abg_interperetation ABG interpretation, BGA, Blood gas analysis.ppt
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Sep 18, 2024
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About This Presentation
ABG interpretation, BGA, Blood gas analysis
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Language: en
Added: Sep 18, 2024
Slides: 55 pages
Slide Content
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
+
]
PCO
2
Partial pressure CO
2
PO
2 Partial pressure O
2
HCO
3
Bicarbonate
BE Base excess
SaO
2
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 PaCO
2
well below nl, pH above nl,
PaO
2 is very low. The blood gas document
Resp. failure due to primary O
2
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 PaCO
2 very high, low pH and PaO
2
is moderately low. The blood gas document
Resp. failure due to primarily ventilatory
insufficiency.
There are two buffers that work in pairs
H
2
CO
3
NaHCO
3
Carbonic acid base bicarbonate
These buffers are linked to the respiratory and
renal compensatory system
Buffers
Respiratory Component
function of the lungs
Carbonic acid H
2
CO
3
Approximately 98% normal metabolites are in the form
of CO
2
CO
2
+ H
2
O H
2
CO
3
excess CO
2
exhaled by the lungs
Metabolic Component
Function of the kidneys
base bicarbonate Na HCO
3
Process of kidneys excreting H
+
into the urine and reabsorbing
HCO
3
-
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 CO
2
in renal epithelial cells
H
2
O + CO
2
H
2
CO
3
HCO
3
+ H
+
Acid/Base Relationship
Respiratory Acidosis
Think of CO
2
as an acid
failure of the lungs to exhale adequate CO
2
pH < 7.35
PCO
2
> 45
CO
2
+ H
2
CO
3
pH
Causes of Respiratory Acidosis
emphysema
drug overdose
narcosis
respiratory arrest
airway obstruction
Metabolic Acidosis
failure of kidney function
blood HCO
3 which results in availability of renal
tubular HCO
3
for H
+
excretion
pH < 7.35
HCO
3
< 22
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
PaCO
2 and decreased pH. Compensation occurs when
the kidneys retain HCO
3
.
Four-step ABG Interpretation
Compensated
Respiratory
Acidosis
CO2
More Abnormal
Respiratory
Acidosis
CO2
Expected
Mixed
Respiratory
Metabolic
Acidosis
CO2
Less Abnormal
CO2 Change
c/w
Abnormality
Metabolic
Metabolic
Acidosis
CO2
Normal
Compensated
Metabolic
Acidosis
CO2 Change
opposes
Abnormality
Acidosis
ABG Interpretation
Compensated
Respiratory
Alkalosis
CO2
More Abnormal
Respiratory
Alkalosis
CO2
Expected
Mixed
Respiratory
Metabolic
Alkalosis
CO2
Less Abnormal
CO2 Change
c/w
Abnormality
Metabolic
Alkalosis
CO2
Normal
Compensated
Metabolic
Alkalosis
CO2 Change
opposes
Abnormality
Alkalosis
ABG Interpretation
Respiratory Acidosis
pH7.30
PaCO
2
60
HCO
3
26
Respiratory Alkalosis
pH7.50
PaCO
2 30
HCO
3 22
Metabolic Acidosis
pH7.30
PaCO
2 40
HCO
3
15
Metabolic Alkalosis
pH7.50
PCO
2 40
HCO
3 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 HCO
3. The ABG will
Show NL pH, CO
2
and HCO
3.
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 PaCO
2
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
pH7.62 BP115/80 mmHg
PCO
230 mmHg Pulse88/min
PO
2
85 mmHg RR10/min
HCO
3
30 mmol/L VT1000ml
BE10 mmol/L MV10L
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:
pH7.15 BP180/110 mmHg
PCO
2
22 mmHg Pulse130/min
PO
2
92 mmHg RR40/min
HCO
3
9 mmol/L VT800ml
BE-30 mmol/L MV32L
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:
pH7.52 BP130/90 mmHg
PCO
255 mmHg Pulse120/min
PO
2
92 mmHg RR25/min
HCO
3
42 mmol/L VT150ml
BE17 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:
pH7.10 BP150/110 mmHg
PCO
2
60 mmHg Pulse150/min
PO
2
125 mmHg RR45/min
HCO
3
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:
pH7.05 BP140/90 mmHg
PCO
212 mmHg Pulse118/min
PO
2
108 mmHg RR40/min
HCO
3
5 mmol/L VT1200ml
BE-30 mmol/L MV48L
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/LAdmin 1/2 over 15 min &
4 repeat ABG
Case No. 7 cont’d
ABG result after bicarb:
pH7.27 BP130/80 mmHg
PCO
2
25 mmHg Pulse100/min
PO
2
92 mmHg RR22/min
HCO
3
11 mmol/L VT600ml
BE-14 mmol/L MV13.2L
Case study No. 8
47 yo was in PACU for 3 hours s/p cholecystectomy. She
had been on 40% oxygen and ABG & VS:
pH7.44 BP130/90 mmHg
PCO
232 mmHg Pulse95/min, regular
PO
2
121 mmHg RR20/min
HCO
3
22 mmol/L VT350ml
BE-2 mmol/L MV7L
SaO
298%
Hb13 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:
pH7.41 BP130/90 mmHg
PCO
210 mmHg Pulse95/min, regular
PO
2
148 mmHg RR20/min
HCO
3
6 mmol/L VT350ml
BE-17 mmol/L MV7L
SaO
299%
Hb7 g/dL
Case No. 8 cont’d
What is going on?
Case No. 8 cont’d
If the picture doesn’t fit, repeat ABG!!
pH7. 45 BP130/90 mmHg
PCO
2
31 mmHg Pulse95/min
PO
2
87 mmHg RR20/min
HCO
3
22 mmol/L VT350ml
BE-2 mmol/L MV7L
SaO
2
96%
Hb13 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:
pH7.36 BP130/90 mmHg
PCO
233 mmHg Pulse100/min
PO
2
55 mmHg RR25/min
HCO
3
18 mmol/L
BE-5 mmol/L MV18L
SaO
2
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:
pH7.44 BP135/95 mmHg
PCO
263 mmHg Pulse110/min
PO
2
52 mmHg RR22/min
HCO
3
42 mmol/L
BE+16 mmol/L MV10L
SaO
2
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:
pH7.36 BP140/100 mmHg
PCO
275 mmHg Pulse105/min
PO
2
65 mmHg RR24/min
HCO
3
42 mmol/L
BE+16 mmol/L MV4.8L
SaO
2
92%
. Pt’s ventilatory pattern has changed to more rapid and
shallow breathing. Although still acceptable the pH and
CO
2
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 SaO
2.
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