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 document

Resp. 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 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

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 Interpretation

Step 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 Relationship

80 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. 4

27 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. 6

43 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’d

This 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