2. OVERVIEW
•VENTILATION
•RELATION BETWEEN VENTILATION AND
PERFUSION
•SHUNT EQUATION AND ALVEOLAR AIR EQUATION
•FACTORS AFFECTING PULMONARY FUNCTION
•PRE-OP ASSESSMENT OF LUNG FUNCTION
•TRANSPORT OF GASES IN BLOOD
•HYPOXIA AND ITS EFFECTS ON BODY SYSTEMS
3. Ventilation
Minute ventilation is amount of air in liters
that a person breathes per minute
Minute ventilation(5L/min)=RR* TV
Alveolar ventilation Va is given by-
Va= RR*(Vt-Vd)
Vd= 2ml/kg, VT= 6ml/kg
Vd/Vt=33%
Vt-Tidal volume
Vd-Dead space volume
4. DISTRIBUTION OF
VENTILATION
Right Lung ventilated more thanLeft Lung(
lower angle of right bronchus branching,
width of right bronchus> left)
Lower lung fields are more venilated than
Upper lung fields because of
transpulmonary pressure(Palveolar-Ppleural
)gradient due to effects of gravity( higher at
apices).
So, Alveoli are maximally inflated at apices
and are relatively non compliant
5. Other factors affecting ventilation-
1. Airway resistance
2. Compliance
Lung inflation
is given by time constant= total compliance
airway resistance
Significance is that in Rapid shallow breathing
Upper areas of lungs are favored in contrast to
normal respiration where lower lung fields are
favored because lower alveoli take time to open
6.
7. Pulmonary PerfusionPulmonary blood flow-5L/min
Pulmonary capillaries contain 70-100ml blood at a time
Pulmonary Perfusion is-
- Increased in-cardiac systole, inspiration, trendelburg
position
- Decreased in – standing position
Local factors-
HYPOXIA affects more than AUTONOMIC SYSTEM- alveolar
hypoxia>arterial hypoxia
-Causes pulmonary vasoconstriction either due to direct
effect on vessels or production of leukotriens or
inhibition of NO
-it helps in reducing intrapulmonary shunting and prevents
hypoxemia
8. DISTRIBUTION OF
PULMONARY PERFUSION
Lower areas> Upper areas due to
gravitational gradient
Perfusion scans show “ onion like” layering
of distribution of perfusion i.e maximum
perfusion at hilum
Perfusion pressure is different at different
parts of lungs that divides lungs in four
distinct zones- WEST’S zones
10. Zone 1 pulmonary Alveolar pressure(PA)
exceeds pulmonary artery pressure(Ppa),which is
negative at this height, so vessels are collapsed-no
blood flow, no gas exchange, hence wasted
ventilation-alveolar dead space.
PA-alveolar preessure,
Pa- pulmonary arterial pressure,
Pv- is pulmonary venous preesure
Under normal conditions little or no
zone 1 exists. But ZONE -1 ENLARGES in
conditions-
where Ppa is greatly reduced-
hypovolemic shock or
where PA is greatly increased-
1. large tidal volume ventilation
2. or high PEEP ventilation during
IPPV-
10
11. In zone 2
The Ppa exceeds PA pressure &
blood flow begins. But, PA still
exceeds Ppv so it’s the Ppa-PA
which determines the flow.
11
12. In zone 3 Ppv becomes
positive and also exceeds
PA and the capillary
systems are thus
permanently open and
blood flow is continuous
down zone 3.
In this region, blood flow
is governed by the
pulmonary arteriovenous
pressure difference (Ppa -
Ppv)
Most Of lung is in ZONE 3
12
13. In zone 4 Ppa > PISF > Ppv > PA
A region of the lung from which a large amount of fluid has
transuded into the pulmonary interstitial compartment or is
possibly at a very low lung volume.
Blood flow is governed by the arteriointerstitial pressure
difference (Ppa - PISF), which is less than Ppa - Ppv
difference, and therefore zone 4 blood flow is less than zone
3.
This produces positive interstitial pressure, which causes
compression of extra-alveolar vessels, increased extra
alveolar vascular resistance, and decreased regional blood
flow.
13
14. Ventilation Perfusion ratio
-Efficacy with which O2 & CO2 exchange at the
alveo-capillary level depends on matching of
capillary perfusion & alveolar ventilation.
-Blood flow in lungs is gravity dependent
-Relationship between pulmonary artery pressure-
Ppa, alveolar pressure PA, and pulmonary venous
pressure Ppv determines the lung perfusion.
14
15. The normal alveolar ventilation (V)is in an
adult is 4 l/min,and total perfusion is 5
l/min (Q).
So proportion of ventilation to perfusion is
4/5= 0.8 ,this ratio is known as
VENTILATION-PERFUSION RATIO.
In an standing person-
Ventilation increase from apex to base
* 0.24 L/min ----> 0.82L/min
Perfusion increase from apex to base
* 0.07 L/min --> 1.29 L/min
Because the increase in perfusion is
greater than that of ventilation
--> V/Q decreases from apex to base
--> 3.3 to 0.63
15
17. Ventilation-Perfusion Relationships
; Concept of shunt
A Pulmonary shunt is a physiological condition
which results when the alveoli of the lung are
perfused with blood as normal, but ventilation (the
supply of air) fails to supply the perfused region.
Perfusion in excess of ventilation ,opposite of dead
space.
The Physiologic shunt : is that portion of the total
cardiac output that returns to the left heart and
systemic circulation without receiving oxygen in the
lung. Normally its less than 5 %
17
18. Venous admixture
It is calculated amount of mixed venous blood
which would be required to mix with the blood draining
ideal alveoli to produce the observed difference
between ideal alveolar and arterial PO2
It can be divided into-
(a)true shunt
(b)low VA/Q ratio
20. SHUNT EQUATION
It is used to calculate venous admixture
QT= QC+QS
(Cc’O2 Qc) + (CvO2 QS) = CaO2 QT
QS/QT=CcO2-CaO2/CcO2-CvO2, it can be calculated by
obtaining mixed venous and ABG measurements, normally
it is <5% (physiological shunt)
Qs =blood flow through physiologic shunt
Qc= blood flow through normally ventilated pulmonary
capillaries
QT=Total cardiac output
CcO2= capillary O2 concentration
CvO2= venous O2 concentration
21. ALVEOLAR GAS EQUATION
Capillary O2 concentration is in equlibrium with
ideal alveolar gas which can’t be sampled because it
gets contaminated with alveolar dead space gas.
Ideal alveolar PO2 can be derived using alveolar gas
equation
PAO2= PiO2-PaCO2(PiO2-PeCO2)/PeCO2,
if patient is breathing 100% O2, alveolar gas
contains only O2 and CO2, then-
IDEAL Alveolar PO2( PAO2)=PiO2-PaCO2
A- alveolar
a-arterial
e-expired
i-inspired
22. Causes of ‘’TRUE-SHUNT’’
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 Atelectasis
Pulmonary edema, Pulmonary
contusions,
Pulmonary hemorrhage
Pulmonary infections
(pneumonia, consolidation)
Pulmonary arteriovenous shunts,
Pulmonary neoplasms including
haemangioma.
22
24. Effect of Posture
Supine position-
ventilation and perfusion become evenly distributed
anterior to posterior gradient develops
Inverted position-
apex>base
Lateral position-
in conscious subjects-ventilation and perfusion greater to
dependent lung
in anaesthetised patients-perfusion is greater to dependent
lung,ventilation more at upper lung
due to reduction in FRC,prevented by PEEP
If chest is opened-
ventilation to upper lung greatly increased
25. Effect of artificial ventilation-
part of the lung becomes overinflated
alveolar pressure rises
enlargement of zone 1
amount of lung with high VA/Q is greater
increase in physiological dead space,upto 50%
or more of tidal volume
26. Effect of premedication
-Atropine - increase in anatomical and
physiological dead space
- Opiates –reduction in alveolar ventilation,
rise in arterial PO2 and depression of
ventilatory response to CO2
27. Effect of anaesthesia on gas
exchangeIncreased dead space, hypoventilation,increased
intrapulmonary shunting.
Venous admixture increases from 5% to 10% due to
atelectasis and airway collapse in dependent areas of lungs
NO inhibits hypoxic pulmonary vasoconstriction
PEEP helps in reducing venous admixture and preventing
hypoxemia during GA until cardiac output is maintained
Giving 100% O2 can cause resorption atelectasis and
increase absolute shunt
Resorption atelectasis occurs in areas of low V/Q ratio
ventilated at 100%O2 because perfusion results in O2 being
transported out of alveoli at a rate faster than it enters
alveoli leading to emptying of alveoli and collapse
28. ALVEOLAR OXYGEN TENSION
Inspired O2 pressure can be calculated by product of % of
O2 in inspired air and its relative pressure in inspired gas
mixture-
PiO2=(PB-PH20)* FiO2
PAO2= PiO2-PaCO2/RQ
PiO2- pressure of oxygen in inspired gas mixture
PB- barometric pressure at sea level
PH2O-water vapor pressure
PAO2-alveolar oxygen tension
PaCO2- arterial CO2 tension
RQ-RESPIRATORY QUOTIENT= CO2 production/ O2 consumption
It implies that a large increase in PaCO2(>75mm Hg)
produces hypoxia at room air but not at high FiO2
29. Arterial O2 tension
Range is 60-100 mm of Hg
PaO2= 120-age/3
Increases with age as closing capacity increases
Hypoxemia is PaO2< 60 mm of Hg ,most common
cause is increased alveolar arterial gradient., which
can be due to-
1. Increased amount of right to left shunt
2. Increased V-Q scatter
3. Low Mixed venous 02 tension- seen in low
cardiac output states and low Hb concentration
and when O2 consumption is increased
30. PULMONARY END CAPILLARY
OXYGEN TENSION
◦ It depends on-
Rate of diffusion across alveolar-
capillary membrane
Pulmonary capillary blood
volume
Transit Time(PBV/Cardiac
output)=0.8sec
31. Binding of O2 to Hb is principal rate
limiting factor in transfer of O2 from
alveolar gas to blood
So O2 uptake is limited by pulmonary
bloodflow, not by O2 Diffusion
O2 diffusion becomes important in normal
individuals at high altitudes, and in patients
with extensive destruction of alveolar-
capillary membrane
32. O2 diffusion capacity-
DLO2=O2 uptake/PAO2-PcO2
Carbon monoxide diffusion capacity is
measured instead of DLO2, as PcO2 can n’t be
measured correctly and PcCO can be taken
zero as CO has HIGH AFFINTY FOR Hb
DLCO= carbon monoxide uptake/PACO
LOW DLCO MEANS- Impediment in gas
transfer
33. Mixed venous oxygen tension,
PvO2
Normal value is 40 mm of Hg
It represents overall balance between O2
consumption and O2 delivery
It is measured by pulmonary artery
catheter
34.
35. •Mixed Venous CO2 Tension,PvCO2
Normaly, it is 46 mm of Hg
It is end result of mixing of blood from tissues of varing
metabolic activity
Higher in blood from heart, lower in blood from skin.
•Alveolar CO2 tension PaCO2
=Total CO2 production, Vco2/alveolar
ventilationVA
It depends more on alveolar ventilation because
CO2 output doesn’t vary appreciably under
most circumstances because of body’s large
capacity to store CO2 buffers acute changes in
CO2 production.
36. •Pulmonary end capillary CO2 tension PcCO2-
Virtually equals to PACO2
•Arterial CO2 Tension-
Normally it is 38+/-4
Even moderate to severe disturbances fail to alter
arterial CO2 because of reflex increase in
ventilation from concomitant hypoxemia.
•End tidal CO2-It is an estimate of arterial PCO2-
arterial and alveolar PCO2 are virtually same PACO2-
PETCO2=5, it represents dilution of alveolar gas with CO2
free gas from non perfused alveoli
37. •The gases of respiratory importance are highly soluble in
cell membrane (all are highly soluble in lipids).
• Also, diffusion of gases through the tissue, including
through the respiratory membrane, is equal to the
diffusion of gases through water.
• CO2 diffusion 20 times more rapidly than O2 because of
its high solubility in tissue fluids.
Diffusion of gases through tissues
38. Factors that affect the rate of gas diffusion through the
respiratory membrane:
1. The thickness of the respiratory membrane.
thickness of the respiratory membrane e.g.,
edema rate of diffusion.
1. Surface area of the membrane.
Removal of an entire lung decreases the surface
area to half normal. In emphysema with dissolution
of the alveolar wall S.A. to 5-folds because of
loss of the alveolar walls.
39. Dissolved Oxygen
Given by Henry’s law-
Gas concentration= @ Partial pressure
@- solubility coefficient (0.003 for O2)
So, even with PaO2=100 mm Hg, O2
dissolved is 0.3ml/dl of blood
40. HAEMOGLOBIN
It is a complex molecule consisting of four
haem and four protein subunits.
Heme is an iron porphyrin compound that
is essential part of O2 binding site.
Only divalent Fe+ form can bind O2
41. Globin(protein) + Heme(iron containing
pigment)
four amino acid chains - porphyrin nucleus-
- two alpha chains(141 AA) four pyrrol rings
joined by
- two beta chains(146 AA) four methine bridges
Iron is in Fe2+ form,attached to N of each pyrrol ring and
N of imidazole group of globin chain.
42. 1g fully oxygenated Hb contains -1.39 ml O2
(expected)
-1.31mlO2
(actual)
-1.31mlO2 (actual)
OXYGEN MIXED VENOUS ARTERIAL
Amount in solution in plasma 0.13 ml% 0.3ml%
Tension 40mmhg(5.3 kPa) 100mmHg(13.3kPa)
Amount combined with hemoglobin 14ml% 19ml%
Saturation 75% 98%
43. Oxygen-haemoglobin dissociation curve
• Haemoglobin is almost
100% saturated at the
normal systemic arterial
PO2 of 100 mm Hg. The fact
that saturation is already
more than 90% at a PO2 of
60 mm Hg permits a
relative normal uptake of
oxygen by the blood even
when alveolar PO2 is
moderately reduced.
• Haemoglobin is 75%
saturated at the normal
systemic venous PO2 of 40
mm Hg. Thus, only 25% of
the oxygen has dissociated
from haemoglobin and
entered the tissues.
44. Complex interaction between Hb subunits
results in non –linear binding with O2
The change in molecular conformation
induce by binding of first three molecules
greatly accelerates binding of fourth O2
molecule this is responsible for saturation
between 25% to 100%
At about 90% saturation, the decrease in
O2 receptors flattens curve until full
saturation is reached.
45. Factors affecting Oxygen Hb
dissociation curve
pH(Bohr effect)
fall in pH -shift to right
rise in pH-shift to left
increase in tissue CO2 tension-fall in pH-shift to right
- dissociates more readily
2,3DPG
2,3 DPG combines with globin and modifies O2 access
to heme chain
High conc.-shift to right
Low conc.-shift to left
46. Temperature
fall in temp.-shift to left
rise in temp-shift to right
Storage of blood
- 2,3 DPG level falls in stored blood-shift to left
- in 10 days 30% reduction,after two weeks complete
depletion in ACD blood
-In CPD blood-nearly normal upto 10 days,then falls
rapidly
49. Abnormal Forms of
haemoglobin
Methhaemoglobin results when iron in heme is oxidized to
is trivalent form +3
Other causes are- presence of nitrates ,nitrites,
sulfonamides and other drugs
All abnormal forms shift O2 Hb dissociation curve to left
Methhaemoglobin can be reduced to normal Hb by giving
mehylene blue and ascorbic acid
Carboxy Hb, HbF2, Hb2, Sickle Hb- all have different O2
saturation characteristics.
50. Bohr Effect
•All the factor which shift O2-Hb
dissociation curve to right,decrease the
affinity of Hb for O2,therefore ,a higher pO2
is required for Hb to bind a given amount of
O2.Therefore,Co2 enter the blood from
tissue and help unloading of O2.This
phenomenon is called Bohr Effect.
51. Total OXYGEN Content-
It is sum of O2 content in solution plus that
carried by haemoglobin.
Total O2 content is expressed by following
equation
O2 Content=(0.003 PO2 ) (SO2 Hb 1.31
ml/dl blood)
Using this normal arterial and mixed venous O2
content can be calculated.
CaO2= (0.003*100)+(0.975*15*1.39)= 19.5 ml/dL
CvO2=(0.003*40)+(0.75*15*1.31)=14.8ml/dL
CaO2-CvO2= 4.7 ml/Dl(measure of O2 delivery to
tissues
52. OXYGEN Transport-
Oxygen Flux-
It is the volume blood delivered by left ventricle
in 1 minute
DO2= CaO2 Cardiac output
DO2 – delivery of O2, it is 1000ml/ min.
O2 Consumption= cardiac output (CaO2-CvO2)
Extraction Fraction= CaO2-CvO2/CaO2= 5/20=25%
It increases when demand increases,if supply exceeds
demand this ratio falls
53. Applied aspect of EXTRACTION
RATIO (ER)
When delivery of oxygen is reduced
moderately, O2 consumption(VO2) remains
normal as ER increases (CvO2 decreases)
With Further reduction in delivery of
O2(DO2), critical point is reached-
VO2 becomes directly proportional to DO2(
seen in progressive lactic acidosis caused by
cellular hypoxia
54. OXYGEN STORES
In lungs ( FRC- 2300 ml)- most important ,
80% is usable
Bound to haemoglobin( myoglobin)
In dissolved form ( very little )
So, to increase FRC and for denitrogenation
patient is preoxygenated with 100%O2 to
delay hypoxemia following apnoea to 4-5
minutes
55. Carriage of Oxygen in Blood.
In Two forms
1.In dissolved form:- Amount of O2 is
0.3ml/100ml of blood/100mmHg PO2
2.In combination with Hb:- 1 gm of Hb
can combine with 1.39 ml of O2
56. Tissues consume the O2
directly.
It depends on the PO2 (so
higher alveolar PO2 will increase
the amount of O2 carried in the
dissolved state e.g., hyperbaric
O2 therapy as in CO poisoning).
The importance of dissolved form
57. •70% carried bound to hemoglobin- Carbaminohemoglobin
• 23%-As carbonic acid buffer system
•7% dissolved in plasma
•Plasma transport- CO2 + H2O <-->H2CO3<-->H+ + HCO3-
•Enzyme is Carbonic Anhydrase present in RBC more than
plasma
•Chloride shift to compensate for bicarbonate moving in and
out of RBC
58.
59. CO2 dissociation curve
•Curve relates the CO2 content of blood to the PCO2 to which it is
exposed.
•The more deoxygenated the blood becomes the more carbon dioxide it
carries at a given PCO2; this is called Haldane effect.
•(Loading of oxygen to the blood causes unloading of CO2 is called
haldane effect.)
•Due to the haldane effect the uptake of CO2 by capillary blood is
facilitated when this blood reaches the lungs and become oxygenated,
elimination of CO2 is facilitated.
60.
61.
62.
63. in the tissues, CO2 content moves up from point a to point
v
low PO2 in the tissues facilitates CO2 loading (reverse
Haldane effect) high PCO2 in the tissues facilitates O2
unloading (Bohr effect)
in the lungs, CO2 content moves down from point v to
point a
high PO2 in the lungs facilitates CO2 unloading (Haldane
effect)
low PCO2 in the lungs facilitates O2 loading (reverse Bohr
effect)
64. HYPOXIA
HYPOXIA: A condition in which the oxygen
available is inadequate at the tissue level
Types of hypoxia:
◦ Hypoxemic Hypoxia
◦ Anaemic Hypoxia
◦ Stagnant (Ischemic) Hypoxia
◦ Histotoxic Hypoxia
65. HYPOXEMIC HYPOXIA
Low PAO2 due to the atmospheric change
Hypoventilation – PCO2 is rising
Diffusion Defects
The PaO2 will be lower in all cases, but the PCO2 may or
may not be increased.
Treatment: Compensatory actions to reduce inequalities,
supplemental oxygen
66. ANAEMIC HYPOXIA
Having a decreased carrying capacity for oxygen, the patient is
with decreased or abnormal Hb.
CAUSES-
Anemia
Carbon monoxide poisoning
Methemoglobinemia
Sickle Cell Disease
Treatment depends on cause of anaemia i. e blood
transfusions, hyperbaric chamber, bone marrow transplant.
67. HISTOTOXIC HYPOXIA
Inability for tissues to utilize oxygen available
Cyanide Poisoning will inhibit cellular metabolism from
occuring; the cells can not process the O2
Treatment: Reversal of poisoning, supplemental oxygen
and/or ventilation
69. DIFFUSION HYPOXIA
The uptake of large volumes of N2O into the alveoli during
recovery.
Occurance of hypoxia … two means-
- directly affects oxygenation by displacing oxygen
- by diluting alveolar CO2 , they may decrease respiratory
drive and ventilation.
70. Causes of Arterial Hypoxemia in the
PACU( post anaesthetic care unit)
Hypoventilation
◦ Residual narcotics
◦ Residual benzodiazepine effect
◦ Residual inhaled anesthetics
◦ Residual muscle relaxants
◦ Pain, splinting
◦ Restrictive Conditions,
abdominal wall binding,
abdominal distension
◦ Airway obstruction
◦ Bronchospasm
V/Q mismatch and Shunt
◦ Atelectasis
◦ Inhibition of Hypoxic Pulmonary
Vasoconstriction.
◦ Pulmonary edema
◦ Aspiration, Pneumonitis
◦ Increased Venous Admixture
71. Cause of Hypoventilation
Normally there is a linear increase in minute ventilation
for increase in CO2.
This linear ventilatory response is blunted in the post
operative period by the effects of drugs.
The alveolar gas equation
PaO2= FIO2 (Patm-PH2O) – PCO2/R
1.-If PaCO2=40
PaO2= 0.21(760-47) – 40/0.8 = 100
2.-If PaCO2=80
PaO2= 0.21(760-47) – 80/0.8= 50
72. Effect of hypoxia on various
systems
Respiratory system
Circulatory system
Hematologic system
Central nervous system
Tissues and cells
74. High Altitude Pulmonary Edema
(HAPE)
A life-threatening form of pulmonary edema (fluid
accumulation in the lungs) that occurs at altitudes typically
above 2.5 km.
The major cause of death related to high-altitude exposure.
Mechanisms of HAPE:
Excitement of the sympathetic nerve
↑ lung artery pressure (due to Hypoxic Pulmonary
Vasoconstriction (HPV)) → Exudation of fluid
↑ permeability of the vascular endothelium
75. Circulatory system
Increased cardiac output (CO) and heart rate (HR)
Redistribution of blood flow
Dilation of heart and brain vessels
Hypoxic Pulmonary Vasoconstriction (HPV)
Capillary proliferation
Hypoxia → HIF (hypoxia-inducible factor) →
VEGF → Capillary growth
76. Central nervous system
Acute hypoxia
Severe Headache- due to cerebral vasodilation.
Poor memory
Inability to make judgment
Depression
Chronic hypoxia
Unable to concentrate
Fatigue
Drowsiness
Cerebral edema and neuron injury → worsen
hypoxia → death
Regulatory centers are affected – death
commences due to respiratory failure
77. Treatment
Identify the Underlying Cause
Hypoventilation
◦ Reversal of drugs
◦ Decrease dead space
ventilation
◦ Supplemental O2
◦ Mechanical ventilation
V/Q Mismatch and Shunt
◦ Sitting position
◦ Incentive Spirometry
◦ Encourage deep breathing.
◦ Positive airway pressure
◦ Supplemental O2, not effective
in true shunt.
◦ Mechanical Ventilation
