Interpretation of the Arterial Blood Gas analysis

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  • Sulfur containing AA ( meth,cysteine=50% in a western diet)
  • Ammonia contributes 60%, TA contributes 40 % and HCO3 excretion is almost zero under basal conditions.
  • Interpretation of the Arterial Blood Gas analysis

    1. 1. Interpretation of theArterial Blood Gas Analysis DM SEMINAR Dr. Vishal Golay 2/11/2011
    2. 2. Overview of thediscussion • 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. 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. 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. 5. pH in humans is tightly regulated between 7.35- 7.45. Chemical Buffers Respiratory regulatory responses Renal regulatory responses
    6. 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. 7. Buffers continued……Extracellular buffers: Examples: Intracellular buffers:• HCO3¯/H2CO3 •Hb HPO42- + (H+•Proteins 4- )↔H2 PO• HPO4²¯/H2PO4 •Organophosphate H2 O + CO2 ↔H2 CO3 ↔H+ + HCO3-• Protein buffers compounds •Bone apatite
    8. 8. Respiratory regulation• 2nd 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. H2 O + CO2 ↔H2 CO3 ↔H+ + HCO3-• Accumulation/loss of Co2 changes pH within minutes
    9. 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. 10. Renal Regulation• Kidneys are the ultimate defense against the addition of non-volatile acid/alkali. HA + NaHCO3↔H2 O + CO2 + 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. 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: 1. NH4⁺ . 2. Titrable acids. (acid excreted that has titrated urinary buffers) 3. Bicarbonate. NAE= NH4⁺ + TA-HCO3¯
    12. 12. 75-80% HCO3 is absorbed in the proximal tubule.
    13. 13. Ammonium excretion 2 2
    14. 14. Interpreting acid-base disorders
    15. 15. ----- XXXX Diagnostics ------Blood248Pt ID Gas 05:36 2570 / 00 Report Jul 22 2000 Normal ABG valuesMeasured 37.0 C o pH 7.35 - 7.45pH 7.463pCO2 44.4 mm Hg PaCO2 35 - 45 mm HgpO2 113.2 mm Hg oCorrected 38.6 C PaO2 70 - 100 mm HgpH 7.439pCO2 47.6 mm HgpO2 123.5 mm Hg SaO2 93 - 98%Calculated Data HCO3¯ 22 - 26 mEq/LTPCO2 49HCO3 act 31.1 mmol / LHCO3 std 30.5 mmol / L %MetHb < 2.0%BE 6.6 mmol / LO2 CT 14.7 mL / dlO2 Sat 98.3 % %COHb < 3.0%ct CO2 32.4 mmol / LpO2 (A - a) 32.2 mm HgpO2 (a / A) 0.79 Base excess -2.0 to 2.0 mEq/LEntered DataTemp 38.6 oCct Hb 10.5 g/dlFiO2 30.0 %
    16. 16. -----XXXX Diagnostics-----Blood Gas Report328 03:44 Feb 5 2006Pt ID 3245 / 00Measured 37.0 0C Measured values…pH 7.452 most importantpCO2 45.1 mm HgpO2 112.3 mm HgCorrected 38.6 0C Temperature Correction :pH 7.436pCO2 47.6 mm Hg Is there any value to it ?pO2 122.4 mm HgCalculated DataHCO3 act 31.2 mmol / L Calculated Data :HCO3 std 30.5 mmol / LBE 6.6 mmol / L Which are useful one?O2 ct 15.8 mL / dlO2 Sat 98.4 %ct CO2 32.5 mmol / LpO2 (A -a) 30.2 mm Hg pO2 (a/A) 0.78 Entered Data :Entered Data ImportantTemp 38.6 0CFiO2 30.0 %ct Hb 10.5 gm/dl
    17. 17. Measured values should be considered AndCorrected values should be discarded
    18. 18. -----XXXX Diagnostics-----Blood Gas Report328 03:44 Feb 5 2006Pt ID 3245 / 00Measured 37.0 0C Bicarbonate is calculated on the basis of thepH 7.452 Henderson equation:pCO2 45.1 mm HgpO2 112.3 mm Hg [H+] = 24 pCO2 / [HCO3-]Corrected 38.6 0CpH 7.436pCO2 47.6 mm HgpO2 122.4 mm HgCalculated DataHCO3 act 31.2 mmol / LHCO3 std 30.5 mmol / LBE 6.6 mmol / LO2 ct 15.8 mL / dlO2 Sat 98.4 %ct CO2 32.5 mmol / LpO2 (A -a) 30.2 mm Hg pO2 (a/A) 0.78Entered DataTemp 38.6 0CFiO2 30.0 %ct Hb 10.5 gm/dl
    19. 19. -----XXXX Diagnostics----- Standard Bicarbonate:Blood Gas Report Plasma HCO3 after equilibration328 03:44 Feb 5 2006 to a PCO2 of 40 mm HgPt ID 3245 / 00 : reflects non-respiratory acid base changeMeasured 37.0 0C : does not quantify the extent of the bufferpH 7.452pCO2 45.1 mm Hg base abnormalitypO2 112.3 mm Hg : does not consider actual buffering capacity ofCorrected 38.6 0C bloodpH 7.436pCO2 47.6 mm HgpO2 122.4 mm HgCalculated Data Base Excess: D base to normalise HCO3 (to 24) with PCO2 at 40HCO3 act 31.2 mmol / L mm HgHCO3 std 30.5 mmol / L (Sigaard-Andersen)BE 6.6 mmol / LO2 ct 15.8 mL / dl : reflects metabolic part of acid base DO2 Sat 98.4 % : no info. over that derived from pH, pCO2ct CO2 32.5 mmol / LpO2 (A -a) 30.2 mm Hg  and HCO3pO2 (a/A) 0.78 : Misinterpreted in chronic or mixed disordersEntered DataTemp 38.6 0CFiO2 30.0 %ct Hb 10.5 gm/dl
    20. 20. "Step –wise approach" for ABG analysis 1. Consider the Clinical Setting. 2. Obtain ABG and Electrolyte values simultaneously. 3. Verify the ABG values. 4. Identify the nature of the disturbance. 5. Calculate the Anion gap in case of MA. 6. Assess ∆AG, ∆ HCO3, ∆Cl & ∆Na 7. Detecting mixed disorders. 8. Clinical correlation
    21. 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. 22. Sampling for ABG analysis Perform Allen’s test. Special mention Clean the site. Use 21 gauze needle with syringe. 1. Specimens held at room temperature must be analyzed within 10-15 minutes of drawing; iced Flush syringe and needle with heparin. samples should be analyzed within 1 hour. Enter skin at 45 angle 2. The PaO2 of samples drawn from subjects with Obtain 2-4ml blood without aspiration. Avoid suction of syringe . elevated white cell counts may decrease very rapidly. If sample contains any air bubble, tap it to the surface and push it out of the syringe. Immediate chilling is necessary. in PaO2 and Air bubbles can lead to increase decrease in PaCO2. Apply firm pressure at punctured site.
    23. 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 patients 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. 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. 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. For every 0.1 decrease in pH, [H+] increases by 10nmol/L• Thus, HCO3 can now be calculated from [H+] and PaCO2 using the Henderson equation. [H+]=24 (PaCO2/ [HCO3])
    26. 26. Step 3 Identify the disorder• Take a look at the pH, as it directs towards the principal disorder. < 7.35• Acidosis >7.45 • Alkalosis • Normal 7.35- • Mixed 7.45 disorder
    27. 27. PCO2HCO3 pHpH
    28. 28. •MetabolicHCO3 Disorder •RespiratoryPaCO2 Disorder
    29. 29. During compensation HCO3¯ & PaCO2 move in the same direction
    30. 30. Compensatory changes (Respiratory disorders).Primary Primary Compensatory Expected Compensation Limits ofdisorder defect response compensationRespiratory ↑ PCO2 ↑ HCO3 Acute: [HCO3]=38acidosis + 1 Meq/L ↑ HCO3 for each ↑ Meq/L PCO2 of 10mmHg Chronic: [HCO3]=45 +4 Meq/L ↑ HCO3 for each ↑ Meq/L PCO2 of 10mmHgRespiratory ↓ PCO2 ↓ HCO3 Acute: [HCO3]=18Alkalosis -2Meq/l ↓ in HCO3 for each ↓ in Meq/L PCO2 of 10mmHg Chronic: [HCO3]=15 -5 Meq/L ↓ in HCO3 for each ↓ in mEq/L PCO2 of 10mmHg 1 4 2 5
    31. 31. Compensatory changes (Metabolic disorders).Primary Primary Compensatory Expected Compensation Limits ofdisorder defect response compensationMetabolic ↓ HCO3 ↓ PCO2 PCO2=1.5[HCO3] + 8 ± 2 PCO2=15mmHgacidosis PCO2= last 2 digits of pH X 100 PCO2= 15+ [HCO3]Metabolic ↑ HCO3 ↑ PCO2 PCO2= + 0.6 mmHg for Δ [HCO3] of PCO2=55mmHgAlkalosis 1 mEq/L PCO2=15+ [HCO3]
    32. 32. Body’s physiologic response to Primary disorderin 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
    33. 33. Step 5 Anion Gap AG= Na⁺ – (Cl¯ + HCO3¯)• 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)
    34. 34. • Anion gap can increase either due to: – Increase in the unmeasured anions. – Decrease in the unmeasured cations ( hypocal, hypomag)• 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)
    35. 35. Step 6 & 7 Detecting mixeddisorders Clues to the presence of a mixed disorder. • Clinical history • pH normal, abnormal PCO2 n HCO3 • PCO2 n HCO3 moving opposite directions • Acid Base map (Flenley Nomogram) • Degree of compensation for primary disorder is inappropriate • Find Delta Gap
    36. 36. Flenley Nomogram
    37. 37. • 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 AlkalosisIf, PCO2 is > 28, Metabolic acidosis + Respiratory Acidosis
    38. 38. Δs 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
    39. 39. Delta gapDelta 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
    40. 40. 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 acidosisIf there is a disproportionate increase of Cl= Metabolic acidosis or Respiratory alkalosis
    41. 41. "Step –wise approach" for ABG analysis 1. Consider the Clinical Setting. 2. Obtain ABG and Electrolyte values simultaneously. 3. Verify the ABG values. 4. Identify the nature of the disturbance. 5. Calculate the Anion gap in case of MA. 6. Assess ∆AG, ∆ HCO3, ∆Cl & ∆Na 7. Detecting mixed disorders. 8. Clinical correlation
    42. 42. Interpretation with examples
    43. 43. Clinical examples
    44. 44. 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, pCO2 16 mmHg, pO2 128 mmHg, HCO3 7.1 mmol/l
    45. 45. • 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 CORRECT• Look at the pH: 7.26 ACIDOSIS• Then find the primary disorder: Low HCO3 along with low pCO2 suggests a METABOLIC disorder.
    46. 46. • Check for compensation: compensation for metabolic acidosis brings pCO2 to 16.5-20.6 mmHg. Thus the acidosis is FULLY COMPENSATED by respiratory regulation and there is NO MIXED disorder. HIGH ANION• Anion Gap= 136-(101+7.1)=28.1 GAP acidosis• ∆AG=27.9-12=15.9, ∆HCO3=24-7.1=14.9• Delta ratio=15.9/14.9=1.07 PURE ANION GAP ACIDOSIS• Na is normal with low Cl (NO HYPERCHLOREMIA) PURE ANION GAP FINAL ABG DIAGNOSIS METABOLIC ACIDOSIS (Etiology, DKA)
    47. 47. 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
    48. 48. • Clinical possibilities: – Severe hypokalemis to be corrected immediately – Respiratory acidosis (respiratory failure) – Respiratory alkalosis (dyspnea) – Metabolic alkalosis (diuretics)• Look at the pH: 7.64 ALKALOSIS• Then find the primary disorder: Low pCO2 along with high HCO3 suggests a MIXED ALKALOSIS.
    49. 49. 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
    50. 50. For the audiencePh 6.99PCo2 10.5 mmHgP02 111 mmHg Expected fall in PCO2BE -29 mmol/L =(1.5 x HCO3)+8HCo3 2.6 = (1.5 x 2.6) +8 2 = 9.9 to 13.9Tco2 45 Thus the compensation isSO2 95 within limits and theNa+ 138 mmol/L diagnosis isK+ 4.2 mmol/L COMPENSATEDiCa+ 1.06 mmol/L METABOLIC ACIDOSISHb 12.6 g/dl
    51. 51. For the audiencePrimary dis- Respiratory alkalosis.For acute Resp. alkalosis---Expected HCO3 = 24- 2(40-19)/10 = 19.8but actual HCO3=13.5 which isless then the expected. So it is mixed disorder with Respiratory alkalosis with Metabolic acidosis
    52. 52. “Understanding ABG is notmagic but an art learned by continued practice”
    53. 53. THANK YOU

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