This document provides guidelines for interpreting arterial blood gas results, including: 1. It describes how to summarize the acid-base and oxygenation status based on pH, PCO2, HCO3, PO2, and other values. 2. It outlines the steps to determine if a disturbance is respiratory or metabolic in nature, and whether it is acute or chronic. 3. Causes and compensation mechanisms for various acid-base imbalances like respiratory acidosis/alkalosis and metabolic acidosis/alkalosis are reviewed.

1. Basics in Arterial Blood Gas Interpretation Crisbert I. Cualteros, M.D.

2. Obtaining Blood Gas Samples Radial artery- best site located superficially, easy to palpate & stabilize excellent collateral circulation via ulnar artery not adjacent to large veins probing needle relatively pain-free if periosteum is avoided

3. Technique for Radial Artery Puncture Explain process to patient. Examine skin, palpate radial & ulnar arteries. Perform modified Allen Test.

4. The Allen Test have the patient clench his/her fist press on both radial and ulnar arteries have the patient unclench fist test for good collateral flow.

5. Technique for Radial Artery Puncture Position patient- hyperextend wrist. Clean site with 70% isopropyl alcohol. Use latex gloves while doing procedure. Local anesthesia may be used. Use G20 or G21 needle. Flush syringe with sodium heparin (10 mg/ml or 1,000 units/ml) & empty. 0.15-0.25 ml of heparin will anticoagulate 2-4 ml of blood.

6. Technique for Radial Artery Puncture Palpate artery with one hand while holding properly prepared syringe & needle with other hand. Hold syringe like a pencil & enter skin at 45 o . Advance needle slowly. Never redirect needle without first withdrawing to subcutaneous tissue. Obtain 2-4 ml blood. If possible don’t aspirate. Remove air bubbles from syringe. Immediately seal syringe with cap. Place sample in ice slush. Analyze blood sample within 10 minutes. Apply pressure to site until bleeding has stopped.

7. Potential Complications Pain Hematoma, hemorrhage Trauma to vessel Arteriospasm Air or clotted-blood emboli Vasovagal response Arterial occlusion Infection

8. Indications for ABG Assess ventilation & acid-base balance Assess oxygenation status

9. Ventilatory/ Acid-Base Status

10. Henderson-Hasselbach Parameters & their normal laboratory ranges pH= [HCO 3 ]p P C02 > 26 < 35 > 7.45 Alkalotic < 22 > 45 < 7.35 Acidotic 22-26 35-45 7.35-7.45 Normal [HCO3]p (mmol/L) PCO2 (mmHg) pH

11. Traditional Metabolic Acid-Base Nomenclature  (+)   N Compensated (chronic)  (+)    Partly compensated (subacute)  (+)  N  Uncompensated (acute) Metabolic alkalosis  (-)   N Compensated (chronic)  (-)     Partly compensated (subacute)  (-)   N  Uncompensated (acute) Metabolic acidosis BE [HCO3]p PCO 2 pH Nomenclature

12. Traditional Respiratory Acid-Base Nomenclature    N Compensated (chronic)     Partly compensated (subacute) N N   Uncompensated (acute) Respiratory alkalosis    N Compensated (chronic)     Partly compensated (subacute) N N   Uncompensated (acute) Respiratory acidosis BE [HCO3]p PCO2 pH Nomenclature

13. Base Excess/ Deficit Blood with large buffering capacity: significant changes in acid content with little change in free H + concentrations (pH) Acidemia or alkalemia:  buffering capacity, > potential for pH change from any given change in H + content Buffering capacity depends on: [HCO 3 - ] RBC mass other factors Base excess/deficit= (measured pH – predicted pH) x 100 x 2/3 Normal metabolic acid-base status: + 3 mmol/L Relatively balanced metabolic acid-base status: + 5 mmol/L Clinically significant imbalance: + 10 mmol/L

14. Nomenclature & Criteria for Clinical Interpretation Clinical Terminology Criteria Ventilatory failure (respiratory acidosis) P a CO 2 > 45 mm Hg Acute ventilatory failure (respiratory acidosis) P a CO 2 > 45 mmHg pH < 7.35 Chronic ventilatory failure (respiratory acidosis) P a CO 2 > 45 mmHg pH 7.36- 7.44 Alveolar hyperventilation (respiratory alkalosis) P a CO 2 < 35 mmHg Acute alveolar hyperventilation (respiratory P a CO 2 < 35 mmHg alkalosis) pH > 7.45 Chronic alveolar hyperventilation (respiratory P a CO 2 < 35 mmHg alkalosis) pH 7.36-7.44

15. Nomenclature & Criteria for Clinical Interpretation Clinical Terminology Criteria Acidemia pH < 7.35 Alkalemia pH > 7.45 Acidosis HCO 3 - < 22 mmol/L BD > 5 mmol/L Alkalosis HCO 3 - > 26 mmol/L BE > 5 mmol/L Combined Respiratory Acidosis & Metabolic Acidosis Respiratory Alkalosis & Metabolic Alkalosis Mixed Respiratory Acidosis & Metabolic Alkalosis Respiratory Alkalosis & Metabolic Acidosis

16. Respiratory Acidosis Acute  pH = 0.08 x (PCO 2 – 40) 10 ex. PCO 2 = 60  pH = 0.08 x (60 - 40) = 0.16 10 expected pH = 7.40 – 0.16 = 7.24 HCO 3 - increases 0.1 – 1 meq/L per 10 mmHg PCO 2 increase Compensation: cellular buffering: HCO 3 renal adaptation: H + secretion, Cl - reabsorption, net acid excretion

17. Respiratory acidosis Chronic  pH = 0.03 x (PCO 2 – 40) 10 ex. PCO 2 = 60  pH = 0.03 x (60 – 40) = 0.06 10 expected pH = 7.40 – 0.06 = 7.34 HCO 3 - increases 1-3.5 meq/L per 10 mmHg PCO 2 increase

18. Respiratory Acidosis COPD O 2 excess in COPD Drugs Barbiturates Anesthetics Narcotics Sedatives Extreme ventilation-perfusion mismatch Exhaustion Inadequate MV Neurologic disorders Neuromuscular disease Poliomyelitis ALL G-B syndrome Electrolyte deficiencies (K + , PO 4 - ) Myasthenia gravis Excessive CO 2 production TPN Sepsis Severe burns NaHCO 3 administration

19. Respiratory Alkalosis Acute  pH = 0.08 x (40 – PCO 2 ) 10 ex. PCO 2 = 20  pH = 0.08 x (40 – 20) = 0.16 10 expected pH = 7.40 + 0.16 = 7.56 HCO 3 - decreases 0-2 meq/L per 10 mmHg PCO 2 decrease Compensation: cellular buffering renal response: retention of endogenous acids, excretion of HCO 3

20. Respiratory Alkalosis Chronic  pH = 0.03 x (40 – PCO 2 ) 10 ex. PCO 2 = 20  pH = 0.03 x (40 – 20) = 0.06 10 expected pH = 7.40 + 0.06 = 7.46 HCO 3 - decreases 2-5 meq/L per 10 mmHg PCO 2 decrease

21. Respiratory Alkalosis Primary central disorders Hyperventilation syndrome, anxiety Cerebrovascular disease Meningitis, encephalitis Pulmonary disease Interstitial fibrosis Pneumonia Pulmonary embolism Pulmonary edema (some patients) Hypoxia Septicemia, hypotension Hepatic failure Drugs Salicylates Nicotine Xanthines Progestational hormones High altitude Mechanical ventilators

22. Metabolic Acidosis Anion Gap artificial disparity between major plasma cations & anions that are routinely measured major plasma cations – major plasma anions [Na + ] – ([Cl - ] + [HCO3 - ]) 12 + 2 (normal) Minor cations: K + , Ca ++ Minor anions: phosphates, sulfates, organic anions

23. Metabolic Acidosis Anion gap acidosis ~ process increases “minor anions” ~ ex. lactatemia, ketonemia, renal failure, excessive organic salt treatment, dehydration, ingestion (salicylates, methanol, ethylene glycol, paraldehyde) ~ process which decreases “minor cations” rare! Non-anion gap acidosis ~ associated with increased plasma Cl - that has replaced HCO 3 - ~ ex. GI loss of HCO 3 - (diarrhea), renal wasting of HCO 3 - (RTA), ingestion of acids, parenteral hyperalimentation, carbonic anhydrase inhibitors

24. Metabolic Acidosis Abnormalities: Overproduction of acids Loss of buffer stores Underexcretion of acids

25. Metabolic Acidosis Expected PCO 2 = ( [HCO 3 - ] x 1.5) + 8 + 2 ex. [HCO 3 - ] = 11 expected PCO 2 = (11 x 1.5) + 8 + 2 = 22.5- 26.5 PCO 2 decreases 1- 1.5 mmHg per 1 meq/L HCO 3 - decrease

26. Metabolic Acidosis Compensation  pCO 2 (hyperventilation) Pathway:  pCO 2 HCO 3 ratio  H + conc Acidification of ECF  ECF  pH Stimulation of brainstem  RR  pCO 2 Normalization of pH  HCO 3

27. Metabolic Acidosis Compensation Ionic shift K + moves extracellularly for H + HCO 3 - generation, H + excretion

28. Corrected [HCO 3 - ] for Anion Gap Metabolic Acidosis Measured serum [HCO 3 - ] + (anion gap – 12)

29. Metabolic Alkalosis Expected PCO 2 = ( [HCO 3 - ] x 0.75 ) + 20 + 5 ex. [HCO 3 - ] = 34 expected PCO 2 = (34 x 0.75) + 20 + 5 = 40.5- 50.5 PCO 2 increases 0.5- 1 mmHg per 1 meq/L HCO 3 - increase

30. Metabolic Alkalosis Pathway HCO 3  PaCO 2 HCO 3 ratio  H + conc Alkalinization of ECF  PaCO 2 with mild hypoxemia Normalization of pH

31. Causes of Metabolic Alkalosis Hypokalemia* Ingestion of large amounts of alkali or licorice Gastric fluid loss: Vomiting, NG suctioning* Hyperaldosteronism 2 0 to nonadrenal factors Bartter’s syndrome Inadequate renal perfusion diuretics (inhibiting NaCl reabsorption)* Bicarbonate administration Sodium bicarbonate overcorrection Blood transfusion Adrenocortical hypersecretion (e.g tumor) Steroids* Eucapnic ventilation posthypercapnia * Common in the ICU

32. Limits of Compensation  0.5- 1/ 1 meq/L [HCO 3 - ]  Metabolic Alkalosis  1- 1.5/ 1 meq/L [HCO 3 - ]  Metabolic Acidosis  2- 5/ 10 mmHg PCO 2  Chronic  0- 2/ 10 mmHg PCO 2  Acute Respiratory Alkalosis  1- 3.5/ 10 mmHg PCO 2  Chronic  0.1- 1/ 10 mmHg PCO 2  Acute Respiratory Acidosis PCO 2 mmHg [HCO 3 - ] meq/L Imbalance

33. Steps for Analyzing Acid- Base Disturbances Is patient acidemic or alkalotic? pH Is disturbance primarily respiratory or metabolic? PCO 2 , [HCO 3 - ] If disturbance respiratory, is it acute or chronic? If disturbance metabolic, is anion gap normal or abnormal? If disturbance metabolic, is the respiratory system compensating adequately? If disturbance is anion gap metabolic acidosis, are there any other metabolic disturbances present?

34. Oxygenation Status

35. Normal Values Seated PO2 = 104.2 – 0.27 (age in years) Supine PO2 = 103.5 – 0.42 (age in years) Patients < 60 y. o. PO2 = 100 + 20 Patients > 60 y. o. PO2 = 80 – (# years > 60)

36. Steps for Analyzing Oxygenation Status

37. 1. Is the patient hypoxemic or normoxemic? Indices of Oxygenation: a. AaDO 2 = PAO 2 – PaO 2 PAO 2 = FiO 2 (713) – PaCO 2 0.8 PaO 2 = obtained from blood gas determination b. aAO 2 = PaO 2 PAO 2 c. P/F ratio = PO 2 FiO 2 Normal Value: patients < 60 y. o. > 400 patients > 60 y. o. expected P/F = 400 – [(age in years – 60) x 5] Actual P/F Ratio < expected = hypoxemic Actual P/F Ratio > expected = normoxemic

38. 2. If hypoxemic, is it uncorrected, corrected, or overcorrected? With O 2 supplementation PaO 2 (mmHg) Uncorrected hypoxemia < 80 Corrected hypoxemia 80 – 120 Overcorrected > 120 FiO 2 to PaO 2 Relationship in Normal Lungs FiO 2 PaO 2 (mmHg) 0.30 > 150 0.40 > 200 0.50 > 250 0.80 > 400 1.00 > 500

39. Room Air (patient < 60 y. o.) PaO 2 (mmHg) Mild hypoxemia 60 to < 80 Moderate hypoxemia 40 to < 60 Severe hypoxemia < 40 For each year > 60 subtract 1 mmHg for limits of mild & moderate hypoxemia. At any age, PaO 2 < 40 mmHg indicates severe hypoxemia.

40. 3. If normoxemic, is oxygenation adequate or more than adequate?

41. Thank you !