Arterial Blood Gas

Mark Joshua S. Cruz RTRP

Gas Exchange
and Transport
Respiration
Process of moving O2 to tissues for aerobic
metabolism and removal of carbon dioxide
– Involves gas exchange at lungs and tissues
• O2 from atmosphere to tissues for aerobic metabolism
• Removal of CO2 from tissues to atmosphere
Diffusion
Whole-body diffusion gradients
– Gas moves across system by simple diffusion
– O2 cascade moves from PO of 159 mm Hg in atmosphere
to intracellular PO of approximately 5 mm Hg
– CO2 gradient is reverse from intracellular CO2
approximately 60 mm Hg to atmosphere where it = 1 mm Hg

Atm = 760 O2 = 21%

760 X .21 = 159 mmHg O2 in the atmoshpere
Normal diffusion gradients
for O2 and CO2. There is a
downward cascade for O2
from air to cells, with a
reverse gradient for CO2.
Determinants of
Alveolar Gas
Tensions
Alveolar Carbon Dioxide
– The alveolar partial pressure of CO2 varies directly with the body’s production of CO2
and inversely with alveolar ventilation
– An increase in dead space, the portion of inspired air that is exhaled without being
exposed to perfused alveoli, can also lead to an increased PACO
– PACO2 decreases if CO2 production decreases or alveolar ventilation increases
– Normal PACO2 is within a range of 35 to 45 mm Hg
Alveolar Partial Pressure Of CO2 (PACO2)

 PACO2 = Alveolar CO2 tension (mm Hg)

 VCO2 = CO2 production (in ml/min standard temperature and pressure, dry [STPD])
 VA = Alveolar ventilation (L/min body temperature and pressure, saturated [BTPS])

 Because VCO2and VA are measured under different conditions

(STPD and BTPS, respectively), a correction factor of K is used.
 K = 0.863.
Example:
Given VCO2 of 200 ml/min and alveolar ventilation of 4 L/min.
2

Compute for PACO2

 PACO2 = (200/4) x 0.863

 PACO2 = 50 x 0.863
 PACO2 = 43.15 mm Hg
Alveolar O2 tensions
– PIO2 is primary determinant
– In lungs, it is diluted by water vapor and CO2
– Alveolar air equation accounts for all these factors
PAO2 = FiO2 × (PB – 47) – (PACO2/0.8)
– Dalton’s law of partial pressures accounts for first part of formula; second part relates
to rate at which CO2 enters lung compared to O2 exiting
• Ratio is normally 0.8.
– If FiO2 > 0.60, (PACO2/0.8) can be dropped from equation
 Alveolar O2 tensions
 FiO2 = Fraction of inspired O2 (expressed in decimals) must always in decimal
ex: 40% = 0.4 30% = 0.3 60% = 0.6 100% = 1
 PB = Barometric pressure (mm Hg) normal is 760
 PH2O = Water vapor tension. At BTPS, a value of 47 mm Hg is usually used.
 PACO2 = Alveolar PCO2 (mm Hg)
 RQ = Respiratory quotient, usually estimated at 0.8.
 PIO2 = FiO2 × (PB − PH2O) represents the partial pressure of O2 in the inspired air and is the most
important determinant of PAO2.
 The expression (PACO2 ÷ RQ) accounts for the alveolar CO2.
 RQ is the ratio of CO2 excretion to O2 uptake, which normally averages 0.8 throughout the lung.
 PaCO2 nearly equals PACO2, PaCO2 can be substituted for PACO2.
If FiO2 is 0.21, PB is 760 mm Hg, and PaCO 2 2

is 40 mm Hg, what is the normal PAO2?

 PAO2 = FiO2 X (PB – PH20) – ( PACO2/RQ )
 PAO2 = 0.21 X (760 – 47) – ( 40/0.8 )
 PAO2 = 0.21 X (713) – ( 50 )
 PAO2 = 149.53 – ( 50 )
 PAO2 = 99.73 mm Hg
Changes in alveolar gas
partial tensions
– O2, CO2, H2O, and N2 normally comprise alveolar
gas
• N2 is inert but occupies space and exerts pressure
• Partial pressure of alveolar nitrogen (PAN2) is determined
by Dalton’s law PAN2 = PB – (PAO2 + PACO2 + PH2O)
– Only changes seen will be in O2 and CO2
• Constant FiO2, PAO2 varies inversely with PACO2
• Prime determinant of PACO2 is VA
Effect of alveolar
ventilation on
alveolar gases.
Mechanisms of Diffusion
• Diffusion occurs along pressure gradients
• Barriers to diffusion
– A/C membrane has three main barriers
• Alveolar epithelium
• Interstitial space and its structures
• Capillary endothelium
– RBC membrane
• Fick’s law: The greater the surface area, diffusion constant,
and pressure gradient, the more diffusion will occur
Pulmonary diffusion
gradients
– Diffusion occurs along pressure gradients
– Time limits to diffusion:
• Pulmonary blood is normally exposed to alveolar gas for
0.75 sec, during exercise may fall 0.25 sec
• Normally equilibration occurs in 0.25 sec
• With diffusion limitation or blood exposure time of less
then 0.25 sec, there may be inadequate time for
equilibration
Ventilation maintains mean
alveolar gas pressures for O2 and
2

CO2 at approximately 100 mm

2

Hg and 40 mm Hg. As blood

enters the venous end of the
capillary, it gives up CO2 and
2

loads O2 until these two gases are

2

in equilibrium with alveolar

pressures. At this point, the blood
is “arterialized.”
Normal Variations From Ideal
Gas Exchange
• PaO normally 5 to 10 mm Hg less than PAO due to:
• Anatomic shunts:
– Portion of cardiac output that returns to left heart without being
oxygenated by exposure to ventilated alveoli
– Two right-to-left anatomic shunts exist
• Bronchial venous drainage
• Thebesian venous drainage
• These drain poorly oxygenated blood into arterial circulation lowering
CaO2
• Regional differences in pulmonary ventilation and blood flow
Ventilation/Perfusion ratio
– Ideal ratio is 1, where V/Q is in perfect balance
– In reality lungs, don’t function at ideal level
• High V/Q ratio at apices greater than 1 V/Q
(approximately 3.3)
– ↑PAO2 (132 mm Hg), ↓PACO2 (32 mm Hg)
• Low V/Q ratio at bases less than 1.0 (approximately 0.66)
– Blood flow is approximately 20X times higher at bases
– Ventilation is greater at apices but not 20X
– ↓PAO2 (89 mm Hg), ↑PACO2 (42 mm Hg)
Summary of Variations in Gas Exchange in
the Upright Lung by Region
Gas Transport
 Oxygen Transport
• Transported in two forms: Dissolved and bound
• Physically dissolved in plasma
– Gaseous O2 enters blood and dissolves.
– Henry’s law allows calculation of amount dissolved
• Dissolved O2 (ml/dl) = PO2 × 0.003
• Chemically bound to hemoglobin (Hb)
– Each gram of Hb can bind 1.34 ml of O2.
– [Hb g] × 1.34 ml O2 provides capacity.
– 70 times more O2 transported bound than dissolved
SaO2 vs PaO2
 SaO2 (and its indirect measurement SpO2) describe the amount of oxygen bound to
hemoglobin in arterial blood. The term "saturation" likens hemoglobin to a sponge that
becomes saturated with oxygen. The measurement is given as a percentage. 
 PaO2 describes the amount of oxygen dissolved in arterial blood plasma.
 Total O2 content of blood
Combination of dissolved and bound to Hb

CaO2 = (0.003 × PaO2) + (Hb × 1.34 × SaO2)

– Normal is 16 to 20 ml/dl

Normal arteriovenous difference (approximately 5

ml/dl)
 Each Hb molecule binds four oxygen atoms in a rapid and reversible
process
 The hemoglobin-oxygen combination is called oxyhemoglobin (HbO2)

 Hemoglobin that has released oxygen is called reduced hemoglobin

(HHb)
• Hemoglobin saturation
– Saturation is % of Hb that is carrying O2 compared to
total Hb
• SaO2 = [HbO2/total Hb] × 100
• Normal SaO2 is 95% to 100%
Oxygen-Hemoglobin
Dissociation Curve
The key feature of the dissociation
 curve is its non-linear, sigmoid
shape. As observed, the saturation of hemoglobin changes
substantially when the partial pressure of oxygen ranges between 20
- 60 mm Hg but tends to plateau at oxygen partial pressures above
80 mm Hg. 
HbO2 dissociation curve
– Relationship between PaO2 and SaO2 is S-shaped
– Flat portion occurs with SaO2 >90%
• Facilitates O2 loading at lungs even with low PaO2
– Steep portion (SaO2<90%) occurs in capillaries
• Facilitates O2 unloading at tissues
pH (Bohr effect)
– Describes affect pH has on Hb affinity for O2
– pH alters position of HbO2 curve
• Low pH shifts curve to right, high pH shifts to left
– Enhances O2 transport
• At tissue pH is approximately 7.37 shift right, more O2 unloaded
• Lungs pH approximately 7.4 shifts back left, enhancing O2 loading
• Body temperature (T) and
HbO2 curve
– Changes in T alter position of HbO2 curve
• Decreased T shifts curve left
• Increased T shifts curve right
• T is directly related to metabolic rate
– When T is higher, right shift facilitates more O2
unloading to meet metabolic demands
– With lower metabolic demands, curve shifts left as not as
much O2 is required.
2,3-Diphosphoglycerate

 2,3-Diphosphoglycerate (2,3-DPG) is a special intermediate of glycolysis in

erythrocytes which is rapidly consumed under conditions of normal oxygen tension.
However, when hypoxia is encountered in peripheral tissues, the concentration of 2,3-
DPG can accumulate to significant levels within hours. At these concentrations, 2,3-
DPG can bind to hemoglobin and reduce its affinity for oxygen, resulting in a right-
ward shift of the Oxygen-Hemoglobin Dissociation Curve discussed in oxygen
transport. This results in enhanced unloading of oxygen by hemoglobin and thus
results in enhanced oxygen transport to tissues encountering long-term hypoxia.
2,3-Diphosphoglycerate (DPG)
and the HbO2 curve
– Found in quantity in RBCs; stabilizes deoxygenated Hb, decreasing oxygen’s affinity
for Hb
• Without 2,3-DPG Hb affinity is so great that O2 cannot unload
– ↑2,3-DPG shifts curve to right, promoting O2 unloading
– ↓2,3-DPG shifts curve to left, promoting loading
• Stored blood loses 2,3-DPG, large transfusions can significantly impair tissue oxygenation
 Abnormal hemoglobins
– HbS (sickle cell): Fragile leads to hemolysis and thrombi
– Acute chest syndrome (ACS), multiple causes
• Most common cause of death
– Methemoglobin (metHb): Abnormal iron (Fe ) cannot 3+ bind with O2 and alters HbO2
affinity (left shift)
• Commonly caused by NO, nitroglycerin, and lidocaine
• Must frequently monitor for MetHb and weigh risk versus benefit
– Carboxyhemoglobin (HbCO): Hb binds CO, has 200 times greater than Hb affinity than
O2
• Displaces O2 and shifts curve left
– O2 which is bound cannot unload (left shift)
– Treat with hyperbaric therapy
Hemoglobin F

 Expression of the F isoform in fetuses is critical for facilitating oxygen transfer from
the maternal to the fetal circulation. Because fetal blood displays a higher affinity for
oxygen than maternal blood, oxygen will diffuse from the pregnant maternal to the
fetal circulation within the placenta, allowing for oxygenation of fetal tissues.
Measurement of Hb affinity for
O2
Bohr Effect
 The Bohr Effect refers to the observation that increases in the carbon dioxide partial
pressure of blood or decreases in blood pH result in a lower affinity of hemoglobin for
oxygen. This manifests as a right-ward shift in the Oxygen-Hemoglobin Dissociation
Curve described in  Oxygen Transport  and yields enhanced unloading of oxygen
by hemoglobin.
 The primary factor determining whether oxygen is loaded or unloaded
onto hemoglobin is the surrounding partial pressure of oxygen. The
quantitative relationship between oxygen partial pressure and the
percent of hemoglobin molecules bound to oxygen is provided by the
"Oxygen-Hemoglobin Dissociation Curve" 
 Carbon Dioxide Transport
Approximately 45 to 55 mL/dL of CO2 is normally carried in
the blood in the following three forms:
– Dissolved in blood: approximately 8% as high solubility coefficient
– Combined with protein: approximately 12% binds with amino
groups on plasma proteins and Hb
– Ionized as bicarbonate: approximately 80% transported as HCO3
due to hydrolysis reaction
• Majority of hydrolysis occurs in RBCs as they contain carbonic anhydrase
—serves as catalyst
• HCO3 diffuses out of RBCs in exchange for Cl , called chloride shift or
hamburger phenomenon
CO2 dissociation curve
– Relationship between PaCO2 and CaCO2
– HbO2 affects this relationship
• Haldane effect describes this relationship
• As HbO2 increases, CaCO2 decreases
– Facilitates CO2 unloading at lungs
• At tissues, HbO2 decreases and facilitates higher CaCO2
for transport to lungs
1. Dissolved Gas
Roughly 5-10% of carbon dioxide is transported from tissues to the lungs in a
simple dissolved form. In this process, metabolically-generated carbon dioxide gas
simply diffuses into local capillaries, travels to the lungs via venous blood, and is
exhaled .
2. Bicarbonate ion in plasma
Transport of carbon dioxide in a chemically-modified form accounts for nearly
80% of total carbon dioxide transport and is achieved by carbon dioxide conversion to
bicarbonate. The processes which are responsible for this transport require multiple
steps as detailed below.
Mechanism
 Gaseous CO2 derived from metabolically-active cells diffuses in a dissolved state
into the cytosol of erythrocytes present in local capillaries.
 This CO2 combines with a water H2O molecule to form Carbonic Acid H2CO3.
This process is naturally very slow. But it is catalyzed by the Carbonic Anhydrase
in the erythrocytes.
  Once generated, carbonic acid spontaneously dissociates into a free hydrogen ion (H+) and
bicarbonate (HCO3-).

 The resultant free hydrogen ions appear to be absorbed by the erythrocytic hemoglobin
molecule which may promote enhanced oxygen unloading in the periphery due to the Bohr
Effect.
 The resultant bicarbonate ion is transported across the erythrocyte membrane into the
plasma in exchange for a chloride ion using an electroneutral Bicarbonate-Cl Antiporter.  -
Hamburger phenomenon

 Bicarbonate then travels in venous plasma to the lungs where the above reactions occur in
reverse, leading to generation of gaseous CO2 which is exhaled. Reversal of these
reactions in the lungs is enhanced by the presence of high oxygen partial pressures as
discussed further in the Haldane Effect.
3. Protein-bound to
hemoglobin
 Transport of carbon dioxide in a protein-bound form accounts for 12% of total carbon
dioxide transport and is achieved by reversible binding of carbon dioxide to
hemoglobin.
CO2 + Hb = HbCO2
 Dissolved CO2 can spontaneously and reversibly react with the free amino-termini in
hemoglobin polypeptides, resulting in the generation of "Carbaminohemoglobin"
molecules.
 The carbaminohemoglobin compounds are transported via venous
blood within eythrocytes to the pulmonary vasculature where the
reaction reverses, releasing a molecule of CO2 that is subsequently
exhaled.

  Release of carbon dioxide bound by hemoglobin is aided by the

higher partial pressures of oxygen in the lungs as described in the 
Haldane Effect.
CO2 dissociation curve
– Relationship between PaCO and CaCO 2 2
– HbO2 affects this relationship
• Haldane effect describes this relationship
• As HbO2 increases, CaCO2 decreases
– Facilitates CO2 unloading at lungs
• At tissues, HbO2 decreases and facilitates higher CaCO2
for transport to lungs
Haldane Effect

 The Haldane Effect describes the phenomenon by which binding of oxygen to

hemoglobin PROMOTES THE RELEASE OF CARBON DIOXIDE. In many ways, the
Haldane Effect is the mirror image of the  Bohr Effect, making clear that oxygen and
carbon dioxide compete for hemoglobin occupancy. This competition is a helpful
biochemical feature which facilitates exchange of carbon dioxide for oxygen in the
pulmonary and peripheral circulations.
Abnormalities of
Gas Exchange
and Transport
Impaired oxygen delivery
(DO2)
– DO2 = CaO2 × CO
– When DO2 is inadequate, tissue hypoxiav ensues
– Hypoxemia: Defined as abnormally low PaO2
• Most common cause is V/Q mismatch
– Because of shape HbO2 curve, areas of high V/Q cannot compensate for areas of low V/Q, so
↓PaO2
• Other causes: Hypoventilation, diffusion defect,
shunting, and low PIO2 (altitude)
Dysoxia
– DO2 is normal, but cells undergo hypoxia
– Cells are unable to adequately utilize O2
• Cyanide poisoning prevents cellular use of O2
• In very sick individuals (sepsis, ARDS), O2
debt may occur at normal levels of DO2
– If O2 uptake increases with increased DO2, then DO2 was
inadequate
– Demonstrates low VO2/DO2 (extraction ratio), thus dysoxia
Reduction in Blood Flow
(Shock or Ischemia)
– Circulatory failure (shock)
• Tissue O2 deprivation is widespread
– Local reductions in perfusion (ischemia)
• Local reductions in blood flow can cause localized
hypoxia
• Can result in anaerobic metabolism, metabolic acidosis,
and eventual death of the affected tissue
Age PaO2
80 60
70 70
60 80
Hemoglobin deficiencies
– Anemias can be either absolute or relative
– Absolute Hb deficiency occurs when the Hb concentration is lower than normal
– Relative Hb deficiencies are caused by either the displacement of O2 from normal Hb
or the presence of abnormal Hb variants
Impaired CO2 removal
Disorders that decrease VA relative to metabolic need
• Inadequate VE
– Usually result of ↓VT, ↓f rare (drug overdose)
• Increased dead space ventilation (VD /VT ) caused by:
– Decreased VT as in rapid shallow breathing or,
– Increased physiologic dead space, as in pulmonary embolus
• Without compensation, alveolar ventilation is lowered per
minute
Ventilation/Perfusion Imbalance

– Typically, CO2 does not rise; instead, increase VE.

There is a direct relationship between VCO2 and
minute ventilation.
• If patient is unable to ↑VE, then hypercarbia with acidosis
occurs
– Seen in severe chronic disorders, that is, COPD
ACID-BASE
BALANCE
Acid-base balance refers to physiological
mechanisms that keep the hydrogen ion
concentration ([H+]) of blood and body fluids in a
range compatible with life.
Hydrogen Ion
Regulation in
Body Fluids
Body fluids must be kept in a narrow pH range of 7.35 to 7.45 to
function normally. This corresponds to [H+] of 45 to 35 nmol/L.

Hydrogen ions react readily with the protein molecules of vital

cellular catalytic enzymes which change the physical contour of
the protein molecule and may render the enzyme inactive.

Hydrogen ions formed in the body come from either volatile or

fixed (nonvolatile) acids.
 Volatile acids are in equilibrium
with a dissolved gas.
The only volatile acid of physiologic importance in the body is carbonic acid (H2CO3),
which is in equilibrium with dissolved carbon dioxide.

Tissue metabolism produces massive amounts of CO2 approximately 13,000 mmol/L each
day, which is hydrolyzed into volatile acid H2CO3 and produces an equal amount of H+ as
shown by the CO2 hydration reaction:
CO2 + H2O → H2CO3 → H+ + HCO3
So basically increase in CO2 will increase H+ that will decrease pH.
Increase CO2 → Increase H+ = Decrease pH (makes it acidic)
 Isohydric Buffering
As CO2 diffuses into the blood at the tissue level most H+ produced in this way causes no
change in pH because hemoglobin (Hb) in the erythrocyte immediately buffers the H+.
When blood reaches the lungs, Hb releases H+ to form CO2 as shown:

In this way, ventilation Most H+ produced in

gets rid of H2CO3 just this way causes no
as fast as it is change in pH because
produced. hemoglobin (Hb) in the
erythrocyte immediately
buffers the H+
Isohydric buffering and ventilation are the two major ways the body
keeps the blood’s pH constant regardless of how much CO2 is produced.
Nonvolatile acids are not in equilibrium with a gas.
They are buffered by bicarbonate ions (HCO3).
Catabolism — the breakdown of proteins continually produces fixed (nonvolatile) acids
such as sulfuric and phosphoric acids. Anaerobic metabolism produces lactic acid another
fixed acid.

H+ of fixed acids can be buffered by bicarbonate ions (HCO3−) and converted to CO2 and
water (H2O). Certain diseases, such as untreated diabetes, increase fixed acid production.
Hydrogen ions produced in this way stimulate respiratory centers in the brain.

In this way, the respiratory

system compensates for
increases in fixed acid;
that is, it prevents [H+]
from rising as sharply as it
otherwise would when
fixed acids are produced.
Strong and Weak
Acids and Bases:
Equilibrium
Constants
Strong acid and base molecules
dissociate or ionize almost completely
in an aqueous (liquid) solution.
An example of a strong acid is hydrochloric acid. Nearly 100% of the HCl molecules
dissociate to form H+ and Cl−

HCl → H+ + Cl−
At equilibrium, when all dissociation stops, the concentration of HCl is extremely small
compared with either [H+] or [Cl−]. There is no arrow pointing to the left, emphasizing
that HCl ionizes almost completely in solution.
Weak acids and bases ionize
only to a small extent.
Carbonic Acid or H2CO3 is an example of a relatively weak acid:

The long arrow pointing to the left indicates that at equilibrium, the concentration of
undissociated H2CO3 molecules is far greater than the concentration of either HCO3 −
or H+.
Equilibrium Constant of an acid is a
measure of the extent to which the acid
molecules dissociate (ionize).
KA is also known as the acid’s ionization or dissociation constant.
KA is a measure of the strength of an acid—that is, how much the acid molecule
dissociates.

A strong acid, such as HCl, has a large KA.

A weak acid, such as H2CO3, has a small KA.
Buffer Solution
Characteristics
A buffer solution resists changes in pH when an
acid or a base is added to it. Buffer solutions are
mixtures of acids and bases.

The acid component is the H+ cation (positively charged ion), formed when a weak acid
dissociates in solution.

The base component is the remaining anion (negatively charged ion) portion of the acid
molecule, known as the conjugate base.
An important blood buffer system is a solution of
carbonic acid and its conjugate base, HCO3 −

In the blood, HCO3 − combines with sodium ions to form sodium bicarbonate (NaHCO3).
Carbonic acid/bicarbonate: in blood exists in reversible combination as NaHCO3 and
H2CO3
If HCl or hydrogen chloride, a strong acid, is added to the H2CO3/NaHCO3 buffer
solution, HCO3 − reacts with the added H+ to form weaker H2CO3 molecules and a
neutral salt: buffered with only small acidic pH change

HCl + NaHCO3 → NaCl + H2CO3

The strong acidity of HCl is converted to the relatively weak acidity of H2CO3,
preventing a large decrease in pH.
If NaOH or sodium hydroxide, a strong base, is added to the buffer solution, it reacts
with the H2CO3 molecule to form the weak base, sodium bicarbonate or NaHCO3, and
H2O: buffered with only slight alkaline pH change.

NaOH + H2CO3 → NaHCO3 + H2O

The strong alkalinity of NaOH is changed to the relatively weak alkalinity of NaHCO3.
Again, pH change is minimized.
Bicarbonate and
Non-bicarbonate
Buffer Systems
 Bicarbonate Buffer System:
consists of H2CO3 and its conjugate
base, HCO3-

• Open buffer system as H2CO3 is hydrolyzed to CO2

• Ventilation continuously removes CO2 preventing equilibration driving reaction to right
HCO3 – + H+ → H2CO3 → H2O + CO2
• Removes vast amounts of acid from body per day
Non-bicarbonate buffer system :
composed of phosphate and proteins
Called a closed buffer system because all the components of acid-base reactions
remain in the system; no gas to remove acid by ventilation.

Hbuf is the weak acid, and Buf− is the conjugate base. When H+ is buffered by Buf−,
the product, HBuf, builds up and eventually reaches equilibrium with the reactants,
preventing further buffering activity:
Classification of Whole Blood
Buffers
OPEN SYSTEM
CLOSED SYSTEM
Bicarbonate Nonbicarbonate
– Plasma – Hemoglobin
– Erythrocyte – Organic
phosphates
– Inorganic
phosphates
– Plasma proteins
Because the HCO3 − is co-produced with the H+, the only buffer system that can buffer the
H+ of volatile acid is the nonbicarbonate buffer system.

However, both nonbicarbonate and bicarbonate buffer systems can buffer the H+ produced
by fixed acids.

Both systems are physiologically important, each playing a unique and essential role in
maintaining pH homeostasis.

Bicarbonate buffers have the greatest buffering capacity because they function in an open
system.
The bicarbonate and nonbicarbonate buffer
systems exist in equilibrium in the plasma.
pH of a Buffer
System: Henderson-
Hasselbalch
Equation
Measuring Hydrogen Ion Concentration:
The Concept of pH
 The concept of pH was developed by Sørenson in 1909. The pH scale ranges from 0 to
14 pH units.

 [H+] in body fluids is extremely small (normally about 40 × 10−9 mol/L, or 40 billionths of 1
mole per liter [0.000000040 mol/L]). The prefix “nano” means billionths; therefore, [H+] of
body fluids is about 40 nmol/L. In clinical medicine, acidity is generally expressed in terms
of pH rather than nmol/L[H+].

 pH is defined as the negative logarithm, or exponent (to the base 10), of [H+]; this is
shown as follows:
Measuring Hydrogen Ion
Concentration:
The Concept of pH
 Because pH is the negative logarithm of [H+], a decrease in pH
indicates an increase in [H+].
Measuring Hydrogen Ion
Concentration:
The Concept of pH
 A chemically neutral solution (neither acidic nor basic) has a pH of 7.0. To the
chemist, a solution with a pH less than 7.0 is acidic, and a solution with a pH greater
than 7.0 is alkaline. By this standard, body fluids are slightly alkaline, as the following
shows:

 Because pH is a logarithmic scale, a change of one pH unit corresponds to a 10-fold

change in [H+].
 In the physiological range, a 1-nmol/L change in [H+] produces a 0.01 change in pH. The
pH-to-[H+] relationship maintains some degree of linearity between pH values of 7.20 and
7.55. However, below a pH of 7.20, linearity deteriorates rapidly
 Henderson-Hasselbalch
Equation
 Describes [H+] as ratio of [H2CO3]/[HCO3 –]
 pH is logarithmic expression of [H+].
 6.1 is the log of the H2CO3 equilibrium constant
 (PaCO2 × 0.03) is in equilibrium with, and directly proportional to blood [H2CO3]

 where pK = 6.1 (an ionization constant) and 0.03 = factor to convert Paco2 to mmol/L
(concentration of dissolved CO2).
 Assuming a normal HCO3 and Paco2, we compute a normal pH as follows:

Note that for a normal pH, the ratio of HCO to dissolved CO2 must
be 20:1. Any major change in this ratio will result in an abnormal
pH.
Clinical Use of Henderson-
Hasselbalch Equation
The H-H equation is useful for checking a clinical blood gas
report to see if the pH, PCO2, and [HCO3−] values are
compatible with one another. In this way, transcription errors
and analyzer inaccuracies can be detected. It is also
clinically useful to predict what effect changing one H-H
equation component will have on the other components. For
example, a clinician may want to know how low the arterial
blood pH will fall for a given increase in PaCO2.
Physiologic Roles of
Bicarbonate and Non-
bicarbonate Buffer
Systems
Bicarbonate Buffer System
HCO3 – can continue to buffer fixed acid H+ as long as ventilation is adequate to
exhale volatile acid CO2
Ventilation

HCO3 – cannot buffer H2CO3 (volatile) acid

In hypoventilation, H2CO3 accumulates; only nonbicarbonate system can serve as buffer
 Nonbicarbonate Buffer System
Hb is most important buffer in this system: it is most abundant
Can buffer any fixed or volatile acid
As closed system, products of buffering accumulate and buffering may slow or stop (H+ +
Buf– ↔ HBuf).

HCO3 – and buf– exist in same blood system so

Ventilation
H+ + HCO3 – → H2CO3 → H2O + CO2
Fixed acid → H+ + Buf– ↔ HBuf
ACID EXCRETION
Bicarbonate and non bicarbonate buffer
systems are the immediate defense
against the accumulation of H+ if the
body fails to eliminate the remaining
acids, these buffers are soon exhausted,
and the pH of body fluids quickly
decreases to life-threatening levels. The
lungs and kidneys are the primary acid-
excreting organs. The lungs can excrete
only volatile acid. The kidneys also
remove fixed acids but at a slow pace.
If acids were not excreted, life-threatening acidosis would follow
Lungs
– Excrete CO2, which is in equilibrium with H2CO3

– Crucial: body produces huge amounts of CO2 during aerobic metabolism (CO2 +
H2O → H2CO3) – In addition, through HCO3

– eliminate fixed acids indirectly as byproducts are CO2 and H2O

– Remove approximately 24,000 mmol/L CO2 removed daily

Kidneys
– Physically remove H+ from body
– Excrete less than 100 mEq fixed acid per day
– Also control excretion or retention of HCO3
– If blood is acidic, then more H are excreted and + all HCO3 – is retained (vice versa )
While lungs can alter [CO2] in seconds, kidneys require hours/days to change HCO3 –
and affect pH
Kidney Functions Terms
• Excretion is the elimination of substances from the body in the urine.
•

Secretion is the process by which renal tubule cells actively transport

substances into the fluid inside the tubule lumen (i.e., the filtrate).
•

Reabsorption is the active or passive transport of filtrate substances

back into the tubule cell and into the blood of nearby
capillaries.
Basic kidney function
– Renal glomerulus filters the blood by passing water,
electrolytes, and nonproteins through semipermeable
membrane.
Filtrate is modified as it flows through renal tubules
– HCO3 is filtered through membrane, while CO2
diffuses into tubule cell, where it is hydrolyzed into H+,
which is then secreted into renal tubule
• H+ secretion increases in the face of acidosis
– That is, hypoventilation or ketoacidosis increases secretion
Reabsorption of HCO3
For every H+ secreted, an HCO3 – is reabsorbed
Reacts in filtrate, forming H2CO3 which dissociates into H2O and CO2
CO2 immediately diffuses into cell, is hydrolyzed, and H is secreted into filtrate; HCO3
– diffuses into blood
Thus, HCO3 – has effectively been moved from filtrate to blood in exchange for H+
If there is excess HCO3 – that does not react with H+, it will be excreted in urine
Renal response to
respiratory
acidosis. Filtrate
HCO3 − is
reabsorbed by
first reacting with
secreted H+.
Renal response
to respiratory
alkalosis.
Excess HCO3 −
is excreted in
the urine with a
positive ion.
Role of urinary buffers in excretion
of excess H+
• Once H+ has reacted with all available HCO3 –, excess reacts with phosphate and
ammonia
• If all urinary buffers are consumed, further H+ filtration ends when pH falls to 4.5
• Activation of ammonia buffer system enhances Cl– loss and HCO3 – gain
SAMPLING AND
ANALYZING
BLOOD GASES
The definition of respiratory failure is
based largely on blood gas
measurements (PaO2, and PaCO2).
Depending on the need, blood gas
samples can be obtained by
percutaneous puncture of a peripheral
artery, from an indwelling catheter:
arterial, central venous, or pulmonary
artery (PA) or by capillary sampling.
Arterial Puncture

An arterial blood sample may be obtained from the radial,

brachial, dorsalis pedis, or femoral arteries.
INDICATIONS
• The need to evaluate ventilation (PaCO2), acid-base balance (pH and
PaCO2), oxygenation status (PaO2 and SaO2), and oxygen-carrying
capacity of blood (PaO2, HbO2, total Hb, and dyshemoglobins)

• The need to assess the patient’s response to therapy or diagnostic

tests (e.g., oxygen or exercise testing)

• The need to monitor the severity and progression of a documented

disease process
Clinical Indications for Arterial
Blood Gas Analysis
• Sudden, unexplained dyspnea
• Cyanosis
• Abnormal breath sounds
• Severe, unexplained tachypnea
• Heavy use of accessory muscles
• Changes in ventilator settings
• Cardiopulmonary resuscitation
• New appearance of diffuse infiltrates in chest radiograph
• Sudden appearance or progression of cardiac arrhythmias
• Acute hypotension
• Acute deterioration in neurologic function
CONTRAINDICATIONS
• Abnormal results of a modified Allen test (lack of collateral circulation) may be
indicative of inadequate blood supply to the hand and suggest the need to select
another puncture site.
• Arterial puncture should not be performed through a lesion or distal to a surgical
shunt. For example, arterial puncture should not be performed on a patient undergoing
dialysis. If there is evidence of infection or peripheral vascular disease involving the
selected limb, an alternative site should be selected.
• Because of the need for monitoring the femoral puncture site for an extended period,
femoral punctures should not be performed outside the hospital.
• Coagulopathy or medium-dose to high-dose anticoagulation therapy, such as heparin
or warfarin (Coumadin), streptokinase, and tissue plasminogen activator (but not
aspirin), may be a relative contraindication.
Recommended Equipment
for Percutaneous Arterial
Blood Sampling
• Standard precautions barrier protection (gloves, safety goggles)
• Preheparinized blood gas kit syringe (1 to 3 ml)
• Short-bevel 20- to 22-gauge needle with a clear hub (23- to 25-gauge for children and
infants)
• Patient and sample label
• Isopropyl alcohol (70%), povidone-iodine (Betadine) (check patient for iodine
sensitivity), or chlorhexidine swabs
• Sterile gauze squares, tape, bandages
Recommended Equipment
for Percutaneous Arterial
Blood Sampling
• Ice slush, depending upon the analyzer. Note: For most point-of-care (bedside)
analyzers, samples should not be chilled and should be run within 1 to 2 minutes after
being obtained.
• Towels
• Sharps container
• Local anesthetic (optional)
• Hypodermic needle (25- or 26-gauge)
• Needle capping device
• Puncture-resistant container
Radial Artery
Puncture
The radial artery is preferred because it is readily
accessible, easy to stabilize, and least likely to cause loss
of distal perfusion if it become obstructed (normally the
ulnar artery provides collateral circulation to the hand).
• It is near the surface and relatively easy to palpate and
stabilize.
• Effective collateral circulation normally exists in the ulnar
artery.
• The artery is not near any large veins.
Procedure for Radial
Artery Puncture
• Check the medical record to (1) confirm the order and indications and (2) determine
the patient’s primary diagnosis, history (especially bleeding disorders or blood-borne
infections), current status, respiratory care orders (especially oxygen therapy or
mechanical ventilation), and anticoagulant or thrombolytic therapy.
• Confirm steady-state conditions (20 to 30 minutes after changes).
• Obtain and assemble necessary equipment and supplies.
• Wash hands and don barrier protection (e.g., gloves, eyewear).
• Identify the patient using current patient safety standards.
• Explain the procedure to the patient.
• Position the patient, extending the patient’s wrist to approximately 30 degrees.
 Perform a modified Allen test, and confirm collateral circulation.

The patient is instructed to make a tight fist. Then the RT compresses both the radial and ulnar
arteries, after which the patient is told to open and relax the hand, which should reveal a blanched
palm and fingers.
 Perform a modified Allen test, and confirm collateral circulation.

Next, the RT releases pressure over the ulnar artery while observing the patient’s hand
for color changes. If collateral flow is adequate, the patient’s hand will “pink up” within
10 to 15 seconds—a positive Allen test. A positive result confirms adequate collateral
flow and that the radial artery is an acceptable sampling site. If the test is negative (the
hand does not pink up rapidly), the radial artery is not an acceptable site for puncture.
In such cases, the other wrist is evaluated, or the brachial artery is used to obtain the
sample.
 Procedure for Radial
Artery Puncture
• Clean site thoroughly with 70% isopropyl alcohol or an equivalent antiseptic.
• Inject a local anesthetic subcutaneously/periarterially, wait 2 minutes for effect
(optional).
• Use a preheparinized blood gas kit syringe, or heparinize a syringe and expel the
excess (fill dead space only).
• Palpate and secure the artery with one hand.
• Insert the needle, bevel up, through the skin at a 45-degree angle until blood pulsates
into the syringe.
• Allow 1 ml of blood to fill syringe (the need to aspirate indicates a venous puncture).
• Apply firm pressure to puncture site with sterile gauze until the bleeding stops.
• Expel any air bubbles from the sample, and cap or plug the syringe.
Procedure for Radial
Artery Puncture
• Mix the sample by rolling and inverting the syringe.
• Place the sample in a transport container and chilled or not, depending on analyzer
manufacturer recommendation. Note: For most point-of-care (bedside) analyzers,
samples should not be chilled and should be run within 1 to 2 minutes after being
obtained.
• Dispose of waste materials and sharps properly.
• Document the procedure and patient status in the medical record and on the
specimen label.
• Check the site for hematoma and adequacy of distal circulation.
Dorsalis Pedis Artery Site
1. Press down on the dorsalis pedis artery to occlude it.
2. Press on the nail of the great toe so that it blanches.
3. Release the pressure on the nail, and watch for a rapid return of color.
4. This normal test finding confirms that a good blood flow exists through the posterior
tibial and lateral plantar arteries. It is safe to draw a sample from the site.
5. A slow return of blood flow indicates poor circulation; another site must be chosen.
PRECAUTIONS AND POSSIBLE
COMPLICATIONS
• Arteriospasm
• Hemorrhage
• Air or clotted blood emboli
• Trauma to the vessel
• Anaphylaxis from local anesthetic
• Arterial occlusion
• Patient or sampler contamination
• Vasovagal response
• Hematoma
• Pain
Rules For Handling The
Needle
• Never recap a used needle without a safety device.
• Never handle a used needle using both hands.
• Never point a used needle toward any part of the body.
• Never bend, break, or remove used needles from syringes by hand.
• Always dispose of used syringes, needles, and other sharp items in
appropriate puncture-resistant sharps containers.
Documentation
(1) date, time, and site of sampling;
(2) results of the modified Allen test, when performed;
(3) patient’s body temperature, position, activity level, and respiratory
rate; and
(4) FiO2 concentration or nasal cannula flow and all applicable
ventilatory support settings.
RULE OF THUMB
To ensure a steady state, waiting up to 30
minutes after any major change in ventilatory
support may be necessary before sampling and
analyzing the blood gases of a critically ill
patient.
Indwelling
Catheters
(Arterial, and Central Venous Pressure, and Pulmonary Artery
Lines)
Indwelling Catheters
 Indwelling catheters provide ready access for blood sampling and allow
continuous monitoring of vascular pressures, without the traumatic risks
associated with repetitive percutaneous punctures.
 However, infection and thrombosis are more likely with indwelling
catheters than with intermittent punctures.
 The most common route for an indwelling arterial vascular line is the
radial artery; less commonly used sites are the dorsalis pedis, brachial,
axillary, and femoral arteries.
COMMON SITES FOR INDWELLING VASCULAR CATHETERS
LOCATION SAMPLE REFLECTS
Peripheral, Arterial blood Pulmonary gas exchange (O2
Umbilical uptake/CO2
artery removal)
Central vein Venous blood Not useful for assessing gas
(unmixed) exchange; can
be used for some other laboratory
tests
Pulmonary artery Mixed venous Gas exchange at tissues (O2
blood consumption/
(balloon deflated) CO2 production)
Capillary Blood
Gases
Capillary Blood Gases
INDICATIONS
 • ABG analysis is indicated, but arterial access is unavailable
 • Noninvasive monitor readings (e.g., PtcCO2 : PETCO2, SpO2) are
abnormal
 • Assessment of initiation, administration, or change in therapy (e.g.,
mechanical ventilation) is indicated
 • A change in patient status is detected by history or physical
assessment
 • Monitoring the severity and progression of a documented disease
process is desirable
CONTRAINDICATIONS
Capillary punctures should not be performed at or through the
following:
 • The posterior curvature of the heel (because it can puncture the bone)
 • The heel of a patient who has begun walking and has callus development
 • The fingers of neonates (because it can cause nerve damage)
 • Previous puncture sites
 • Inflamed, swollen, or edematous tissues
 • Cyanotic or poorly perfused tissues
 • Localized areas of infection
 • Peripheral arteries
CONTRAINDICATIONS
Capillary punctures should not be performed:
 • On patients less than 24 hours old (because of poor peripheral perfusion)
 • When there is a need for direct analysis of oxygenation
 • When there is a need for direct analysis of arterial blood

Relative contraindications
include: :
 • Peripheral vasoconstriction
 • Polycythemia (caused by shorter clotting times)
 • Hypotension
PRECAUTIONS AND POSSIBLE
COMPLICATIONS
• Contamination and infection of the patient, including calcaneus osteomyelitis and
cellulitis
• Inappropriate patient management may result from reliance on capillary PO2 value
• Inadvertent puncture or incision and consequent infection
• Tibial artery laceration (puncture of posterior sample of
medial aspect of heel)
• Burns
• Hematoma
• Bruising
• Scarring
• Bleeding
Equipments
 Lancet,
 Preheparinized Capillary Tubes,
 Small Metal Stirrer Bar (Metal Flea),
 A Magnet,
 Clay Or Wax Sealant Or Caps,
 Gauze Or Cotton Balls, Bandages, Ice, Gloves,
 Skin Antiseptic,
 Warming Pads (42° C),
 Sharps Container,
 Labeling Materials.
Procedure for Capillary
Blood Sampling
 • Check the medical record (as per arterial puncture).
 • Confirm steady-state conditions (20 to 30 minutes after changes).
 • Obtain and assemble necessary equipment and supplies.
 • Wash hands and don barrier protection (e.g., gloves, eyewear).
 • Select site (e.g., heel, earlobe, great toe, finger).
 • Warm site to 42° C for 10 minutes using a compress, heat lamp, or commercial hot
pack.
 • Clean skin with an antiseptic solution.
 • Puncture the skin (<2.5 mm) with the lancet.
 • Wipe away the first drop of blood and observe free flow (do not squeeze).
Procedure for Capillary
Blood Sampling
 • Fill the sample tube from the middle of the blood drop until it is completely full (75 to
100 mcl).
 • Place the metal flea in the capillary tube, and then seal the tube ends.
 • Tape sterile cotton or a bandage over the puncture wound.
 • Mix the sample by moving the magnet back and forth along the capillary tube.
 • Sample should be immediately chilled or analyzed within 10 to 15 minutes if left at
room temperature.
 • Dispose of waste materials properly.
 • Document the procedure and patient status in the medical record and on the
specimen label.
Noninvasive
Measurements
Pulse Oximetry
 Pulse oximetry is a noninvasive technique for measuring oxygen
saturation of hemoglobin (Hb) in the blood, with the reported measure
being abbreviated as Spo2.
 As the “fifth vital sign,” pulse oximetry is widely used.
 The pulse oximeter combines the principle of spectrophotometry, as
used by hemoximeters, with photoplethysmography.
Photoplethysmography uses light to detect the tiny volume changes
that occur in living tissue during pulsatile blood flow.
 The probe is noninvasive and may be attached to the finger, toe, or ear
of an adult or the ankle or foot of an infant.
 The standard device probe transmits two wavelengths of light—red and infrared—
through capillary beds such as the earlobe or digit. A more or less constant level of
light is absorbed by the tissues and venous blood.
 However, a portion of the light is absorbed by the pulsatile flow of arterial blood,
yielding variable rates of absorption for oxygenated Hb (HbO2) and reduced Hb
(HHb). The oximeter circuitry then compares these differences in light absorption and
computes the Spo2 as follows:

 the Spo2 often is called the functional saturation because it is based solely on the
presence of normal Hb, that is, the amount available for binding with oxygen.
INDICATIONS
 • To monitor the adequacy of arterial oxyhemoglobin saturation
 • To quantify the response of arterial oxyhemoglobin saturation to
therapeutic intervention or to diagnostic procedures, such as
bronchoscopy
 • To comply with mandated regulations or recommendations by
authoritative groups
 The sensor has two sides. From one side, separate red and infrared light-emitting
diodes (LEDs) alternately transmit light through the tissue. The transmitted light
intensity is measured by a photodetector on the other side. The resulting output signal
is filtered and amplified by instrument electronics, with processing and display
functions controlled by a microprocessor.
 By comparing light absorbance during the pulsatile phase with the baseline value at
each wavelength, a pulse-added measure is obtained. Arterial oxyhemoglobin
saturation is computed as the ratio of the pulse-added absorbances at the two
different wavelengths. The accuracy of pulse oximetry readings is usually within ± 3%
to 5% of invasive hemoximetry readings. Generally, the lower the actual SaO2, the
less accurate and reliable is the SpO2 measurement.
RULE OF THUMB

If the pulse oximeter is reading a critically low value

(<90%) but the patient appears in no distress, then it is
likely that there is an erroneous pulse oximeter reading.
In such situations is best to further assess the patient’s
clinical status and troubleshoot the pulse oximetry
equipment setup. If further examination suggests that
the patient is stable, it is likely that the problem is the is
equipment related and the setup, including the sensor,
should be checked.
Key Points for Performing
Pulse Oximetry
 • Always follow manufacturer’s recommended protocol.
 • Never mix sensors among different devices.
 • Ensure the sensor is the correct size for the site chosen.
 • Ensure the sensor is properly applied (not too tight or loose).
 • Before taking or recording a reading, confirm the adequacy and accuracy of the
pulse signal.
 • When doing spot checks, allow sufficient response time before taking a reading
because response times vary greatly.
Key Points for Performing
Pulse Oximetry
 • For continuous monitoring of adults and children, set the low alarm at 88% to 92%.
 • Whenever possible, validate the initial SpO2 reading against the actual SaO2.
 • Clean multiuse sensors and disinfect the instrument housing between patients.
 • Inspect the sensor site frequently throughout the duration of continuous monitoring
and change it as needed.
 • Never act on SpO2 readings alone.
 • Avoid using pulse oximetry to monitor hyperoxia in neonates.
Transcutaneous
Monitoring of
Carbon Dioxide
and Oxygen
INDICATIONS
• The need to monitor continuously the adequacy of arterial oxygenation
or ventilation
• The need to quantify the real-time responses to diagnostic and
therapeutic interventions, as evidenced by PtcO2 or PtcCO2 values
When direct measurement of arterial blood is unavailable or not readily
accessible, PtcO2 or PtcCO2 measurements may suffice temporarily if
the limitations of the data are appreciated.
•For continuous and prolonged monitoring (e.g., during mechanical
ventilation, continuous positive airway pressure [CPAP], and
supplemental oxygen administration).
Transcutaneous Blood Gas
Monitoring
 Transcutaneous blood gas monitoring provides continuous,
noninvasive estimates of arterial PO2 and PCO2 through a surface skin
sensor.
 As with capillary sampling, the device arterializes the underlying blood
by heating the skin(the safe upper limit is approximately 42° C).
Warming also increases the permeability of the skin to O2 and CO2,
which enhances diffusion from the capillaries to the sensor, where they
are measured as transcutaneous partial pressures (PtcO2 and
PtcCO2).
 As a safety precaution, change the electrode on all patients at least
every 4 hours, or at least every 3 hours if the patient is hypothermic.
 Optimal Neonatal Sites
 Upper part of the chest.
 Right upper chest if a preductal PtCO2 value is desired.
 Abdomen.
 Inner aspect of either thigh.
Optimal Child or Adult Sites
 Upper part of the chest.
 Inner aspect of the upper arm.
Sites to Avoid
 Large fat deposit.
 Bony prominence.
 Pressure point.
 Thick skin.
 Skin edema.
 Hands and feet.
Should Not be Used
 Locally cold skin or general, deep hypothermia.
 Locally decreased peripheral perfusion or general hypotension.
 Patient receiving vasoconstricting drugs such as tolazoline or
dopamine.
 Cardiac index less than 1.9 L/min/m2 of body surface area.
 Halothane anesthesia will give erroneously high transcutaneous O2
values unless a Teflon membrane is used
Preparation and Application
 An airtight seal between the skin and the electrode is necessary for accurate
readings. An air leak (21% oxygen) will falsely increase or decrease the PtCO2
reading from the patient’s actual value. A room air leak will always cause a decrease
in the PtcCO2 reading.

1. Clean the skin. Usually, cleaning with an alcohol

swab is enough to remove perspiration. Oily skin
should be cleaned with soap and water.
2. Adults may need to have hair shaved from the site.
3. Adults may have dead skin cells removed by placing
sticky adhesive tape against the site and pulling it off.
4. Apply the adhesive ring to the skin. Make sure there
are no wrinkles that could result in a leak.
Preparation and Application
5. Prepare the electrode according to the manufacturer’s
guidelines. This usually includes placing a drop
of the electrolyte solution on the electrode surface
and placing a gas-permeable membrane with a double
adhesive ring over the electrode.
6. Screw the electrode into the adhesive ring to form
an airtight seal
7. As the electrode warms the skin, the patient values
will fluctuate. Stabilization usually requires several
minutes, after which the patient values should be
clinically useful.
Normal acid-base
balance
– Kidneys maintain HCO3 – of 22 to 26 mEq/L
– Lungs maintain CO2 of 35 to 45 mm Hg
– These produce pH of 7.35 to 7.45 (H-H equation)
pH = 6.1 + log (24/(40 × 0.03) → pH = 7.40
– Note pH determined by ratio of HCO3 to
dissolved CO2
• Ratio of 20:1 will provide normal pH (7.40)
• Increased ratio results in alkalemia
• Decreased ratio results in acidemia
Primary respiratory
disturbances
– PaCO2 is controlled by the lung, changes in pH caused by PaCO2 are considered
respiratory disturbances

• Hyperventilation lowers PaCO2, which raises pH; referred to as respiratory alkalosis

• Hypoventilation (↑PaCO2) decreases the pH; called respiratory acidosis

Primary metabolic
disturbances
– Involve gain or loss of fixed acids or HCO3
– Both appear as changes in HCO3 – as changes in fixed acids will alter amount of
HCO3 used in buffering

– Decrease in HCO3 – results in metabolic acidosis

– Increase in HCO3 – results in metabolic alkalosis

Compensation: Restoring pH
to normal
– Any primary disturbance immediately triggers compensatory response
• Any respiratory disorder will be compensated for by kidneys (process takes hours to
days)
• Any metabolic disorder will be compensated for by lungs (rapid process, occurs within
minutes)
Compensation: Restoring pH
to normal
– Respiratory acidosis (hypoventilation)
• Renal retention HCO3/elimination of H+ – raises pH toward normal
– Respiratory alkalosis
• Renal elimination HCO3/retention of H+ – lowers pH toward
normal
– Metabolic acidosis
• Hyperventilation ↓CO2, raising pH toward normal
– Metabolic alkalosis
• Hypoventilation ↑CO2, lowering pH toward normal
 The CO2 hydration reaction’s
effect on [HCO3 ]

– Large portion of CO2 is transported as HCO3

– As CO2 increases, it also increases HCO3
– In general, effect is increase of approximately 1 mEq/L
HCO3 for every 10 mm Hg increase in PaCO2 above 40
mmHg
• An increase in CO2 of 30 would increase HCO3 by
approximately 3 mEq/L
pH-PCO2 diagram
Because of the hydration
reaction between CO2 and H2O,
acute increases in PCO2
increase the plasma HCO3 −
concentration along line CADB.
An acute increase in PCO2 from
40 mm Hg to 80 mm Hg (point A
to point D) increases [HCO3 −]
from 24 mEq/L to approximately
29 mEq/L.
 Primary Acid-Base Disorders and
Compensatory Responses

→, No change; ↓, decrease; ↑, increase.

Clinical Acid-Base
States
Respiratory acidosis
(alveolar hypoventilation)
– Any process that raises PaCO > 45 mm Hg and
lowers pH below 7.35
• Increased PaCO2 produces more carbonic acid

– Causes
• Anything that results in Alveolar Ventilation (VA) that fails
to eliminate CO2 equal to carbon dioxide produced (VCO2)
Common Causes of
Respiratory Acidosis
Respiratory acidosis
– Compensation is by renal reabsorption of HCO3
• Partial compensation: pH improved but not normal
• Full compensation: pH restored to normal
– Correction (goal is to improve VA)
• May include: – Improved bronchial hygiene and lung
expansion – Noninvasive positive pressure ventilation,
endotracheal intubation and mechanical ventilation
• If chronic condition with renal compensation, lowering
PaCO2 may be detrimental for patient
Acute Ventilatory Failure
(Acute Respiratory Acidosis)
Defined as a pH below 7.35 and a PaCO2 level above 45 mm Hg and an HCO3 level
up slightly but still in normal range
Acute ventilatory failure can develop in response to any ventilatory pattern that does
not provide adequate alveolar ventilation. When an increased PaCO2 is accompanied
by acidemia (decreased pH), then acute ventilatory failure, or respiratory acidosis, is
said to exist.
Clinically, this is a medical emergency that may require mechanical ventilation.
Acute ventilatory failure is a condition in which the lungs are unable to meet the metabolic
demands of the body in terms of CO2 homeostasis—and, typically, tissue oxygenation. In
other words, the patient is unable to provide the muscular, mechanical work necessary to
move gas into and out of the lungs to meet the normal CO2 production of the body. This
condition leads to an increased PACO2 and, subsequently, an increased PaCO2. The
increased PACO2 causes a decrease in the PAO2, which, in turn, leads to a decreased
PaO2 in the arterial blood.
Chronic Ventilatory Failure
(Compensated Respiratory Acidosis)
 defined as a greater-than normal PaCO2 level with a normal pH status—and,
typically, a decreased PaO2 on room air.
 as a respiratory disorder gradually worsens, the work of breathing progressively
increases to a point at which more oxygen is consumed than is gained. The patient
slowly develops a breathing pattern that uses the least amount of oxygen for the
energy expended. In essence, the patient selects a breathing pattern based on work
efficiency rather than ventilatory efficiency.
 As a result, the patient’s alveolar ventilation slowly decreases, which in turn causes the
PaO2 to decrease and the PaCO2 to increase further. As the PaCO2 increases, the pH
falls. When an individual hypoventilates for a long period of time, the kidneys work to
correct the decreased pH by retaining HCO3 .
 Renal compensation in the presence of chronic hypoventilation can be shown when the
calculated HCO3 − and pH readings are higher than expected for a particular PCO2 level.
When the HCO3 − level increases enough to return the acidic pH to normal, complete
renal compensation is said to have occurred (chronic ventilatory failure).
 The lungs play an important role in maintaining the PaCO2, HCO3 − , and pH levels on a
moment-to-moment basis. The kidneys play an important role in maintaining the HCO3 −
and pH levels during long periods of hyperventilation or hypoventilation.
Respiratory Diseases Associated with Chronic
Ventilatory Failure during the Advanced Stages
Chronic Obstructive Pulmonary Disorders
(Most Common)
• Chronic bronchitis
• Emphysema
• Bronchiectasis
• Cystic fibrosis
Restrictive Respiratory Disorders
• Tuberculosis
• Fungal diseases
• Kyphoscoliosis
• Chronic interstitial lung diseases
• Bronchopulmonary dysplasia
Respiratory alkalosis
(alveolar hyperventilation)
– Lowers arterial PaCO2 decreases carbonic acid, thus
increasing pH
– Causes
• Any process that increases VA so that CO2 is eliminated at rate
higher than VCO2.
• Most common cause is hypoxemia
• Anxiety, fever, and pain
– Clinical signs: early paresthesia; if severe, may have
hyperactive reflexes, tetanic convulsions, and dizziness
Causes
 Any process in which ventilatory
elimination of CO2 exceeds the body’s
production of CO2 causes respiratory
alkalosis.
Respiratory alkalosis
– Compensation is by renal excretion of HCO3
• Partial compensation returns pH toward normal
• Full compensation returns pH to high normal range
– Correction
• Involves removing stimulus for hyperventilation
– That is, hypoxemia: give oxygen (O2) therapy
Acute Alveolar Hyperventilation
(Acute Respiratory Alkalosis)
Defined as a pH above 7.45 and a PaCO2 level below 35 mm Hg and an HCO3 level
down slightly but still within normal range
The most common cause of acute alveolar hyperventilation is hypoxemia.
The decreased PaO2 seen during acute alveolar hyperventilation usually develops from
a decreased V/Q ratio, capillary shunting (or a relative shunt or shuntlike effect), and
venous admixture associated with the pulmonary disorder.
The PaO2 continues to drop as the pathologic effects of the disease intensify.
Eventually the PaO2 may decline to a point low enough (a PaO2 of about 60 mm Hg) to
significantly stimulate the peripheral chemoreceptors, which in turn causes the
ventilatory rate to increase.
The increased ventilatory response in turn causes the PaCO2 to decrease and the pH
to increase.
Pathophysiologic Mechanisms That Lead
to a Reduction in the Paco2
• Decreased lung compliance
• Stimulation of the central chemoreceptors
• Activation of the deflation reflex
• Activation of the irritant reflex
• Stimulation of the J receptors
• Pain and anxiety
Expected Effect of Acute Changes in PaCO2 on
Arterial pH
Acute Ventilatory
Changes
Superimposed on
Chronic Ventilatory
Failure
Acute Alveolar
Hyperventilation
Superimposed On Chronic
Ventilatory Failure
 the patient with chronic ventilatory failure can also experience acute periods of
hyperventilation. For example, the patient with chronic ventilatory failure can acquire
an acute shunt-producing disease (e.g., pneumonia)—and hypoxemia. Some of these
patients have the mechanical reserve to increase their alveolar ventilation significantly
in an attempt to maintain their baseline PaO2.
 However, in regard to the patient’s baseline PaCO2 level, the increased alveolar
ventilation is often excessive. When excessive alveolar ventilation occurs, the
patient’s PaCO2 rapidly decreases. This action causes the patient’s PaCO2 to
decrease from its normally “high baseline” level. As the PaCO2 decreases, the arterial
pH increases.
 As this condition intensifies, the patient’s baseline ABG values can quickly change from
chronic ventilatory failure to acute alveolar hyperventilation superimposed on chronic
ventilatory failure.
 If the clinician does not know the past history of the patient with acute alveolar
hyperventilation superimposed on chronic ventilatory failure, he or she might initially
interpret the ABG values as signifying partially compensated metabolic alkalosis with
severe hypoxemia.
 However, the clinical situation that offsets this interpretation is the presence of marked
hypoxemia. A low oxygen level is not normally seen in patients with pure metabolic
alkalosis. Thus, whenever the ABG values appear to reflect partially compensated
metabolic alkalosis but the condition is accompanied by significant hypoxemia, the
respiratory therapist should be alert to the possibility of acute alveolar hyperventilation
superimposed on chronic ventilatory failure.
Acute Ventilatory Failure
Superimposed
on Chronic Ventilatory Failure
(Acute Hypoventilation on
Compensated Respiratory Acidosis)
 Often patients with chronic ventilatory failure do not have the mechanical reserve to meet
the hypoxemic challenge of a respiratory disorder. When these patients attempt to
maintain their baseline PaO2, by increasing their alveolar ventilation, they often consume
more oxygen than is gained and/or become fatigued, or experience a combination of both.
 When this happens, the patient begins to breathe less. This action causes the PaCO2 to
increase and eventually to rise above the patient’s normally high PaCO2 baseline level.
This action causes the patient’s arterial pH level to fall or become acidic. In short, the
patient’s baseline ABG values shift from chronic ventilatory failure to acute ventilatory
failure superimposed on chronic ventilatory failure.
Overview Examples of Acute Changes in
Chronic Ventilatory Failure
Metabolic acidosis
– Low HCO3 –, with a low pH
defined as a bicarbonate level of less than 22 mEq/L with
a pH of less than 7.35.
– Causes:
• Increased fixed acid accumulation
– Lactic acidosis in anaerobic metabolism
• Excessive loss of HCO3
– Diarrhea
• Anion gap can help identify cause
Metabolic acidosis
– Low HCO3 –, with a low pH
defined as a bicarbonate level of less than 22 mEq/L with
a pH of less than 7.35.
– Causes:
• Increased fixed acid accumulation
– Lactic acidosis in anaerobic metabolism
• Excessive loss of HCO3
– Diarrhea
• Anion gap can help identify cause
Causes
(1) fixed (nonvolatile) acid build-up in the blood
 Renal failure
 Diabetic ketoacidosis
 Anaerobic metabolism
 Starvation
 Salicylate intoxication
(2) an excessive loss of HCO3 − from the body
severe diarrhea
intestinal fistulas
Anion Gap
 The law of electroneutrality states that the total number of positive charges must
equal the total number of negative charges in the body’s fluids.

 140 mEq/L for Na+, 105 mEq/L for Cl−, and 24 mEq/L for HCO3 −, yielding an “anion
gap” of 11 mEq/L (140 mEq/L − [105 mEq/L + 24 mEq/L] = 11 mEq/L).
 The normal anion gap range is 9 to 14 mEq/L.
 An increased anion gap (>14 mEq/L) is caused by a metabolic acidosis in which
abnormal fixed acids accumulate in the body.
 Metabolic acidosis caused by HCO3 − loss from the body does not cause a further
increase in the anion gap.
• Increased anion gap metabolic acidosis
– Normal anion gap = 9 to 14 mEq/L
– As fixed acids increase, they dissociate and H
+ binds with HCO3 –, leaving unmeasured anion
behind
• Increasing anion gap
• Normal anion gap metabolic acidosis
– HCO3 loss does not cause increased gap
• As HCO3 – is lost, it is offset by gain in Cl–
• Also called hyperchloremic acidosis
Compensation for metabolic
acidosis
– Hyperventilation is main compensatory mechanism
• Acidosis activates CNS receptors, signaling need to increase
VE
– Compensation happens very quickly
• Lack of compensation implies ventilatory defect
– Symptoms
• Patients often complain of dyspnea due to hyperpnea
• Kussmaul’s respiration seen with ketoacidosis
• Neurologic response may range from lethargy to coma
Medical intervention to
correct metabolic acidosis
– If pH is greater than 7.2, no correction is
required
• Hyperventilation usually brings it above this level
– pH below 7.2 can cause serious cardiac
arrhythmias
• In severe acidosis, treat with IV NaHCO3
Metabolic Alkalosis
 Metabolic alkalosis is defined as a bicarbonate level greater
than 26 mEq/liter with a pH greater than 7.45.
 Either an excess of base or a loss of acid within the body can
cause metabolic alkalosis.
Metabolic alkalosis
– Increased [HCO3 –], with elevated pH
– Causes:
• Due to increased buffer base or loss of fixed acids
• Loss of fixed acids occurs during vomiting (HCl)
• Often, it is iatrogenic due to diuretic use or gastric
drainage
Causes
 (1) loss of fixed acids or

(
Causes
 2) gain of blood buffer base
Metabolic alkalosis
– Compensation
• Hypoventilation, despite ensuing hypoxemia
• Metabolic alkalosis blunts hypoxemic stimulation of ventilation
– PaO2 as low as 50 mm Hg with continued compensation

– Correction
• Restore normal fluid volume, K+, and Cl– levels
• In severe alkalosis, may give dilute HCl in central line
Mixed Acid-Base States
Combinations of acid-base disorders may occur in the
same patient
– Primary respiratory and primary metabolic disorders
occurring simultaneously
• That is, pH 7.62, PaCO2 32, and HCO3 29
• High pH caused by low PaCO2 and high HCO3:
combined alkalosis
• Compensation is not possible
Even small changes in hydrogen ion
concentration [H+] can cause vital metabolic
processes in the body to fail.
Normal metabolism continually generates H+,
which means
H+ regulation is extremely important.
Several physiologic mechanisms work
together to keep [H+] of body fluids in a range
that supports life.
H+ means hydrogen ions
ABG
INTERPRETATION
Components of
the Arterial Blood
Gas
pH

 Measurement of acidity or alkalinity, based on the hydrogen (H+) ions

present.
 The normal range is 7.35 to 7.45
 Remember:
 pH > 7.45 = alkalosis
 pH< 7.35 = acidosis
PaCO2

 The amount of carbon dioxide dissolved in arterial blood.

 The normal range is 35 to 45 mm Hg.
 Remember:
 pCO2 >45 = acidosis
 pCO2 <35 = alkalosis
HCO3
 The calculated value of the amount of bicarbonate in the
bloodstream.
 The normal range is 22 to 26 mEq/liter
 Remember:
 HCO3 > 26 = alkalosis
 HCO3 < 22 = acidosis
B.E.
 The base excess indicates the amount of excess or
insufficient level of bicarbonate in the system.
 determined by equilibrating a blood sample in the laboratory
to a PCO2 of 40 mm Hg (at 37° C) and recording the amount
of acid or base needed to titrate 1 L of blood to a pH of 7.40.
A normal BE is ±2 mEq/L. A “positive BE” (>+ 2 mEq/L)
indicates a gain of base or loss of acid from nonrespiratory
causes. A “negative BE” (<−2 mEq/L) indicates a loss of base
or a gain of acid from Non respiratory causes.
 The normal range is -2 to +2 mEq/liter.
PaO2
 The partial pressure of oxygen that is dissolved in arterial
blood.
 The normal range is 80 to 100 mm Hg.
SaO2
 The arterial oxygen saturation.
 The normal range is 95% to 100%.
Step One
 Identify whether the pH, pCO2 and HCO3 are abnormal. For each component, label it
as “normal”, “acid” or “alkaline”.
Step two
Step 3 – Find the
compensation
 Fully Compensated (Chronic) = if the pH is within
normal range
 Partially Compensated = if both PaCO2 or HCO3 is
abnormal
 Uncompensated or Acute = if either PaCO2 or HCO3
is within normal range
Step 4 – Assess oxygenation
 If patient breathing room air ( 21% FiO2)
PaO2 80 – 100 = Normal Oxygenation
PaO2 79-60 = mild hypoxemia
PaO2 59-40 = Moderate hypoxemia
PaO2 <40 = Severe Hypoxemia
 If patient has oxygen support or breathing greater than room
air (>21%)
PaO2 >100 = Overcorrected Oxygenation
PaO2 80 – 100 = Normal Oxygenation
PaO2 <80 = Uncorrected Hypoxemia
The patient is on a nonrebreathing mask at 15
L/min and his ABG results are below.
pH 7.23 =
PaCO2 21 torr =
PaO2 174 torr =
HCO3 12 mEq/L =
BE -13
SaO2 68%
The following data has been obtained from a 36-year-old
patient in ICU with pneumonia on a 50% venturi mask.
Arterial blood gases:
pH 7.46 =
PaCO2 33 torr =
PaO2 54 torr =
HCO3 24 mEq/L =
The following blood gases have been
obtained from a ventilator patient with
100% FiO2 in ICU.
pH 7.26 =
PaCO2 51 torr =
PaO2 70 torr =
HCO3 15 mEq/L =
A patient on room air has the following arterial
blood gas values:
pH 7.44 =
PaCO2 32 torr =
PaO2 96 torr =
HCO3 19 mEq/L =
BE +5
The patient is on room air with his ABG results are
below.
pH 7.50 =
PaCO2 51 torr =
PaO2 74 torr =
HCO3 35 mEq/L =
BE -13
SaO2 78%
ASSURING VALID
MEASUREMENT
AND USE OF
BLOOD GAS DATA
ASSURING VALID
MEASUREMENT
 In general, the types of ABG errors can be classified as
 (1) Preanalytic Errors,
 (2) Analytic Errors,
 (3) Postanalytic Errors,
 (4) Interpretation Errors.
Preanalytic Errors
include errors that occur either before or after the sample analysis—
for example, improper sample or data handling.
Error Effects How to Recognize How to Avoid
Air in sample Lowers Pco2 Visible bubbles or froth Discard frothy samples
Raises pH Low Pco2 inconsistent Fully expel bubbles
Raises low Po2 with patient Mix only after air
Lowers high Po2 status expelled
Cap syringe quickly
Venous blood or Raises Pco2 Failure of syringe to fill Avoid femoral site
venous Lowers pH by pulsations Do not aspirate
admixture Can greatly lower Po2 Patient has no sample
symptoms of Use short-bevel
hypoxemia needles
Avoid artery
“overshoot”
Cross-check with
Spo2
1. Preanalytic Errors
Error Effects How to Recognize How to Avoid
Excess liquid heparin Lowers Pco2 Visible liquid heparin Visible liquid heparin
Raises pH remains in syringe remains in syringe
Raises low Po2 before sampling before sampling
Lowers high Po2
Metabolic effects Raises Pco2 Excessive time lag Analyze within 30
Lowers pH since sample minutes
Lowers Po2 collection If analysis cannot
Values inconsistent occur with
with patient status 30 minutes, place
sample in
ice slush
2. Analytic Errors
 Include errors that occur during the actual analysis of the ABG sample
—for example, blood gas machine malfunctions and poor individual
technique.
 Blood gas quality control measures help avoid errors during sample
analysis. To minimize analytic errors requires regular calibration of the
measurement device.
 Calibration involves exposing the analyzer to calibration media at two
or more known levels of measurement
Quality control
 Defined as a system that includes analysis of control samples (with a
known pH, PCO₂ and PO₂), assessment of the measurement against
defined limits, identification of problems and specification of corrective
action.
 Internal Quality Control are designed to ensure that the instruments (i.e.,
electrodes) within a laboratory perform with precision.
 External quality control, known as proficiency testing, is a system by
which laboratories can compare the accuracy of their results with the results
obtained from other labs.
Internal Statistical Quality
Control
 Internal quality control takes calibration verification a step further by
applying statistical and rule-based procedures (Westgard rules) to help
detect, respond to, and correct instrument error.
 In one common approach, the results of control media analyses are
plotted on a graph and compared with statistically derived limits, usually
± 2 standard deviation (SD) ranges. Control results that fall outside
these limits indicate analytic error.
Levey-Jennings quality
control chart for PaCO2

Open
 Point A circles, calibration
represents a values that are within
random 2 SDs of the
error; mean value. They are
considered to be in
 Point B control. Black
represents circles, calibration
systematic values that are out of
errors. control.
Internal Statistical Quality
Control
 Applies statistical and rule-based procedures to help identify and
correct instrument error. The results of control media analyses are
plotted on a graph and compared with statistically derived limits,
typically 2 standard deviation (SD) ranges. Analytical error is indicated
when the control results fall outside these limits.
 There are two categories of analytic error:
(1) random error and
(2) systematic error.
Random error
 Random error is observed when sporadic, out-of-range data points occur.
 Random errors are errors of precision or, more precisely, imprecision.
 Conversely, either a trending or an abrupt shift in data points outside the statistical
limits is sometimes observed. This phenomenon is called systematic error or
sometimes bias.
 Bias plus imprecision equals total instrument error, or INACCURACY.
 A single random error is insignificant and should be disregarded. However, if the
frequency of random error increases, the machine and techniques should be
evaluated. Frequent random errors are known as dispersion. They may be caused by
statistical probability, sample contamination, or sample mishandling. The samples
should be rerun or analysis repeated on a different machine.
Systematic error
 : also referred to as bias or trending and indicated by a recurrent shift in data points
outside the statistical limits. This maybe caused by aging mercury batteries, an aging
electrode, contaminated buffers, incorrect gas concentrations, or protein
contamination of the electrode.
External Quality Control
(Proficiency Testing)
 is a system by which laboratories can compare the accuracy of their
results with the results obtained from other laboratories. Based on the
data obtained, individual discrepancies can be identified and evaluated.
 Proficiency testing requires analysis and reporting on externally
provided control media with unknown values, usually three times per
year, with five samples per test.
 Acceptable performance is indicated by a specified range around a
target value, for example ±0.04 for pH.
QUALITY ASSURANCE
 Quality assurance is a systematic process used to monitor,
document, and regulate the accuracy and reliability of a
procedure or laboratory measurement.
 Refers to the broader concern that the results of the blood
gas measurement are not only accurate and reliable but also
clinically useful.
 This involves recordkeeping, performance validation,
preventive maintenance and calibration.
CALIBRATION
 is the systematic standardization of the graduations of the
blood gas analyzer against known values to ensure
consistency. Proper calibration of the electrodes is essential
to the accuracy of the blood gas values. Some general
calibration steps are discussed later. The manufacturer’s
guidelines must be followed for the specific steps in
calibration.
pH electrode – Sanz Electrode
One-point calibration
1. Should be done before every sample is analyzed if one-point
calibration is not automatically performed every 30 minutes
2. Performed with the near-normal QC material of 7.384 ± 0.005 pH used
to set the balance potentiometer
3. Recommended every 30 minutes
4. Should be rechecked after a suspicious pH result; the blood sample
should then be rerun
pH electrode – Sanz Electrode
Two-point calibration
1. Should be done at least once every 8 hours when patient samples are
being analyzed
2. Recommended for every 25 patient samples
3. Performed with the slope potentiometer set with a QC material of
6.840 ± 0.005 pH (this is the same pH as the reference electrode
solution)
4. Performed with the balance potentiometer set with a QC material of
7.384 ± 0.005 pH
pH electrode – Sanz Electrode
Three-point calibration
1. Should be done at least every 6 months on existing equipment
2. Should be done whenever a new electrode is put into use
3. Covers the physiologic range to confirm linearity; QC materials of
6.840 ± 0.005, 7.384 ± 0.005, and 7.874 ± 0.005 pH are used
PCO2 electrode - Severinghaus
One-point calibration .
1. Should be done before every sample is analyzed if one-
point calibration is not automatically performed every 30
minutes
2. Performed with 5% ± 0.03% CO2 used to set the balance
potentiometer
3. Recommended every 30 minutes 4. Should be rechecked
after a suspicious PCO2 result; the blood sample should then
be rerun
PCO2 electrode - Severinghaus
Two-point calibration
1. Should be done at least once every 8 hours when patient
samples are being analyzed
2. Recommended for every 25 patient samples
3. Performed with 10% ± 0.03% CO2 to set the slope
potentiometer
4. Performed with 5% ± 0.03% CO2 to set the balance
potentiometer
PCO2 electrode - Severinghaus
Three-point calibration
1. Should be done at least every 6 months on existing equipment
2. Should be done whenever a new electrode is put into use
3. Covers the physiologic range to confirm linearity; three PCO2 values between 0 and
80 mm Hg should be determined
4. Room air or a gas cylinder containing up to 0.03% CO2 can be used to set the zero
point
PO2 electrode – Clark electrode

One-point calibration
1. Should be done before every sample is analyzed if one-point calibration is not
automatically performed every 30 minutes
2. Performed with 12% ± 0.03% O2 used to set the balance potentiometer; some
analyzers are designed to use 20% ± 0.03% O2 from a gas cylinder or draw room air
(20.95% oxygen) into the unit
3. Recommended every 30 minutes
4. Should be rechecked after a suspicious PO2 result; the blood sample should then
be rerun
PO2 electrode – Clark electrode

Two-point calibration
1. Should be done at least once every 8 hours when patient samples are
being analyzed
2. Should be done whenever readjustment of one point calibration is
greater than 3 torr
3. Recommended for every 25 patient samples
4. Performed with 0% ± 0.03% O2 to set the slope potentiometer
5. Performed with 12% ± 0.03% O2 to set the balance potentiometer;
some analyzers are designed to use 20% ± 0.03% O2 from a gas
cylinder or draw room air (20.95% oxygen) into the unit
PO2 electrode – Clark electrode

Three-point calibration
1. Should be done at least every 6 months on existing equipment
2. Should be done whenever a new electrode is put into use
3. Should be done to confirm linearity whenever the PO2 value could be
more than 150 torr, assuming that the balance point is set on room
oxygen content; the third point should be set on 100% ± 0.03% O2 from
a gas cylinder
Blood gas analyzers
 should undergo one- and twopoint calibrations on a routine basis. The process should
include high and low values for pH, PCO2, and PO2 electrodes.
 A one-point calibration should be performed before a blood gas sample is run unless
the analyzer automatically performs the calibration at programmed intervals. 3.
 A two-point calibration is usually performed every 8 hours.
 The criteria for acceptable results are below:
 a. pH must be within ±0.04 of the target value.
 b. PCO2 must be within ± 3 mm Hg of the target value.
 c. PO2 must be within ± 3 mm Hg of standard deviations.