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1. Ventilation, Transport of gases and
oxygen delivery
Dr. Megha Jain
University College of Medical Sciences & GTB Hospital,
Delhi

2. Contents





Lung volumes
Mechanics of ventilation
Work of breathing
Diffusion of gases
Transport of gases and oxygen delivery

3. Lung volumes

Tidal volume- Volume of air breathed in or out of the lungs, during
quiet respiration. Average: 500ml in adult.

Inspiratory reserve volume- Maximal volume of air which can
be inspired after normal tidal inspiration.
Average: 3000 ml.

Expiratory reserve volume- Maximal volume that can be
expired below normal tidal expiration. Average: 1100ml.

Residual volume- Volume of air remaining in lungs after maximal
expiration. Average: 1200ml.

Total lung capacity- Volume of air contained in lungs after
maximal inspiration. Average: 5800ml.

4. Lung volumes

Vital capacity- Maximal volume of air that can be
exhaled following maximal inspiration. Average: 60-70
ml/kg.

Functional residual capacity- Lung volume at the
end of normal exhalation. Average: 2300ml.

Closing capacity- Volume at which the small airways
begins to close in the dependent parts of the lung.
Normally – well below FRC, but ↑ with age.
It equals FRC in supine position( at around 44 yrs)
in upright position( at around 66 yrs)
Unlike FRC unaffected by posture.

5. Lung volumes

6. Spirometry

7. Ventilation






Defined as mechanical movement of air into and out of
the lungs.
Primary mechanism for excretion of Carbon dioxide
Cyclic activity- 2 components
Inward flow of air- Inhalation- active process
Outward flow of air- Exhalation- passive process
Minute ventilation- sum of all exhaled gas volumes in
one minute.
MV= RR X TV
MV= RR X TV.
Normal range= 5 to 10 lts/min in resting state.

8. Ventilation

Dead space ventilation- some of the minute volume occupies
space in conducting zones, does not participate in gas exchange
and forms anatomic dead space
Average in upright position – 150 ml or 2 ml/kg
Alveolar dead space- adequately ventilated alveoli not
participating in gas exchange as perfusion is absent.
Physiologic dead space- sum of anatomic and alveolar dead
space.

Alveolar ventilation- volume of inspired gas actually taking part
in gas exchange in one minute.
AV= RR X (TV – DV) = 12 X (500-150) = 4200 ml/min

9. Ventilation

Dead space to tidal volume ratio: a numeric index of the total
amount of wasted ventilation
Vd/Vt = PAco2 – PEco2/PAco2 (N value=0.2 - 0.4)

It represents the primary clinical measure of efficiency of
ventilation
Clinical significance:
Alveolar ventilation depends on relationship b/w RR and TV.
* High RR and low TV result in higher prop. of wasted ventilation per
min.

* Most efficient breathing pattern is slow and deep breathing.

10. Ventilation
RR
Normal
High rate,low
volume
Low rate,high
volume
↑ed dead
space
Compensatio
n for ↑ed dead
space
TV
MV
Physio.
Alveolar
ventilation
12
24
500
250
6000
6000
Dead
space
150
150
06
1000 6000
150
5100
12
500
6000
300
2400
12
650
7800
300
4200
4200
2400

11. Effectiveness of ventilation

Ventilation is effective when the body’s need for removal of CO2 is
adeqately met.

Under resting metabolic conditions the body produces about 200 ml
CO2 per min.

The relative balance b/w CO2 production and alveolar
ventilation determines the level of CO2 in lungs and in the blood.
PAco2 = V CO2/V A or total CO2 production/CO2 elimination

Normal- alveolar and arterial partial pressures of CO2 are in close
equilibrium at approx 40 mmhg.

12. Effectiveness of ventilation

In cases where alveolar ventilation is ↓ed:
rate of CO2 production > rate of excretion
thus PA CO2 will rise above its normal value.

Thus, ventilation that is insufficient to meet metabolic needs –
hypoventilation

Very high arterial PaCO2 – depress ventilatory response
(CO2 narcosis)

Alveolar hypoventilation: by definition it exists when arterial PaCO2
↑ses above normal range of 37 to 43 mmhg(hypercarbia)

13. Mechanics of ventilation
Forces opposing lung inflation
ELASTIC
Lung, thorax,
surface
tension
FRICTIONAL
Airflow
Tissue movement

14. 
In intact thorax,
Lungs & thorax recoil in opposite directions

Point at which these forces balance = resting vol of
lung

AT THIS POINT
Ppulm =Patm
No air flows
Vol. retained in lungs = FRC = 40% of TLC

15. Elastance
Physical tendency to return to original state after deformation
Lung vol at any
given P is
slightly more
during deflation
than it is
during inflation.
↓
HYSTERESIS
↓
(Due to surface
tension)

16. GRAVITY DEPENDENT ventilation exploited to direct ventilation
towards healthy lung by changing position of patient

17. Frictional forces opposing inflation
Tissue viscous
resistance(20%)
Due to tissue displacement during
ventilation (lungs, thorax,
diaphragm)
↑ by obesity, fibrosis, ascites
Airway resistance(80%)
Raw = ∆P(driving P)/ ∆V(flow rate)
= transrespiratory P/flow rate
= 0.5-2.5 cmH2O/L/sec
Flow measured by
PNEUMOTACHOMETER
P measured by
PLETHYSMOGRAPH
Affected by pattern of flow

19. Distribution of airway resistance
80%
Nose, mouth, large airways
TURBULENT FLOW
20%
Airways < 2 mm diameter
LAMINAR FLOW
Branching of airway ↑ total
cross sectional area with each
generation
↑ area → ↓ velocity→ + laminar flow
Deflation - ↑ airway diameter → ↑ resistance
Wheezing heard during EXPIRATION

20. Types of airflow
LAMINAR
TRANSITIONAL
Governed by Poiseulle’s
Hagon equation
TURBULENT

21. LAMINAR
∆P = 8ηL X flow
π r4
η – viscosity
L – length of tube
r – radius
∆P – driving P
↑ Reynold’s number
Re = ρ D V
η
TURBULENT
∆P = flow2 X ρ
r5
ρ -density
1. Helium is less dense but more viscous than air
Advantageous in turbulent flow but not laminar flow

22. Inferences from poiseulle’s hagen equation

∆P = 8ηL X
flow
Reducing tube diameter by half requires 16 fold ↑in
π r4 P to maintain same flow

∆P α flow
r4

Small changes in bronchial caliber can markedly
change flow rates.
Basis for - 1. bronchodilator therapy
2. using largest practical size of artificial
Flow α ∆P X r4
airway

23. Flow – volume loops
To diagnose lung
pathologies as
Extra / intrathoracic
Variable / fixed
Obstructive / restrictive

24. AIRWAY OBSTRUCTION
FIXED
Circumferential narrowing
Not affected by thoracic P
VARIABLE
INTRATHORACIC
EXTRATHORACIC
Below 6th tracheal ring Above suprasternal notch
Expiratory curve
Inspiratory curve plateaus
plateaus

25. Fixed
Variable
extrathoracic
Variable
intrathoracic

27. Work of breathing

Done by respiratory msls to overcome elastic &
frictional forces opposing inflation.
W = F X S ( force X distance)
= ∆P X ∆V
= area under P-V curve
Normal breathing – active inhalation
- passive exhalation ( work of
exhalation recovered from potential energy stored in
expanded lungs & thorax during inspiration)

28. Area 1 = work done against elastic forces ( compliance) = 2/3
Area 2 = work done against frictional forces ( resistance work) = 1/3
Area 1+2 = total work done = 2/3 + 1/3 = 1

29. ↑TV → ↑ elastic component of work
↑ RR ( flow) → ↑ frictional work
People with diseased lungs assume a ventilatory pattern
optimum for minimum work of breathing.
FIBROSIS
Restrictive disease
Rapid shallow breathing
(↓elastic work)
COAD
Obstructive disease
Slow breathing with pursed lips
(↓ frictional work)

30. Transport of gases


Diffusion: gas movement b/w the lungs and tissue
occurs via simple diffusion.
For O2 there is a stepwise downward cascade of
“partial” pressure.
PP of oxygen
Atmospheric = 147
Alveolar = 100
Arterial = 97
Venous = 40
Tissue = 5

31. Mechanism of diffusion


Physical process whereby gas molecules move from
area of high partial pressure to low one.
Five barriers
* RBC
* Capillary membrane
* Interstitial fluid
* Alveolar membrane
* Surfactant

32. Fick’s law of diffusion

Describes bulk movement of gases through biological
membranes
V gas = A X D X (P 1 – P 2 )/T
A = Cross sectional area
D
= Diffusion coefficient of gases
T=
Thickness of memb.
P1 – P2 = Diff. in partial pressure

Pulmonary end capillary O2 tension (Pc’O2) depends on:
# rate of O2 diffusion
#
pulmonary capillary blood volume
#
transit time

33. 
Capillary transit time = pulm cap bld vol/CO
= 70 ml/5000 ml per min
= 0.8 seconds.

High fever, septic shock often cause ↑ed CO, limit
diffusion time due to ↑ed blood flow

Maximum Pc’O2 attained after only 0.3 sec ,providing a
large safety margin (like exercise where transit time ↓
due to ↑ blood flow)

For practical purposes, Pc’O2 is considered identical to
PAO2.

34. Diffusion of gases

35. Diffusion capacity

Defined as no. of ml of a specific gas that diffuses across
the ACM into the bloodstream each min for each mmhg
diff in pressure gradient
DLO 2 = O 2 uptake/ PAO2 - Pc’O2

Carbon monoxide is preferred over O2 as test gas since
its higher affinity for Hb keeps its cap pp very low, so
Pc’O2 can be considered as zero
DL CO = CO uptake/PA CO

Reduction in DL CO implies impaired gas transfer
seen in * abnormal V/Q ratio
* destruction of memb
* very short capillary transit time

36. Determinants of alveolar gas tensions


Alveolar O 2 tension:
* pp of O2 in air (Pi O2 = PB x Fi O2) = 760x0.21 =
159.6 mmhg
* accounting for humidification for inspired gases Pi
O2 = PB – PH2O x Fi O2 = 760 - 47X0.21 = 149 mmhg
* accounting for residual CO2 from previous breaths
final alveolar O2 tension is defined by: alveolar air equan:
PAO2 = Fi O2 x (PB – 47) – (PA CO2/0.8)
= 0.21 x (760 – 47) – (40/0.8)
= 99
mmhg.
Arterial O 2 tension: approximated by
PaO2 = 102 – age/3, n range = 60 – 100 mmhg

37. Determinants of alveolar gas tensions

Alveolar CO 2 tension:
PA CO2 = V CO2 x 0.863/V A = 40 mmhg

Arterial CO 2 tension:
readily measured, n = 38+/-4 mmhg

End tidal CO 2 tension:
used clinically as an estimate of PaCO2.
PA CO2 – PETCO2 gradient is normally < 5 mmhg.

38. Compliance



Compliance = Distensibility of lung
Elastance = resisting deformation
Compliance = 1/ elastance = ∆V/ ∆P = 0.2L/cm H2O (lung)
= 0.2L/cm H2O (Thorax)
= 0.1L/cm H2O (lung+ thorax)
Affected by
Obesity
Kyphoscoliosis
Ankylosing spondylitis
Fibrosis
Emphysema

39. Steep curve + Lt shift = ↑compliance
(loss of elastic tissue)
Flat curve + Rt shift = ↓compliance
(↑ connective tissue)

40. Compliance
Static compliance: measured when air flow is absent,
reflects elastic resistance of lung & chest wall.
=Corrected tidal vol./(plateau pressure – PEEP)
n value: 40 to 60 ml/cm H2O.
Dynamic compliance: measured when air flow is present,
reflects airway + elastic resistance,
=
Corrected tidal vol./(peak airway pressure – PEEP) n
value: 30 to 40 ml/cm H2O.
LOW Compliace: Lung expansion difficult.
HIGH Compliance: Incomplete CO2 elimination.

41. Compliance is reduced in
STATIC
DYNAMIC
Atelectasis
ARDS
Tension Pneumothorax
Obesity
Retained secretions
Bronchospasm
Kinking of ET tube
Airway obstruction

42. Transport of oxygen
 2 forms:
RBC

1. Small amount dissolved in plasma
2. Chemically combined with Hb in
Dissolved oxygen: henry’s law
Gas conc = S x PP in soln
* S - gas solubility coefficient for given
soln at a given temp
Dissolved O2 = 0.003 x 100 = 0.3ml/dl

43. Transport of oxygen

Chemically combined with Hb:
accounts for max blood oxygen

Hemoglobin - conjugated protein:
four polypeptide (globin) chain,
each combined with a porphyrin
complex called heme.
each heme complex has a central
ferrous ion to which O2 binds
converting Hb into oxygenated state.


1 gram of normal Hb carries 1.34 ml of O2, if Hb is 15 g/dl ,
O2 carrying capacity of blood = 1.34 ml x 15 g/dl
= 20.1 ml/dl

44. Transport of oxygen



O2 content: dissolved + combined with Hb
O2 content = (0.003 x PO2) + (Hb x 1.34 x SaO2)
= (0.003 x 100) + (15 x 1.34 x 0.975)
= 19.5 ml/dl (arterial)
O2 content = (0.003 x 40) + (15 x 1.31 x 0.75)
= 14.8 ml/dl (venous)
O2 content
Arterial
Venous
Combined
19.5
14.7
Dissolved
0.3
0.1
Total
19.8
14.8

45. Transport of oxygen

Total oxygen delivery to tissues:
= oxygen content x CO
= 20 ml/dl x 50 dl blood/min
= 1000 ml/min.

O 2 Flux: amount of O2 leaving the left ventricle per min in
the arterial blood.

Fick equation describes O 2 consumption (VO 2 )
= CO x diff b/w arterial and venous oxygen content
= 250 ml/min.
Extraction ratio for O 2 = (Ca O2 - Cv O2)/ Ca O2
= 5/20 = 25%


46. Oxygen stores

Normally in adults = 1500 ml
* O2 remaining in lungs
* bound to Hb
* dissolved in body fluids

O2 contained within lungs at FRC – most imp source of
oxygen.
Apnea in pt breathing room air = FiO2 x FRC
= 0.21 x 2300
= 480 ml depleted in 90 sec
Preoxygenation with 100% oxygen for 4-5 min leaves
2300 ml of oxygen – delays hypoxemia following apnea



47. HbO2 Dissociation Curve

Relates SpO2 to the PO2
Sigmoid shaped
(comb of 1st heme Hb
molecule with O2↑ affinity
of other heme
molecules)

SHIFTING AFFINITY

48. Measure of Hb affinity for O2



quantified by P50.
P50 - PO2 at which Hb is 50% saturted.
P50 = 26 mmhg at PCO2 40 mmhg, pH 7.4, temp.
37°C.
↓ Hb affinity,
Rt shift of ODC
↑ P50
(facilitates O2 release)

49. Factors affecting O2 loading and
unloading




Blood pH
Body temp
Organic phosphates in RBC
Variations in structure of Hb

50. Shift of curve to right




Fall in blood pH due to
a. ↑ CO2
b. Presence of any acid in blood
↑ temp
Inhalational anesthetics: Isoflurane shifts P50 to right
by 2.6 mmhg.
↑ conc of 2,3- DPG
By product of glycolysis (accumulates in anaerobic met.)
Competes with O2 for binding sites on Hb
↓ in: acidosis, blood stored in acid citrate dextrose sol in blood bank
↑ in: high altitude, chronic anemia, exercise

51. Bohr effect
↑ in blood H+ ion
reduces oxygen binding to Hb
Rt shift of ODC
O2 release

Double Bohr Effect * 2 – 8% of the trans placental transfer of oxygen

* concomitant fetal to maternal transfer of CO 2 makes
maternal blood more acidic & fetal blood more alkalotic
right shift in maternal
ODC
left shift in fetal
ODC

52. Shift of curve to left






Carbon monoxide – inhibits synthesis of 2,3 DPG.
Affinity of CO for Hb is 200 times than that of O 2
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

53. Transport of CO2

CO 2 is carried in blood in 3 forms:
* Ionized as bicarbonate
* Chemically combined with proteins
* Dissolved in physical soln

54. Transport of CO2

Ionized as bicarbonates (80%)
a. In plasma – partly in soln,
- remaining combines with water
forming carbonic acid.
CO2 + H2O → H2CO3 (slow reaction)
b. In RBC – this reaction is rapid due to presence of
enzyme carbonic anhydrase.

55. Transport of CO2

As carbamino compds
CO2 can react with amino group on proteins
a. In plasma – with plasma proteins (slow rxn)
b. In RBC – with Hb – carbaminoHb (fast rxn)
* Deoxygenated Hb has a higher affinity(3.5 times)
for CO2, thus venous blood carries more CO2

As dissolved CO2 (8%)
CO2 is more soluble in blood than oxygen with a
solubility coefficient of 0.067 ml/dl/mmhg at 37°C

56. Transport of CO2


Hb acts as a buffer at physiologic pH
* In tissue capillaries deoxygenated Hb behaves like
a base, takes up H+ ions, ↑ bicarb formn.
CO2 + H2O + HbO2 → HbH+ + HCO 3 + O2
Thus, deoxyHb ↑ amount of CO2 that is carried in venous
blood as bicarbonate.

57. Transport of CO2

Chloride shift
or hamburger
phenomenon
To maintain
electrical
neutrality Cl¯
ions shift from
plasma to
RBCs in
exchange of
HCO3 ions.

58. Transport of CO2

In lungs oxyHb
behaves as acid,
release H+ ions, favour
CO2 production
HbH+ + HCO 3 + O2→ CO2
+ H2O + HbO2
Thus CO2 is
eliminated from lungs.

59. CO2 dissociation curve
•Depicts relationship b/w
PCO2 & CO2 content
•Haldane effectwhen oxygen combines
with Hb it ↓
affinity of Hb for CO2

60. Haldane and Bohr effect

61. Transport of CO2
CO2 content of blood(mmol/lt)
Arterial
Venous
Dissolved
1.2
1.4
Bicarbonate
24.4
26.2
Carbamino
negligible
negligible
Total
25.6
27.6

62. References
1. Respiratory physiology, the essentials. John
B.West.2003, 3rd ed.
2. Egan’s fundamentals of respiratory care 9th ed.
3. A practice of anaesthesiology. Wylie 5th, 7th ed.
4. Lee’s synopsis of anaesthesia 13th ed.
5. Miller’s Anaesthesia 6th ed.
6. Clinical Anaesthesiology, Morgan 4th ed.