Lecture 12: Blood Gas Transport
1. Partial Pressures of Gases throughout the Circulatory System
In blood flowing through the pulmonary artery into the lungs, oxygen levels are relatively low (40
mmHg) and CO levels quite high (46 mmHg). Note: mmHg is often referred to as 'Torr'; they are the
same unit. The blood reaches the lungs, where it interactswith alveolar air. Alveolarair is not the same as
atmospheric air; atmospheric air has a PO of2160 mmHg and a PCO2 of 0.3 mmHg, whilst alveolar air
has a PO 2of 100 mmHg and a P CO 2 of 40mmHg. There areseveral reasons for this: firstly, gas exchange
occurs through the capillaries in the alveoli with the atmospheric air before it has a chance to reach the
blood of the systemic circuit; secondly, there is mixing of the air in the anatomical dead space; and
thirdly, the alveoli are filled with water vapour as well, with a relative humidity of approximately - and
we have to subtract the partial pressure of water vapour from the partial pressure of oxygen and carbon
The blood flowing through the lungs equalizes with thepartial pressures of the alveolar air (100 Torr O 2
and 40 Torr CO 2) and remains at these valuesthroughout the systemic arteries. When the blood enters the
systemic capillaries (tissues) and begins oxygenating the tissues and carrying away carbon dioxide, the
partial pressure of oxygen drops to 40 Torr and the partial pressure of carbon dioxide rises to 46 Torr.
Within the mitochondria oxygen levels can be as low as 1 Torr. The deoxygenated blood flows through
the venous system back to the right side of the heart, maintaining these partial pressure values until it
returns to the lungs. 2
2. Perfusion versus Diffusion Limitation
In human lungs), the uptake of O2 and the excretion of CO2 areperfusion limited. This refers to the fact
that the limiting factor in the oxygenation of our tissues (and the removal of CO2 from our tissues) is the
rate of blood flow to our lungs and tissues. However, some animals such as fish, and humans in certain
circumstances, are instead diffusion limited, meaning that the limiting factor in oxygenation of the
tissues is the diffusion rate of oxygen from the lung gas into the blood flowing through the lungs.
The rate of O 2uptake, and CO exc2etion, is a function ofthe distance the blood has to travelthrough the
pulmonary capillaries. Within the first third of the length of a pulm onary capillary, the blood has changed
from being deoxygenated and high in CO (40mmHg2O ; 46mmHg CO )2to being oxygena2ed and low in
CO (200mmHg O ; 40mmH2 CO ). What this2means is that we havea large reserve distance in the lungs
for gas exchange; two thirds of the capillary length is not even used in normal gas exchange. In very
highly-trained athletes, at the peak of their performance, however, diffusion limitations do begin to
3. Determination of Alveolar Ventilation
The rate of gas exchange at the lungs depends upon our metabolic demands. The amount of oxygen that
is being consumed, or carbon dioxide excreted, will aff ect the amount of alveolarventilation. The ratio of
CO p2oduction to O co2sumption in our tissues is called therespiratory quotient and it is a measure of
our metabolic rate (in the lungs this ratio is referred to as the respiratory exchange ratio). Regular
breathing which is sufficient to meet our metabolic demands is called eupnea or eupneic breathing.
When metabolic demands increase, for example during exercise, alveolar ventilation must increase to
meet this heightened demand; this is called hyperpnea. Apnea is the term for the absence of breathing,
and dyspnea is the term for difficult or laboured breathing.
4. Hyperventilation and Hypoventilation
Everyone has heard the terms hyperventilation and hypoventilation before; colloquially we use these
terms to refer to an increase or decrease in breathing, but clinically they are defined in terms of blood gas
levels. If breathing is reduced enough that the partial pressure of oxygen in the arterial blood falls below
100mmHg and/or the P CO 2 rises above 40Hg, we refer to this as hypoventilation. If breathing increases
such that PO 2 rises above 100mmHg, and CO fall2 below 40mmHg, then we refer to this as
5. Daily Oxygen Consumption
Minute ventilation is about 6 L per minute. Of this 6 litres of air that we breathe every minute, some
ventilates the dead space of theconducting zone so only approximately4.2 L per minute actually reaches
the alveoli. We know that air contains about 21% oxygen so therefore approximately 882 ml (4 200 ml x
21%) of oxygen reaches the alveoli every minute. Only about 250 ml of this 882 ml of oxygen actually
diffuses into the blood. If we multiply this by the number of minutes in a day, we find that per day, a
human consumes about 360 litres of oxygen. We can't ge t this amount of oxygen toour tissues by relying
on oxygen dissolved in the blood - if we did, cardiac output would have to be 83.3 L of blood a minute,
far more than the 5 L of blood actually pumped per minute. So how do we get so much oxygen to the
The answer is haemoglobin. Haemoglobin contains 98.5% of the O in the blood.2Each molecule of
haemoglobin consists of 4 globin subunits (2 alpha and 2 beta) with each subunit containing a heme
group which consists of a porphyrin ringwith an iron molecule in the centre. The iron molecule is the site
of O 2inding so each haemoglobin molecule can bind up to four O molecules. 2
7. Linking Oxygen and Carbon Dioxide Transport in the Blood
Carbonic anhydrase (CA) is an enzyme that is found throughout the body. CA’s function is to catalyse
the reversible hydration/dehydration reaction whereby CO reacts w2th water to form an H ion and a +
HCO 3 ion. Carbonic anhydrases are found in the red blood cells, in the kidney tissues (where it is
important for bicarbonate reabsorptionand acid-base balance), in the parietal cells lining the stomach and
in other tissues. However it is not present in the plasma.
The CO hy2ration/dehydration reaction (H O + CO ↔2HCO + H 2 is critic3l for O and CO transport 2 2
in the blood.
The other reaction involved in this process describes the binding of oxygen to haemoglobin.
These two equations summarize the relationship between CO and O transport in the blood and we can
model gas exchange in a red blood cell in the lung (and tissues) using these two equations. 5
In the lungs O 2iffuses into the blood and then into the redcell. It binds to haemoglobin, and as shown in
the equation, causing haemoglobin to lose H ions. These free H ions react with HCO ions in the3cell
(these enter the cell via chloride bicarbonate exchanger gates) to produce CO and H2O, and t2en this
CO 2diffuses out into the alveolar gas and is lost as we expire.
In the tissues, CO 2iffuses into the red cell andreacts with water to form a proton and a bicarbonate ion.
The proton then binds to oxygenated Hb causing the oxygenmolecule to come off the Hb molecule. It is
then free to diffuse into the tissues.
Both +he CO 2hydration/dehydration reaction and the oxygenation/deoxygenation of Hb are influenced
by H ions. Given this, pH can have a significant effect on oxygen-haemoglobin binding.
CO 2in the systemic arterial blood can be found in many forms, but primarily (89.6%) it is found as
bicarbonate ions in the blood. 5.5% is dissolved in the blood directly, and another 4.8% is bound to
8. The Oxygen Equilibrium Curve (OEC)
We can quantify the binding of oxygen to haemoglobin using an oxygen equilibrium (or
disassociation) curve, which plots the partial pressure of oxygen in mmHg onthe x-axis. The Y-axis can
be the level of oxygen-Hb saturation (as a percentage value) or it can be a measure of oxygen content
(units of oxygen or units of oxygen per units of Hb such as volume %, or molO /molHb2 or gO /gHb). 2
The curve issigmoidal in shape. It is relatively flat at the lowest PO 2 levels and then becomes quite steep
before reaching a plateau at higher P O2 levels. The sigmoidal nature of this curve results from positive
cooperativity, in which the binding of one O mol2cule to a Hb subunit facilitates the binding of a
second, and so on. When we have very low partial pressures, the hemoglobin molecule does not a have a
particular high affinity for oxygen - but as one molecule becomes bound, it causes the other heme groups