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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 - PowerPoint PPT Presentation
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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-baseabnormalities
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. 160 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. 260 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 PaO2
is moderately low. The blood gas documentResp. failure due to primarily ventilatoryinsufficiency.
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
Buffers
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 tubules1) active exchange Na+ for H+ between the tubular
cells and glomerular filtrate2) carbonic anhydrase is an enzyme that accelerates
hydration/dehydration CO2 in renal epithelial cells
H2O + CO2 H2CO3 HCO3 + H+
Acid/Base Relationship
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
PCO2 > 45
HCO3 < 22
pH > 7.45
PCO2 < 35
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 ABG1. PO2 NL = 80 – 100 mmHg
2. pH NL = 7.35 – 7.45Acidotic <7.35Alkalotic >7.45
3. PCO2 NL = 35 – 45 mmHgAcidotic >45Alkalotic <35
4. HCO3 NL = 22 – 26 mmol/LAcidotic < 22Alkalotic > 26
Four-step ABG InterpretationStep 1:
Examine PaO2 & SaO2
Determine oxygen status
Low PaO2 (<80 mmHg) & SaO2 means hypoxia
NL/elevated oxygen means adequate oxygenation
Step 2:
pH acidosis <7.35alkalosis >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 workingto try to correct the pH.
ie: if have primary respiratory acidosis will have increasedPaCO2 and decreased pH. Compensation occurs whenthe kidneys retain HCO3.
Four-step ABG Interpretation
~ PaCO2 – pH Relationship80 7.20
60 7.30
40 7.40
30 7.50
20 7.60
CompensatedRespiratory
Acidosis
CO2More Abnormal
RespiratoryAcidosis
CO2Expected
MixedRespiratoryMetabolicAcidosis
CO2Less Abnormal
CO2 Changec/w
Abnormality
MetabolicMetabolic Acidosis
CO2Normal
CompensatedMetabolicAcidosis
CO2 Changeopposes
Abnormality
Acidosis
ABG Interpretation
CompensatedRespiratoryAlkalosis
CO2More Abnormal
RespiratoryAlkalosis
CO2Expected
MixedRespiratoryMetabolicAlkalosis
CO2Less Abnormal
CO2 Changec/w
Abnormality
MetabolicAlkalosis
CO2Normal
CompensatedMetabolicAlkalosis
CO2 Changeopposes
Abnormality
Alkalosis
ABG Interpretation
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 willattempt to compensate and visa versa.
In chronic respiratory acidosis (COPD) the kidneys increasethe elimination of H+ and absorb more HCO3. The ABG willShow NL pH, CO2 and HCO3.
Buffers kick in within minutes. Respiratory compensationis rapid and starts within minutes and complete within 24 hours. Kidney compensation takes hours and up to 5 days.
Mixed Acid-Base AbnormalitiesCase Study No. 3:
56 yo neurologic dz required ventilator support for severalweeks. She seemed most comfortable when hyperventilatedto PaCO2 28-30 mmHg. She required daily doses of lasix toassure 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 mmHgPCO2 30 mmHg Pulse 88/minPO2 85 mmHg RR 10/minHCO3 30 mmol/L VT 1000mlBE 10 mmol/L MV 10LK+ 2.5 mmol/L
Interpretation: Acute alveolar hyperventilation (resp. alkalosis) and metabolic alkalosis with corrected hypoxemia.
Case study No. 427 yo retarded with insulin-dependent DM arrived at ERfrom the institution where he lived. On room air ABG & VS:
pH 7.15 BP 180/110 mmHgPCO2 22 mmHg Pulse 130/minPO2 92 mmHg RR 40/minHCO3 9 mmol/L VT 800mlBE -30 mmol/L MV 32L
Interpretation: Partly compensated metabolic acidosis.
Case study No. 574 yo with hx chronic renal failure and chronic diuretic therapywas admitted to ICU comatose and severely dehydrated. On40% oxygen her ABG & VS:
pH 7.52 BP 130/90 mmHgPCO2 55 mmHg Pulse 120/minPO2 92 mmHg RR 25/minHCO3 42 mmol/L VT 150mlBE 17 mmol/L MV 3.75L
Interpretation: Partly compensated metabolic alkalosis with corrected hypoxemia.
Case study No. 643 yo arrives in ER 20 minutes after a MVA in which heinjured 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 mmHgPCO2 60 mmHg Pulse 150/minPO2 125 mmHg RR 45/minHCO3 18 mmol/L VT ? mlBE -15 mmol/L MV ? L.Interpretation: Acute ventilatory failure (resp. acidosis) and
acute metabolic acidosis with corrected hypoxemia
Case study No. 717 yo, 48 kg with known insulin-dependent DM came to ERwith Kussmaul breathing and irregular pulse. Room airABG & VS:
pH 7.05 BP 140/90 mmHgPCO2 12 mmHg Pulse 118/minPO2 108 mmHg RR 40/minHCO3 5 mmol/L VT 1200mlBE -30 mmol/L MV 48L
Interpretation: Severe partly compensated metabolicacidosis without hypoxemia.
Case No. 7 cont’dThis patient is in diabetic ketoacidosis.IV glucose and insulin were immediately administered. 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)
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 mmHgPCO2 25 mmHg Pulse 100/minPO2 92 mmHg RR 22/minHCO3 11 mmol/L VT 600mlBE -14 mmol/L MV 13.2L
Case study No. 847 yo was in PACU for 3 hours s/p cholecystectomy. Shehad been on 40% oxygen and ABG & VS:
pH 7.44 BP 130/90 mmHgPCO2 32 mmHg Pulse 95/min, regularPO2 121 mmHg RR 20/minHCO3 22 mmol/L VT 350mlBE -2 mmol/L MV 7LSaO2 98%Hb 13 g/dL
Case No. 8 cont’dOxygen was changed to 2L N/C. 1/2 hour pt. ready to be D/Cto floor and ABG & VS:
pH 7.41 BP 130/90 mmHgPCO2 10 mmHg Pulse 95/min, regularPO2 148 mmHg RR 20/minHCO3 6 mmol/L VT 350mlBE -17 mmol/L MV 7LSaO2 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 mmHgPCO2 31 mmHg Pulse 95/minPO2 87 mmHg RR 20/minHCO3 22 mmol/L VT 350mlBE -2 mmol/L MV 7LSaO2 96% Hb 13 g/dLTechnical error was presumed.
Case study No. 967 yo who had closed reduction of leg fx without incident.Four days later she experienced a sudden onset of severe chestpain and SOB. Room air ABG & VS:
pH 7.36 BP 130/90 mmHgPCO2 33 mmHg Pulse 100/minPO2 55 mmHg RR 25/minHCO3 18 mmol/LBE -5 mmol/L MV 18LSaO2 88% Interpretation: Compensated metabolic acidosis withmoderate hypoxemia. Dx: PE
Case study No. 1076 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:
pH 7.44 BP 135/95 mmHgPCO2 63 mmHg Pulse 110/minPO2 52 mmHg RR 22/minHCO3 42 mmol/LBE +16 mmol/L MV 10LSaO2 86%. Interpretation: Chronic ventilatory failure (resp. acidosis)with uncorrected hypoxemia
Case No. 10 cont’dShe was placed on 3L and monitored for next hour. She remained alert, oriented and comfortable. ABG wasrepeated:
pH 7.36 BP 140/100 mmHgPCO2 75 mmHg Pulse 105/minPO2 65 mmHg RR 24/minHCO3 42 mmol/LBE +16 mmol/L MV 4.8LSaO2 92%. Pt’s ventilatory pattern has changed to more rapid andshallow breathing. Although still acceptable the pH andCO2 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 BloodGases; 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 DirtyProduction
Practice ABG’s1. PaO2 90 SaO2 95 pH 7.48 PaCO2 32 HCO3 242. PaO2 60 SaO2 90 pH 7.32 PaCO2 48 HCO3 253. PaO2 95 SaO2 100 pH 7.30 PaCO2 40 HCO3 184. PaO2 87 SaO2 94 pH 7.38 PaCO2 48 HCO3 285. PaO2 94 SaO2 99 pH 7.49 PaCO2 40 HCO3 306. PaO2 62 SaO2 91 pH 7.35 PaCO2 48 HCO3 277. PaO2 93 SaO2 97 pH 7.45 PaCO2 47 HCO3 298. PaO2 95 SaO2 99 pH 7.31 PaCO2 38 HCO3 159. PaO2 65 SaO2 89 pH 7.30 PaCO2 50 HCO3 2410. PaO2 110 SaO2 100 pH 7.48 PaCO2 40 HCO3 30
Answers to Practice ABG’s
1. Respiratory alkalosis2. Respiratory acidosis3. Metabolic acidosis4. Compensated Respiratory acidosis5. Metabolic alkalosis6. Compensated Respiratory acidosis7. Compensated Metabolic alkalosis8. Metabolic acidosis9. Respiratory acidosis10. Metabolic alkalosis