Interpretation of the Arterial Blood Gas analysis

1. Interpretation of the Arterial Blood Gas Analysis DM SEMINAR Dr. Vishal Golay 2/11/2011

2. Overview of the discussion Basics of acid-base balance. Role of kidneys in acid-base homeostasis. Step-wise approach in diagnosis of acid-base disorders. Some practical examples.

3. Basic terminology pH – signifies free hydrogen ion concentration. pH is inversely related to H + ion concentration. Acid – a substance that can donate H + ion, i.e. lowers pH. Base – a substance that can accept H + ion, i.e. raises pH. Anion – an ion with negative charge. Cation – an ion with positive charge. Acidemia – blood pH< 7.35 with increased H + concentration. Alkalemia – blood pH>7.45 with decreased H + concentration. Acidosis – Abnormal process or disease which reduces pH due to increase in acid or decrease in alkali. Alkalosis – Abnormal process or disease which increases pH due to decrease in acid or increase in alkali.

4. Endogenous sources of acid. Daily production ~ 1 mEq of H+/kg/day Sulfuric acid ( from S containing AA) Organic acids (from intermediary metabolism) Phosphoric acid ( hydrolysis of PO4 containing proteins) Hydrochloric acid (from metab of cationic AA-Lysine, Arg , Histidine )

5. pH in humans is tightly regulated between 7.35-7.45.

6. Buffers Buffers are chemical systems which either release or accept H + and minimize change in pH induced by an acid or base load. First line of defense blunting the changes in [ H +] A buffer pair consists of: A base (H+ acceptor) & An acid (H+ donor)

7. Buffers continued…… Extracellular buffers: HCO3 ¯ /H2CO3 HPO4² ¯ /H2PO4 Protein buffers Intracellular buffers: Hb Proteins Organophosphate compounds Bone apatite Examples: HPO 4 2-  + (H + )↔H 2   PO 4 - H 2  O + CO 2  ↔H 2  CO 3  ↔H +  + HCO 3 -

8. Respiratory regulation 2 nd line of defense 10-12 mol/day CO2 is accumulated and is transported to the lungs as Hb -generated HCO3 and Hb -bound carbamino compounds where it is freely excreted. H 2  O + CO 2  ↔H 2  CO 3  ↔H +  + HCO 3 - Accumulation/loss of Co2 changes pH within minutes

9. Respiratory regulation contd ….. Balance affected by neurorespiratory control of ventilation. During Acidosis, chemoreceptors sense ↓pH and trigger ventilation decreasing pCO2. Response to alkalosis is biphasic. Initial hyperventilation to remove excess pCO2 followed by suppression to increase pCO2 to return pH to normal

10. Renal Regulation Kidneys are the ultimate defense against the addition of non-volatile acid/alkali. HA  + Na HCO 3 ↔ H 2  O + CO 2 + NaA Addition of Acid causes loss of HCO3 ¯ Kidneys play a role in the maintenance of this HCO3¯ by: Conservation of filtered HCO3 ¯ Regeneration of HCO3 ¯

11. Net Acid Excretion(NAE) Kidneys balance nonvolatile acid generation during metabolism by excreting acid. Each mEq of NAE corresponds to 1 mEq of HCO3 ¯ returned to ECF. NAE has three components: NH4⁺ . Titrable acids. (acid excreted that has titrated urinary buffers) Bicarbonate. N AE = NH4⁺ + TA-HCO3 ¯

12. 75-80% HCO3 is absorbed in the proximal tubule.

13. Ammonium excretion 2 2

14. Interpreting acid-base disorders

15. Normal ABG values pH 7.35 - 7.45 PaCO 2 35 - 45 mm Hg PaO 2 70 - 100 mm Hg SaO 2 93 - 98% HCO 3 ¯ 22 - 26 mEq /L % MetHb < 2.0% % COHb < 3.0% Base excess - 2.0 to 2.0 mEq /L ----- XXXX Diagnostics ------ Blood Gas Report 248 05:36 Jul 22 2000 Pt ID 2570 / 00 Measured 37.0 o C pH 7.463 pCO 2 44.4 mm Hg pO 2 113.2 mm Hg Corrected 38.6 o C pH 7.439 pCO 2 47.6 mm Hg pO 2 123.5 mm Hg Calculated Data TPCO2 49 HCO 3 act 31.1 mmol / L HCO 3 std 30.5 mmol / L BE 6.6 mmol / L O 2 CT 14.7 mL / dl O 2 Sat 98.3 % ct CO 2 32.4 mmol / L pO 2 (A - a) 32.2 mm Hg pO 2 (a / A) 0.79 Entered Data Temp 38.6 o C ct Hb 10.5 g/dl FiO 2 30.0 %

16. -----XXXX Diagnostics----- Blood Gas Report 328 03:44 Feb 5 2006 Pt ID 3245 / 00 Measured 37.0 C pH 7.452 pCO2 45.1 mm Hg pO2 112.3 mm Hg Corrected 38.6 C pH 7.436 pCO2 47.6 mm Hg pO2 122.4 mm Hg Calculated Data HCO3 act 31.2 mmol / L HCO3 std 30.5 mmol / L B E 6.6 mmol / L O2 ct 15.8 mL / dl O2 Sat 98.4 % ct CO2 32.5 mmol / L pO2 (A -a) 30.2 mm Hg  pO2 (a/A) 0.78 Entered Data Temp 38.6 0C FiO2 30.0 % ct Hb 10.5 gm/dl Measured values… most important Temperature Correction : Is there any value to it ? Calculated Data : Which are useful one? Entered Data : Important

17. Measured values should be considered And Corrected values should be discarded

18. Bicarbonate is calculated on the basis of the Henderson equation: [H + ] = 24 pCO 2 / [HCO 3 - ] Act Bicarbonate: -----XXXX Diagnostics----- Blood Gas Report 328 03:44 Feb 5 2006 Pt ID 3245 / 00 Measured 37.0 C pH 7.452 pCO2 45.1 mm Hg pO2 112.3 mm Hg Corrected 38.6 C pH 7.436 pCO2 47.6 mm Hg pO2 122.4 mm Hg Calculated Data HCO3 act 31.2 mmol / L HCO3 std 30.5 mmol / L B E 6.6 mmol / L O2 ct 15.8 mL / dl O2 Sat 98.4 % ct CO2 32.5 mmol / L pO2 (A -a) 30.2 mm Hg  pO2 (a/A) 0.78 Entered Data Temp 38.6 0C FiO2 30.0 % ct Hb 10.5 gm/dl

19. -----XXXX Diagnostics----- Blood Gas Report 328 03:44 Feb 5 2006 Pt ID 3245 / 00 Measured 37.0 C pH 7.452 pCO2 45.1 mm Hg pO2 112.3 mm Hg Corrected 38.6 C pH 7.436 pCO2 47.6 mm Hg pO2 122.4 mm Hg Calculated Data HCO3 act 31.2 mmol / L HCO3 std 30.5 mmol / L B E 6.6 mmol / L O2 ct 15.8 mL / dl O2 Sat 98.4 % ct CO2 32.5 mmol / L pO2 (A -a) 30.2 mm Hg  pO2 (a/A) 0.78 Entered Data Temp 38.6 0C FiO2 30.0 % ct Hb 10.5 gm/dl Standard Bicarbonate: Plasma HCO 3 after equilibration to a PCO 2 of 40 mm Hg : reflects non-respiratory acid base change : does not quantify the extent of the buffer base abnormality : does not consider actual buffering capacity of blood Base Excess: D base to normalise HCO 3 (to 24) with PCO 2 at 40 mm Hg ( Sigaard -Andersen) : reflects metabolic part of acid base D : no info. over that derived from pH, pCO2 and HCO3 : Misinterpreted in chronic or mixed disorders

20. "Step – wise approach" for ABG analysis Consider the Clinical Setting. Obtain ABG and Electrolyte values simultaneously. Verify the ABG values. Identify the nature of the disturbance. Calculate the Anion gap in case of MA. Assess ∆AG, ∆ HCO3, ∆ Cl & ∆Na Detecting mixed disorders. Clinical correlation

21. Steps 1 & 2 Basic clinical scenario gives an idea about the type of the underlying disorder. ABG samples should be taken properly. Excess of heparin should be avoided during sampling.

22. S ampling for ABG analysis Perform Allen’s test. Clean the site. Use 21 gauze needle with syringe. Flush syringe and needle with heparin. Enter skin at 45° angle Obtain 2-4ml blood without aspiration. Avoid suction of syringe . If sample contains any air bubble, tap it to the surface and push it out of the syringe. Air bubbles can lead to increase in PaO 2 and decrease in PaCO 2 . Apply firm pressure at punctured site. Special mention Specimens held at room temperature must be analyzed within 10-15 minutes of drawing; iced samples should be analyzed within 1 hour. The PaO2 of samples drawn from subjects with elevated white cell counts may decrease very rapidly. Immediate chilling is necessary .

23. Indications for performing an ABG analysis The need to evaluate the adequacy of ventilatory (PacO2) acid-base (pH and PaCO2) , and oxygenation (PaO2 and SaO2) status, and the oxygen-carrying capacity of blood (PaO2, HbO2, Hbtotal , and dyshemoglobins ) .  The need to quantitate the patient's response to therapeutic intervention and/or diagnostic evaluation ( eg , oxygen therapy, exercise testing ) The need to monitor severity and progression of a documented disease process .

24. Steps 2 Verify the ABG values. The values should be checked for internal consistency. In ABG samples, pH and PaCO2 are measured and HCO3 calculated by the HH equation. Simultaneously measured plasma HCO3 should be within ±2-3 mmol /L of each other.

25. Steps 3 continued……. Most ABG reports do not give HCO3. It can be calculated indirectly from pH an PaCO2 values. Normal [H+] 40 nmol /L first 2 decimals of pH value. Thus, HCO3 can now be calculated from [H+] and PaCO2 using the Henderson equation. For every 0.1 decrease in pH, [H+] increases by 10nmol/L [H+]=24 (PaCO2/ [HCO3 ])

26. Step 3 Identify the disorder Take a look at the pH, as it directs towards the principal disorder.

27. During compensation HCO3¯ & PaCO2 move in the same direction

28. Compensatory changes (Respiratory disorders). Primary disorder Primary defect Compensatory response Expected Compensation Limits of compensation Respiratory acidosis ↑ PCO2 ↑ HCO3 Acute: + 1 Meq /L ↑ HCO3 for each ↑ PCO2 of 10mmHg [HCO3]=38 Meq /L Chronic: +4 Meq /L ↑ HCO3 for each ↑ PCO2 of 10mmHg [HCO3]=45 Meq /L Respiratory Alkalosis ↓ PCO2 ↓ HCO3 Acute: - 2Meq/l ↓ in HCO3 for each ↓ in PCO2 of 10mmHg [HCO3]=18 Meq /L Chronic: -5 Meq /L ↓ in HCO3 for each ↓ in PCO2 of 10mmHg [HCO3]=15 mEq /L 1 4 2 5

29. Compensatory changes (Metabolic disorders). Primary disorder Primary defect Compensatory response Expected Compensation Limits of compensation Metabolic acidosis ↓ HCO3 ↓ PCO2 PCO2= 1.5[ HCO3] + 8 ± 2 PCO2= last 2 digits of pH X 100 PCO2= 15+ [HCO3] PCO2=15mmHg Metabolic Alkalosis ↑ HCO3 ↑ PCO2 PCO2= + 0.6 mmHg for Δ [HCO3] of 1 mEq /L PCO2= 15+ [HCO3] PCO2=55mmHg Remember ……. Respiratory compensation is always FAST … 12-24 hrs Metabolic compensation is always SLOW ...5 -7 days

30. Body’s physiologic response to Primary disorder in order to bring pH towards NORMAL limit Full compensation Partial compensation No compensation…. (uncompensated) BUT never overshoots, If a overshoot pH is there, Take it granted it is a MIXED disorder

31. Step 5 Anion Gap Normal range is 10 ± 2 mEq /L It represents unmeasured anions. These unmeasured anions can be; Anionic proteins SO4, PO4, organic anions Acid anions ( acetoacetate , lactate, uremic anions) AG = Na⁺ – ( Cl ¯ + HCO3¯)

32. Anion gap can increase either due to: Increase in the unmeasured anions. Decrease in the unmeasured cations ( hypocal , h ypomag ) Anion gap may decrease due to: Increase in unmeasured cations (Ca, Mg, K) Addition of abnormal cations (Li) Decrease in albumin ( each 1g/dl decrease of alb decrease AG by 2.5 mEq /L)

33. Step 6 & 7 Detecting mixed disorders Clues to the presence of a mixed disorder. Clinical history pH normal, abnormal PCO 2 n HCO 3 PCO 2 n HCO 3 moving opposite directions Acid Base map ( Flenley Nomogram ) Degree of compensation for primary disorder is inappropriate Find Delta Gap

34. Flenley Nomogram

35. Compensation in excess points towards a mixed disorder. Example: In a case of primary metabolic acidosis, HCO3=12 Expected compensated PCO3 will be 24-28 (PCO2=1.5XHCO3 + 8 ± 2) If, PCO2 is < 24, Metabolic acidosis + Respiratory Alkalosis If, PCO2 is > 28, Metabolic acidosis + Respiratory Acidosis

36. Δ s for metabolic acidosis Every increase in unmeasured anion ( Δ AG), should be met with similar decrease in HCO3 ( Δ HCO3). Thus, Δ AG= Δ HCO3 in a case of simple AG metabolic acidosis However, If, Δ AG is > Δ HCO3= AG Metabolic acidosis + Metabolic alkalosis

37. Delta gap Delta ratio =∆AG/ ∆HCO3 = (observed AG-12)/ (24- obs HCO3) <1 =High anion gap & normal AG acidosis 1-2= Pure anion gap metabolic acidosis >2 = High anion gap acidosis with concurrent metabolic alkalosis

38. Significance of Δ Cl Normally the values of Cl change according to the hydration stature or Na If this proportional change is absent, then it indicates an acid base disorder. If there is a disproportionate decrease of Cl = Metabolic alkalosis or Respiratory acidosis If there is a disproportionate increase of Cl = Metabolic acidosis or Respiratory alkalosis

39. "Step – wise approach" for ABG analysis Consider the Clinical Setting. Obtain ABG and Electrolyte values simultaneously. Verify the ABG values. Identify the nature of the disturbance. Calculate the Anion gap in case of MA. Assess ∆AG, ∆ HCO3, ∆ Cl & ∆Na Detecting mixed disorders. Clinical correlation

40. Interpretation with examples

41. Clinical examples

42. Example 1 A 19 year old pregnant insulin dependent diabetic patient was admitted with a history of polyuria and thirst. She now felt ill and presented to hospital. There was a history of poor compliance with medical therapy. She was afebrile . Chest was clear. Circulation was adequate . Urinalysis : 2+ ketones , 4+ glucose . Na +  136, K +  4.8, Cl -   101 , pH 7.26, pCO 2  16 mmHg, pO 2  128 mmHg, HCO 3  7.1 mmol /l

43. Clinical possibilities: Diabetic ketoacidosis Lactic acidosis Hyperchloremic metabolic acidosis Respiratory acid-base disturbances Check the internal validity of the report. Observed HCO3 report= 7.1, calculated HCO3= 7 Look at the pH : 7.26 Then find the primary disorder : Low HCO3 along with low pCO2 suggests a METABOLIC disorder. ACIDOSIS CORRECT

44. Check for compensation : compensation for metabolic acidosis brings pCO2 to 16.5-20.6 mmHg. Thus the acidosis is by respiratory regulation and there is Anion Gap = 136-(101+7.1)=28.1 ∆AG=27.9-12=15.9, ∆HCO3=24-7.1=14.9 Delta ratio =15.9/14.9=1.07 Na is normal with low Cl (NO HYPERCHLOREMIA) FINAL ABG DIAGNOSIS PURE ANION GAP METABOLIC ACIDOSIS (Etiology, DKA) PURE ANION GAP ACIDOSIS HIGH ANION GAP acidosis NO MIXED disorder. FULLY COMPENSATED

45. Example 2 A 60 year old woman was admitted with lobar pneumonia. She was on a thiazide diuretic for 9 months following a previous admission with congestive cardiac failure. The admission arterial blood results were : pH 7.64 pCO2 32 mmHg pO2 75 mmHg HCO3 33 mmol /l K +  2.1 mmol /l

46. Clinical possibilities: Severe hypokalemis to be corrected immediately Respiratory acidosis (respiratory failure) Respiratory alkalosis ( dyspnea ) Metabolic alkalosis (diuretics) Look at the pH : 7.64 Then find the primary disorder : Low pCO2 along with high HCO3 suggests a MIXED ALKALOSIS. ALKALOSIS

47. Check for compensation : Considering Chronic respiratory alkalosis, expected HCO3 is 20mEq/l on maximal compensation. Observed value is much higher so a Metabolic alkalosis should be present. Considering Metabolic alkalosis, predicted pCo2 after compensation is 43mmHg. The observed value is much lower so a respiratory alkalosis should be present. FINAL ABG DIAGNOSIS MIXED METABOLIC & RESPIRATORY ALKALOSIS

48. Ph 6.99 PCo 2 10.5 mmHg P0 2 111 mmHg BE -29 mmol /L HCo3 2.6 Tco2 45 SO2 95 Na+ 138 mmol /L K+ 4.2 mmol /L iCa+ 1.06 mmol /L Hb 12.6 g/dl For the audience Expected fall in PCO 2 =( 1.5 x HCO 3 )+ 8 = (1.5 x 2.6) + 8 ±2 = 9.9 to 13.9 Thus the compensation is within limits and the diagnosis is COMPENSATED METABOLIC ACIDOSIS

49. For the audience Primary dis - Respiratory alkalosis. For acute Resp. alkalosis--- Expected HCO3 = 24- 2(40-19)/10 = 19.8 but actual HCO3=13.5 which is less then the expected. So it is mixed disorder with Respiratory alkalosis with Metabolic acidosis

50. “Understanding ABG is not magic but an art learned by continued practice”

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