ABG INTERPRETATION

Debbie Sander PAS-II

Objectives
 What’s an ABG?

 Understanding Acid/Base Relationship

 General approach to ABG Interpretation

 Clinical causes Abnormal ABG’s

 Case studies

 Take home
 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 from primary metabolic acid-base
abnormalities
What Is An ABG?
pH [H+]

PCO2 Partial pressure CO2

PO2 Partial pressure O2

HCO3 Bicarbonate

BE Base excess

SaO2 Oxygen Saturation

Acid/Base Relationship
 This relationship is critical for homeostasis

 Significant deviations from normal pH ranges are

poorly tolerated and may be life threatening

Achieved by Respiratory and Renal systems

Case Study No. 1
60 y/o male comes ER c/o SOB.
Tachypneic, tachycardic, diaphoretic and
Cyanotic. Dx acute resp. failure and ABG’s
Show PaCO2 well below nl, pH above nl,
PaO2 is very low. The blood gas document
Resp. failure due to primary O2 problem.
 Case Study No. 2
60 y/o male comes ER c/o SOB.
Tachypneic, tachycardic, diaphoretic and
Cyanotic. Dx acute resp. failure and ABG’s
Show PaCO2 very high, low pH and PaO2
is moderately low. The blood gas document
Resp. failure due to primarily ventilatory
insufficiency.
Buffers
There are two buffers that work in pairs

H2CO3 NaHCO3
Carbonic acid base bicarbonate

These buffers are linked to the respiratory and

renal compensatory system
Respiratory Component

 function of the lungs

 Carbonic acid H2CO3

 Approximately 98% normal metabolites are in the form

of CO2
CO2 + H2O  H2CO3
 excess CO2 exhaled by the lungs
 Metabolic Component
 Function of the kidneys

 base bicarbonate Na HCO3

 Process of kidneys excreting H+ into the urine and reabsorbing
HCO3- into the blood from the renal tubules
1) active exchange Na+ for H+ between the tubular
cells and glomerular filtrate
2) carbonic anhydrase is an enzyme that accelerates
hydration/dehydration CO2 in renal epithelial cells
Acid/Base Relationship

H2O + CO2  H2CO3  HCO3 + H+

Normal ABG values
pH 7.35 – 7.45

PCO2 35 – 45 mmHg

PO2 80 – 100 mmHg

HCO3 22 – 26 mmol/L

BE -2 - +2

SaO2 >95%
Acidosis Alkalosis

pH < 7.35 pH > 7.45

PCO2 > 45 PCO2 < 35

HCO3 < 22 HCO3 > 26

Respiratory Acidosis
 Think of CO2 as an acid

 failure of the lungs to exhale adequate CO2

 pH < 7.35
 PCO2 > 45

 CO2 + H2CO3   pH
Causes of Respiratory Acidosis

 emphysema

 drug overdose

 narcosis

 respiratory arrest

 airway obstruction
Metabolic Acidosis
 failure of kidney function

  blood HCO3 which results in  availability of renal

tubular HCO3 for H+ excretion

 pH < 7.35
 HCO3 < 22
Causes of Metabolic Acidosis
 renal failure

 diabetic ketoacidosis

 lactic acidosis

 excessive diarrhea

 cardiac arrest
 Respiratory Alkalosis
 too much CO2 exhaled (hyperventilation)

  PCO2, H2CO3 insufficiency =  pH

 pH > 7.45
 PCO2 < 35
 Causes of Respiratory Alkalosis
 hyperventilation

 panic d/o

 pain

 pregnancy

 acute anemia

 salicylate overdose
 Metabolic Alkalosis
  plasma bicarbonate

 pH > 7.45
 HCO3 > 26
 Causes of Metabolic Alkalosis

  loss acid from stomach or kidney

 hypokalemia

 excessive alkali intake

How to Analyze an ABG
1. PO2 NL = 80 – 100 mmHg

2. pH NL = 7.35 – 7.45
Acidotic <7.35
Alkalotic >7.45

3. PCO2 NL = 35 – 45 mmHg
Acidotic >45
Alkalotic <35

4. HCO3 NL = 22 – 26 mmol/L
Acidotic < 22
Alkalotic > 26
 Four-step ABG Interpretation
Step 1:

 Examine PaO2 & SaO2

 Determine oxygen status

 Low PaO2 (<80 mmHg) & SaO2 means hypoxia

 NL/elevated oxygen means adequate oxygenation

 Four-step ABG Interpretation
Step 2:

 pH acidosis <7.35
alkalosis >7.45
 Four-step ABG Interpretation
Step 3:

 study PaCO2 & HCO 3

 respiratory irregularity if PaCO2 abnl & HCO3 NL

 metabolic irregularity if HCO3 abnl & PaCO2 NL

Four-step ABG Interpretation
Step 4:

Determine if there is a compensatory mechanism working

to try to correct the pH.

ie: if have primary respiratory acidosis will have increased

PaCO2 and decreased pH. Compensation occurs when
the kidneys retain HCO3.
~ PaCO – pH Relationship
2

80 7.20

60 7.30

40 7.40

30 7.50

20 7.60
 ABG Interpretation
Acidosis

CO2 Change CO2 CO2 Change

c/w Normal opposes
Abnormality Abnormality

CO2 CO2 CO2 Metabolic Compensated

Metabolic
More Abnormal Expected Less Abnormal Metabolic
Acidosis Acidosis

Compensated Respiratory Mixed

Respiratory Acidosis Respiratory
Acidosis Metabolic
Acidosis
 ABG Interpretation
Alkalosis

CO2 Change CO2 CO2 Change

c/w Normal opposes
Abnormality Abnormality

CO2 CO2 CO2 Metabolic Compensated

More Abnormal Expected Less Abnormal Alkalosis Metabolic
Alkalosis

Compensated Respiratory Mixed

Respiratory Alkalosis Respiratory
Alkalosis Metabolic
Alkalosis
Respiratory Acidosis
pH 7.30

PaCO2 60

HCO3 26
Respiratory Alkalosis
pH 7.50

PaCO2 30

HCO3 22
Metabolic Acidosis

pH 7.30

PaCO2 40

HCO3 15
Metabolic Alkalosis

pH 7.50

PCO2 40

HCO3 30
 What are the compensations?
Respiratory acidosis  metabolic alkalosis

Respiratory alkalosis  metabolic acidosis

In respiratory conditions, therefore, the kidneys will

attempt to compensate and visa versa.

In chronic respiratory acidosis (COPD) the kidneys increase

the elimination of H+ and absorb more HCO3. The ABG will
Show NL pH, CO2 and HCO3.
Buffers kick in within minutes. Respiratory compensation
is rapid and starts within minutes and complete within 24
hours. Kidney compensation takes hours and up to 5 days.
 Mixed Acid-Base Abnormalities
Case Study No. 3:

56 yo   neurologic dz required ventilator support for several

weeks. She seemed most comfortable when hyperventilated
to PaCO2 28-30 mmHg. She required daily doses of lasix to
assure adequate urine output and received 40 mmol/L IV K+
each day. On 10th day of ICU her ABG on 24% oxygen & VS:
ABG Results
pH 7.62 BP 115/80 mmHg
PCO2 30 mmHg Pulse 88/min
PO2 85 mmHg RR 10/min
HCO3 30 mmol/L VT 1000ml
BE 10 mmol/L MV 10L
K+ 2.5 mmol/L

Interpretation: Acute alveolar hyperventilation

(resp. alkalosis) and metabolic alkalosis with corrected
hypoxemia.
 Case study No. 4
27 yo retarded  with insulin-dependent DM arrived at ER
from the institution where he lived. On room air ABG & VS:

pH 7.15 BP 180/110 mmHg

PCO2 22 mmHg Pulse 130/min
PO2 92 mmHg RR 40/min
HCO3 9 mmol/L VT 800ml
BE -30 mmol/L MV 32L

Interpretation: Partly compensated metabolic acidosis.

 Case study No. 5
74 yo  with hx chronic renal failure and chronic diuretic therapy
was admitted to ICU comatose and severely dehydrated. On
40% oxygen her ABG & VS:

pH 7.52 BP 130/90 mmHg

PCO2 55 mmHg Pulse 120/min
PO2 92 mmHg RR 25/min
HCO3 42 mmol/L VT 150ml
BE 17 mmol/L MV 3.75L

Interpretation: Partly compensated metabolic alkalosis with

corrected hypoxemia.
 Case study No. 6
43 yo  arrives in ER 20 minutes after a MVA in which he
injured his face on the dashboard. He is agitated, has mottled,
cold and clammy skin and has obvious partial airway obstruction.
An oxygen mask at 10 L is placed on his face. ABG & VS:

pH 7.10 BP 150/110 mmHg

PCO2 60 mmHg Pulse 150/min
PO2 125 mmHg RR 45/min
HCO3 18 mmol/L VT ? ml
BE -15 mmol/L MV ? L
.
Interpretation: Acute ventilatory failure (resp. acidosis) and
acute metabolic acidosis with corrected hypoxemia
 Case study No. 7
17 yo, 48 kg  with known insulin-dependent DM came to ER
with Kussmaul breathing and irregular pulse. Room air
ABG & VS:

pH 7.05 BP 140/90 mmHg

PCO2 12 mmHg Pulse 118/min
PO2 108 mmHg RR 40/min
HCO3 5 mmol/L VT 1200ml
BE -30 mmol/L MV 48L
Interpretation: Severe partly compensated metabolic
acidosis without hypoxemia.
 Case No. 7 cont’d
This patient is in diabetic ketoacidosis.
IV glucose and insulin were immediately administered. A
judgement was made that severe acidemia was adversely
affecting CV function and bicarb was elected to restore pH to
 7.20.
Bicarb administration calculation:
Base deficit X weight (kg)
4

30 X 48 = 360 mmol/L Admin 1/2 over 15 min &

4 repeat ABG
Case No. 7 cont’d
ABG result after bicarb:

pH 7.27 BP 130/80 mmHg

PCO2 25 mmHg Pulse 100/min
PO2 92 mmHg RR 22/min
HCO3 11 mmol/L VT 600ml
BE -14 mmol/L MV 13.2L
 Case study No. 8
47 yo  was in PACU for 3 hours s/p cholecystectomy. She
had been on 40% oxygen and ABG & VS:

pH 7.44 BP 130/90 mmHg

PCO2 32 mmHg Pulse 95/min, regular
PO2 121 mmHg RR 20/min
HCO3 22 mmol/L VT 350ml
BE -2 mmol/L MV 7L
SaO2 98%
Hb 13 g/dL
 Case No. 8 cont’d
Oxygen was changed to 2L N/C. 1/2 hour pt. ready to be D/C
to floor and ABG & VS:

pH 7.41 BP 130/90 mmHg

PCO2 10 mmHg Pulse 95/min, regular
PO2 148 mmHg RR 20/min
HCO3 6 mmol/L VT 350ml
BE -17 mmol/L MV 7L
SaO2 99%
Hb 7 g/dL
Case No. 8 cont’d
What is going on?
Case No. 8 cont’d
If the picture doesn’t fit, repeat ABG!!

pH 7. 45 BP 130/90 mmHg
PCO2 31 mmHg Pulse 95/min
PO2 87 mmHg RR 20/min
HCO3 22 mmol/L VT 350ml
BE -2 mmol/L MV 7L
SaO2 96%
Hb 13 g/dL
Technical error was presumed.
 Case study No. 9
67 yo  who had closed reduction of leg fx without incident.
Four days later she experienced a sudden onset of severe chest
pain and SOB. Room air ABG & VS:

pH 7.36 BP 130/90 mmHg

PCO2 33 mmHg Pulse 100/min
PO2 55 mmHg RR 25/min
HCO3 18 mmol/L
BE -5 mmol/L MV 18L
SaO2 88%

Interpretation: Compensated metabolic acidosis with

moderate hypoxemia. Dx: PE
 Case study No. 10
76 yo  with documented chronic hypercapnia secondary to
severe COPD has been in ICU for 3 days while being tx for
pneumonia. She had been stable for past 24 hours and was
transferred to general floor. Pt was on 2L oxygen & ABG &VS:

pH 7.44 BP 135/95 mmHg

PCO2 63 mmHg Pulse 110/min
PO2 52 mmHg RR 22/min
HCO3 42 mmol/L
BE +16 mmol/L MV 10L
SaO2 86%
.Interpretation: Chronic ventilatory failure (resp. acidosis)
with uncorrected hypoxemia
Case No. 10 cont’d
She was placed on 3L and monitored for next hour. She
remained alert, oriented and comfortable. ABG was
repeated:

pH 7.36 BP 140/100 mmHg

PCO2 75 mmHg Pulse 105/min
PO2 65 mmHg RR 24/min
HCO3 42 mmol/L
BE +16 mmol/L MV 4.8L
SaO2 92%
.
Pt’s ventilatory pattern has changed to more rapid and
shallow breathing. Although still acceptable the pH and
CO2 are trending in the wrong direction. High-flow
oxygen may be better for this pt to prevent intubation
Take Home 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 four steps.

A quick assessment of patient oxygenation can be achieved

with a pulse oximeter which measures SaO2.
It’s not magic understanding
ABG’s, it just takes a little
practice!
Any Questions?
References

1. Shapiro, Barry A., et al; Clinical Application of Blood

Gases; 1994

2. American Journal of Nursing1999;Aug99(8):34-6

3. Journal Post Anesthesia Nursing1990;Aug;5(4)264-72

4. Irvine, David;ABG Interpretation, A Rough and Dirty

Production
 Practice ABG’s
1. PaO2 90 SaO2 95 pH 7.48 PaCO2 32 HCO3 24
2. PaO2 60 SaO2 90 pH 7.32 PaCO2 48 HCO3 25
3. PaO2 95 SaO2 100 pH 7.30 PaCO2 40 HCO3 18
4. PaO2 87 SaO2 94 pH 7.38 PaCO2 48 HCO3 28
5. PaO2 94 SaO2 99 pH 7.49 PaCO2 40 HCO3 30
6. PaO2 62 SaO2 91 pH 7.35 PaCO2 48 HCO3 27
7. PaO2 93 SaO2 97 pH 7.45 PaCO2 47 HCO3 29
8. PaO2 95 SaO2 99 pH 7.31 PaCO2 38 HCO3 15
9. PaO2 65 SaO2 89 pH 7.30 PaCO2 50 HCO3 24
10. PaO2 110 SaO2 100 pH 7.48 PaCO2 40 HCO3 30
 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