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ArteriaI BIood Gases

ArteriaI bIood gas anaIysis provides information on the


foIIowing:
1] Oxygenation of blood through gas exchange in the lungs. 2]
Carbon dioxide (CO2) elimination through respiration. 3] Acid-base
balance or imbalance in extra-cellular fluid (ECF).

NormaI BIood Gases
Arterial Venous
pH 7.35 - 7.45 7.32 - 7.42
Not a gas, but a measurement of acidity or
alkalinity, based on the hydrogen (H+) ions
present. The pH of a solution is equal to the
negative log of the hydrogen ion
concentration in that solution: pH = - log
[H+].
PaO2
80 to 100 mm
Hg.
28 - 48 mm
Hg
The partial pressure of oxygen that is
dissolved in arterial blood.
New Born - Acceptable range 40-70 mm
Hg. Elderly: Subtract 1 mm Hg from the
minimal 80 mm Hg level for every year over
60 years of age: 80 - (age- 60) (Note: up
to age 90)
HCO3
22 to 26
mEq/liter
(21-28 mEq/L)
19 to 25
mEq/liter
The calculated value of the amount of
bicarbonate in the bloodstream. Not a blood
gas but the anion of carbonic acid.
PaCO2 35-45 mm Hg 38-52 mm Hg
The amount of carbon dioxide dissolved in
arterial blood. Measured. Partial pressure
of arterial CO2. (Note: Large A= alveolor
CO2). CO2 is called a "volatile acid
because it can combine reversibly with H2O
to yield a strongly acidic H+ ion and a weak
basic bicarbonate ion (HCO3 -) according to
the following equation: CO2 + H2O <--- -->
H
+
+ HCO3
B.E.
-2 to +2
mEq/liter

Other

sources:
normal
reference
range is
between -5 to
+3.
The base excess indicates the amount of
excess or insufficient level of bicarbonate in
the system. (A negative base excess
indicates a base deficit in the blood.) A
negative base excess is equivalent to an
acid excess. A value outside of the normal
range (-2 to +2 mEq) suggests a metabolic
cause for the abnormality. Calculated
value. The base excess is defined as the
amount of H+ ions that would be required to
return the pH of the blood to 7.35 if the
pCO2 were adjusted to normal.

It can be estimated by the equation:
Base excess = 0.93 (HCO3 - 24.4 + 14.8(pH
- 7.4))
Alternatively: Base excess = 0.93HCO3 +
13.77pH - 124.58

A base excess > +3 = metabolic alkalosis a
base excess < -3 = metabolic acidosis
$aO2 95% to 100% 50 - 70%
The arterial oxygen saturation.

$tep by $tep ABG AnaIysis
$tep One - Assessing pH
Look at pH and determine if it is acidotic (<7.35),
normal (7.35 - 7.45), or alkalotic (> 7.45).

pH is the best overall indicator in determining the
acid-base status of the patient.
$tep Two - Determine respiratory invoIvement
#eview the PaCO2 to assess respiratory involvement
[The lungs control the level of carbon dioxide in the
arterial blood]. The PaCO2 must be evaluated in light
of the arterial pH. That is, if the pH is abnormal, we
then ask ourselves: would this observed PaCO2, by
itself, cause this pH abnormality? For example,
suppose that the pH is below 7.35 (denoting
acidosis) and the PaCO2 is above 45 mmHg.
According to the Henderson-Hasselbalch equation, a
high PaCO2 would indeed cause a low pH (i.e.,
acidosis). Therefore we know that the respiratory
system is at least in part, if not entirely, responsible
for the acidosis. On the other hand, if the pH is less
than 7.35 and the PaCO2 is in the normal range,
then we know that the acidosis must be of non-
respiratory (metabolic) origin.

PaCO2:
Normal: 35 - 45 mmHg (4.6 - 6
kPa)
Respiratory acidosis: > 45
mmHg (> 6 kPa)
Respiratory alkalosis: <35
mmHg (< 4.6 kPa)

$tep Three - Determine metaboIic invoIvement
#eview the plasma [HCO3-] or B.E. (Base excess) to
determine metabolic involvement (both controlled by
non-respiratory factors.) Each of these components
must be evaluated based on the current pH. If the
pH is abnormal, we ask: would this observed [HCO3-
] by itself, cause this pH abnormality? For example,
suppose that the pH is less that 7.35 (denoting
acidosis) and the [HCO3-] is below 22 mEq/L.
Indeed, according to the Henderson-Hasselbalch
equation, the low [HCO3-] is consistent with acidosis.
Thus, we know that non-respiratory factors are in
part, if not entirely, responsible for the acidosis. If
[HCO3-] were in the normal range in the presence of
this acidosis, then we would know that the acidosis
must be of respiratory origin.
HCO
3
-
--------------------------
Normal: 22 - 26 mEq/L
Metabolic acidosis: <22 mEq/L
Metabolic alkalosis: > 26
mEq/L

[Standard Bicarbonate:
Calculated value. Similar to the
base excess. It is defined as the
calculated bicarbonate
concentration of the sample
corrected to a PCO2 of 5.3kPa
(40mmHg).

BE (Base Excess):
--------------------------
Normal: -2 to +2 mmol/L
Metabolic acidosis: < -2
mmol/L
Mild -4 to -6
Moderate -6 to -9
Marked -9 to -13
Severe to < -13

Metabolic alkalosis: > +2
mmol/L
Severe > +13
Marked 9 to 13
Moderate 6 to 9
Mild 4 to 6


[Base excess (BE) is the mmol/L
of base that needs to be removed
to bring the pH back to normal
when PCO2 is corrected to 5.3
kPa or 40 mmHg. During the
calculation any change in pH due
to the PCO2 of the sample is
eliminated, therefore, the base
excess reflects only the metabolic
component of any disturbance of
acid base balance.]

$tep Four - Assess for compensation
ook at the pH, PaCO
2
, and B.E. / HCO
3
- to
decide whether compensatory mechanisms are
at work.

Once the acid-base disorder is identified as
respiratory or metabolic, we must look for the degree
of compensation that may or may not be occurring.
we know that the system not primarily responsible
for the acid-base abnormality must assume the
responsibility for returning the pH to the normal
range. This compensation may be complete (pH is
brought into the normal range) or partial (pH is still
out of the normal range but is in the process of
moving toward the normal range.) In pure
respiratory acidosis (high PaCO2, normal [HCO3-],
and low pH) we would expect an eventual
compensatory increase in plasma [HCO3-] that would
work to restore the pH to normal. Similarly, we
expect respiratory alkalosis to elicit an eventual
compensatory decrease in plasma [HCO3-]. A pure
metabolic acidosis (low [HCO3-], normal PaCO2, and
a low pH) should elicit a compensatory decrease in
PaCO2, and a pure metabolic alkalosis (high [HCO3-],
normal PaCO2, and high pH) should cause a
compensatory increase in PaCO2. All compensatory
responses work to restore the pH to the normal range
(7.35 - 7.45)

[ $ee sample problems near the bottom of the
page]
$tep Five - Further anaIysis in cases of
METABOLIC ACIDO$I$
Metabolic acidosis:

1] Calculate the anion gap:
Anion gap = Na+ - [CL- +
HCO3-]

Difference between calculated
serum anions and cations.
Based on the principle of
electrical neutrality, the serum
concentration of cations (positive
ions) should equal the serum
concentration of anions (negative
ions).
However, serum Na+ ion
concentration is higher than the
sum of serum Cl- and HCO3-
concentration.
Na+ = CL- + HCO3- +
unmeasured anions (gap).

Normal anion gap: 12 mmol/L
(10 - 14 mmol/L)

2] Based on the anion gap and patient history -
review potential causes:

Normal anion gap (hyperchloremic) metabolic
acidosis:
Normal anion gap acidosis: The most common
causes of normal anion gap acidosis are GI or renal
bicarbonate loss and impaired renal acid excretion.
Normal anion gap metabolic acidosis is also called
hyperchloremic acidosis, because instead of
reabsorbing HCO3- with Na, the kidney reabsorbs Cl-
. Many GI secretions are rich in bicarbonate (eg,
biliary, pancreatic, and intestinal fluids); loss from
diarrhea, tube drainage, or fistulas can cause
acidosis. In ureterosigmoidostomy (insertion of
ureters into the sigmoid colon after obstruction or
cystectomy), the colon secretes and loses
bicarbonate in exchange for urinary Cl- and absorbs
urinary ammonium, which dissociates into NH3+ and
H+.

Loss of HCO3 ions is accompanied by an increase in
the serum Cl- concentration. The anion gap remains
normal. Disease processes that can lead to normal
anion gap (hyperchloremic) acidosis. Useful
mnemonic (DU#HAM):
a) Diarrhea (HCO3- and water is lost).
b) Ureteral diversion: Urine from the ureter may be
diverted to the sigmoid colon due to disease
(uretero-colonic fistula) or after bladder surgery. In
such an event urinary Cl- is absorbed by the colonic
mucosa in exchange for HCO3-, thus increases the
gastrointestinal loss of HCO3-.
c) Renal tubular acidosis: dysfunctional renal tubular
cells causes an inappropriate wastage of HCO3- and
retention of Cl-.
d) Hyperalimentation
e) Acetazolamide
f) Miscellaneous conditions: They include pancreatic
fistula, cholestyramine, and calcium chloride (CaCl)
ingestion, all of which can increase the
gastrointestinal wastage of HCO3-.

Increased anion gap metabolic acidosis
High anion gap acidosis: The most common causes
of a high anion gap metabolic acidosis are
ketoacidosis, lactic acidosis, renal failure, and toxic
ingestions. #enal failure causes anion gap acidosis by
decreased acid excretion and decreased bicarbonate
reabsorption. Accumulation of sulfates, phosphates,
urate, and hippurate accounts for the high anion
gap. Toxins may have acidic metabolites or trigger
lactic acidosis.

In increased anion gap metabolic acidosis, the
nonvolatile acids are organic or other inorganic acids
(e.g., lactic acid, acetoacetic acid, formic acid,
sulphuric acid). The anions of these acids are not Cl-
ions. The presence of these acid anions, which are
not measured, will cause an increase in the anion
gap. Useful mnemonic (MUD PILES):

Methanol poisoning: Methanol is metabolized by
alcohol dehydrogenase in the liver to formic acid.
Uremia: In end-stage renal failure in which
glomerular filtration rate falls below 10-20 ml/min,
acids from protein metabolism are not excreted and
accumulate in blood.

Diabetic ketoacidosis: incomplete oxidation of fatty
acids causes a build up of beta-hydroxybutyric and
acetoactic acids (ketoacids).

Paraldehyde poisoning.

Ischemia: causes lactic acidosis.

actic acidosis: Lactic acid is the end product of
glucose breakdown if pyruvic acid, the end
product of anaerobic glycolysis, is not oxidized to
CO2 and H2O via the Tricarboxylic Acid Cycle.
(Causes: hypoxia, ischemia, hypotension, sepsis).

Ethylene glycol poisoning: Ethylene is
metabolized by alcohol dehydrogenase to oxalic acid
in the liver. Usually there is also a coexisting lactic
acidosis.

$alicylate poisoning


Causes of common acid-base disturbances:
MetaboIic acidosis (non-respiratory)
High anion gap.
Ketoacidosis (diabetes,
Renal HCO3- loss:
Tubulointerstitial renal
chronic alcoholism,
malnutrition, fasting).
Lactic acidosis.
#enal failure.

%oxins metabolized to
acids:
Methanol (formic acid)
Ethylene glycol (oxalate)
Paraldehyde (acetate,
chloracetate)
Salicylates

%oxins causing lactic
acidosis
CO2
Cyanide
Iron
Isoniazid
Toluene (initially high
gap, subsequent
excretion of metabolites
normalizes gap)

#habdomyolysis (rare)

oss of base -
Normal anion gap
(hyperchloremic acidosis)
GI HCO3- loss (diarrhea,
ileostomy, colostomy,
enteric fistulas, use of
ion-exchange resins)

Ureterosigmoidostomy,
ureteroileal conduit
disease.
#enal tubular acidosis,
types 1, 2, 4.
Hyperparathyroidism.

Ingestions
(acetazolamide, CaCl2,
MgSO4) Others

Hypoaldosteronism,
Hyperkalemia
Parenteral infusion of
arginine, lysine, NH4Cl.
#apid NaCl infusion.
Toluene (late).

Formulas
(Compensation):
pCO2 decreases 1.2 for
each mEq/L change in
HCO3 or
pCO2 = last two digits of
pH

Compensation
Ventilation of the lungs
increases through
stimulation of central
chemoreceptors (H+ ion
receptors) in the medulla
and peripheral
chemoreceptors in the
carotid and aortic bodies.
Consequently PCO2 falls
below normal, and H+
ion concentration falls.
#espiratory compensation
increases the acidic pH
towards normal. The
respiratory system
responds to metabolic
acidosis quickly and
predictably by
hyperventilation, so much
so that pure metabolic
acidosis is seldom seen.
#espiratory AIkaIosis:
CNS disorders or lesions, Compensation:
hypoxia [Hypoxia-causing
conditions], pulmonary
receptor stimulation
(asthma, pneumonia,
pulmonary edema, PE),
Pulmonary vascular
disease, anxiety, fear,
pain, drugs (ASA,
theophylline), liver
failure, sepsis.

Formulas
(Compensation):
- Acute: HCO3 decreases
0.22 for every mmHg
change in pCO2

- Chronic: HCO3
decreases 0.5 for every
mmHg change in pCO2
In the presence of
respiratory alkalosis the
kidneys compensate for
the increase in pH by
retaining H+ ions and
excreting HCO3 - ions. As
a result, pH falls towards
normal and HCO3 -
concentration falls below
normal. #enal
compensation to
respiratory alkalosis is a
slow process and the pH
does not completely
return to normal.
MetaboIic (non-resp)
aIkaIosis:
#espiratory Acidosis:
Increase in base
Administration/ingestion
of HCO3-
Hypochloremia (HCO3
retained).
Diuretic therapy
Contraction of blood
volume.
Loss of fixed acid.
Severe vomiting (loss of
H+).
Nasogastric suction.
Hypokalemia - Potassium
deficiency.
Corticosteroid
administration.

Formulas
(Compensation):
pCO2 increases 0.6 for
each mmol/L change in
HCO3

Compensation:
The respiratory response
to metabolic alkalosis is
Central nervous
depression: sedatives
etc.
Neuromuscular disease
(Guillain-Barr,
myasthenia gravis).
Trauma.
Severe restrictive
disorders: scoliosis.
COPD. Acute airway
obstruction: choking etc.
CVA, pneumothorax,
chest wall disorder,
tumor. Acute and chronic
lung disease.

Formulas
(Compensation):
- Acute: HCO3 increases
0.1 for every mmHg
change in pCO2

- Chronic: HCO3
increases 0.35 for every
mmHg change in pCO2

hypoventilation. PCO2
rises above normal.
#espiratory compensation
to metabolic alkalosis is
variable and
unpredictable. It is
unlikely that a conscious
patient breathing
spontaneously will
hypoventilate to a PCO2
> 7.3 kPa (55 mmHg) to
compensate for metabolic
alkalosis.
Compensation: In the
presence of respiratory
acidosis the kidneys
compensate for the fall in
pH by excreting H+ ions
and retaining HCO3 -
ions. As a result, pH rises
towards normal and
HCO3 - concentration
rises above normal. #enal
compensation (also called
metabolic compensation)
to respiratory acidosis is
a slow process.
Compensation is not
obvious for several hours
and takes 4 days to
complete.



$ampIe ProbIems - ArteriaI BIood
Gases
#espiratory
alkalosis
(chronic alveolar
hyperventilation)
pH:
PaCO2:
HCO
3:

BE:
7.44
24
16
-6
#espiratory
acidosis.
Chronic ventilation
failure
pH:
PaCO2:
HCO
3:

BE:
7.38
76
42
+14
Uncompensated
metabolic alkalosis
pH:
PaCO2:
HCO
3:

BE:
7.56
44
38
+14
(#espiratory
acidosis.
acute ventilation
failure
pH:
PaCO2:
HCO
3:

BE:
7.26
56
24
-4
uncompensated
metabolic alkalosis
pH:
PaCO2:
HCO
3:

BE:
7.56
40
34
+11
#espiratory
alkalosis (chronic
pH:
PaCO2:
7.44
26
alveolar
hyperventilation)
HCO
3:

BE:
18
-4
#espiratory
acidosis.

Chronic ventilation
failure
pH:
PaCO2:
HCO
3:

BE:
7.40
56
34
+7
#espiratory
alkalosis.
Chronic alveolar
hyperventilation
pH:
PaCO2:
HCO
3:

BE:
7.44
20
16
-7
Uncompensated
metabolic acidosis
pH:
PaCO2:
HCO
3:

BE:
7.24
36
14
-13
#espiratory
alkalosis (acute
alveolar
hyperventilation)
pH:
PaCO2:
HCO
3:

BE:
7.52
28
22
+1
Acute #espiratory
Acidosis
Dx - heroin overdose.
Breathing - shallow,
slow.
ABGs:
pH: 7.30
PaCO2: 55 mm/Hg
HCO3-: 27 mEq/L
Chronic #espiratory
Acidosis
Hx/Dx: 73yo,
emphysema, labored
breathing at rest.
ABGs:
pH: 7.36
PaCO2: 64 mmHg
HCO3-: 35 mEq/L
Acute #espiratory
Alkalosis
Hx/Dx: 77yo, anxiety,
psychosomatic origin.
#apid breathing and
slurred speech.
ABGs:
pH: 7.57
PaCO2: 23 mmHg
HCO3-: 21 mEq/L
Compensated
#espiratory
Alkalosis
Persistent bacterial
pneumonia. Mild
cyanosis and labored
breathing.
ABGs:
pH: 7.44
PaCO2: 26 mmHg
HCO3-: 17 mEq/L
PaO2: 53 mmHg
Metabolic Alkalosis
80 yo with heart
disease. #: diuretic
ABGs:
pH: 7.58
PaCO2: 48 mmHg
HCO3-: 44 mEq/L
BE: + 19 mEq/L
Serum CL- 95 mEq/L