Acid base (A.B.G)

How I interpret an ABG?
Vijish Venugopal

Disclosures
• Interactive session. Pen and paper please with calc.
• No intention to talk on physiology or management of acid base
disorders

What is an ABG ?
Arterial Blood Gas
Drawn from artery- radial, brachial, femoral
It is an invasive procedure.
Caution must be taken with patient on anticoagulants.
Helps differentiate oxygen deficiencies from primary
ventilatory deficiencies and primary metabolic acid-base
abnormalities

What Is In An ABG?
pH [H+
]
PCO2 Partial Pressure CO2
PO2 Partial Pressure O2
HCO3 Bicarbonate
BE Base Excess
SaO2 Oxygen Saturation

Normal Arterial Blood Gas Values*
pH 7.35-7.45
PaCO2 35-45 mm Hg
PaO2 70-100 mm Hg**
SaO2 93-98%
HCO3
-
22-26 mEq/L
%MetHb <2.0%
%COHb <3.0%
Base excess -2.0 to 2.0 mEq/L
CaO2 16-22 ml O2/dl
•* At sea level, breathing ambient air
•** Age-dependent

•Acid base status
•Oxygenation
–Dissolved O2 (pO2)
–Saturation of hemoglobin
•CO2 elimination
Information Obtained from an ABG:

•Assess the ventilatory status,
oxygenation and acid base status
•Assess the response to an intervention
Indications:

•Pulse oximetry uses light absorption at two
wavelengths to determine hemoglobin
saturation.
•Pulse oximetry is non-invasive and provides
immediate and continuous data.
ABG v/s Pulse oximetry
BEER LAMBERT LAW

•Pulse oximetry does not assess ventilation
(pCO2) or acid base status.
•Pulse oximetry becomes unreliable when
saturations fall below 70%.
•Technical sources of error (ambient or
fluorescent light, hypoperfusion, nail polish,
skin pigmentation)
Why an ABG instead of Pulse
oximetry?

•The radial artery is superficial, has
collaterals and is easily compressed. It
should almost always be the first choice.
•Other arteries (femoral, dorsalis pedis,
brachial) can be used in emergencies.
Which Artery to Choose?

•Make sure you and the patient are
comfortable.
•Assess the patency of the radial and
ulnar arteries.
Preparing to perform the Procedure

•Type of syringe
–Plastic vs. glass
•Use of heparin
•Air bubbles
•Specimen handling and transport
Collection Problems:

•Glass-
–Impermeable to gases
–Expensive and impractical
•Plastic-
–Somewhat permeable to gases
–Disposable and inexpensive
Type of Syringe

•Liquid
–Dilutional effect if <2-3 ml of blood
collected
•Preloaded dry heparin powder
–Eliminates dilution problem
–Mixing becomes more important
–May alter sodium or potassium levels
Heparin

•Gas equilibration between ambient air
(pO2 ~ 150, pCO2~0) and arterial blood.
•pO2 will begin to rise, pCO2 will fall
•Effect is a function of duration of
exposure and surface area of air bubble.
Air bubbles

•After specimen collected and air bubble
removed, gently mix and invert syringe.
•Because the WBC s are metabolically active,
they will consume oxygen.
•Plastic syringes are gas permeable.
•Key: Minimize time from sample acquisition
to analysis.
Transport

•Placing the AGB on ice may help
minimize changes, depending on the
type of syringe, pO2 and white blood cell
count.
•Its probably not as important if the
specimen is delivered immediately.
Transport

•Put on gloves
•Prepare the site
–Drape the bed
–Cleanse the radial area with a alcohol
•Position the wrist (hyper-extended, using a
rolled up towel if necessary)
•Palpate the arterial pulse and visualize the
course of the artery.
Performing the Procedure:

•If you are going to use local anesthetic,
infiltrate the skin with 2% xylocaine.
•Open the ABG kit
•Line the needle up with the artery, bevel
side up.
•Enter the artery and allow the syringe to fill
spontaneously.

•Withdraw the needle and hold pressure
on the site.
•Protect needle
•Remove any air bubbles
•Gently mix the specimen by rolling it
between your palms
•Place the specimen on ice and transport
to lab immediately.

9 Sequential Rules:
• Rule #1
– Must know the pH; pH determines whether the
primary disorder is an acidosis or an alkalosis
• Rule #2
– Must know the PaO2, PaCO2 and serum HCO3
-
• Rule #3
– Must be able to establish that the available data
(pH, PaCO2, and HCO3
-
) are consistent

PaO2
• Depends on FiO2.(usually 4-5 times)
• Depends on the barometric pressure and age
• PaO2age adjusted = 102- (age in yrs/3)
• Calculate PAO2- PaO2
• PAO2
normal A–a gradient is less than [age in years]/4 + 4
For every decade a person has lived, their A–a gradient is
expected to increase by 1 mmHg

Are the data consistent?
• The Henderson Equation:
[ ] −
+
×=
3
2
24
HCO
PaCO
H

Convert pH to [H+
] :
• Subtract the last two digits of a pH from 80
example: calculated [H+
] of 24
pH of (80-56)~7.56
example: calculated [H+
] of 53
pH of (80-27)~7.27

Relationship between [H+
] & pH

Disorders
• 1. Look at pH.
Down: Acidosis
Up: Alkalosis
• 2. Look at HC03 and PCO2
HC03 : Metabolic disorder
PCO2 :Respiratory Disorder
• 3. Look for compensatory changes

Simple Acid-Base Disorders:
Type of Disorder pH PaCO2 [HCO3]
Metabolic Acidosis ↓ ↓
Metabolic Alkalosis
Acute Respiratory Acidosis
Chronic Respiratory Acidosis
Acute Respiratory Alkalosis
Chronic Respiratory Alkalosis

Metabolic Acidosis ↓ ↓ ↓
Metabolic Alkalosis

Metabolic Acidosis
Metabolic Alkalosis ↑ ↑

Metabolic Acidosis
Metabolic Alkalosis ↑ ↑ ↑
Metabolic Acidosis

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Acidosis ↓ ↑
Chronic Respiratory Acidosis ↓ ↑

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Acidosis ↓ ↑ ↑
Chronic Respiratory Acidosis ↓ ↑ ↑↑

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Alkalosis ↑ ↓
Chronic Respiratory Alkalosis ↑ ↓

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Alkalosis ↑ ↓ ↓
Chronic Respiratory Alkalosis ↑ ↓ ↓↓

Metabolic Acidosis ↓ ↓ ↓
Acute Respiratory Acidosis ↓ ↑ ↑
Chronic Respiratory Acidosis ↓ ↑ ↑↑
Acute Respiratory Alkalosis ↑ ↓ ↓
Chronic Respiratory Alkalosis ↑ ↓ ↓↓

• The compensatory variable always changes
in the SAME DIRECTION as the primarily
deranged variable
• Compensation is always more pronounced
in CHRONIC RESPIRATORY disorders
than in acute respiratory disorders

Rule #4: Obtain relevant clinical history!
a. Metabolic acidosis:
DM/renal failure/muscle overactivity/ hypotension/
diarrhoea/ diamox, metformin/ alcoholism.
b. Metabolic alkalosis:
Vomiting, RT aspiration/hypovolemia, diuretic/
NaHCO3 administration/ hypokalemia (paraletic ileus)
c. Respiratory acidosis:
COPD, muscular weakness, post-op.
d. Respiratory alkalosis:
Tachypnea, hepatic coma, sepsis

Who has better lungs? Why?
A B
PO2 70 140
PCO2 36 36
PH 7.44 7.44
HCO3 24 24

Who has better lungs? Why?
A B Never interpret
without adequate
clinical information
!!!
FiO2 0.21 1.00
PO2 70 140
PCO2 36 36
PH 7.44 7.44
HCO3 24 24

Patient on room air. What is wrong?
How severe is it? What will you do?
FiO2 0.21
PO2 48
PCO2 40
pH 7.40
HCO3 24
Na -
Cl -

Patient on room air. What is wrong?
How severe is it? What will you do?
FiO2 0.21 Hypoxemia
Increase FiO2
PO2 48
PCO2 40
pH 7.40
HCO3 24
Na -
Cl -

Patient on Ventilator. What is
wrong? How are the lungs? Can the
patient be weaned? What will you
do?
FiO2 0.80
PO2 220
PCO2 34.6
pH 7.48
HCO3 26
Na -
Cl -

Patient on Ventilator. What is
wrong? How are the lungs? Can the
patient be weaned? What will you
do?
FiO2 0.80
Expected PaO2=5x 80= 400.
PaO2/fiO2(old)=PaO2/fiO2(new)
PaO2(new)=220x .21/.80 =57.8
Therefore patient would be hypoxic on room air.
Not advisable to wean
Reduce fiO2 to 36-40%to get PaO2 of 100
PO2 220
PCO2 34.6
pH 7.48
HCO3 26
Na -
Cl -

Patient on ventilator FiO2 =40% TV=
500 RR=12. What is wrong? What will
you do?
FiO2 0.40
PO2 128
PCO2 60
pH 7.21
HCO3 24
Na -
Cl -

you do?
FiO2 0.40
PCO2 high, therefore increase
minute ventilation (RR x TV)
RR x PCO2(old)= RR x PCO2(new)
12 x 60 = RR x 40
RR = 18 (increase RR to 18)
PO2 128
PCO2 60
pH 7.21
HCO3 24
Na -
Cl -

you do?
FiO2 0.70
PO2 180
PCO2 28
pH 7.51
HCO3 22.4

you do?
FiO2 0.70
PCO2 is low therefore RR
needs to be reduced
RR x PCO2 = RR x PCO2
RR x 40 = 24 x 28
RR = 16.8 (17)
PO2 180
PCO2 28
pH 7.51
HCO3 22.4

Patient chronic smoker comes to OPD
for ABG. What is wrong? What will
you do?
FiO2 0.21
PO2 46
PCO2 62
pH 7.38
HCO3 35

Patient chronic smoker comes to OPD
for ABG. What is wrong? What will
you do?
FiO2 0.21 COPD
PH OK therefore don’t
worry about PCO2
Careful with giving
supplemental oxygen
TREAT THE PATIENT NOT THE
ABG REPORT.
PO2 46
PCO2 62
pH 7.38
HCO3 35

Patient on ventilator FiO2
=60% What is wrong? What will
you do?
FiO2 0.60
PO2 300
PCO2 20
pH 7.40
HCO3 18

Patient on ventilator FiO2 =60%
What is wrong? What will you do?
FiO2 0.60 Check compatibility
H x HCO3/PCO2 = 24
40 x 18/20 = 36 !!!
Cannot comment on this
ABG. DON’T TREAT BUT
RECHECK ABG.
PO2 300
PCO2 20
pH 7.40
HCO3 18

9 Sequential Rules:
• Rule #5:
– must know if compensation is appropriate
– compensation never overshoots
• Must have known “rules of thumb” to
interpret appropriateness of compensation

Rules of Compensation:
• Metabolic Acidosis
– PaCO2 should fall by 1 to 1.5 mm Hg x the fall in
plasma [HCO3]
– Winters formula
• PaCO2 = 1.5 x HCO3 + 8 (+/-2)
• Metabolic Alkalosis
– PaCO2 should rise by .5 to 1 mm Hg x the rise in
plasma [HCO3]
– Modified formula
• PaCO2 = 0.7 x HCO3 + 20

• Acute Respiratory Acidosis
– Plasma [HCO3] should rise by ~1mmole/l for
each 10 mm Hg increment in PaCO2
• Chronic Respiratory Acidosis
– Plasma [HCO3] should rise by ~4mmoles/l for

• Acute Respiratory Alkalosis
– Plasma [HCO3] should fall by ~2 mmole/l for
each 10 mm Hg decrement in PaCO2, usually
not to less than 18 mmoles/l
• Chronic Respiratory Alkalosis
– Plasma [HCO3] should fall by ~5 mmole/l for

Practice ABG’s
1. PaO2 90 SaO2 95 pH 7.48 PaCO2 32 HCO3 24

Answers to Practice ABG’s
1. Respiratory alkalosis
2. Respiratory acidosis
3. Metabolic acidosis
4. Compensated Respiratory acidosis
5. Metabolic alkalosis
6. Compensated Respiratory acidosis
7. Compensated Metabolic alkalosis
8. Metabolic acidosis
9. Respiratory acidosis
10. Metabolic alkalosis

It’s not magic understanding
ABG’s, it just takes a little
practice!

Case #1:
• A 4 year old with chronic renal failure
presents to the ER with history of
increasing azotemia, weakness, and
lethargy. Exam reveals the patient to be
modestly hypertensive, and tachypneic.
Labs reveal BUN=100, and Creatinine=8.
• How can we tell if an acid-base disorder is
present?

Case #1:
• Steps 1&2: must know pH, PaCO2, HCO3
• pH=7.33, PaCO2=24, and HCO3=12
• Step 3: are the available data consistent?
[ ] −
+
×=
3
2
24
HCO
PaCO
H

Case #1:
• [H+]=48, equates to pH~7.32; data are thus
consistent
• What is the primary disorder?
• “_________Acidosis”
• Which variable (PaCO2, HCO3) is deranged
in a direction consistent with acidosis?
• Primary disorder is “Metabolic Acidosis”

Is compensation appropriate?
• HCO3 is decreased by 12 mmoles/l
• PaCO2 should decrease by 1 to 1.5 times the
fall in HCO3; expect PaCO2 to decrease by
12-18 mm Hg or be between 22-28 mm Hg
• Since PaCO2 is 24 mm Hg, compensation is
appropriate, and the data are consistent with
a simple metabolic acidosis with respiratory
compensation

9 Sequential Rules:
• Rule #6:
– If the data are consistent with a simple disorder,
it does not guarantee that a simple disorder
exists; need to re examine the patient’s
history
• Rule #7:
– When compensatory responses do not lie within
the accepted range, by definition a combined
disorder exists.

Case #2:
• A 15 year old female is brought to the ER in
an obtunded state. Per her family, patient
history is notable for progressive
weakness/“malingering” over two months.
A recent “complete physical” demonstrated
decreased DTRs symmetrically, without
other abnormal findings. Exam shows
shallow, tachypneic respiratory effort.

Case #2: Steps 1, 2, and 3
• What baseline information is required?
• PaCO2=40 mm Hg, HCO3=7, pH=6.88
• Are the data internally consistent?
[ ] −
+
×=
3
2
24
HCO
PaCO
H

Case #2:
• [H+
]~140, which equates to a pH~6.85, so
data are internally consistent
• What is the primary disturbance?
• “___________ Acidosis”
• Which variable is deranged in a direction
which is consistent with acidosis?
• PaCO2 WNL, ergo, “Metabolic Acidosis”

Is compensation appropriate?
– PaCO2 should fall by 1 to 1.5 mm Hg x the fall
in plasma [HCO3]
• HCO3 decreased by 17, so we expect PaCO2
to be decreased by 17-26
• PaCO2 WNL; since PaCO2 inappropriately
high, there is a combined metabolic acidosis
and respiratory acidosis

Case #3:
• A 16 year old male with sickle cell anemia,
hemochromatosis, & subsequent cirrhosis,
presents with a several day history of
emesis. At presentation to the ER, he is
hypotensive, orthostatic, and confused.
• What acid-base disorders might be
anticipated based on the above information?

Case #3:
• 16 yo male with sickle cell anemia, hemo-
chromatosis, & subsequent cirrhosis, and
several days of emesis. In the ER, he is
hypotensive, orthostatic, and confused.
• Emesis-loss of H+
(HCl)-metabolic alkalosis
• Orthostatic hypotension-?lactic acidosis
• SCD-decreased O2 delivery-?lactic acidosis
• Cirrhosis-decreased lactate metabolism

Case #3:
• What baseline information is available?
• pH=7.55, PaCO2=66
• ‘lytes: Na+
=166, K+
=3.0, Cl-
=90, HCO3=56
[ ] −
+
×=
3
2
24
HCO
PaCO
H

Case #3:
• [H+]~28, equates to pH~7.55; consistent
• What is the primary abnormality?
• “_________ Alkalosis”
• PaCO2↑ed, HCO3 ↑ed, therefore…….
• “Metabolic Alkalosis” presumed due to
emesis
• Is compensation appropriate?

Case #3:
• Metabolic Alkalosis
– PaCO2 should rise by .5 to 1 mm Hg x the rise
in plasma [HCO3]
• HCO3 ↑ed by 32; PaCO2 should ↑ by 16-32
• PaCO2 ↑ed by 26, so compensation appears
appropriate
• What about multiple risk factors for lactic
acidosis?

Case #3:
• Could there be a concealed lactic acidosis?
• What is the anion gap?
• Na+
- (Cl-
+ HCO3), normally 12-14
• Anion gap here is 166 - (90 + 56) = 20
∀↑ed anion gap implies metabolic acidosis
• Combined metabolic alkalosis & metabolic
acidosis therefore present

9 Sequential Rules:
• Rule #8: Always calculate the anion gap and Delta
gap
• Often it is the only sign of an occult metabolic
acidosis
– acidotic patients partially treated with HCO3
– acidotic patients with emesis
• May be the only sign of metabolic acidosis
“concealed” by concomitant acid-base disorders

Causes of Anion Gap Acidosis:
• Endogenous acidosis
– Uremia (uncleared organic acids)
– Ketoacidosis, Lactic acidosis (increased organic
acid production), Rhabdomyolosis
• Exogenous acidosis
– ingestions: salicylate, iron; paraldehyde use
• Other Ingestions:
– Methanol toxicity, Ethylene Glycol toxicity

Anion Gap:
• Based on the concept of electroneutrality; the
assumption that the sum of all available cations=
the sum of all available anions. Restated as:
• Na+
+ Unmeasured Cations (UC) = Cl-
+ HCO3 +
Unmeasure Anions (UA); conventionally restated:
• Na+
-(Cl-
+HCO3)=UA-UC=Anion Gap=12 to 14

Anion Gap:
• Na+
-(Cl-
+HCO3)=UA-UC
• Serum albumin contributes ~1/2 of the total
anion equivalency of the “UA” pool.
Assuming normal electrolytes, a 1gm/dl
decline in serum albumin decreases the
anion gap factitiously by 3 mEq/L. this is an
important correction factor in settings of
chronic illness or malnourished patients

Case #4:
• A 3 year old is brought to the ER at ~3am,
stuporous and tachypneic. History is
remarkable for his parents having cleaned
out their medicine cabinet earlier that day.
An ABG and electrolytes have been
accidentally drawn by the nurse.

Case #4:
• Available data: pH=7.53, PaCO2=12;
Na+
=140, K+
=3.0, Cl-
=106, HCO3=10
[ ] −
+
×=
3
2
24
HCO
PaCO
H

Case #4:
• [H+]~29, so pH~7.51; data consistent
• “__________ Alkalosis”
in a direction consistent with alkalosis?
∀↓ed PaCO2, ↓ed HCO3; so “Respiratory
Alkalosis”

Case #4:
• Acute respiratory alkalosis
– Plasma [HCO3] should fall by ~1-3 mmole/l for
• PaCO2 ↓ed by ~30 mm Hg; HCO3 should
fall by 3-9 mmole/l; HCO3 ↓ is too great, so
superimposed metabolic acidosis

Case #4:
• 140 - (106 + 10) = 24; elevated anion gap
consistent with metabolic acidosis
• What is the differential diagnosis?
• Combined (true) respiratory alkalosis and
metabolic acidosis seen in sepsis, or
salicylate intoxication

Case #5:
• A 5 year old with Bartter’s Syndrome is
brought to clinic, where she collapses. She
has recently been febrile, but history is
otherwise unremarkable. An ABG and
serum electrolytes are obtained: pH=6.9,
PaCO2=81; Na+
=142, K+
=2.8, Cl-
=87,
HCO3=16

Case #5:
• Are the data consistent?
• [H+
]=122, pH~6.9; data are consistent
[ ] −
+
×=
3
2
24
HCO
PaCO
H

Case #5:
• “_________ Acidosis”
in a direction consistent with acidosis?
• Both; pick most abnormal value--
• “Respiratory Acidosis”

Case #5:
• Acute Respiratory Acidosis
– Plasma [HCO3] should rise by ~1mmole/l for
• Since HCO3 is inappropriately depressed,
compensation is not appropriate, and there
is a concomitant metabolic acidosis as well
• AG=39, confirms metabolic acidosis

Case #5:
• Combined Respiratory Acidosis and
Metabolic Acidosis; are there other
disorders present?
• What about the dx of Bartter’s Syndrome?
• Bartter’s Syndrome characterized by
hypokalemic metabolic alkalosis
• Does this patient have a concealed
metabolic alkalosis?

Case #5:
• Anion gap is 39, or 25-27 greater than normal
• Typically, increases in anion gap correlate with
decreases in HCO3
• Gap gap ratio : deltaAG/ delta HCO3
• Gap gap < 1: conc NAG acidosis
• Gap gap >2 : conc metab alkalosis
• Here gap gap is 27/8 = 3.2.

Case #5:
• Therefore, gap gap >1, consistent with
expected metabolic alkalosis. This
metabolic alkalosis was “concealed” by the
supervening profound metabolic and
respiratory acidoses associated with her
arrest event.
• Final diagnosis: Metabolic alkalosis,
metabolic acidosis, & respiratory acidosis

9Sequential Rules; Rule #9
• Rule #9: Mixed Acid-Base Disorders
• Coexistent metabolic acidosis and
metabolic alkalosis may occur. Always
check the change in the anion gap vs.
decrement in bicarbonate to rule out a
concealed metabolic disorder.

Case #6:
• A 3 year old toddler is brought to the ER at
3 am after being found unarousable on his
bedroom floor, with urinary incontinence.
EMS monitoring at the scene revealed sinus
bradycardia. One amp of D50W and 5 mg of
naloxone were given IV without response.
Vital signs are stable; respiratory effort is
regular, but tachypneic. He is acyanotic.

Case #6:
• Initial lab studies (lytes, ABG & urine tox
screen) are sent. Initial dextrostick is >800.
• Initial available data are:
• Na+
=154, K=5.6, Cl=106, HCO3=5, BUN=6
creatinine=1.7, glucose=804, PO4=12.3, Ca+
+
=9.8, NH4=160, serum osms=517
• pH=6.80, PaCO2=33, PaO2=298

Case #6:
• ________ Acidosis
• No; PaCO2 level is inappropriately high
• Are other disorders present?
• Respiratory acidosis (due to evolving coma)

Case #6:
• What is our differential thus far?
– Anion gap vs. non-anion gap metabolic acidosis
– DKA, lactic acidosis, renal failure, ingestion
• The urine tox screen comes back negative
• The patient’s IV falls out. He then has a
seizure, is incontinent of urine, and fills the
specimen bag you placed on ER arrival.

Case #6:
• What is the calculated serum osmolality,
and does an osmolal gap exist?
• 2(Na) + BUN/2.8 + Glucose/18
– Calculated=355, Measured=517
• What is the most likely diagnosis?
• How can this be confirmed definitively?
– Review of urinalysis
– Serum ethylene glycol level

Case #6:
Anion gap metabolic acidosis
Osmolal gap
Methanol, ethylene glycol
ethyl alcohol, isopropyl alcohol

Take Home (to work) Message:
Valuable information can be gained from an
ABG as to the patients physiologic condition
Remember that ABG analysis if only part of the patient
assessment.
Be systematic with your analysis, start with ABC’s as always
and look for hypoxia (which you can usually treat quickly),
then follow the basic steps.
A quick assessment of patient oxygenation can be achieved
with a pulse oximeter which measures SaO2.

Acid base (A.B.G)

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