ABG INTERPRETATION

Debbie Sander PAS-II

Objectives
Whats an ABG? Understanding Acid/Base Relationship General approach to ABG Interpretation Clinical causes Abnormal ABGs 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 ABGs 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 ABGs 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 PCO2 PO2 HCO3 BE SaO2 7.35 7.45 35 45 mmHg 80 100 mmHg 22 26 mmol/L -2 - +2 >95%

Acidosis
pH < 7.35

Alkalosis
pH > 7.45

PCO2 > 45 HCO3 < 22

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 ABG

1. PO2
2. pH

NL

= 80 100 mmHg

NL = 7.35 7.45 Acidotic <7.35 Alkalotic >7.45 NL = 35 45 mmHg Acidotic >45 Alkalotic <35 NL = 22 26 mmol/L Acidotic < 22 Alkalotic > 26

3. PCO2

4. HCO3

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 60 40 30 20

7.20 7.30 7.40 7.50 7.60

ABG Interpretation
Acidosis CO2 Change c/w Abnormality CO2 Normal CO2 Change opposes Abnormality

CO2 More Abnormal

CO2 Expected

CO2 Less Abnormal

Metabolic

Metabolic

Acidosis

Compensated Metabolic Acidosis

Compensated Respiratory Acidosis

Respiratory Acidosis

Mixed Respiratory Metabolic Acidosis

ABG Interpretation
Alkalosis
CO2 Change c/w Abnormality CO2 Normal CO2 Change opposes Abnormality

CO2 More Abnormal

CO2 Expected

CO2 Less Abnormal

Metabolic Alkalosis

Compensated Metabolic Alkalosis

Compensated Respiratory Alkalosis

Respiratory Alkalosis

Mixed Respiratory Metabolic Alkalosis

Respiratory Acidosis
pH 7.30

PaCO2
HCO3

60
26

Respiratory Alkalosis
pH 7.50

PaCO2
HCO3

30
22

Metabolic Acidosis
pH PaCO2 HCO3 7.30 40 15

Metabolic Alkalosis
pH 7.50

PCO2
HCO3

40
30

What are the compensations?

Respiratory acidosis Respiratory alkalosis metabolic 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

BP Pulse RR VT MV

180/110 mmHg 130/min 40/min 800ml 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 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 contd

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 contd

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 contd

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 contd

What is going on?

Case No. 8 contd

If the picture doesnt 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 130/90 mmHg 95/min 20/min 350ml 7L

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 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 contd

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% . Pts 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 ABCs 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.

Its not magic understanding ABGs, 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 ABGs
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 ABGs

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