Gas Exchange

The lungs are the major organ of gas exchange, but it must also be remembered that gas exchange
takes place with all living cells in the body.

Arterial Blood Gas Analysis

Oxygen Status
The single most useful measure of a patient's oxygen status is the
PaO2 [mmHg]. Note that the unit
of measure is pressure and that is because this reflects the driving pressure of Oxygen in the blood,
and hence the bloods ability to oxygenate tissue and cells. This comprises of oxygen bound with
haemoglobin and that dissolved in plasma. It is known as a partial pressure since there are other
gases in air and blood that exert their pressures too.

The Alveolar air equation.

If the oxygen journey is viewed as starting with the inspired air then the partial pressure oxygen (PO 2)
exerts is equal to the barometric pressure multiplied by the fraction of oxygen in the inspired air. This
fraction is usually 0.209 or 20.9%. Mean barometric pressure at sea level is 760 [mmHg], yet this
contains moisture and the vapour pressure the moisture exerts is known to be 47[mmHg]. So the total
pressure of gases in our inspired sample is 713[mmHg](760 - 47 = 713).
Therefore the partial pressure of oxygen is 20.9% of 713, giving 149[mmHg]. This inspired air is
diluted by the air in the physiological dead space of the upper respiratory tract and trachea, bronchi,
and non-respiratory bronchioles. The degree of dilution dependant on the dead space to tidal volume
ratio (Vd/Vt). For the average person at rest this further reduces the partial pressure of oxygen in the
alveoli to approx 115[mmHg].

Other factors, including membrane diffusion reduce this to a pulmonary end capillary PO 2 of approx
102[mmHg] and then venous admixture (blood passing through unventilated alveoli), and plasma
solubility reduce this again, such that the normal systemic arterial oxygen partial pressure (PaO 2) is
between 80 and 100 mmHg. Hypoxaemia would be considered mild between 70-80 mmHg, moderate

between 55-70mmHg and severe when less than 55mmHg. If chronically low then
oxygen therapy may be warranted.

long term

Disease that changes the diffusion membrane thickness, or rate of alveolar ventilation, or rate of
perfusion, will all have an effect on the PaO2. Changes in alveolar membrane thickness are
associated with pulmonary fibrosis, cor-pulmonale, and diffuse interstitial lung disease, all can cause
a reduced PaO2. In obstructive lung disease the physiological dead space may increase as a result of
infection or worsening disease, without a corresponding increase in tidal volume there will be a
reduction of alveolar ventilation also producing a reduced PaO 2. Arterio-venous shunts will by
definition reduce the PaO2, as will right heart failure.

The oxyhaemoglobin dissociation curve

Haemoglobin molecules have four binding sites for oxygen. Curiously the affinity of haemoglobin for
oxygen increases as successive molecules of O2 bind. Fortunately this makes for a rapid "fill-up" at
the lungs and then a quick "offload" at the tissues where the opposite occurs and as the first oxygen
molecule moves off down the concentration gradient the others soon follow. This gives a characteristic
sigmoid shape to the dissociation curve.

Oxygen dissociation curve modified from "Pulmonary Pathophysiology" by Grippi.

The position of the dissociation curve may shift left or right - influenced by pH, temperature, PaCO 2,
and levels of 2,3 -DPG (the Bhor effect). Note that the steep downward part of the curve at normal pH
starts at a stauration about 90% and a PaO2 about 70mmHg. If there is a shift to the right it means a
higher PO2 is required to "pick-up" oxygen in the lungs, with the converse happening with a shift to the
left. At PaO2 values less than 55mmHg it takes only a small fall in PaO2 to cause a large fall in SaO2.

Acid-Base Balance

Together with the kidneys the lungs act as the regulator of the bodies blood pH, in response to
changes in the rate of metabolism or cellular respiration. The principles of homeostasis come to the
for in that the normal arterial pH of 7.35 to 7.45 is very tightly controlled by the body. Indeed the
chemoreceptors are exquisitely sensitive to changes in pH. The breathing process eliminates carbondioxide (CO2) from the body, CO2 that when dissolved in plasma forms carbonic acid, lowering the
pH. The other latent form of carbon-dioxide in blood is that in the bi-carbonate ion [HCO3-]. This can
be regulated by the secretion of H+ ions and control of filtration of HCO3- ions at the countercurrent
multiplier mechanism of the loop of Henle in the kidney. Even when the rate of filtration remains
unchanged the volume of micturition may affect blood concentrations of HCO3.
The basis of the above was demonstrated by the Henderson-Hasselbach equation:
pH = pK + log ([HCO3-]/0.03 PaCO2)
Where the constant pK has a value of 6.1 for plasma. Here it can be seen that the ratio of CO 2 to
HCO3 will determine the pH of the blood. This chemical balance can be represented with it's clinical
link by the equation below
H2O + CO2
Respiratory regulation

H2CO3

H+ +

HCO3-

Renal regulation

It is referred to as a balance as it may move in either direction. If, as sometimes in chronic lung
disease, CO2 is retained then gradually the pH may be "normalised" by a retention of HCO3 by the
kidneys. This is usually a slow response and can take several days. Since the primary change was
the raised PCO2 it is referred to as Respiratory Acidosis with metabolic compensation, or chronic
respiatory acidosis (see Flenley diagram below).
mmol/L

Flenley diagram, modified from Crofton & Douglas's "Respiratory Diseases" 4th Ed..
A respiratory alkalosis may occur during acute hyperventilation where the CO 2 is "blown off" and there
is a reduced PaCO2, raising the pH (see Flenley diagram above). This is rarely chronic and it is rare
for the pH to remain high long enough for significant amounts of compensation to occur, an insult to
the pneumotaxic centre of the brain might be one cause due to drug abuse or physical injury.
The buffering capacity of the lungs is about 2-3 times that of the sum of the bio-chemical buffering
capacity of the system, and it is capable of reacting much more rapidly. Those of you familiar with
electronic circuits may think of this as a whetstone bridge balance.

The level of pH being regulated by changes in any of the four areas, Metabolism, Respiration,
Micturition, and Renal Filtration.

Typical Blood Gas Results

COPD
Parame
ter

Stable

PaO2
PaCO2
pH
BE
SBC
(HCO3)
SaO2

60mmHg
45mmHg
7.38
2.6
28.4mmol

Acute
End
Exacerbatio Stage
n
42mmHg
50mmHg
59mmHg
55mmHg
7.26
7.37
3.5
6.9
31.2
33.8

90%

71%

85%

DILD
Paramete Stable
r
PaO2
PaCO2
pH
BE
SBC
(HCO3)
SaO2

80mmHg
35mmHg
7.35
1.6
27.2mmol

Acute
Exacerbatio
n
65mmHg
24mmHg
7.49
-3.5
20.2

94%

87%

Hyperventilation Syndrome
Paramete Stable
r
PaO2
PaCO2
pH
BE
SBC
(HCO3)
SaO2

90mmHg
35mmHg
7.44
-0.5
24.0mmol

Acute
Exacerbatio
n
99mmHg
22mmHg
7.56
-5.5
19.2

99%

100%

Pneumonia
Paramete Stable
r
PaO2
PaCO2
pH
BE
SBC
(HCO3)
SaO2

65mmHg
42mmHg
7.38
0.6
24.4mmol

Acute
Exacerbatio
n
42mmHg
40mmHg
7.36
-1.5
21.2

90%

71%