Publication of the Association of Polysomnographic Technologists • Winter 2006 • www.aptweb.org
What is a Blood Gas?
BY WILLIAM W. ECKHARDT, RPSGT, CRT, A2Zzz MAGAZINE ASSOCIATE EDITOR
his article is not about the invasive procedure of obtaining a “blood
gas.” Rather, it is about gas molecules and their movement from
outside the body to the cells within the body. Arterial blood gases
(ABGs), commonly called blood gases, are introduced to the blood via
the thoracic pump driving air in and out of the lungs (convection). In the
lung, the air (a mixture of gases) exchanges gases with the blood (diffusion). This is done through the alveolar capillary membrane. Whichever
side of the alveolar capillary membrane (lung or blood) has the greater
concentration of a particular gas, the higher concentration will diffuse to
the side with the lesser concentration trying to equilibrate gas pressures
on both sides of the alveolar capillary membrane.
the other). Eventually the movements from
greater to lesser stop as both sides are
equal called dynamic equilibrium (we are in
a dynamic system where there is always
new blood to reach equilibrium, so this
process never really stops). When a gas
meets a liquid there is also an exchange of
molecules as long as the gas is soluble in
the liquid such as O2 in blood, the molecules then become dissolved unless they
combine chemically with the liquid.
The air or earth’s atmosphere is made up of different gas molecules
(we like oxygen quite a bit) and they are all important to the big picture.
These molecules have mass and are attracted to the earth by its gravitational force. This pressure of course is greatest at the earth’s surface
(more molecules pushing down from above). This is atmospheric pressure. Water vapor or humidity is a gas and acts like the other gases in
the air and exerts a pressure. Once the air reaches the lungs, it is
100% humidified often exerting a greater partial pressure than in the
atmosphere. The partial pressure of oxygen in arterial blood when
breathing ambient air for healthy individuals is 80-100 mm Hg, but when
supplemental oxygen is given, it can be as high as 600 mm Hg. See
Sidebar 1 for calculation of partial pressure of gases ambient and alveolar at standard conditions (BTPS — Barometric pressure the body is
exposed to 750 mm Hg or one atmosphere (atm), body temperature at
37° C and water vapor at maximum for 37° C being 47 mmHg).
Henry’s Law — The amount of gas that can be dissolved in a liquid is
proportional to the partial pressure of the gas to which the liquid is exposed.
T
Gas
Percentage Within Mixture of Gases Partial Pressure
Air at Sea Level (760 mm Hg)
Oxygen
20.9%
159
Nitrogen
79%
600
Inerts
1%
1
Alveolar Gas at Sea Level (760 mm Hg)
Oxygen
13.3%
101
Nitrogen
75.2%
572
Carbon Dioxide
5.3%
40
Water Vapor
6.2
47
760 mm Hg (standard pressure of 1 atm) x .20.9 (percentage of
oxygen in the atmosphere expressed as a decimal) = 159
William W. Eckhardt
Why do we care about diffusion? O2 and CO2 are dissolved in the
blood. O2 comes from the air we breathe and CO2 comes from metabolism within the cells of our bodies (small amounts are of course in the
air we breathe). So, these gases are in differing quantities and states
e.g. dissolved or combined chemically when in the lungs, in pulmonary
circulation or within cells.
Within our blood we have red blood cells. Red blood cells contain
hemoglobin, lots of hemoglobin (280 million molecules). Each hemoglobin molecule contains 4 atoms of iron and can have a reversible bond
with O2. The fact that the bond is reversible helps when transporting O2
from one area to another. So, if this “affinity” of hemoglobin for O2
changes it will gain or lose its hold on the O2. This is good as blood
needs to pick up O2 in the lungs (we want the affinity to be high). In the
cells the reverse is true, we want the hemoglobin to release the O2 to
the cell (we want a lower affinity). There are factors that affect this affinity e.g. temperature, carbon dioxide, and carbon monoxide (CO).
Carbon dioxide is also carried in direct chemical combination with
hemoglobin called carbamino-CO2. It also is transported in the form of
carbonic acid via the bicarbonate ion mechanism. O2 and CO2 also
travel dissolved in the plasma, albeit in small amounts. The measurement of blood gases are derived from the partial pressure of the dissolved gases.
Bohr Effect
Dalton’s Law — In a mixture of gases, the total pressure is equal to
the sum of the partial pressures of the separate components.
There is a relationship between O2 and CO2. The addition of CO2 to
the blood enhances O2 release (decreases the affinity). If we think about
this — it is good. When oxygenated blood reaches the cell, the cell has
a large amount of CO2 compared to the blood. The blood will pickup the
CO2 (higher partial pressure so it wants to diffuse to the side with the
lesser partial pressure) the affinity therefore decreases and O2 is
released to the cell.
Why Do Gases Diffuse?
Haldane Effect
Diffusion is the movement of gas molecules from high concentration
to a lower concentration. This can take place in the atmosphere and
across cell membranes. Each gas works independently. If Carbon Dioxide
(CO2) and Oxygen (O2) are both moving across the alveolar capillary membrane they will likely move at different rates and amounts due to a difference in their respective gradients (pressure differences from one side to
The addition of O2 to the blood enhances CO2 release. This too is
good! When blood reaches the lung it will pickup O2 (higher partial pressure of O2 in the lung causes the O2 to diffuse across the alveolar capillary membrane). This addition of O2 to the blood causes enhanced CO2
release at a time conducive to its elimination.
Sidebar 1
Gas Laws
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Publication of the Association of Polysomnographic Technologists • Winter 2006 • www.aptweb.org
Blood gas measurements are generally done after performing an arterial puncture and using a blood gas analyzer. This analyzer works by measuring the dissolved form of the gases partial pressure. The blood gas measurement is seldom done in the sleep lab for various practical reasons.
What we do measure in the sleep lab is the O2 saturation of the
blood and sometimes the end tidal CO2 of expired gases. These are noninvasive methods and the values can change over time as the patients
status changes, even on a breath by breath basis.
The Oxy-hemoglobin dissociation curve gives us a representation of oxygen partial pressure in relation to the oxyhemoglobin (percent hemoglobin
saturated with oxygen) at differing partial pressures. At the alveolar capillary
membrane the amount of oxygen that can be dissolved in the blood is proportional to the partial pressure of the oxygen to which the blood is exposed
(Henry’s Law). Most the oxygen attaches to hemoglobin and once the pressure gradient equilibrates the hemoglobin is maximally saturated for that
blood oxygen tension. It is possible to increase the saturation by increasing
the oxygen tension (increased inspired oxygen concentration or FiO2). The
oxy-hemoglobin dissociation curve is a sigmoid shape between 0 and 100
mm Hg. This shape shows that hemoglobin’s affinity for O2 progressively
increases as more and more molecules of O2 combine with the hemoglobin. At the beginning of the curve O2 saturation increases significantly as
the partial pressure of O2 increases. At the flatter part of the curve only
slight increases in saturation are seen with increases in partial pressure.
The curve can shift, right or left, showing the relationship certain factors have on hemoglobin’s affinity for oxygen. A shift to the right presents
with a decreased oxygen affinity. For a given partial pressure of oxygen the
oxygen content is decreased. Oxygen content being the sum of the oxygen
dissolved in the blood and that attached to hemoglobin. A left shift presents with a increased oxygen affinity. For a given partial pressure of oxygen
the oxygen content is increased. So, this affects the availability of the oxygen to the tissues. At higher affinity there is less oxygen available for a given
partial pressure. Some factors that affect availability or shifts are carbon
dioxide tension (Bohr Effect), blood pH, and temperature. An increase in
these causes decreased oxygen affinity. Blood needs to pick up O2 in the
lungs (we want the affinity to be high) the decreased CO2 (carbon dioxide
partial pressure is higher in the blood and diffuses across the alveolar capillary membrane) increases the affinity for oxygen and the oxygen content
increases. In the cells the reverse is true, we want the hemoglobin to
release the O2 to the cell (we want a lower affinity) and the tissue metabolism produces carbon dioxide resulting in a slight shift to the right.
Fig. 1 Oxyhemoglobin Dissociation Curve — A left shift means that
smaller increases in the partial pressure of O2 correspond to higher hemoglobin saturations. A right shift would require (reduced affinity) greater
increases in partial pressure of O2 to maintain saturation. Left shifts are
good for the uptake of O2 (Haldane effect — seen as the blood enters the
lungs. The addition of O2 to the blood enhances CO2 release) and right
shifts are good for the release of O2 to the tissues (Bohr Effect — the addition of CO2 to the blood enhances O2 release from hemoglobin).
So how do we measure the oxygen level? You know the answer, with
an oximeter. The oximeter uses Spectrophotometry to determine the
amounts of oxyhemoglobin and deoxygenated hemoglobin. This method
shines light of two different wavelengths through the sensor site. These
are absorbed differently by the hemoglobin depending on its state with the
oxygen molecules. The oximeter calculates these into a saturation value
which is given as a percentage of saturation. Knowing this value you can
look at the curve and determine
where on the curve it lays, giving
you the partial pressure. The difference between the value of an
oximeter and that of a blood gas
is the oximeter gives us arterial
oxyhemoglobin saturation whereas the blood gas gives us the
partial pressure of oxygen in the
arterial blood. The blood gas
also gives values of other
gases/parameters that the
Figure 1
oximeter can not but the
patient’s oxygenation status can
be evaluated with either the blood gas (PaO2) or the saturation (SpO2).
There are of course technical and physiological factors that can influence
the accuracy of either test. Blood oxygen measurements need to be evaluated relative to the patient status, history, and other clinical tests.
Another important aspect of blood gas partial pressure is in the regulation of breathing. The drive to breathe is controlled by The Respiratory
Control System that uses the partial pressure of O2 and CO2 for the feedback in which to modify system controls. Sensors or chemoreceptors
with in the medulla in the brainstem (central chemoreceptors) and the
carotid and aortic bodies (peripheral chemoreceptors) send afferent input
back to the controllers (negative feedback). So, the controller takes input
and this precipitates an action which affects the “plant” or controlled system (here the lungs) which in turn changes the system output. The feedback is sent to the controller utilizing output from these receptors that
react to partial pressures of the gases O2 and CO2. This is a negative
feedback system largely run from values of the blood gases.
Why Do I Need To Know All This?
Because the oxygen saturation of our patient’s blood is one of the
most important parameters we measure in the sleep lab. When measuring something you should know where that value comes from. A
patient may need support to enhance their oxygenation. This may be
done by enhancing ventilation such as with PAP therapy or increasing the
patients inspired oxygen concentration (FiO2). Please refer to the APT
CORE COMPETENCY: Monitoring Pulse Oximetry in Polysomnographic
Technology and APT CORE COMPETENCY: Supplemental Low Flow
Oxygen Titration in Polysomnographic Technology. This is an aspect of
care in which polysomnographic technologists need to gain competency,
in order to provide the best possible patient care. #
References
Clinical Application of Blood Gases, Barry A. Shapiro, Ronald A. Harrison, John R. Walton,
Third Edition, Year Book Medical Publishers
Mosby’s Respiratory Care Equipment, J.M. Cairo, Susan P. Pilbeam, Seventh Edition, Mosby
Ventilatory Control and the Thoracic Pump, William W. Eckhardt, A2Zzz Magazine, Volume
14 Number 1
About the Author
Will Eckhardt, RPSGT, CRT is a member of the APT Board of Directors, and serves the APT
Board Liaison for the APT Standards and Guidelines Committee. He is a board member of
the New England Polysomnographic Society (NEPS) and is NEPS Education Committee Chair.
His full time position is with Sleep HealthCenters where he is the Director of Education.
Eckhardt also is a faculty member at Northern Essex Community College where he teaches
in the polysomnography program and is a member of the advisory board. He is a member of
the A2Zzz Magazine Editorial board and a recipient of the APT Dr. Allen DeVilbiss Literary
Award in 2004. He is also a member of the American Academy of Sleep Medicine Committee
on Polysomnographic Technologists Issues.
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