

14. 2. Loss of tone of scalene , sternocleidomastoid & intercostal muscle.
3. Loss of tone of diaphragm leading to cephalad displacement
4. Supine or Trendelenburg position
In a healthy young adult , FRC is above CC, increase in CC or decrease in FRC can results in
closure of the small airways during certain period of normal tidal ventilation. This airway
closure produces shunting , with perfusion of unventilated lung. Therefore shunt is increased
and arterial oxygenation is decreased.
Closing Capacity (CC) : It is the lung volume at which small airways in the dependent part of
lung begins to close. CC= CV+RV.
If CC = FRC , some airway remain closed , even with normal tidal volume breathing
If CC> FRC, airway closure occur , causing V/Q mismatch

15. • TV+IRV+ERV
• Varies with age, height, weight, physical training & normal VC is about 60–70 mL/kg.
Decreased by
1. Lesions in brain, nerve, neuromuscular mechanism
2. Pulmonary disease- asthma, chronic bronchitis, pulm.fibrosis
3. Chest Space occupying lesions- Pericardial and pleural effusions, pneumothorax, tumours, consolidation,etc
4. Abdominal tumors impeding diaphragmatic descent
5. Abdominal pain: 70-75% in upper abdominal & 50% in lower abdominal operations
6. Tight abdominal binders, strapping or bandaging
7. Alterations in posture→alter blood volume in the lung → maximum decrease with lithotomy
VITAL CAPACITY

16. Significance of Vital Capacity :
• During anaesthesia:
• minimal change unless alteration in vital capacity is significantly pronounced, e.g., tension
pneumothorax, etc.
•Post operative period:
• Reduction in VC may impede expulsion of secretions.
• If VC falls below 3 times of TV artificial help may be needed to maintain airway free of secretions.

17. CLOSING CAPACITY
Closing capacity : Lung volume at which small airways begin to close during expiration.
Closing volume :The volume above RV at which airways begin to close during expiration.
CC = Residual volume + Closing Volume

18. CC ↑es with :
•Age
• Smokers
• Obesity
• COPD
• LVF
• After surgery
Relation of CC with FRC :
• Normally FRC > CC
• CC= FRC :
At 66 yrs in upright position
At 44 yrs in supine position
• Beyond this CC >> FRC
When FRC ↓ below CC → small airways close at the end of normal tidal expiration →
hypoxaemia, atelectasis and worsening gas exchange (d/t increasing V/Q mismatch)

19. • PEEP ↑es FRC and hence improving gas exchange
• FRC with age ( because of loss of elastic tissue)
• Step with supine ( diaphragm elevation by abdominal contents)
• Further with anesth. + supine
• CC – more steep increase with age- airway closure above FRC in upright subjects(>65 yrs) and in
supine subjects(>45 yrs).

20. 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

21.  ANATOMICAL DEAD SPACE
Volume of the conducting air passages i.e. from nostrils and mouth down to
but not including respiratory bronchioles.
• ~ 150 ml in most adults in upright position ( approx. 2ml/kg )
Factors affecting anatomical dead space :
Size of subject => increases with body size.
Age , sex => at infancy, anatomical dead space is higher for body weight
(3.3ml/kg) ,it may be 100 ml in young woman and 200 ml in old man.
Position of neck and jaw => Depression of jaw with flexion of head ( as
occurs in respiratory obstruction in anesthetized person) can reduce dead space
by 30 ml, on contrary protrusion of jaw with neck extension may increase by 40
ml.
Drugs e.g. bronchodilator will increase dead space.

22. Measurement of anatomical dead space
Fowler's method
Based on rapid dilution of gas already in lung (N2 or CO2) by inspired gas
(100% O2).
1.Single breath of 100% O2
2.During the following expiration, [N2] increases from 0% (pure dead space
gas) to equilibrium (pure alveolar gas) (i.e. plateau)
=> as per [N2] vs time graph
3.Using [N2] vs expired volume graph, anatomical dead space is taken to be
at the mid-point of the transition from conducting zone to gas exchange zone.

24. • 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
 ALVEOLAR DEAD SPACE
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

26.  PHYSIOLOGICAL DEAD SPACE
That fraction of the tidal volume which is not available for gaseous exchange.
• Includes both anatomical and alveolar dead space.
• In normal humans anatomical and physiological dead space are almost equal ~ 30% of tidal volume, i.e., the V
D/ VT ratio is 0.3(0.25-0.4)
Physiological dead space is increased by :
• Old age
• Upright> Supine position
• Large tidal volume
• High RR
• Bronchodilator
• Inspiratory time is ≤ 0.5 sec during controlled ventilation
• Lung diseases with altered V/Q ratio

27. Estimation of physiological dead space during anaesthesia with
passive ventilation : Cooper’s formula
V D/ VT = [33 + Age/3 ] %
Where PACO2 is alveolar CO2 tension
PECO2 is mixed expired CO2 tension
Bohr equation : Measures physiological dead space

28. ALVEOLAR VENTILATION
That part of minute volume which participates in gas exchange.
• 2 – 2.4 L/min/m2 BSA
• ~ 3.5 - 4.5 L/ min in adults
• VA = (VT – VD Phy ) x RR
Where VA – Alveolar Ventilation
VT - Tidal volume
VD Phy - Physiological dead space
RR – Respiratory rate
• It is the pulmonary factor controlling the excretion of carbon dioxide by the lungs.
• Alveolar ventilation depends on relationship b/w RR and TV.
• * High RR and low TV result in higher proportion of wasted ventilation per min.
• * Most efficient breathing pattern is slow and deep breathing.

29. MUSCLES OF RESPIRATION

30. CONTROL OF BREATHING
• Respiratory centres:
1. Inspiratory centre- dorsal part of medulla,on each
side, basic rhythm.
2. Pneumotaxic centre- upper pons, limits inspiration,
faster RR.
3. Apneustic centre (excitatory)- lower pons,
overridden by pneumotaxic centre.
4. Expiratory centre-ventral medulla,- inspiratory mscl.
For passive expiration

31. CO2 RESPONSE CURVE
• Relationship between PaCO2 and minute volume
is nearly linear
• Slope is a measure of subject’s ventilatory
senstivity to CO2
• Shift to right: signify depression of ventilation
• The PaCO2 at which ventilation is zero ( x-
intercept) is known as the apneic threshold .
Spontaneous respirations are typically absent
under anesthesia when PaCO2 falls below the
apneic threshold.

32. Factors influencing CO2 Curve :
1.Individual responses
2.Hypoxia: steeper curve; reinforces the ventilatory response to CO2
3.Metabolic alkalosis: right shift
4.Metabolic acidosis: left shift
5.Chronic bronchitis and other chronic diffuse airway obstructive diseases- flattened curve
6.Opiates depress ventilatory response to CO2 (morphine – right, pethidine- right + depressed slope)
7.Inhalational agents-ventilatory responses to inhaled CO2 progressively reduced as anaesthesia
becomes deeper and eventually becomes flat.

34. • Central Chemoreceptors
• Lie on the anterolateral surface of the medulla
• Respond primarily to changes in cerebrospinal fluid (CSF) [H+]
• Blood–brain barrier is permeable to dissolved CO2 but not to bicarbonate ions.
• Acute changes in PaCO2 , but not in arterial [HCO3-], are reflected in CSF
• ↑PaCO2 → ↑ CSF [H+] concentration → activate the chemoreceptors → stimulates
adjacent respiratory medullary centers → alveolar ventilation ↑→ PaCO2 ↓ back to
normal.

35. • Peripheral Chemoreceptors
Include :
• carotid bodies (at the bifurcation of the common carotid arteries)
• aortic bodies (surrounding the aortic arch)
 Carotid bodies are the principal peripheral chemoreceptors and are sensitive to
changes in PaO2 (most sensitive to PaO2), PaCO2, pH and arterial perfusion presssure.
• also stimulated by cyanide, doxapram, and large doses of nicotine
• Receptor activity does not appreciably increase until PaO2 decreases below 50 mm Hg

36. Respiratory tract reflexes
1. Hering- Breuer Inflation Reflex - inhibition of inspiration when the lung is inflated to
excessive volumes.
2. Deflation Reflex - shortening of exhalation when the lung is deflated.
3. Irritant receptors in the tracheobronchial mucosa react to noxious gases, smoke, dust, and
cold gases; activation produces reflex increases in respiratory rate, bronchoconstriction,
and coughing.
4. J (juxta-capillary) receptors located in alveolar walls → induce dyspnea,
bronchoconstriction and contraction of adductor muscles of larynx in response to
expansion of interstitial fluid like in pulmonary oedema, microembolism and pnemonia.

37. BASIC MECHANISM OF BREATHING
• The pressure within alveoli is always greater than the
surrounding (intrathoracic) pressure unless the alveoli are
collapsed.
• Alveolar pressure is atmospheric (zero for reference) at
end-inspiration and end-expiration
• Pleural pressure is used as a measure of intrathoracic
pressure - At end-expiration, intrapleural pressure
normally averages about –5 cm H2O
• Transpulmonary pressure is the pressure needed
to keep the lung inflated at a certain level

38. 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)
RESPIRATORY MECHANICS
 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
Lungs have a tendency to collapse due to high elastin content and surface tension forces
acting at the air-fluid interface in the alveoli

39. SURFACE TENSION
• Acts in the air-fluid 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 :
o lowers surface tension
o effect is directly proportional to its concentration within the
alveolus.

40. 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

41. COMPLIANCE
• Defined as change in volume per unit change in pressure.
• Measure of elastic recoil.
•Compliance = ∆V/∆P
Factors affecting compliance :
1.Lung elastic recoil  Due to:
a) Surface tension in the alveoli (accounts for 70% of the elastic recoil)
b) Stretched elastic fibers in the lung parenchyma

42. 2.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
3.Disease state.

43. • Static compliance: measured when airflow has ceased as during breath holding or during
apnea in anaesthesia.
o Reflects elastic resistance of lung & chest wall.
o Decreased in:
1. Atelectasis
2. ARDS
3. Tension pneumothorax
4. Obesity
5. Retained secretions

44. Static Compliance Curves
-18
-16
-14
-12
-10
-8
-6
-4
-2
0
2
Fibrosis
(low compliance)
Normal
Emphysema
(high compliance)
VT
FRCN
VT
FRCF
VT
FRCE
Pleural Pressure, Ppl (cm H2O)
Lung
Volume
In restrictive lung disease
• Curve shifts to right
• Smaller FRC
• Lower lung compliance
In obstructive lung disease
• Curve shifts to left
• Increasing FRC (gas trapping)
• High compliance in emphysema
• Elastic recoil is minimal

45. • Dynamic compliance: measured when air flow is present.
o Reflects airway + elastic resistance.
o Decreased in :
1. Bronchospasm
2. Kinking of ETT
3. Airway obstruction

46. • Lung Compliance(CL ) is defined as :
CL is normally 150–200 mL/cm H2 O
•Chest wall compliance is given by :
o Where transthoracic pressure equals atmospheric pressure minus intrapleural pressure.
o Normal chest wall compliance is 200 mL/cm H2 O
• Total compliance (lung and chest wall together) is 100 mL/cm H2 O and is expressed by the
following equation:

47. 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)
Factors affecting airway resistance
1. Lung volume
2. Density and viscosity of inspired gas
3. Small airway obstruction
• Constriction of bronchial smooth muscles
• Oedema of bronchiolar tissues, mucosal congestion, inflammation
• Plugging of the lumen by mucus, oedema fluid, exudate, or foreign bodies

48.  LAMINAR FLOW
• Consists of concentric cylinders of gas flowing at different velocities, velocity is highest in the
centre & ↓ towards periphery
•During laminar flow,
Flow = Pressure gradient
Airway resistance
•Using Poiseuille’s equation
R = 8 x length x viscosity = __Δ P__
π x (radius)4 Flow
• Laminar flow-distal to small bronchioles (<1mm)

49.  TURBULENT FLOW
• Characterised by random movement of the gas molecules in air passages
∆P = FLOW2 x GAS DENSITY
Radius5
• Is extremely sensitive to airway calibre
• Turbulence occurs at
- High gas flows - Sharp angles
- Bifurcations - Abrupt change in airway diameter
- large airways

50. REYNOLD’S NUMBER
• Predicts flow
• = linear velocity x diameter x gas density
gas viscosity
• < 1000 = Laminar flow
• > 1500 = Turbulent flow
Helium has lower density to viscosity ratio → He-O2 mixture reduces turbulent flow & airway resistance

51. INFERENCES FROM POISEULLE’S HAGEN EQUATION
Reducing tube diameter by half requires 16 fold ↑in
Pressure to maintain same flow
Small changes in bronchial caliber can markedly
change flow rates.
Basis for - 1. bronchodilator therapy
2. using largest practical size of artificial
airway

52. WORK OF BREATHING
Done by respiratory muscles to overcome
• elastic resistance of lung and chest wall
• airflow resistance at tracheo-bronchial tree
• tissue frictional resistance or structural resistance
Normal breathing – active inhalation
- passive exhalation
( work of exhalation recovered from potential energy stored in expanded lungs & thorax during inspiration)
WORK = FORCE x DISTANCE
FORCE = PRESSURE x AREA
Distance = volume / area
WORK = PRESSURE x VOLUME
= Area under P-V curve

53. Components of Work of breathing
Elastic work - work to overcome:
•lung elastic recoil
•thoracic cage displacement
•abdominal organ displacement
Frictional work - work to overcome:
•air-flow resistance (major)
•viscous resistance (lobe friction, minor)
Inertial work - work to overcome:
•acceleration and deceleration of air (negligible due to low mass of air)
•acceleration and deceleration of chest wall and lungs (negligible due to over damping)

54. Minimizing work of breathing
Among the factors influencing work of breathing, two factors are important in minimizing work:
• Lung volume (at FRC)
• Respiratory rate
 Lung volume
Work of breathing is minimized at FRC, because..
 high pulmonary compliance (on steep part of the pressure-volume curve)
--> Elastic work is low
Low airway resistance
--> Resistance work is low (but not lowest)
Partial inflation and being at a volume above the closing capacity
--> No work required to open collapsed parts of the lung or closed airways
At low lung volume, resistance work is increased (due to increased airway resistance)
At high lung volume, elastic work is increased (due to already stretched fiber).

55.  Respiratory rate
Given the same minute volume,
 There is a optimal RR which minimizes the total work required.
 RR > Optimal rate
--> Decreased tidal volume
--> Increased work due to airway resistance
 RR < Optimal rate
--> Increase work due to elastic recoil

56. 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, valsalva, haemorrhage, systemic vasodilation.
Pulmonary artery hypertension:
Pulmonary artery systolic pressure> 30 mmHg
Due to back pressure changes,
↑ PBF (left to right shunt)
↑ PVR (advanced chronic bronchitis due to chronic hypoxia)
PULMONARY CIRCULATION

57. PULMONARY VASCULAR RESISTANCE (PVR)
Pulmonary vascular resistance (PVR) is about 1/8 to 1/10 of the systemic vascular resistance
Mean pulmonary blood pressure = 15
Left atrium blood pressure = 5
Pulmonary blood flow = 5~6 L/min
PVR = Pressure difference / blood flow
= (15-5)/5 or (15-5)/6
= about 1.7~2.0 mmHgL-1min
Alternatively,
PVR = (Mean pulmonary artery pressure - mean pulmonary capillary wedge pressure)/cardiac
output
All 3 of these variables can be measured with a Swan-Ganz catheter

58. Factors affecting PVR
1. Viscosity of blood
2. Radius of vessel( inversely proportional to 4th power)
3. Pulmonary blood flow: As pulmonary blood flow increases, PVR drops because of:
recruitment - some capillaries, which were closed or open but with no blood flow, begins to conduct
blood
distension - capillaries change from near flattened to more circular
Both mechanisms contribute, but:
at low pulmonary arterial pressure, recruitment dominate
at high pulmonary arterial pressure, distension dominate
4. Lung volume: At high lung volumes : Resistance is increased because:
stretching of alveolar walls
=> decreased caliber of alveolar capillary
=> increased resistance
At low lung volumes : Resistance is increased because:
reduction in radial traction by lung parenchyma
=> decreased caliber of extra-alveolar capillary
Lowest PVR occurs at functional residual capacity.

59. 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)
• 50 % of the final shift in blood flow occurs in 2 minutes of onset of alveolar hypoxia.
• And is complete after 7 minutes.
• Response occurs locally and may have some autonomic contribution.

60. 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

61. VENTILATION
&
PERFUSION

62. VENTILATION
The rate at which air enters or leaves the lungs.
 Types : i) Pulmonary Ventilation
ii) Alveolar Ventilation
1)Pulmonary Ventilation (minute ventilation or
respiratory minute volume): Is the volume of air
moving in and out of respiratory tract in a given unit of
time during quiet breathing.
INTRODUCTION


63. 
 Pulmonary Ventilation= Tidal volume X Respiratory a
= 500 ml x 12/minute
= 6000 ml/minute
2) Alveolar ventilation: It is the amount of air utilized for
gaseous exchange every minute.
Alveolar ventilation
= (Tidal volume – Dead space) X Respiratory Rate
= ( 500 – 150 ) ml x 12/minute
= 4200ml/minute
TYPES OF
VENTILATION.....

64. 
 PERFUSION: The movement of blood
into lung through pulmonary capillaries.
 VENTILATION/PERFUSION RATIO:
It is the ratio of alveolar ventilation and
the amount of blood that perfuse the alveoli.
Mathematically, V/Q = 0.84
VENTILATION AND PERFUSION

65. 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 mm Hg.
• Blood flow in upright position: Base > Apex
supine position: Base = Apex
Posterior > anterior

66. WEST ZONES OF LUNG

67. 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

68. 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.

69. 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

70. DISTRIBUTION OF VENTILATION
During quiet breathing, most gas goes to the lower, dependent regions
• basal, diaphragmatic areas in the upright or sitting position and
• dorsal units in the supine position  Alveolar pressure is constant all over the lung.
 Intrapleural pressure is less negative at the bottom than
the top of the lung d/t gravity.
1 cm H2O decrease per 3 cm decrease in lung
height
 Transpulmonary pressure ( pressure needed to keep
the lung inflated at a certain level)
PTP = Alveolar pressure – Intrapleural pressure
 PTP apex > PTP base in an upright posture
 Alveoli in upper lung areas are near-maximally inflated and relatively noncompliant, and they undergo
little expansion during inspiration.
While the smaller alveoli in dependent areas are more compliant, and undergo greater expansion during
inspiration.

71. VENTILATION/PERFUSION RELATIONSHIPS
Normal alveolar ventilation (V) = 5 l/min
Total perfusion = 5 l/min (Q).
VENTILATION-PERFUSION RATIO = 1
• Both V and Q increase down the lung but ↑ in Q > ↑ in V
• Bottom of the lung :
• Q>V → low V/Q ratio ~ 0.63
• Blood leaving the base is slightly hypoxic and
hypercapnic.
• Passing up the lung → both V & Q decrease → ↓ in Q is 3 times > ↓ in V
• Top of the lung:
• V>Q → high V/Q ratio ~ 3.3 → wasted ventilation
• Blood leaving apices is almost 100% saturated with slightly low CO2 content.

72. 
VENTILATION AND PERFUSION
(5ml/minute)
(0.56ml/minute
)
(10.3ml/minute
)

73. 
• Zone 1: Ventilation(V) >>> Perfusion(Q)
• V/Q= 3.4 (high)
• Zone 2: Ventilation(V) = Perfusion(Q)
• V/Q= 0.8 (average)
• Zone 3: Perfusion(Q) >>> Ventilation(V)
• V/Q=0.63(low)
V/Q IN DIFFERENT
ZONES OF LUNGS

74. ALVEOLAR – ARTERIAL PO₂ DIFFERENCE (PAO₂ - PaO₂)
•Normally PAo₂ = 101 mm Hg and Pao₂ = 97 mm Hg.
•PAo₂ - Pao₂ ranges from 5-25 mm Hg.
•Increases with age(for every decade  by 1 mm Hg).
FACTORS responsible for increase :
1. Increased partial pressure of oxygen in inspired gas
2. Venous admixture
i. LOW V/Q RATIO
ii. TRUE SHUNT
3. Reduced partial pressure of O₂ in mixed venous blood (PѵO₂)

75. 1. Increased partial pressure of oxygen in inspired gas – higher the alveolar Po ₂, greater is the
alveolar – arterial Po₂ difference, due to the shape of ODC. A small difference in the O₂ content of blood
at high levels of Po₂ is reflected by a large change in Po₂.
2. Venous admixture -Amount of mixed venous blood that would have to be mixed with pulmonary end
capillary blood to account for difference in O ₂ tension between arterial and pulmonary end capillary
blood. Normally – upto 5 % of CO.
1. TRUE SHUNT – blood which has passed from right to left side of circulation and picked up no
oxygen in the lungs
2. LOW V/Q RATIO – blood has picked up some O₂ in the lungs but is still less than fully
oxygenated, having passed through relatively overperfused or underventilated zones.
3. Reduced partial pressure of O₂ in mixed venous blood (PѵO₂) – The lower the PѵO₂ the greater will
be the effect of a given amount of venous admixture on PAo₂ - Pao₂ difference. The commonest cause of
a reduced PѵO₂, apart from arterial hypoxia is a low cardiac output

76. Desaturated, mixed venous blood from the right heart returns to the left heart without being resaturated
with O2 in the lungs.
SHUNTS
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.

77. Physiological Shunt
(NORMAL SHUNT)
Pathological Shunt
(ABNORMAL SHUNT)
Extra-Pulmonary Thebesian veins Congenital disease of heart or great vessels
with RIGHT TO LEFT SHUNT.
Intra-Pulmonary Bronchial veins
Possibly some slight degree of
atelectasis
Atelectasis
Pulmonary edema, Pulmonary contusions,
Pulmonary hemorrhage
Pulmonary infections (pneumonia,
consolidation)
Pulmonary arteriovenous shunts,
Pulmonary neoplasms including
haemangioma.
CLASSIFICATION OF CAUSES OF ‘’TRUE-SHUNT’’

78. Normal = upto 2% of cardiac output
(physiological shunt)

79. POSITIONING
SUPINE: - distribution of ventilation & perfusion is even from top to bottom
- anterior to posterior gradient appears
LATERAL: - blood flow is greater to dependent lung.
 Normal conscious : Ventilation is also greater to the dependent lung, preventing substantial fall in V/Q ratio
of this lung.
 Anaesthetised : Ventilation is greater to the upper part/area of the lung, so the V/Q ratio of the lower lung
falls.
 If Chest wall is opened - ventilation to the upper lung is greatly ,this causes further  in V/Q mismatch
and reduction in PaO2.
PRONE : The vertical pleural pressure gradient may be smaller in the prone position than when supine. This may
be due to the weight of the heart, which is compressing the dependent parts of the lung in the supine position and
permitting the nondependent regions to expand. In the prone position, the heart is resting on the sternum with less
effect on the shape of the lung.

80. • Thank You !