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ABG
INTERPRETATIONDebbie
Sander
PAS-II1Objectives2What’sanABG?Understanding
Acid/Base
RelationshipGeneral
approach
to
ABG
InterpretationClinical
causes
Abnormal
ABG’sCase
studiesTake
homeWhat
is
an
ABG3Arterial
Blood
GasDrawn
from
artery-
radial,
brachial,
femoralIt
is
an
invasive
procedure.Caution
must
be
taken
with
patient
onanticoagulants.Helps
differentiate
oxygen
deficiencies
from
primaryventilatory
deficiencies
from
primary
metabolic
acid-baseabnormalitiesWhat
Is AnABG?pH
[H+]PCO2
Partial
pressure
CO2PO2
Partial
pressure
O2HCO3
BicarbonateBE Base
excessSaO2Oxygen
Saturation4Acid/Base
Relationship5
This
relationship
is
critical
for
homeostasis
Significant
deviations
from
normal
pH
ranges
arepoorly
tolerated
and
may
be
life
threatening
Achieved
by
Respiratory
and
Renal
systemsCase
Study No.
1660
y/o
male
comes
ER
c/o
SOB.Tachypneic,
tachycardic,
diaphoretic
andCyanotic.
Dx
acute
resp.
failure
and
ABG’sShow
PaCO2
well
below
nl,
pH
above
nl,PaO2
is
very
low.
The
blood
gas
documentResp.
failure
due
to
primary
O2
problem.Case
Study No.
2760
y/o
male
comes
ER
c/o
SOB.Tachypneic,
tachycardic,
diaphoretic
andCyanotic.
Dx
acute
resp.
failure
and
ABG’sShow
PaCO2
very
high,
low
pH
and
PaO2is
moderately
low.
The
blood
gas
documentResp.
failure
due
to
primarily
ventilatoryinsufficiency.
There
are
two
buffers
that
work
in
pairs8
H2CO3CarbonicacidNaHCO3base
bicarbonate
These
buffers
are
linked
to
the
respiratory
andrenal
compensatory
systemBuffersRespiratory
Component9
function
of
the
lungs
Carbonic
acid
H2CO3Approximately
98%
normal
metabolites
are
in
theform ofCO2CO2
+
H2O
H2CO3
excess
CO2
exhaled
by
the
lungsMetabolic
Component10
Function
of
the
kidneys
base
bicarbonate Na
HCO3Process
of
kidneys
excreting
H+into
the
urine
and
reabsorbingHCO
-
intothe
blood
from
the
renaltubules3active
exchange
Na+
for
H+
between
the
tubularcells
and
glomerular
filtratecarbonic
anhydrase
is
an
enzyme
that
accelerates hydration/dehydration
CO2
in
renal
epithelial
cellsH2O
+
CO2
H2CO311
HCO3
+H+Acid/Base
RelationshipNormal
ABG
values12pH 7.35
–7.45PCO2
35–45
mmHgPO2
80–100mmHgHCO3
22
–26mmol/LBE -2-+2SaO2
>95%Acidosis13AlkalosispH <
7.35PCO2
>
45HCO3
<
22pH >
7.45PCO2
<
35HCO3
>
26Respiratory
Acidosis14
Think
of
CO2
as
an
acid
failure
of
the
lungs
to
exhale
adequate
CO2pH<
7.35
PCO2
>
45
CO2
+
H2CO3
pHCauses
of
Respiratory
Acidosis15
emphysema
drug
overdose
narcosis
respiratory
arrest
airway
obstructionMetabolic
Acidosis16
failure
of
kidney
function
blood
HCO3
which
results
in
availability
of
renaltubularHCO3
forH+
excretion
pH
<
7.35
HCO3
<
22Causes
of Metabolic
Acidosis17
renal
failure
diabetic
ketoacidosis
lactic
acidosis
excessive
diarrhea
cardiac
arrestRespiratory
Alkalosis18
too
much
CO2
exhaled
(hyperventilation)
PCO2,
H2CO3
insufficiency
=
pH
pH
>
7.45
PCO2
<
35Causes
of
Respiratory
Alkalosis19
hyperventilation
panic
d/o
pain
pregnancy
acute
anemia
salicylate
overdoseMetabolic
Alkalosis20
plasma
bicarbonate
pH
>
7.45
HCO3
>
26Causes
of Metabolic
Alkalosis21
loss
acid
from
stomach
or
kidney
hypokalemia
excessive
alkali
intakeHow
to Analyze
an
ABGPO2
NL
= 80–100mmHgpH
NL
= 7.35
–7.45AcidoticAlkalotic<7.35>7.453.
PCO2NL
= 35–45mmHgAcidoticAlkalotic>45<354.
HCO3NL
= 22–26mmol/LAcidoticAlkalotic<
22>
2622Four-step ABG
Interpretation23Step
1:
Examine
PaO2
&
SaO2
Determine
oxygen
status
Low
PaO2
(<80
mmHg)
&
SaO2
means
hypoxia
NL/elevated
oxygen
means
adequate
oxygenationStep
2:
pHacidosisalkalosis<7.35>7.45Four-step ABG
Interpretation24Step
3:
study
PaCO2
&
HCO
3
respiratoryirregularity
if
PaCO2
abnl
&
HCO3
NL
metabolic
irregularity
if
HCO3
abnl
&
PaCO2
NL25Four-step ABG
InterpretationStep
4:Determine
if
there
is
a
compensatory
mechanism
workingto
try
to
correct
the
pH.ie: if
have
primary
respiratory
acidosis
will
have
increasedPaCO2
and
decreased
pH. Compensation
occurswhenthe
kidneys
retain
HCO3.26Four-step ABG
Interpretation~
PaCO2
–
pH
Relationship27807.20607.30407.40307.50207.60CompensatedRespiratoryAcidosisCO2More
AbnormalRespiratoryAcidosisCO2ExpectedMixedRespiratoryMetabolicAcidosisCO2Less
AbnormalCO2
Changec/wAbnormalityMetabolicMetabolicAcidosisCO2NormalCompensatedMetabolicAcidosisCO2
ChangeopposesAbnormalityAcidosisABG
Interpretation28CompensatedRespiratoryAlkalosisCO2More
AbnormalRespiratoryAlkalosisCO2ExpectedMixedRespiratoryMetabolicAlkalosisCO2Less
AbnormalCO2
Changec/wAbnormalityMetabolicAlkalosisCO2NormalCompensatedMetabolicAlkalosisCO2
ChangeopposesAbnormalityAlkalosisABG
Interpretation29Respiratory
Acidosis30pH
7.30PaCO2
60HCO3
26Respiratory
Alkalosis31pH
7.50PaCO2
30HCO3
22Metabolic
Acidosis32pH
7.30PaCO2
40HCO3
15Metabolic
Alkalosis33pH
7.50PCO2
40HCO3
30What
are
thecompensations?34Respiratory
acidosis
metabolic
alkalosisRespiratory
alkalosis
metabolic
acidosisIn
respiratory
conditions,
therefore,
the
kidneys
willattempt
to
compensate
and
visa
versa.In
chronic
respiratory
acidosis
(COPD)
the
kidneysincreasethe
eliminationofH+
andabsorbmore
HCO3.
The
ABG
willShow
NL
pH,
CO2and
HCO3.Buffers
kick
in
withinminutes. Respiratory
compensationis
rapid
and
starts
within
minutes
and
complete
within
24hours.
Kidney
compensation
takes
hours
and
up
to
5
days.Mixed
Acid-Base
Abnormalities35Case
Study
No.
3:56
yo
neurologic
dz
required
ventilator
support
for
severalweeks. She
seemed
most
comfortable
when
hyperventilatedto
PaCO2
28-30mmHg. She
required
daily
doses
of
lasix
toassure
adequate
urine
output
and
received
40
mmol/L
IV
K+each
day.
On
10th
day
ofICU
her
ABG
on24%
oxygen
&
VS:ABG
Results36pH7.62BP115/80
mmHgPCO230mmHgPulse88/minPO285mmHgRR10/minHCO330mmol/LVT1000mlBE10mmol/LMV10LK+2.5mmol/LInterpretation:
Acute
alveolar
hyperventilation(resp.
alkalosis)
and
metabolic
alkalosis
with
correctedhypoxemia.Case
study No.
43727
yoretarded
with
insulin-dependent
DM
arrivedat
ERfrom
the
institution
where
he
lived. On
room
air
ABG
&
VS:pH7.15BP180/110
mmHgPCO222mmHgPulse130/minPO292mmHgRR40/minHCO3
9mmol/LBE -30mmol/LVT
800mlMV
32LInterpretation:Partly
compensated
metabolic
acidosis.Case
study No.
53874
yo
with
hx
chronic
renal
failure
and
chronic
diuretictherapywas
admitted
to
ICU
comatose
and
severelydehydrated.
On40%
oxygen
her
ABG
&
VS:pH7.52BP130/90
mmHgPCO255mmHgPulse120/minPO292mmHgRR25/minHCO342mmol/LVT150mlMV
3.75LPartly
compensated
metabolic
alkalosis
withBE 17mmol/LInterpretation:corrected
hypoxemia.Case
study No.
643
yo
arrives
in
ER
20
minutes
after
a
MVA
in
which
heinjured
his
face
on
thedashboard. He
is
agitated,
has
mottled,cold
and
clammy
skin
and
has
obvious
partial
airwayobstruction.An
oxygen
mask
at
10
L
is
placed
on
hisface. ABG
&
VS:pH7.10BP150/110
mmHgPCO260mmHgPulse150/minPO2125mmHgRR45/minHCO318mmol/LVT?
mlBE-15mmol/LMV?
LIn.
terpretation: Acute
ventilatory
failure
(resp.
acidosis)andacute
metabolic
acidosis
with
corrected
hypoxemia39Case
study No.
74017yo,48kg
with
knowninsulin-dependent
DM
came
to
ERwith
Kussmaul
breathing
and
irregular
pulse. Room
airABG
&
VS:pH7.05BP140/90
mmHgPCO212mmHgPulse118/minPO2108mmHgRR40/minHCO35mmol/LVT1200mlBE-30mmol/LMV48LInterpretation:
Severe
partly
compensated
metabolicacidosis
without
hypoxemia.Case
No.
7
cont’d41This
patient
is
in
diabetic
ketoacidosis.IV
glucose
and
insulin
were
immediatelyadministered.
Ajudgement
was
made
that
severe
acidemia
was
adverselyaffecting
CV
function
and
bicarb
was
elected
to
restore
pH
to
7.20.Bicarb
administration
calculation:Base
deficit
X
weight
(kg)430X
48 =
360mmol/L4Admin
1/2
over
15
min
&repeat
ABGCase
No.
7
cont’d42ABG
result
after
bicarb:pH7.27BP130/80
mmHgPCO225mmHgPulse100/minPO292mmHgRR22/minHCO311mmol/LVT600mlBE-14mmol/LMV13.2LCase
study No.
84347
yo
was
inPACU
for
3
hours
s/pcholecystectomy.
Shehad
been
on
40%
oxygen
and
ABG
&
VS:pH7.44BP130/90
mmHgPCO232mmHgPulse95/min,
regularPO2121mmHgRR20/minHCO322mmol/LVT350mlBE-2mmol/LMV7LSaO2Hb98%13
g/dLCase
No.
8
cont’d44Oxygen
was
changed
to
2L
N/C. 1/2
hour
pt.
ready
to
be
D/Cto
floor
and
ABG
&
VS:pH7.41BP130/90
mmHgPCO210mmHgPulse95/min,
regularPO2148mmHgRR20/minHCO36mmol/LVT350mlBE-17mmol/LMV7LSaO2Hb99%7g/dLCase
No.
8
cont’dWhat
is
going
on?45Case
No.
8
cont’d46If
the
picture
doesn’t
fit,
repeat
ABG!!pH7.45BP130/90
mmHgPCO231mmHgPulse95/minPO287mmHgRR20/minHCO322mmol/LVT350mlBE-2mmol/LMV7LSaO2Hb96%13
g/dLTechnical
error
was
presumed.Case
study No.
94767
yo
who
had
closed
reduction
of
leg
fx
withoutincident.Four
days
later
she
experienced
a
sudden
onset
of
severe
chestpain
and
SOB. Room
air
ABG
&
VS:pH7.36BP130/90
mmHgPCO233mmHgPulse100/minPO2HCO3BE55mmHg18mmol/L-5mmol/LRRMV25/min18LSaO288%Interpretation:
Compensated
metabolic
acidosis
withmoderate
hypoxemia.
Dx:
PECase
study No.
104876
yo
with
documented
chronic
hypercapnia
secondary
tosevere
COPD
has
been
in
ICU
for
3
days
while
being
tx
forpneumonia. She
had
been
stable
for
past
24
hours
and
wastransferred
to
general
floor. Pt
was
on
2L
oxygen
&
ABG
&VS:pHPCO27.4463mmHgBPPulse135/95
mmHg110/minPO2HCO352mmHg42mmol/LRR22/minSaO2BE +16
mmol/L86%.Interpretation:MV
10LChronic
ventilatory
failure
(resp.
acidosis)with
uncorrected
hypoxemiaCase
No.
10
cont’dShe
was
placed
on
3L and
monitored
for
nexthour.
Sheremained
alert,
oriented
and
comfortable. ABGwasrepeated:pH7.36BP140/100
mmHgPCO275mmHgPulse105/minPO2HCO3BE65mmHg42mmol/L+16
mmol/LRRMV24/min4.8LSaO292%.Pt’s
ventilatory
pattern
has
changed
to
more
rapid
andshallow
breathing. Although
still
acceptable
the
pH
andCO2are
trending
in
the
wrongdirection.
High-flowoxygen
may
be
better
for
this
pt
to
preventintubation49Take
Home
Message:50
Valuable
information
can
be
gained
from
anABG
as
to
the
patients
physiologic
condition
Remember
that
ABG
analysis
if
only
part
of
thepatientassessment.
Be
systematic
with
your
analysis,
start
with
ABC’s
as
alwaysand
look
for
hypoxia
(which
you
can
usual
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