Transcript ABG INTERPRETATION

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
Carbonic acid
NaHCO3
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
pH
< 7.35
Alkalosis
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
= 80 – 100 mmHg
1. PO2
NL
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
alkalosis
<7.35
>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
c/w
Abnormality
CO2
More Abnormal
CO2
Expected
CO2
Less Abnormal
Compensated
Respiratory
Acidosis
Respiratory
Acidosis
Mixed
Respiratory
Metabolic
Acidosis
CO2
Normal
CO2 Change
opposes
Abnormality
Metabolic
Compensated
Metabolic
Acidosis
Metabolic
Acidosis
ABG Interpretation
Alkalosis
CO2 Change
c/w
Abnormality
CO2
More Abnormal
CO2
Expected
CO2
Less Abnormal
Compensated
Respiratory
Alkalosis
Respiratory
Alkalosis
Mixed
Respiratory
Metabolic
Alkalosis
CO2
Normal
CO2 Change
opposes
Abnormality
Metabolic
Alkalosis
Compensated
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
PCO2
PO2
HCO3
BE
K+
7.62
30 mmHg
85 mmHg
30 mmol/L
10 mmol/L
2.5 mmol/L
BP
Pulse
RR
VT
MV
115/80 mmHg
88/min
10/min
1000ml
10L
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
PCO2
PO2
HCO3
BE
7.15
22 mmHg
92 mmHg
9 mmol/L
-30 mmol/L
Interpretation:
BP
Pulse
RR
VT
MV
180/110 mmHg
130/min
40/min
800ml
32L
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
PCO2
PO2
HCO3
BE
7.52
55 mmHg
92 mmHg
42 mmol/L
17 mmol/L
BP
Pulse
RR
VT
MV
130/90 mmHg
120/min
25/min
150ml
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
PCO2
PO2
HCO3
BE
7.05
12 mmHg
108 mmHg
5 mmol/L
-30 mmol/L
BP
Pulse
RR
VT
MV
140/90 mmHg
118/min
40/min
1200ml
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
4
Admin 1/2 over 15 min &
repeat ABG
Case No. 7 cont’d
ABG result after bicarb:
pH
PCO2
PO2
HCO3
BE
7.27
25 mmHg
92 mmHg
11 mmol/L
-14 mmol/L
BP
Pulse
RR
VT
MV
130/80 mmHg
100/min
22/min
600ml
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
PCO2
PO2
HCO3
BE
SaO2
Hb
7.44
32 mmHg
121 mmHg
22 mmol/L
-2 mmol/L
98%
13 g/dL
BP
Pulse
RR
VT
MV
130/90 mmHg
95/min, regular
20/min
350ml
7L
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
PCO2
PO2
HCO3
BE
SaO2
Hb
7.41
10 mmHg
148 mmHg
6 mmol/L
-17 mmol/L
99%
7 g/dL
BP
Pulse
RR
VT
MV
130/90 mmHg
95/min, regular
20/min
350ml
7L
Case No. 8 cont’d
What is going on?
Case No. 8 cont’d
If the picture doesn’t fit, repeat ABG!!
pH
PCO2
PO2
HCO3
BE
SaO2
Hb
7. 45
31 mmHg
87 mmHg
22 mmol/L
-2 mmol/L
96%
13 g/dL
BP
Pulse
RR
VT
MV
Technical error was presumed.
130/90 mmHg
95/min
20/min
350ml
7L
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
PCO2
PO2
HCO3
BE
SaO2
7.36
33 mmHg
55 mmHg
18 mmol/L
-5 mmol/L
88%
BP
130/90 mmHg
Pulse 100/min
RR
25/min
MV
18L
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
2. PaO2
3. PaO2
4. PaO2
5. PaO2
6. PaO2
7. PaO2
8. PaO2
9. PaO2
10. PaO2
90
60
95
87
94
62
93
95
65
110
SaO2 95
SaO2 90
SaO2 100
SaO2 94
SaO2 99
SaO2 91
SaO2 97
SaO2 99
SaO2 89
SaO2 100
pH 7.48
pH 7.32
pH 7.30
pH 7.38
pH 7.49
pH 7.35
pH 7.45
pH 7.31
pH 7.30
pH 7.48
PaCO2 32
PaCO2 48
PaCO2 40
PaCO2 48
PaCO2 40
PaCO2 48
PaCO2 47
PaCO2 38
PaCO2 50
PaCO2 40
HCO3
HCO3
HCO3
HCO3
HCO3
HCO3
HCO3
HCO3
HCO3
HCO3
24
25
18
28
30
27
29
15
24
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