1. ABG INTERPRETATION Debbie Sander PAS-II

2. Objectives What’s an ABG? Understanding Acid/Base Relationship General approach to ABG Interpretation Clinical causes Abnormal ABG’s Case studies Take home

3. 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

4. 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

5. 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

6. 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.

7. 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.

8.  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

9. 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

10. 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

11. H 2 O + CO 2  H 2 CO 3  HCO 3 + H + Acid/Base Relationship

12. Normal ABG values pH7.35 – 7.45 PCO 2 35 – 45 mmHg PO 2 80 – 100 mmHg HCO 3 22 – 26 mmol/L BE-2 - +2 SaO 2 >95%

13. AcidosisAlkalosis pH< 7.35 PCO 2 > 45 HCO 3 < 22 pH> 7.45 PCO 2 < 35 HCO 3 > 26

14. 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

15. Causes of Respiratory Acidosis  emphysema  drug overdose  narcosis  respiratory arrest  airway obstruction

16. 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

17. Causes of Metabolic Acidosis  renal failure  diabetic ketoacidosis  lactic acidosis  excessive diarrhea  cardiac arrest

18. Respiratory Alkalosis  too much CO 2 exhaled (hyperventilation)   PCO 2, H 2 CO 3 insufficiency =  pH  pH > 7.45  PCO 2 < 35

19. Causes of Respiratory Alkalosis  hyperventilation  panic d/o  pain  pregnancy  acute anemia  salicylate overdose

20. Metabolic Alkalosis   plasma bicarbonate  pH > 7.45  HCO 3 > 26

21. Causes of Metabolic Alkalosis   loss acid from stomach or kidney  hypokalemia  excessive alkali intake

22. How to Analyze an ABG 1.PO 2 NL = 80 – 100 mmHg 2. pHNL = 7.35 – 7.45 Acidotic<7.35 Alkalotic>7.45 3.PCO 2 NL = 35 – 45 mmHg Acidotic>45 Alkalotic<35 4.HCO 3 NL = 22 – 26 mmol/L Acidotic < 22 Alkalotic> 26

23. Four-step ABG Interpretation Step 1:  Examine PaO 2 & SaO 2  Determine oxygen status  Low PaO 2 (<80 mmHg) & SaO 2 means hypoxia  NL/elevated oxygen means adequate oxygenation

24. Step 2:  pHacidosis<7.35 alkalosis>7.45 Four-step ABG Interpretation

25. Step 3:  study PaCO 2 & HCO 3  respiratory irregularity if PaCO 2 abnl & HCO 3 NL  metabolic irregularity if HCO 3 abnl & PaCO 2 NL Four-step ABG Interpretation

26. 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

27. ~ PaCO 2 – pH Relationship 807.20 607.30 407.40 307.50 207.60

28. Compensated Respiratory Acidosis CO2 More Abnormal Respiratory Acidosis CO2 Expected Mixed Respiratory Metabolic Acidosis CO2 Less Abnormal CO2 Change c/w Abnormality Metabolic Acidosis CO2 Normal Compensated Metabolic Acidosis CO2 Change opposes Abnormality Acidosis ABG Interpretation

29. 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

30. Respiratory Acidosis pH7.30 PaCO 2 60 HCO 3 26

31. Respiratory Alkalosis pH7.50 PaCO 2 30 HCO 3 22

32. Metabolic Acidosis pH7.30 PaCO 2 40 HCO 3 15

33. Metabolic Alkalosis pH7.50 PCO 2 40 HCO 3 30

34. 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.

35. 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:

36. ABG Results pH7.62BP115/80 mmHg PCO 2 30 mmHgPulse88/min PO 2 85 mmHgRR10/min HCO 3 30 mmol/LVT1000ml BE10 mmol/LMV10L K + 2.5 mmol/L Interpretation:Acute alveolar hyperventilation (resp. alkalosis) and metabolic alkalosis with corrected hypoxemia.

37. 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: pH7.15BP180/110 mmHg PCO 2 22 mmHgPulse130/min PO 2 92 mmHgRR40/min HCO 3 9 mmol/LVT800ml BE-30 mmol/LMV32L Interpretation:Partly compensated metabolic acidosis.

38. 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: pH7.52BP130/90 mmHg PCO 2 55 mmHgPulse120/min PO 2 92 mmHgRR25/min HCO 3 42 mmol/LVT150ml BE17 mmol/LMV 3.75L Interpretation:Partly compensated metabolic alkalosis with corrected hypoxemia.

39. 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: pH7.10BP150/110 mmHg PCO 2 60 mmHgPulse150/min PO 2 125 mmHgRR45/min HCO 3 18 mmol/LVT? ml BE-15 mmol/LMV? L. Interpretation:Acute ventilatory failure (resp. acidosis) and acute metabolic acidosis with corrected hypoxemia

40. 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: pH7.05BP140/90 mmHg PCO 2 12 mmHgPulse118/min PO 2 108 mmHgRR40/min HCO 3 5 mmol/LVT1200ml BE-30 mmol/LMV48L Interpretation:Severe partly compensated metabolic acidosis without hypoxemia.

41. 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

42. Case No. 7 cont’d ABG result after bicarb: pH7.27BP130/80 mmHg PCO 2 25 mmHgPulse100/min PO 2 92 mmHgRR22/min HCO 3 11 mmol/LVT600ml BE-14 mmol/LMV13.2L

43. Case study No. 8 47 yo  was in PACU for 3 hours s/p cholecystectomy. She had been on 40% oxygen and ABG & VS: pH7.44BP130/90 mmHg PCO 2 32 mmHgPulse95/min, regular PO 2 121 mmHgRR20/min HCO 3 22 mmol/LVT350ml BE-2 mmol/LMV7L SaO 2 98% Hb13 g/dL

44. 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: pH7.41BP130/90 mmHg PCO 2 10 mmHgPulse95/min, regular PO 2 148 mmHgRR20/min HCO 3 6 mmol/LVT350ml BE-17 mmol/LMV7L SaO 2 99% Hb7 g/dL

45. Case No. 8 cont’d What is going on?

46. Case No. 8 cont’d If the picture doesn’t fit, repeat ABG!! pH7. 45BP130/90 mmHg PCO 2 31 mmHgPulse95/min PO 2 87 mmHgRR20/min HCO 3 22 mmol/LVT350ml BE-2 mmol/LMV7L SaO 2 96% Hb13 g/dL Technical error was presumed.

47. 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: pH7.36BP130/90 mmHg PCO 2 33 mmHgPulse100/min PO 2 55 mmHgRR25/min HCO 3 18 mmol/L BE-5 mmol/LMV18L SaO 2 88% Interpretation:Compensated metabolic acidosis with moderate hypoxemia. Dx: PE

48. 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: pH7.44BP135/95 mmHg PCO 2 63 mmHgPulse110/min PO 2 52 mmHgRR22/min HCO 3 42 mmol/L BE+16 mmol/LMV10L SaO 2 86%. Interpretation:Chronic ventilatory failure (resp. acidosis) with uncorrected hypoxemia

49. Case No. 10 cont’d She was placed on 3L and monitored for next hour. She remained alert, oriented and comfortable. ABG was repeated: pH7.36BP140/100 mmHg PCO 2 75 mmHgPulse105/min PO 2 65 mmHgRR24/min HCO 3 42 mmol/L BE+16 mmol/LMV4.8L 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

50. 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.

51. It’s not magic understanding ABG’s, it just takes a little practice!

52. Any Questions?

53. 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

54. Practice ABG’s 1.PaO 2 90SaO 2 95 pH 7.48 PaCO 2 32 HCO 3 24 2.PaO 2 60SaO 2 90 pH 7.32 PaCO 2 48 HCO 3 25 3.PaO 2 95SaO 2 100 pH 7.30 PaCO 2 40 HCO 3 18 4.PaO 2 87SaO 2 94 pH 7.38 PaCO 2 48 HCO 3 28 5.PaO 2 94SaO 2 99 pH 7.49 PaCO 2 40 HCO 3 30 6. PaO 2 62SaO 2 91 pH 7.35 PaCO 2 48 HCO 3 27 7.PaO 2 93SaO 2 97 pH 7.45 PaCO 2 47 HCO 3 29 8.PaO 2 95SaO 2 99 pH 7.31 PaCO 2 38 HCO 3 15 9.PaO 2 65SaO 2 89 pH 7.30 PaCO 2 50 HCO 3 24 10. PaO 2 110SaO 2 100 pH 7.48 PaCO 2 40 HCO 3 30

55. 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