V/Q and Oxygen

Anuja Abayadeera
Part 1B Anaesthsiology

What is?
Hypoxia
Hypoxaemia
Aim oxygen delivery to tissues

OXYGEN CASCADE
PIO2
150
100
95

PAO2

PaO2

40

Tissue PO2
10

mmHg

OXYGEN CASCADE
PIO2 = 0.21 x760 mmHg
= 159 mm Hg
PIO2 = 0.21 x(760 47)
= 149 mm Hg

PAO2
Depends on
removal of oxygen by pul.capillary blood
Replenishment by alveolar ventilation
(PACO2)
Removal = oxygen consumption = 250ml/min

PAO2
Inspired gas come to alveoli,
PCO2 increase from 0 to 40 mmHg.
If O2 leaving alveoli = CO2 diffusing into alveoli
PAO2 = PIO2- PACO2 ; 149 - 40 = 109 mmHg
VCO2/ VO2 = 200/250 = 0.8 = R (respiratory exchange ratio)
Ideal alveolar gas equation
PAO2 = PIO2- PACO2/ R or PAO2 = PIO2 PACO2 x1.2

PAO2 = 150-50(40/0.8) =100

OXYGEN CASCADE
PIO2
150
100
95

PAO2

PaO2

40

Tissue PO2
10

mmHg

Normal Gas Exchange

Affected by
Diffusion
Shunt
V/Q scatter
PAO2 PaO2

Diffusion
Ficks Law
0

Vgas = A x D x (P1 P2)

T
D = diffusion coefficient = sol
mw

Diffusion

Perfusion limited

Diffusion limited

Diffusion
P1 P2 =60
Exercise

P1-P2 =30

High Altitude

Diffusion
At rest blood spends sec in the capillary
At rest, PO2 of blood reaches that of alveolar
gas in 1/3 rd of the time in the capillary
On exercise time reduced to sec
Diffusion process challenged by
Exercise
Alveolar hypoxia
Thick blood gas barrier

Shunt
Blood that enters the arterial system without
going through ventilated areas of lung
Physiological
Bronchial veins to pulmonary veins
Thebesian veins to left ventricle
2%-5% of cardiac output

V/Q Scatter
If pulmonary blood perfuses ventilated lung regions
normal gas exchange occurs.

Riley Analysis

Absolute shunt

Relative shunt

Absolute dead space

Relative dead space

Oxygen carbon dioxide diagram

V/Q PAO2

PACO2

3.3

132

28

1.0

100

40

0.6

89

42

Regional differences in V/Q give

regional differences in PAO2 &
PACO2 in alveoli & similarly in
end capillary blood.

Depression of arterial
PO2 by V/Q inequality.
High V/Q units cannot
change the desaturating
effect of low V/Q units.
Note that PaO2 is not
equal to PO2. (no Hb
involved)

CaO2 change by V/Q inequality

The reduction in O2 content in arterial blood caused by alveoli with low

V/Q is more than the increase in O2 content caused by alveoli with high
V/Q.

Normal A a gradient
5-10 mmHg when breathing room air
30-56 mmHg when breathing 100% oxygen
Due to
Physiological shunt
Normal V/Q scatter
Diffusion

Abnormal gas exchange

Effect hypoxaemia low PaO2
CO2 elimination may be affected

Causes of hypoxaemia
PaO2
1. Alveolar O2 partial pressure
overall hypoventilation
2. Alveolar to arterial O2 partial pressure
gradient
Aa
abnormal diffusion, pathological shunt,
V/Q mismatch (relative shunt; low V/Q
ratio)

Effect of overall hypoventilation

Drug overdose
Muscle paralysis
PCO2 = VCO2
VA

Abnormal A -a
Diffusion no effect
Unless thick alv.capillary membrane

Abnormal A -a
Shunt pathological shunts
cardiac A V shunts
pulmonary absolute shunt (venous admixture)
Causes
Pneumonia
Pulmonary oedema
Alveolar collapse

Absolute shunt

Depression of arterial PO2 by

shunted blood

V/Q
mismatch
Commonest cause
Regional hypoventilation

Partial airway obstruction:

asthma, COPD, low
compliance

V/Q mismatch on O2 & CO2

Low V/Q
Theoretically cause hypoxaemia and
hypercapnia.
Actually, have normal or low PaCO2
Rising PaCO2 stimulates ventilation above
requirement
Wasted or dead space ventilation

A 61 year old man with myasthenia gravis is

admitted to ETU. He c/o progressive weakness and
shortness of breath.
ABG on air shows: PaO2 = 59mmHg
PaCO2= 63 mmHg
pH= 7.22; HCO3- = 25meq/L

Vital capacity and maximum inspiratory force are low. A

previous ABG on air is found which is
PaO2 =80 mmHg; PaCO2=40 mmHg; pH= 7.39;
HCO3- = 24meq/L
Why is he having hypoxaemia? Is it abnormal gas
exchange ?

28yr old man after chest trauma develops

ARDS and is ventilated in ITU.
ABG on 50% oxygen:
PaO2 =45mmHg; PaCO2= 38mmHg;
pH= 7.41; SaO2= 80%.
Ventilator is adjusted. PEEP of 10 cmH2O
added.
ABG on 50% oxygen after 1 hr;
PaO2 = 65mmHg; PaCO2= 36mmHg;
pH= 7.42; SaO2= 92%.
How do you explain this change?

55 yr old male is ventilated in the ITU for left

lower lobe pneumonia.
ABG done when lying on the left side
PaO2 = 68mmHg; PaCO2 = 40mmHg
pH= 7.43; SaO2 = 92%.
2hrs later when lying on the right side
PaO2 = 110mmHg; PaCO2= 40mmHg
pH= 7.42; SaO2=99%.
How did the oxygenation improve?

22yr old patient is admitted with bronchial

asthma.
ABG on air:
PaO2= 60mmHg; PaCO2= 35mmHg; pH= 7.35;
SaO2= 90%
Treated with bronchodilators and oxygen is
increased to 28%; ABG 1 hr later
PaO2= 90mmHg; PaCO2=38mmHg; pH=7.37;
SaO2= 96%.
Was the hypoxaemia due to hypoventilation, shunt
or V/Q mismatch?

Low PaO2
Cause
Hypoventilation
Shunt

Mechanism
VA

P(A-a)O2

PACO2 Normal

Venous blood
mixing with arterial
blood

Response
to O2
good

Increased poor

(venous admixture)

Ventilationperfusion
mismatch

Underoxygenated
blood mixing with
arterial blood
(venous admixture)

Increased good

Causes of hypoxaemia
PaO2
1. Alveolar O2 partial pressure
2. Alveolar to arterial O2 partial pressure
gradient
A-a

Measurement of shunt
A a gradient
Normal 5 10 mmHg breathing 21% O2
30 56 mmHg breathing 100% O2
A ideal alveolar gas equation
a blood gases
Normal value increase with age.
Varies with FiO2- limit value

Measurement of shunt
PaO2 / PAO2
More stable with FiO2 changes
Lower normal limit 0.75
Useful to follow patients lung function
when FiO2 is changed
Used to predict FiO2 required to achieve a
desired PaO2

Measurement of shunt
PaO2 /FiO2
Oxygenation ratio (P/F ratio)
Affected by PaCO2
Least accurate indicator of shunt
None of these consider CvO2
(mixed venous oxygen content)
Misleading in patients with cardiovascular instability

Shunt equation
Calculation (shunt fraction)
QT x CaO2 = QS x CVO2 + (QT Qs) x CcO2
QS = CcO2 - CaO2= oxygen lost by mixing with Qs
QT CcO2 - CVO2 = total amount of oxygen uptake
Most reliable method for oxygen transfer efficiency
a - arterial
C end capillary = oxygen delivery equation ; ideal alveolar equation
V mixed venous

Shunt <10% = normal lungs

Clinical significance
Shunt fraction percentage

Clinical significance

<10%

Clinically compatible with

normal lungs

10%-19%

Intrapulmonary
abnormality; ? support

20%-29%

Significant abnormality;
need CPAP/PEEP

30% or more

Severe disease;
aggressive support with
PEEP

Points to remember
V/Q abnormalities are more likely to create
hypoxaemia than hypercapnia
High V/Q regions cannot compensate for
hypoxaemic effects of low V/Q regions.