Arterial Blood Gas
Arterial Blood Gas
Arterial Blood Gas
– Normal is 16 to 20 ml/dl
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.
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:
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.
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.
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
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.
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-
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:
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
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
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
– 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
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.