Acid Base Physiology
and
Arterial Blood Gas
Interpretation
By:
Dr.behzad barekatain,MD
Assistant professor of pediatrics
neonatalogist
Selected Acid-Base Web Sites
http://www.acid-base.com/
http://www.qldanaesthesia.com/AcidBaseBook/
http://www.virtual-anaesthesia-textbook.com
/vat/acidbase.html#acidbase
http://ajrccm.atsjournals.org/cgi/content/full/162/6/2246
http://www.osa.suite.dk/OsaTextbook.htm
http://www.postgradmed.com/issues/2000/03_00/fall.htm
http://medicine.ucsf.edu/housestaff/handbook/HospH2002_C5.htm
Indications for ABG
•
•
•
•
•
•
•
•
•
•
(1) Severe respiratory or metabolic disorders
(2) Clinical features of hypoxia or hypercarbia
(3) Shock
(4) Sepsis
(5) Decreased cardiac output
(6) Renal failure
(7) Ideally any baby on oxygen therapy
(8) Inborn errors of metabolism
(9) ventilated infant
………………….
INTRODUCTION
An arterial blood gas (ABG) is a test that measures the oxygen tension
(PaO2), carbon dioxide tension (PaCO2), acidity (pH), oxyhemoglobin
saturation (SaO2), and bicarbonate (HCO3) concentration in arterial
blood.
Some blood gas analyzers also measure the methemoglobin,
carboxyhemoglobin, and hemoglobin levels.
Such information is vital when caring for patients with critical illness
or respiratory disease.
As a result, the ABG is one of the most common tests performed on
patients in intensive care units (ICUs).
The sites, techniques, and complications of arterial sampling
are reviewed here, as well as the transport and analysis of the
arterial blood.
Normal ABG values are provided and a common clinical
situation in which the ABG results may be misleading is also
described.
Interpretation of abnormal ABG values and venous blood
gases are also discussed
ARTERIAL SAMPLING
Arterial blood is required for an ABG.
It can be obtained by percutaneous needle puncture or from an
indwelling arterial catheter.
• A) Needle puncture — Percutaneous needle puncture refers to
the withdrawal of arterial blood via a needle stick. It needs to be
repeated every time an ABG is performed, since an indwelling
catheter is not inserted.
Site selection
The initial step in percutaneous needle puncture is locating a palpable
artery.
Common sites include the radial, femoral, brachial, dorsalis pedis, or
axillary artery.
There is no evidence that any site is superior to the others. However,
the radial artery is used most often because it is accessible, easily
positioned, and more comfortable for the patient than the alternative
sites.
1.The radial artery is best palpated between the distal radius and the
tendon of the flexor carpi radialis when the wrist is extended.
To get the wrist into this position, the arm should be positioned on an
arm-board with the palm facing upward and a large roll of gauze should
be placed between the wrist and the arm-board in a position that
extends the wrist. Taping the forearm and palm to the arm-board helps
maintain the position.
2.The brachial artery is best palpated medial to the biceps tendon
in the antecubital fossa, when the arm is extended and the palm is
facing up. The needle should be inserted just above the elbow
crease.
3.The femoral artery is best palpated just below the midpoint of the
inguinal ligament, when the lower extremity is extended.
The needle should be inserted at a 90 degree angle just below the
inguinal ligament.
4.The dorsalis pedis artery is best palpated lateral to the extensor
hallucis longus tendon.
It receives collateral flow from the lateral plantar artery through an
arch similar to that in the hand.
5.The axillary artery is best palpated in the axilla, when the arm is
abducted and externally rotated.
There is good collateral flow to the arm through the thyrocervical
trunk and subscapular artery; thus, the risk of ischemic complications
to the arm is low.
The needle should be inserted as high into the axilla as possible
Collateral circulation
We believe that patients undergoing radial or dorsalis pedis artery
puncture should have the collateral flow to those vessels evaluated
prior to puncture, even though studies have found variable accuracy
associated with such evaluations.
Our belief is based upon the notion that the evaluation can be
performed quickly at the bedside at no cost and with little risk for
harm, but has substantial potential for benefit (ie, to identify patients
who have impaired collateral circulation and, therefore, may be at
increased risk of an ischemic complication).
The Allen test or modified Allen test can be performed in patients
undergoing radial artery puncture. These are bedside tests that
demonstrate collateral flow through the superficial palmar arch.
To perform the modified Allen test, the patient's hand is initially held
high with the fist clenched and both the radial and ulnar arteries
compressed.This allows the blood to drain from the hand. The hand is
then lowered, the fist is opened, and pressure is released from the
ulnar artery. Color should return to the hand within six seconds,
indicating that the ulnar artery is patent and the superficial palmar
arch is intact. The test is considered abnormal if ten seconds or more
elapses before color returns to the hand.
• The Allen test (from which the modified Allen test evolved) is
performed identically, except these steps are executed twice:
once with release of pressure from the ulnar artery and once with
release of pressure from the radial artery.
For patients undergoing dorsalis pedis artery puncture, the
dorsalis pedis artery can be occluded, followed by compression
of the nailbed of the great toe and assessment of the rapidity with
which color returns to the nailbed after pressure is released from
the great toe
Technique
Once a palpable artery has been located, blood is withdrawn using the
following steps.
1.The planned puncture site should be sterilely prepped.
2.Local analgesia prior to arterial puncture should be considered,
since it appears to prevent pain without adversely impacting the
success of the procedure.
This was illustrated by a trial that randomly assigned 101 patients
undergoing arterial puncture to receive 2 percent lidocaine, normal
saline, or no agent prior to the procedure.The lidocaine decreased pain
without increasing the difficulty of the procedure (ie, the number of
attempts), compared to the other groups.
3.The seal of a heparinized syringe should be broken by pulling its
plunger. The plunger can then be pushed back into the syringe,
leaving a small empty volume (eg, less than 1 mL) in the syringe. A
small needle (eg, 22 to 25 gauge) should then be attached to the
syringe. Arterial blood gas kits are available, which contain a
heparinized plastic syringe with the plunger already pulled back to
allow for the collection of 2 mL of blood without the need to break
the seal.
4.Using one hand to gently palpate the artery and the other to
manipulate the syringe and needle, the artery should be punctured
with the needle at a 30 to 45 degree angle relative to the skin. The
syringe will fill on its own (ie, pulling the plunger is unnecessary).
Approximately 2 to 3 mL of blood should be removed.
5.To prevent coagulation, the syringe should be rolled between
the hands for a few seconds to allow blood to mix with the
heparin.
6.After withdrawing a sufficient volume of blood, the needle
should be removed and pressure applied to the puncture site for
five to ten minutes to achieve hemostasis.
Complications
Complications due to percutaneous needle puncture are rare.
They include:
*persistent bleeding
*Bruising
*injury to the blood vessel
*Circulation distal to the puncture site may also be impaired
following percutaneous needle puncture, presumably due to
thrombosis at the puncture site.
. B) Indwelling catheters
Arterial blood can also be obtained via an indwelling arterial catheter.
Indwelling catheters provide continuous access to arterial blood,
which is helpful when frequent blood gases are needed (eg, respiratory
failure).
Venous blood gases and other
alternatives to arterial blood gases
An arterial blood gas (ABG) is the traditional method of estimating the
systemic carbon dioxide tension and pH, usually for the purpose of
assessing ventilation and/or acid-base status.
However, the necessary sample of arterial blood can be difficult to
obtain due to diminished pulses or patient movement. Diminished
pulses may reflect poor peripheral circulation or low blood pressure,
while patient movement is frequently caused by the pain associated
with arterial puncture.
A venous blood gas (VBG) is an alternative method of estimating
systemic carbon dioxide and pH that does not require arterial blood
sampling. Performing a VBG rather than an ABG is particularly
convenient in the intensive care unit, since most patients have a
central venous catheter from which venous blood can be quickly and
easily obtained.
Sampling sites
A VBG can be performed using a peripheral venous sample (obtained
by venipuncture), a central venous sample (obtained from a central
venous catheter), or a mixed venous sample (obtained from the distal
port of a pulmonary artery catheter).
Central venous blood gases are preferred because their correlation
with arterial blood gases is the most well-established by research and
clinical experience.
Peripheral venous blood gases are an alternative for patients who do
not have central venous access.If a tourniquet is used to facilitate
venipuncture, it should be released about one minute before the
sample is drawn to avoid changes induced by local ischemia.
Mixed venous blood gases are a reasonable alternative for
patients whose venous access is a pulmonary artery catheter;
however, a pulmonary artery catheter should not be inserted
for the sole purpose of venous blood sampling
Measurements
A VBG measures the venous oxygen tension (PvO2), carbon dioxide
tension (PvCO2), acidity (pH), oxyhemoglobin saturation (SvO2), and
serum bicarbonate (HCO3) concentration:
• PvCO2, venous pH, and venous serum HCO3 concentration are
used to assess ventilation and/or acid-base status
• SvO2 is used to guide resuscitation during severe sepsis or septic
shock, a process called early goal-directed therapy
• PvO2 has no practical value at this time. It is not useful in
assessing oxygenation because oxygen has already been extracted
by the tissues by the time the blood reaches the venous circulation.
The inability of a VBG to measure oxygenation is the major
drawback compared with an ABG. To overcome this limitation,
VBGs are often considered in combination with pulse oximetry.
Correlation with arterial blood gases
Central venous
*The central venous pH is usually 0.03 to 0.05 pH units lower than the
arterial pH
*the PCO2 is usually 4 to 5 mmHg higher
*little or no increase in serum HCO3.
Mixed venous blood gives results similar to central venous blood.
peripheral venous
*The pH is approximately 0.02 to 0.04 pH units lower than the arterial
pH
*the venous serum HCO3 concentration is approximately 1 to 2 meq/L
higher
*the venous PCO2 is approximately 3 to 8 mmHg higher.
There are no venous to arterial conversions for the central venous,
mixed venous, or peripheral venous PvO2 or SvO2.
Misleading results
The correlation between arterial and venous blood gas measurements
varies with the hemodynamic stability of the patient.
This observation has two practical consequences:
First, clinicians should be wary of VBG results and preferentially
obtain an ABG in hypotensive patients.
Second, periodic correlation of the venous measurements with arterial
measurements should be performed whenever venous measurements
are used for serial monitoring.
END-TIDAL CARBON DIOXIDE
Measurement of end tidal carbon dioxide (PetCO2) is another method
of non-invasively estimating the arterial carbon dioxide tension
(PaCO2).
This technique, called capnography, requires a closed system of gas
collection, either with a tight fitting mask or a ventilator circuit.
A sample of expired gas is analyzed by infrared or mass spectrometry,
and then displayed as a numerical value or a graph.
The PetCO2 is usually within 1 mm of the PaCO2 in healthy adults, but
it is far less accurate in critically ill adults because of the dependence
of CO2 production on cardiac output .Thus, routine use of
PetCO2 exists primarily in newborn ICUs, operating rooms, and
emergency departments, to provide early warning of endotracheal tube
complications. PetCO2 is reviewed in detail separately.
TRANSCUTANEOUS CARBON DIOXIDE
Systems that measure both transcutaneous carbon dioxide (ptcCO2)
and pulse oximetry are an attractive option because they overcome the
major limitations of both ABGs (invasive arterial sampling) and VBGs
(lack of information about oxygenation).
Such combination systems generally have a heating element that raises
the skin temperature to 42 to 45ºC to increase local perfusion, an
electrode to measure ptcCO2, and a light emitter and sensor to measure
arterial oxyhemoglobin saturation.
Older studies suggested that ptcCO2 measurements are accurate in
neonates, but not critically ill adults because of poor peripheral
perfusion (peripheral artery disease, hypotension, vasopressors).
Devices have since improved and more recent observational studies
suggest that the newer systems may be more accurate in critically ill
patients, although their accuracy diminishes when the arterial carbon
dioxide tension (PaCO2) is greater than 56 mmHg.
Such combination systems have limitations:
1.They may be difficult to keep calibrated
2.may be difficult to mount in a way that prevents air trapping
3.may take up to an hour to sufficiently warm the skin.
4.the devices must be attached to an ear, which may be difficult in
agitated patients or in those who had neurosurgery
Given the limitations of noninvasive monitoring, any persistent or
unexpected change in the ptcCO2 or oxyhemoglobin saturation should
be confirmed with an ABG. Clinical trials are necessary before
combined pulse oximetry and ptcCO2 monitoring become routine care.
Comparison of Blood Gas Analysis at
different sites
•
•
•
•
•
Arterial
PH
Same
PO2 Higher
PCO2 Lower
HCO-3 Same
Recommendation
Good
Capillary
---------------------------Fair
Venous
Lower
Lower
Higher
Same
Bad
SPECIMEN CARE
Regardless of the method used to withdraw the arterial blood, several
issues should be considered prior to sending the specimen to the
laboratory:
1.Gas diffusion through the plastic syringe is a potential source of
error. However, it appears that the clinical significance of the error is
minimal if the sample is placed on ice and analyzed within 15 minutes.
Using a glass syringe will also prevent this error.
2.The heparin that is added to the syringe as an anticoagulant can
decrease in the pH if acidic heparin is used. It can also dilute the
PaCO2, resulting in a falsely low value.Thus, the amount of heparin
solution should be minimized and at least 2 mL of blood should be
obtained.
3.Air bubbles that exceed 1 to 2 percent of the blood volume can
cause a falsely high PaO2 and a falsely low PaCO2.
The magnitude of this error depends upon the difference in gas
tensions between blood and air, the exposure surface area (which
is increased by agitation), and the time from specimen collection
to analysis.
The clinical significance of this error can be decreased by gently
removing the bubbles without agitation and analyzing the sample
as soon as possible.
4.This reduces oxygen consumption by leukocytes (ie, leukocyte
larceny), which can cause a factitiously low PaO2.This effect is
most pronounced in patients whose leukocytosis is profound. In
addition, it reduces the likelihood that error due to gas diffusion
through the plastic syringe or air bubbles will be clinically
significant.
TRANSPORT
The arterial blood should be placed on ice during transport to the lab
and then analyzed as quickly as possible.
ANALYSIS
Analysis of arterial blood is usually performed by automated blood
gas analyzers, which automatically transport the specimen to
electrochemical sensors to measure pH, PaCO2, and PaO2:
• The PaCO2 is measured using a chemical reaction that consumes
CO2 and produces a hydrogen ion, which is sensed as a change in
pH
• The PaO2 is measured using oxidation-reduction reactions that
generate measurable electric currents
• Automated blood gas analyzers rinse the system, calibrate the
sensors, and report the results. Rigorous quality control by the
laboratory is essential for accurate results.
• Arterial blood gas measurements are effected by temperature.
Specifically, pH increases and both PaO2 and PaCO2 decrease as
temperature declines.
The effect of temperature on blood gas measurements
Modern automated blood gas analyzers can report the pH, PaO2,
and PaCO2 at either 37ºC (the temperature at which the values
are measured by the blood gas analyzer) or at the patient's body
temperature.
Most centers report the values of pH, PCO2, and PO2 at 37ºC,
even if the patient's body temperature is different. However, this
practice is controversial
Terminology of ABG
• Acidemia — An arterial pH below the normal range (less than 7.36).
• Alkalemia — An arterial pH above the normal range (greater than
7.44).
• Acidosis — A process that tends to lower the extracellular fluid pH
(hydrogen ion concentration increases). This can be caused by a fall
in the serum bicarbonate (HCO3) concentration and/or an elevation
in PCO2.
• Alkalosis — A process that tends to raise the extracellular fluid pH
(hydrogen ion concentration decreases). This can be caused by an
elevation in the serum HCO3 concentration and/or a fall in PCO2.
• Metabolic acidosis — A disorder that causes reductions in the serum
HCO3 concentration and pH.
• Metabolic alkalosis — A disorder that causes elevations in the serum
HCO3 concentration and pH.
• Respiratory acidosis — A disorder that causes an elevation in arterial
PCO2 and a reduction in pH.
• Respiratory alkalosis — A disorder that causes a reduction in arterial
PCO2 and an increase in pH.
• Simple acid-base disorder — The presence of one of the above four
disorders with the appropriate respiratory or renal compensation for
that disorder.
• Mixed acid-base disorder — The simultaneous presence of more
than one acid-base disorder.
Mixed acid-base disorders can be suspected from the patient's history,
from a lesser- or greater-than-expected compensatory respiratory or
renal response, and from analysis of the serum electrolytes and anion
gap.
As an example, a patient with severe vomiting would be expected to
develop a metabolic alkalosis due to the loss of acidic gastric fluid. If,
however, the patient developed hypovolemic shock from the fluid loss,
the ensuing lactic acidosis would lower the elevated serum HCO3
possibly to below normal values, resulting in acidemia
INTERPRETATION
ABGs provide information about oxygenation, ventilation, and acidbase balance
• Acid-Base & ventilation Information
• pH
• PCO2
• HCO3 [calculated vs measured]
• Oxygenation Information
• PO2 [oxygen tension]
• SO2 [oxygen saturation]
Each day approximately 15,000 mmol (considerably more with
exercise) of carbon dioxide (CO2, which can generate carbonic acid as
it combines with water) and 50 to 100 meq of nonvolatile acid (mostly
sulfuric acid derived from the metabolism of sulfur-containing amino
acids) are produced.
Acid-base balance is maintained by normal pulmonary and renal
excretion of carbon dioxide and nonvolatile acid, respectively.
General principles in ABG interpretation
The Henderson-Hasselbalch equation shows that the pH is determined
by the ratio of the serum bicarbonate (HCO3) concentration and the
PCO2, not by the value of either one alone. Each of the simple acidbase disorders is associated with a compensatory respiratory or renal
response that limits the change in ratio and therefore in PH.
pH = 6.10 + log ([HCO3-] ÷ [0.03 x PCO2])
Hydrogen Ions
H+ is produced as a by-product of metabolism.
[H+] is maintained in a narrow range.
Normal arterial pH is around 7.4.
A pH under 7.0 or over 7.8 is compatible with life for only short
periods.
PH and [H+]
[
+
H]
in nEq/L = 10
(9-pH)
A normal [H+] of 40 nEq/L
corresponds to a pH of 7.40.
Because the pH is a negative
logarithm of the [H+],
changes in pH are inversely
related to changes in [H+]
(e.g., a decrease in pH is
associated with an increase
in [H+]).
pH
[H+]
7.7
7.5
7.4
7.3
7.1
7.0
6.8
20
31
40
50
80
100
160
Hydrogen Ion Regulation
The body maintains a narrow pH range by 3 mechanisms:
1.
Chemical buffers (extracellular and intracellular) react instantly
to compensate for the addition or subtraction of H+ ions.
2.
CO2 elimination is controlled by the lungs (respiratory system).
Decreases (increases) in pH result in decreases (increases) in
PCO2 within minutes.
3. HCO3- elimination is controlled by the kidneys. Decreases
(increases) in pH result in increases (decreases) in HCO3-. It
takes hours to days for the renal system to compensate for
changes in pH.
CENTRAL EQUATION OF
ACID-BASE PHYSIOLOGY
The hydrogen ion concentration [H+] in extracellular fluid is
determined by the balance between the partial pressure of
carbon dioxide (PCO2) and the concentration of bicarbonate
[HCO3-] in the fluid. This relationship is expressed as follows:
[H+] in nEq/L = 24 x (PCO2 / [HCO3 -] )
where [ H+] is related to pH by [ H+] in nEq/L = 10 (9-pH)
NORMAL VALUES
Using a normal arterial PCO2 of 40 mm Hg and a normal serum
[HCO3- ] concentration of 24 mEq/L, the normal [H+] in arterial
blood is
24 × (40/24) = 40 nEq / L
When a primary acid-base disturbance alters one component of the
PCO2/[HCO3- ]ratio, the compensatory response alters the other
component in the same direction to keep the PCO2/[HCO3- ]
ratio constant.
PCO2/[HCO3- ] Ratio
Since [H+] = 24 x (PCO2 / [HCO3-]), the stability of the
extracellular pH is determined by the stability of the
PCO2/HCO3- ratio.
Maintaining a constant PCO2/HCO3- ratio will maintain a
constant extracellular pH.
The respiratory compensation:
When a metabolic acid-base disorder causes the serum HCO3 to
decrease (metabolic acidosis) or increase (metabolic alkalosis), there is
usually an appropriate respiratory compensation that causes the PCO2
to change in the same direction as the serum HCO3 (falling in
metabolic acidosis and rising in metabolic alkalosis).
The respiratory compensation mitigates the change in the ratio of the
serum HCO3 to PCO2 and therefore in the pH.
The respiratory compensation in metabolic acidosis or alkalosis is a
rapid response that, in metabolic acidosis, begins within 30
minutes and is complete within 12 to 24 hours
The ventilatory control system provides the compensation for
metabolic acid-base disturbances, and the response is prompt.
The changes in ventilation are mediated by H+ sensitive
chemoreceptors located in the carotid body (at the carotid
bifurcation in the neck) and in the lower brainstem.
*A metabolic acidosis excites the chemoreceptors and initiates a
prompt increase in ventilation and a decrease in arterial PCO2.
*A metabolic alkalosis silences the chemoreceptors and produces a
prompt decrease in ventilation and increase in arterial PCO2.
Control System for Respiratory Regulation of Acid-base Balance
Control
Element
Controlled
variable
Physiological or
Anatomical
Correlate
Arterial pCO2
Sensors
Central and peripheral
chemoreceptors
Central
integrator
The respiratory center in
the medulla
Effectors
The respiratory muscles
Comment
A change in arterial pCO2 alters arterial pH
(as calculated by use of the HendersonHasselbalch Equation).
Both respond to changes in arterial pCO2
(as well as some other factors)
An increase in minute ventilation
increases alveolar ventilation and thus
decreases arterial pCO2 (the controlled
variable).
The renal compensation:
When a respiratory acid-base disorder causes the PCO2 to increase
(respiratory acidosis) or decrease (respiratory alkalosis), there is
usually a renal compensation that causes the HCO3 to change in
the same direction as the PCO2, thereby mitigating the change in pH.
These compensations are mediated by increased hydrogen ion
secretion (which raises the serum HCO3 concentration) in respiratory
acidosis and decreased hydrogen ion secretion and urinary HCO3 loss
in respiratory alkalosis.
The renal compensation takes three to five days for completion. As a
result, the expected findings are different in acute (little or no renal
compensation) and chronic (full renal compensation) respiratory acidbase disorders.
Renal excretion of acid is achieved by combining hydrogen ions with
either urinary buffers to form titratable acid, mainly phosphate
(HPO42- + H+ → H2PO4-), or with ammonia to form ammonium
(NH3 + H+ → NH4+)
When increased quantities of acid must be excreted by the kidney, the
major adaptive response consists of increases in ammonia production
(derived from the metabolism of glutamine) with a resultant increase
in ammonium excretion into the urine.
The compensatory renal and respiratory responses are thought to be
mediated, at least in part, by parallel pH changes within sensory and
regulatory cells including renal tubule cells and cells in the respiratory
center.
The magnitude of the compensatory response is proportional to the
severity of the primary acid-base disturbance.
An important clinical consequence of these compensations is that the
diagnosis of an acid-base disorder requires measurement of the
extracellular (usually arterial) pH.
The diagnosis cannot be made from the serum HCO3 alone. A low
value could represent either metabolic acidosis or the renal
compensation to respiratory alkalosis, while a high value could
represent either metabolic alkalosis or the renal compensation to
respiratory acidosis. In addition, mixed acid-base disorders may be
present.
The expected compensation for any given acid-base disorder has been
determined empirically by observations in humans with either
spontaneous or experimentally induced simple acid-base disorders
The degree of compensation is usually calculated from the decrease or
increase in arterial PCO2 from its normal range (in metabolic acid-base
disorders) or the decrease or increase in serum HCO3 from its normal
range (in respiratory acid-base disorders).
This approach presumes that the patient had normal values prior to the
onset of the acid-base disorder. Thus, in the absence of known baseline
values, there is the potential for error if the patient had abnormal
baseline values.
Metabolic acid-base disorders
1.Metabolic acidosis
*The respiratory compensation to metabolic acidosis results in an
approximately 1.2 mmHg fall in arterial PCO2 for every 1 meq/L
reduction in the serum HCO3 concentration.
*The respiratory response to metabolic acidosis begins within 30
minutes and is complete within 12 to 24 hours.
*The lag in respiratory compensation is not seen when the metabolic
acidosis develops slowly (eg, 4 meq/L fall in serum HCO3 over 15
hours).
*An inability to generate the expected respiratory response is usually
indicative of significant underlying respiratory or neurologic disease,
but can also be seen in patients with acute metabolic acidosis in whom
there has not been adequate time for respiratory compensation to
achieve completion.
*Several other relationships have been used to determine the
appropriate respiratory compensation to metabolic acidosis. These
include:
• Arterial PCO2 = 1.5 x serum HCO3 + 8 ± 2 (Winters' equation)
• Arterial PCO2 = Serum HCO3 + 15
• Arterial PCO2 should be similar to the decimal digits of the arterial pH (eg, 25
mmHg when the arterial pH is 7.25, a setting in which the serum HCO3
concentration would be approximately 11 meq/L)
These formulas generally give similar results and there are no data on
comparative efficacy
A reasonable approach is to use the relationship rule that is easiest to
remember and implement.
*There is a limit to the maximum respiratory compensation that can be
attained. In severe metabolic acidosis (eg, serum HCO3 concentration
less than 6 meq/L), the PCO2 can be reduced to a minimum of 8 to 12
mmHg in individuals with normal neuro-respiratory function.
*In addition to assessing the respiratory compensation, another
component in the evaluation of patients with metabolic acidosis is
calculation of the serum anion gap to determine if it is normal or
elevated.
*Metabolic acidosis may be of the
-high anion gap type
-normal anion gap type (hyperchloremic)
-combined normal and elevated anion gap acidosis. The latter often
occurs with severe diarrhea, which generates a normal anion gap
metabolic acidosis but can also lead to hypovolemia-induced lactic
acidosis
With high anion gap metabolic acidosis, comparing the change in
anion gap (or the Δ anion gap) with the change in bicarbonate (or the
Δ bicarbonate) may be helpful.
2.Metabolic alkalosis
The respiratory compensation to metabolic alkalosis should raise the
PCO2 by 0.7 mmHg for every 1 meq/L elevation in the serum HCO3
concentration
In severe metabolic alkalosis, the arterial PCO2 can be as high as 55
mmHg, suggesting that hypoxia in individuals without underlying lung
disease does not usually limit the respiratory compensation
• Limitations of the respiratory compensation
It has been shown in dog studies that respiratory compensation for
metabolic acidosis or alkalosis most effectively blunts changes in pH
acutely.
If the metabolic disorder persists, on the other hand, respiratory
compensation becomes less effective and can even have a detrimental
effect on pH
The acute hyperventilatory response to metabolic acidosis causes a fall
in PCO2 and this will initially raise the arterial pH toward normal.
However, over time, the reduction in PCO2 causes a further decrease in
the serum HCO3 concentration due to both reduced renal acid secretion
and urinary HCO3 loss; these changes are similar to those induced by
primary respiratory alkalosis
The net effect of these two processes is that they tend to cancel one
another out so that the arterial pH with chronic metabolic acidosis is
often the same whether or not respiratory compensation occurs.
Furthermore, in studies in dogs, the respiratory response was
occasionally maladaptive, and the secondary fall in serum HCO3
actually caused the arterial pH to fall below the level that would have
existed in the absence of respiratory compensation.
Analogous findings have been demonstrated in chronic metabolic
alkalosis in which the respiratory compensation (hypoventilation
leading to a rise in PCO2) causes increased renal acid secretion and a
rise in the serum HCO3 concentration similar to that induced by
primary respiratory acidosis.
The renal response to a high PCO2 mitigates the pH benefit of
hypoventilation. As with chronic metabolic acidosis, studies in dogs
showed that this effect could become maladaptive and raise the arterial
pH to a value higher than that which would have occurred in the
absence of respiratory compensation
Respiratory acid-base disorders
The compensatory response to respiratory acid-base disorders occurs in
two stages:
• The initial acute response is generated by blood, extracellular fluid,
and cell buffering that causes the serum HCO3 to increase (in
respiratory acidosis) or decrease (in respiratory alkalosis) within
minutes. The acute response is relatively modest.
• A larger response generated by the kidney is called chronic
compensation. This response begins soon after the onset of the
primary respiratory disorder but requires 3 to 5 days to become
complete. Because of this variation with time, different
compensatory responses are expected with acute and chronic
respiratory disorders
• With chronic respiratory acidosis, the kidney increases acid
excretion in the form of titratable acid and ammonium, and also
increases HCO3 reabsorption to maintain the higher HCO3
concentration
• With chronic respiratory alkalosis, the kidney reduces acid
excretion, and also excretes some HCO3 to reduce the HCO3
concentration. Renal tubular reabsorption of HCO3 is also reduced.
• These renal responses are carefully regulated. As an example,
administering exogenous HCO3 in the setting of chronic respiratory
acidosis and relatively normal renal function results in the urinary
excretion of the excess alkali without a further elevation in the
serum HCO3 concentration.
1.Respiratory acidosis
The compensatory response to acute respiratory acidosis causes the
serum HCO3 concentration to increase by about 1 meq/L for every 10
mmHg elevation in the PCO2
If the elevated PCO2 persists, the serum HCO3 will continue to
gradually increase and, after three to five days, the disorder is
considered chronic. Studies mostly performed in hospitalized patients
found that the serum HCO3 increases by 3.5 to 4.0 meq/L for every 10
mmHg elevation in PCO2 in patients with chronic respiratory acidosis
However, a later study in stable outpatients with chronic respiratory
acidosis found a greater compensatory rise in serum HCO3 of about
5.0 meq/L per 10 mmHg elevation in PCO2.
The compensatory response to mild to moderate chronic respiratory
acidosis (PCO2 less than 70 mmHg) results in an arterial pH that is
usually modestly reduced or in the low-normal range.Thus, moderate
to severe acidemia in a patient with mild to moderate chronic
respiratory acidosis is usually indicative of concurrent metabolic
acidosis or superimposed acute respiratory acidosis. An arterial pH of
7.40 or higher suggests a concurrent metabolic alkalosis or acute
respiratory alkalosis.
2.Respiratory alkalosis
The compensatory response to acute respiratory alkalosis causes the
serum HCO3 concentration to fall by 2 meq/L for every 10 mmHg
decline in the PCO2 .
If the reduced PCO2 persists for more than 3 to 5 days, then the
disorder is considered chronic and the serum HCO3 concentration
should fall by about 4 to 5 meq/L for every 10 mmHg reduction in the
PCO2.
DIAGNOSIS
There are four primary acid-base disorders: metabolic acidosis,
metabolic alkalosis, respiratory acidosis, and respiratory alkalosis.
Because the renal compensation to respiratory disorders takes 3 to 5
days to complete, the primary respiratory disorders can be further
divided into acute and chronic respiratory acidosis and respiratory
alkalosis.
An important clinical consequence of the respiratory and renal
compensations to acid-base disorders is that the diagnosis cannot be
made with certainty from the serum HCO3 alone. As an example, a low
value could represent either metabolic acidosis or the renal
compensation to respiratory alkalosis, while a high value could
represent either metabolic alkalosis or the renal compensation to
respiratory acidosis.
PRIMARY AND SECONDARY ACID-BASE DERANGEMENTS
End-Point: A Constant PCO2/[HCO3- ] Ratio
Acid-Base Disorder
Primary Change Compensatory Change
Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis
PCO2 up(10)
PCO2 down(10)
HCO3 down(1)
HCO3 up(1)
HCO3 up(1),(5)
HCO3 down(2),(4-5)
PCO2 down(1.2)
PCO2 up(0.7)
Expected Compensation in Acid-Base
Disorders
EXPECTED CHANGES IN ACID-BASE DISORDERS
Primary Disorder
Metabolic acidosis
Metabolic alkalosis
Acute respiratory acidosis
Chronic respiratory acidosis
Acute respiratory alkalosis
Chronic respiratory alkalosis
Expected Changes
PCO2 = 1.5 × HCO3 + (8 ± 2)
PCO2 = 0.7 × HCO3 + (21 ± 2)
delta pH = 0.008 × (PCO2 - 40)
delta pH = 0.003 × (PCO2 - 40)
delta pH = 0.008 × (40 - PCO2)
delta pH = 0.003 × (40 - PCO2)
Normal Neonatal ABG values
• PH: 7.35 – 7.45
• pCO2: 35 – 45 mm Hg
• pO2: 50 – 70 mm Hg
• HCO3: 20 – 24 mEq/L
• BE: +/- 5
NORMAL VALUES ACCORDING TO SITE OF SAMPLING — The range
of normal values for acid-base parameters is different for arterial and
venous samples and also varies among laboratories.
• Arterial sample — For an arterial sample, the normal range for
pH is 7.36 to 7.44; for bicarbonate (HCO3) concentration, 21 to 27
meq/L; and for PCO2, 36 to 44 mmHg.
• Peripheral venous sample — Normal values for peripheral
venous blood differ from those of arterial blood due to the uptake
and buffering of metabolically produced CO2 in the capillary
circulation. If a tourniquet is used to facilitate phlebotomy, it
should be released about one minute before the sample is drawn to
avoid changes induced by ischemia
In different studies, the peripheral venous range for pH is
approximately 0.02 to 0.04 pH units lower than in arterial blood, the
HCO3 concentration is approximately 1 to 2 meq/L higher, and the
PCO2 is approximately 3 to 8 mmHg higher
If venous measurements are used for serial monitoring, periodic
correlation with arterial measurements should be performed.
• Central venous sample — Central venous samples may be used in
patients with central venous catheters. The central venous pH is
usually 0.03 to 0.05 pH units lower than in arterial blood and the
PCO2 is 4 to 5 mmHg higher, with little or no increase in serum
HCO3.
ABG values vary with age of neonate:
ABG values vary with gestational age:
The Steps
Approach to
Solving
Acid-Base
Disorders
Accurate diagnosis of an acid-base disorder requires measurement of
serum electrolytes to determine the serum HCO3 concentration, the
serum potassium (looking for hypokalemia or hyperkalemia which can
accompany many metabolic acid-base disorders), and the serum sodium
and chloride concentrations to detect possible hyponatremia or
hypernatremia and calculation of the serum anion gap.
In addition, in patients with a high anion gap metabolic acidosis,
analysis of the increase of the anion gap from its baseline divided by the
reduction in bicarbonate from normal (ie, the Δ anion gap divided by
the Δ bicarbonate, or "Δ/Δ") may be helpful.
A definitive diagnosis of acid-base disorders requires measurement of
the arterial pH and PCO2 to identify the underlying disorder and to
determine whether a mixed acid-base disorder exists.
However, measurement of arterial pH may not be required when the
history and serum electrolytes clearly point toward a particular
diagnosis. As an example, arterial blood gas analysis might not be
required in a previously healthy patient with a recent history of severe
diarrhea who has a low serum bicarbonate, hypokalemia, a normal
anion gap, and no apparent cause of chronic respiratory alkalosis in
which a low serum bicarbonate would represent the compensatory
response.
Measurement of peripheral venous pH and PCO2 is an alternative, less
invasive and more convenient approach than arterial measurements.
However, venous measurements have some important limitations. As a
result, arterial measurements are preferred. If venous measurements are
used for serial monitoring, periodic correlation with arterial
measurements should be performed. These issues are discussed in
detail elsewhere.
• We suggest the following three-step approach in most patients:
Step 1: Establish the primary diagnosis:
*Metabolic acidosis is characterized by a low serum HCO3 and a low
arterial pH; the serum anion gap may be increased or normal
*Metabolic alkalosis is characterized by an elevated serum HCO3 and
an elevated arterial pH
*Respiratory acidosis is characterized by an elevated arterial PCO2 and
a low arterial pH
*Respiratory alkalosis is characterized by low arterial PCO2 and an
elevated arterial pH
• Compensatory responses do not usually return the arterial pH to
normal. Thus, a normal arterial pH in the presence of substantial
changes in both serum HCO3 and arterial PCO2 is usually
indicative of a mixed acid-base disorder (which could include an
acute respiratory alkalosis produced by hyperventilation due to the
discomfort of obtaining the blood sample).
• However, there are two exceptions in which a simple acid-base
disorder may be accompanied by a normal arterial pH. Specifically,
compensatory responses may return the arterial pH to the highnormal range with mild to moderate chronic respiratory alkalosis,
and to the low-normal range with mild to moderate chronic
respiratory acidosis.
Step 2: Assess the degree of compensation
A substantially reduced or excessive compensation is indicative of
a mixed acid-base disorder.
The degree of compensation is usually calculated from the change in
arterial PCO2 (in metabolic acid-base disorders) or serum HCO3 (in
respiratory acid-base disorders) from their presumed baseline normal
values.
The assumption that the patient had normal values prior to the onset of
the acid-base disorder may be incorrect and introduces potential error.
The compensatory response must be correlated with the history. This is
particularly true in respiratory acid-base disorders since the renal
compensation occurs over 3 to 5 days. Thus, the expected
compensation is smaller with acute compared with chronic disorders.
As noted above, the normal compensatory response to respiratory
acidosis is an increase in the serum HCO3 concentration by about 1
meq/L for every 10 mmHg elevation in the PCO2 acutely and about
3.5 to 5.0 meq/L for every 10 mmHg elevation in the PCO2 if the
underlying respiratory problem persists for three to five days or more.
Step 3: In patients with metabolic acidosis, determine if the anion
gap is elevated
If it is, then analyze the ratio of the increase in anion gap to the
decrease in the HCO3 concentration. This is the Δanion gap/ΔHCO3
ratio. Interpretation of the anion gap and the Δanion gap/ΔHCO3 ratio
are discussed elsewhere.
Step 4: Establish the clinical diagnosis
Once the acid-base disorder is identified, the underlying cause or
causes of the disorder should be determined and corrected.
• Case 1 — A patient with respiratory distress and an uncertain past
history presents with an arterial pH of 7.32, an arterial PCO2 of 70
mmHg, and a serum HCO3 concentration of 35 meq/L, which is
approximately 11 meq/L above the value seen in normal
individuals.
• These values are compatible with the expected renal compensation
to chronic respiratory acidosis, although they are also compatible
with a mixed acid-base disorder.
• As an example, an acute respiratory acidosis causing a rise in PCO2
to 70 mmHg should increase the serum HCO3 by 3 meq/L to about
27 meq/L. If, however, this respiratory disturbance is superimposed
on a metabolic alkalosis that raises the serum HCO3 by an
additional 8 meq/L to 35 meq/L, the resulting findings would be the
same as those seen with a simple chronic respiratory acidosis. The
history usually helps to distinguish among these possibilities.
• Case 2 — A patient with diarrhea has an arterial pH of 7.24, HCO3
concentration of 10 meq/L, and arterial PCO2 of 24 mmHg.
• The low pH indicates acidemia, and the low serum HCO3
concentration indicates metabolic acidosis. The serum HCO3
concentration of 10 meq/L is approximately 14 meq/L below
normal. This should generate a 17 mmHg fall in the PCO2 (14 x 1.2
= 17) from 40 to 23 mmHg.Thus, this patient has a simple metabolic
acidosis.
• The other estimation equations for the degree of compensation cited
above give similar results. Winters' equation predicts a PCO2 of 23
mmHg (1.5 x 10 +8 ± 2), the "HCO3 + 15" rule predicts a PCO2 of
25 mmHg, and the pCO2 is the same as the decimal digits of the
arterial pH.
• A PCO2 significantly higher than the expected value would indicate
a concurrent respiratory acidosis, as might occur if the patient were
obtunded and had respiratory center depression. If, on the other
hand, the PCO2 were lower than 20 mmHg, then a concurrent
respiratory alkalosis would be present. The combination of
metabolic acidosis and respiratory alkalosis is often seen with
salicylate intoxication or septic shock.
• Mixed acid-base disorders — Some patients have two, three, or
more relatively independent acid-base disorders.
• These mixed disorders include combinations of metabolic disorders
(eg, vomiting-induced metabolic alkalosis plus hypovolemiainduced lactic acidosis), mixed metabolic and respiratory disorders
(eg, metabolic acidosis and respiratory alkalosis in salicylate
intoxication), and more complex combinations.
• As discussed in the preceding section, the evaluation of patients
with acid-base disorders initially requires identification of the major
disorder, and then determination if the degree of compensation is
appropriate. If the compensation is not appropriate, then this is
indicative of a second acid-base disorder (ie, a mixed acid-base
disorder is present).
The following examples are illustrative:
• If metabolic acidosis is the primary disorder, an arterial PCO2
substantially higher than the expected compensatory response
defines the mixed disorder of metabolic acidosis and respiratory
acidosis, while an arterial PCO2 substantially lower than expected
defines the mixed disorder of metabolic acidosis and respiratory
alkalosis (which could be produced by acute hyperventilation due to
the discomfort of obtaining the blood sample).
• If respiratory acidosis is the major disorder, then the serum HCO3
should be appropriately increased. If the serum HCO3 is not as high
as expected, then metabolic acidosis also exists and the arterial pH
may be substantially reduced. In contrast, if the serum HCO3 is
higher than expected, then metabolic alkalosis complicates the
respiratory acidosis and the arterial pH may be inappropriately
"normal."
• In patients with a high anion gap metabolic acidosis, a diagnosis of a
mixed metabolic acidosis and a metabolic alkalosis generally
requires calculation and interpretation of the Δ anion gap and the Δ
HCO3.
• Case 3 — Establishing the correct diagnosis may be more difficult
with respiratory acid-base disorders, because of the difference
between the acute and chronic compensatory responses. Consider
the following arterial blood values: arterial pH 7.27, arterial PCO2
70 mmHg, and serum HCO3 31 meq/L. The low pH and
hypercapnia indicate that the patient has respiratory acidosis. If this
is acute hypercapnia, then the 30 mmHg rise in PCO2 should
increase the serum HCO3 concentration by 3 meq/L (to about 27
meq/L). If this is chronic hypercapnia, the serum HCO3 should
increase by 11 meq/L (to about 35 meq/L).
The observed value of 31 meq/L is between these expected levels and
could have multiple explanations, including:
1.Chronic respiratory acidosis with a superimposed metabolic acidosis
that has reduced the serum HCO3 from 35 to 31 meq/L. This might
occur in a patient with chronic obstructive pulmonary disease who
developed diarrhea due to viral gastroenteritis or lactic acidosis from
sepsis.
2.Acute respiratory acidosis with a superimposed metabolic alkalosis
that has increased the HCO3 from 27 to 31 meq/L. This could occur in
a patient with respiratory depression due to a sedating drug who also
developed vomiting or was taking diuretics.
3.Acute respiratory acidosis superimposed on mild chronic respiratory
acidosis. Suppose, for example, that a patient has chronic respiratory
acidosis with a PCO2 of 55 mmHg and an appropriate serum HCO3 of
30 meq/L. The patient then develops pneumonia, which acutely
increases the pCO2 to 70 mmHg. The serum HCO3 would rise further
to about 31 meq/L.
4.Acute respiratory acidosis that is evolving into a chronic disorder
(between 1 and 3 days).
• Thus, the correct diagnosis in a primary respiratory acid-base
disorder can be established only when correlated with the clinical
history and physical examination.
• This is true even when the arterial blood values appear to represent a
simple disorder. If the serum HCO3 concentration had been 35
meq/L in this example, the findings would have been compatible
with an uncomplicated chronic respiratory acidosis. However,
similar findings could have been induced by acute respiratory
acidosis plus metabolic alkalosis.
• The history usually helps to distinguish among the possibilities and
serial blood gas measurements and serum chemistries should be
performed.
Some Aids to Interpretation of Acid-Base Disorders
"Clue"
Significance
High anion gap
Always strongly suggests a metabolic
acidosis.
Hyperglycaemia
If ketones present also diabetic ketoacidosis
Hypokalemia and/or hypochloremia
Suggests metabolic alkalosis
Hyperchloremia
Common with normal anion gap acidosis
Elevated creatinine and urea
Suggests uremic acidosis or hypovolemia
(prerenal renal failure)
Elevated creatinine
Consider ketoacidosis: ketones interfere in
the laboratory method (Jaffe reaction) used
for creatinine measurement & give a falsely
elevated result; typically urea will be
normal.
Elevated glucose
Consider ketoacidosis or hyperosmolar nonketotic syndrome
Urine dipstick tests for glucose and ketones
Glucose detected if hyperglycaemia;
ketones detected if ketoacidosis
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