"Mastering Arterial Blood Gas (ABG) Analysis: A Practical Guide for Clinicians" - by Dr Bodhisatwa Choudhuri

Dive into the essentials of Arterial Blood Gas (ABG) analysis with this comprehensive presentation by Dr. Bodhisatwa Choudhuri, an expert in Critical Care and Emergency Medicine. This guide covers the critical components of ABG—including pH, PaCO₂, PaO₂, and bicarbonate (HCO₃)—and demonstrates their significance in diagnosing and managing respiratory and metabolic imbalances. Learn when to order ABG tests, interpret results systematically, and apply clinical insights to optimize patient outcomes. Ideal for medical professionals aiming to strengthen their understanding of ABG interpretation and management in emergency and ICU settings.

It includes the following -

Introduction
Indication
Technique
Evaluation
A-a Gradient
Steps of Interpretation
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
Mixed Acid-Base Disorders
Delta Gap
Compensation
Sequalae
Cases

1. ARTERIAL BLOOD GAS Dr Bodhisatwa Choudhuri MBBS, MD(Med), MEM(USA), MRCEM(UK), MRCP Acute Medicine, FCCS, Dip Rheumatology (UK), CCEBDM, CCIDC Consultant & In-charge, Critical Care & Emergency, Rheumatology, Parkview Super-specialty Hospital, Saltlake, Kolkata

2. What is an ABG? The Components pH / PaCO 2 / PaO 2 / HCO 3 / O 2 sat / BE Desired Ranges ABG VBG pH 7.35-7.45 7.32-7.42 PaCO2 35-45 mmHg 38-52 mmHg PaO2 80-100 mmHg 28-48 mmHg HCO3 21-27 19-25 SO2 95-100% 60-74% Base Excess +/-2 mEq /l +/-2 mEq /l

3. Why Order an ABG? Aids in establishing a diagnosis Helps guide treatment plan Aids in ventilator management Improvement in acid/base management allows for optimal function of medications Acid/base status may alter electrolyte levels critical to patient status/care

4. Indications for Ordering an ABG When there are concerns about VENTILATION (or, are they breathing enough?): Not awake enough to breathe: Obtunded COPD patient (due to hypercarbia) To verify no hypercarbia in a patient with altered mental status/obtundation Breathing too fast/concern for poor gas exchange or muscle fatigue: Anxious asthmatic/COPD breathing fast Septic patient breathing fast with concern for “tiring out”

5. Indications for Ordering an ABG When there are concerns about OXYGENATION when O 2 Sat doesn’t suffice Concern for Carbon Monoxide Intoxication ( carboxyhemoglobinemia ) or Methemoglobinemia (e.g. Benzocaine intoxication, congenital) On day of discharge to verify PO 2 >60, for the patient to qualify for home oxygen To determine the A-a gradient

6. Indications for Ordering an ABG When there are concerns about ACID-BASE BALANCE: Sepsis DKA Poly-drug overdose Increased anion gap or decreased bicarbonate To assess “adequacy of resuscitation” in both sepsis and trauma (Lactic Acid may be substituted for ABGs)

7. Indications for Ordering an ABG Miscellaneous: After intubation in all patients To monitor progression of disease or response to therapy in ventilated ICU patients or COPD patients on BiPap/after other interventions For rapid (<10 minutes) assessment of sodium, potassium, chloride, ionized calcium (“ABG Plus”) During the “Apnea Test” to determine brain death To assess for candidacy for extubation as one of many criteria (ABG not required in every patient)

8. Keys to proper ABG Management Order the test when you need it Interpret the ABG fully everytime , and SYSTEMATICALLY Don’t stop there: Treat the patient based on your interpretation Always interpret the ABG in the context of the patient you are treating (particularly when looking at the PCO2)

9. Technique Prior to drawing blood the syringe should be heparinised . About 0.05-0.1 ml heparin(1000units/ml) anticoagulates 1 ml blood. Excess heparin alters pH, PO2, PCO2. Pre- filled syringes are available. About 2-3 ml blood is required for analysis. ABG samples should be drawn in strict anaerobic conditions, placed in ice and held at 0 c till analysis to prevent ongoing cellular metabolism and o2 consumption. Air bubbles in sample overestimates Po2 & underestimates Pco2. Prior to drawing ABG, check for the status of distal circulation. Perform modified Allen test prior to radial art puncture. Low predictive value. When using the femoral and brachial artery, check distal pulses and signs of peripheral arterial disease and arterial insufficiency.

10. 0 10 20 30 40 50 60 70 80 90 100 PaO 2 20 40 60 80 100 Rt. Shift Normal arterio/venous difference Shift of the curve ……changes saturation for a given PaO 2 Normal Oxygen delivered to tissues with normally placed curve Delivered oxygen with Rt. Shift curve

11. Evaluate Oxygenation and Adequacy of Ventilation PaO2 < 80 mm hg, consider Hypoxemia Causes: Alveolar Hypoventilation, VQ mismatch, Rt-Lt shunting, Diffusion impairment, Reduced inspired oxygen tension. Pt remains hypoxic in spite of adequate oxygenation and ventilation, calculate the A-a gradient (Alveolar Arterial oxygen gradient)

12. A-a Gradient Tells you whether oxygen is appropriately getting into the blood through the lungs or not A = Alveolar (or, the partial pressure of oxygen that you’re breathing) a = arterial (or, the partial pressure of oxygen getting into your blood stream) At sea level on room air, Alveolar O2 =150 – (PaCO2/0.8). The A-a gradient is calculated by subtracting the MEASURED arterial O2 from this value

13. A-a gradient (continued) “Normal” = (Age/4) + 4 28 year olds should have an A-a gradient of 11; 80 year olds should have an A-a gradient of 24 A-a gradient goes up as your FiO2 goes up (that’s normal) NOTE: A “normal” A-a gradient still does not rule out pulmonary embolism. Abnormal A-a gradient Indicative of some sort of Ventilation-Perfusion (V-Q) mismatch

14. Alveolar-arterial Difference Inspired O 2 = 21 % p i O 2 = (P atm O 2 – P H2O O 2 ) x FiO2 = (760-45) x .21 = 150 mmHg O 2 CO 2 p alv O 2 = p i O 2 – pCO 2 / RQ = 150 – 40 / 0.8 = 150 – 50 = 100 mm Hg PaO 2 = 90 mmHg p alv O 2 – p art O 2 = 10 mmHg

15. Alveolar- arterial Difference O 2 CO 2 Oxygenation Failure WIDE GAP p i O 2 = 150 pCO 2 = 40 p alv O 2 = 150 – 40/.8 =150-50 =100 PaO 2 = 45 (A-a) = 100 - 45 = 55 Ventilation Failure NORMAL GAP p i O 2 = 150 pCO 2 = 80 p alv O 2 = 150-80/.8 =150-100 = 50 PaO 2 = 45 (A-a) = 50 - 45 = 5

16. Oxygenation Treatment Keep the PaO2>60 mm Hg (>=70 mm Hg is reasonable for all except CO2 retainers, where the goal should be 60 mm Hg, or an O2 Sat of 90-93%) Minimize damage to the lungs (FiO2 at >60% for prolonged periods of time may lead to free radical formation and lung toxicity; get the FiO2 down to 60% or less as soon as the patient’s oxygenation allows)

17. 20 × 5 = 100 Expected PaO 2 = FiO 2 × 5 = PaO 2 Normal situation

18. 5 The Steps for Successful Blood Gas Analysis

19. INTERPRETATION OF ABG LOOK FOR pH WHO IS THE CULPRIT ? IF RESPIRATORY, ACUTE / CHRONIC ? IF METABOLIC, COMP. / ANION GAP CLINICAL CORRELATION

20. Check Validity of ABG Assess the internal consistency of the report using the Henderson- Hasselbach equation [H+] =24(PaCO2)/HCO3- If the H+ and HCO3 are inconsistent, the ABG is not valid pH is inversely related to [H + ]; a pH change of 1.00 represents a 10-fold change in [H + ] pH [H + ] in nanomoles/L 7.00 100 7.10 80 7.30 50 7.40 40 7.52 30 7.70 20 8.00 10

21. Step 2 Who is responsible for this change in pH - CO 2 will change pH in opposite direction - Bicarb will change pH in same direction Acidemia : With HCO 3 < 20 mmol/L = metabolic With PCO 2 >45 mm Hg = respiratory Alkalemia : With HCO 3 >28 mmol/L = metabolic With PCO 2 <35 mm Hg = respiratory Step 1 Look at the pH Is the patient acidemic pH < 7.35 alkalemic pH > 7.45

22. Step 3 If there is a primary respiratory disturbance, is it acute or chronic? 0.08 change in pH (Acute) 0.03 change in pH (Chronic) 10 mm Change PaCO 2 =

23. Step 4 If the disturbance is metabolic is the respiratory compensation appropriate? For metabolic acidosis: Expected PaCO 2 = (1.5 x [HCO 3 ]) + 8) + 2 or simply… expected PaCO 2 = last two digits of pH For metabolic alkalosis: Expected PaCO 2 = 7mm for 10 mEq . rise in Bicarb. Suspect if ............. actual PaCO 2 is more than expected : additional …respiratory acidosis actual PaCO 2 is less than expected : additional …respiratory alkalosis

24. Step 4 cont . If there is metabolic acidosis, is there an anion gap ? Na + + Unmeasured cation = (HCO3 - + Cl - ) + Unmeasured anion Anion Gap = Unmeasured anion - Unmeasured cation = Na + - ( HCO3 - + Cl - ) usually <12 If >12, High Anion Gap Metabolic Acidosis Common Causes : M ethanol U remia D iabetic Ketoacidosis P araldehyde I nfection (lactic acid) E thylene Glycol S alicylate Common pediatric causes Lactic acidosis Metabolic disorders Renal failure

25. th step Clinical correlation 5

26. HCO3 META. pH PaCO 2 pH RESP. Same direction Opposite direction

27. Metabolic Acidosis  pH,  HCO 3 12-24 hours for complete activation of respiratory compensation  PCO 2 by 1.2mmHg for every 1 mEq /L  HCO 3 The degree of compensation is assessed via the Winter’s Formula: Expected PCO 2 = [1.5(HCO 3 ) +8]  2

28. The Causes High Anion Gap Metabolic Acidosis M - Methanol U - Uremia D - DKA P - Paraldehyde I - INH L - Lactic Acidosis E - Ehylene Glycol S - Salicylate Non Anion Gap Metabolic Acidosis Hyperalimentation Acetazolamide RTA (Calculate urine anion gap) Diarrhea Pancreatic Fistu la

29. If AG is high, calculate the osmolar gap in compatible clinical scenarios like a suspected toxic ingestion. Osmolar gap = 2[Na+]+ Glucose/18- BUN/2.8 Normal < 10 Causes of High OG: Methanol Glycine (TRUP) Ethylene Glycol Propylene Glycol Sorbitol Polyethylene Glycol Mannitol Maltose (IV IG)

30. NAGMA Urinary anion gap = (Urine Na + + Urine K + ) - Urine Cl - In RTA - Urine anion gap is positive RTA Urine pH > 6.0 – Type I RTA Urine pH < 5.5 – Type II/IV RTA In GI causes - Urine anion gap is negative

31. Primary lesion Compensation pH Bicarbonate PaCO 2 METABOLIC ACIDOSIS HYPER VENTILATION BICARB CHANGES pH in same direction Low Alkali

32. Metabolic Alkalosis  pH,  HCO 3  PCO 2 by 0.7 for every 1mEq/L  in HCO 3 In a metabolic alkalosis, the patient will breathe slower to retain CO2. The formula for compensation is as follows: Expected PCO2 = [0.9 (HCO3) + 15] +/-5 Causes Vomiting Diuretics Chronic diarrhea Rapid correction of chr hypercapnea Cystic Fibrosis Laxative Abuse “Chloride Unresponsive” (Urine Na> 20 ) “Chloride Responsive” (Urine Na <10) Hypokalemia Renal Failure Excess Mineralocorticoid (Cushing’s, ACTH excess) Bartter’s Syndrome

33. Primary lesion Compensation pH Bicarbonate PaCO 2 METABOLIC ALKALOSIS HYPO VENTILATION BICARB CHANGES pH in same direction High Alkali

34. Respiratory Acidosis  pH,  CO 2,  Ventilation Causes CNS depression Pleural disease COPD/ARDS Musculoskeletal disorders Compensation for metabolic alkalosis

35. Respiratory Acidosis Acute vs Chronic Acute - little kidney involvement. Buffering via titration via Hb pH  by 0.08 for 10mmHg  in CO 2 pH = 0.008 x [PCO2-40]) Chronic - Renal compensation via synthesis and retention of HCO 3 (  Cl to balance charges) pH  by 0.03 for 10mmHg  in CO 2 pH = 0.003 x [PCO2-40])

36. Primary lesion compensation pH PaCO 2 BICARB Respiratory acidosis CO 2 CHANGES pH in opposite direction High CO 2

37. Respiratory Alkalosis  pH,  CO 2,  Ventilation  CO 2  HCO 3 (  Cl to balance charges hyperchloremia) Causes Intracerebral hemorrhage Salicylate and Progesterone drug usage Anxiety Cirrhosis of the liver Sepsis (Early stage)

38. Respiratory Alkalosis Acute -  HCO 3 by 2 mEq/L for every 10mmHg  in PCO 2 Chronic - Ratio increases to 4 mEq/L of HCO 3 for every 10mmHg  in PCO 2 Decreased bicarb reabsorption and decreased ammonium excretion to normalize pH

39. Primary lesion compensation pH PaCO 2 BICARB Respiratory alkalosis PaCO 2 CHANGES pH in opposite direction Low PaCO 2

40. Mixed Acid-Base Disorders Patients may have two or more acid-base disorders at one time

41. Delta Gap Delta gap = (change in anion gap) - (change in bicarbonate) = (AG – 12) – (24 – HCO3) (The normal anion gap is assumed to be 12, and the normal HCO 3  is assumed to be 24) Simplified Delta gap = Na +  - Cl -  - 36 Interpretation of the generated gap: -6 = Mixed high and normal anion gap acidosis -6 to 6 = Only a high anion gap acidosis exists over 6 = Mixed high anion gap acidosis and metabolic alkalosis

42. Delta Ratio or Delta Delta Gap Delta ratio = (change in anion gap) / (change in bicarbonate) = ∆AG/ ∆HCO3 = (AG-12)/(24–HCO3) (The normal anion gap is assumed to be 12, and the normal HCO 3  is assumed to be 24) Interpretation of the generated ratio: 0.4 = normal anion gap metabolic acidosis 0.4-0.8 = mixed high and normal anion gap acidosis exists. 0.8-1.0 = purely due to a high anion gap metabolic acidosis 1.0-2.0 = still purely a high anion gap metabolic acidosis Over 2.0 = high anion gap acidosis with pre-existing metabolic alkalosis

43. compensation considered complete when the pH returns to normal range

44. COMPENSION LIMITS METABLIC ACIDOSIS PaCO2 = Up to 10 ? METABOLIC ALKALOSIS PaCO2 = Maximum 60 RESPIRATORY ACIDOSIS BICARB = Maximum 40 RESPIRATORY ALKALOSIS BICARB = Up to 10

45. Sequalae of Severe Acidosis (pH<7.2) Cardiovascular Decreased contractility Centralized blood volume Decreased CO and BP Increased arrhythmias Decreased responsiveness to catecholamines Respiratory Hyperventilation Resp. muscle fatigue Dyspnea Metabolic Increased metabolic demands Hyperkalemia (H-K) Insulin Resistance Obtundation, Coma

46. Squeal of Severe Alkalosis (pH>7.50) Cardiovascular Arteriolar constriction Decreased coronary blood flow Decreased angina threshold Predisposition to arrhythmias Respiratory hypoventilation Metabolic Stimulation of organic acid production Hypokalemia (H-K) Decreased ionized Ca Hypo Mg, Hypo Phos Cerebral Reduced blood flow Tetany, seizures, lethargy, delirium, stupor

47. Blood Gas Report Measured 37.0 o C pH 7.523 PaCO 2 30.1 mm Hg PaO 2 105.3 mm Hg Calculated Data HCO 3 act 22 mmol / L O 2 Sat 98.3 % PO 2 (A - a) 8 mm Hg D PO 2 (a / A) 0.93 Entered Data FiO 2 21.0 % Case 1 16 year old female with sudden onset of dyspnea . No Cough or Chest Pain Vitals normal but RR 56, anxious. Acute respiratory alkalosis

48. Case 2 6 year old male with progressive respiratory distress Muscular dystrophy . Blood Gas Report Measured 37.0 o C pH 7.301 PaCO 2 76.2 mm Hg PaO 2 45.5 mm Hg Calculated Data HCO 3 act 35.1 mmol / L O 2 Sat 78 % PO 2 (A - a) 9.5 mm Hg D PO 2 (a / A) 0.83 Entered Data FiO 2 21 % pH <7.35 :acidemia Res. Acidemia : High PaCO 2 and low pH Hypoxemia Normal A-a gradient ∆ CO 2 =76-40=36 Expected ∆ pH for ( Acute ) = .08 for 10 Expected ( Acute ) pH = 7.40 - 0.29=7.11 Chronic resp. acidosis Hypoventilation Chronic respiratory acidosis With hypoxia due to hypoventilation

49. 8-year-old male asthmatic; 3 days of cough, dyspnea and orthopnea not responding to usual bronchodilators. O/E: Respiratory distress; suprasternal and intercostal retraction; tired looking; on 4L O 2 NC. Blood Gas Report Measured 37.0 o C pH 7. 24 PaCO 2 49.1 mm Hg PaO 2 66.3 mm Hg Calculated Data HCO 3 act 18.0 mmol / L O2 Sat 92 % PO 2( A – a) 68 mm Hg D PO 2 (a/A) 0.4 Entered Data FiO 2 30 % pH <7.35 ; acidemia PaCO 2 >45; respiratory acidemia p i O 2 = 715x.3=214 / p alv O 2 = 214-49/.8=153 Wide A - a gradient Hypoxia WITH INCREASE IN CO 2 BICARB MUST RISE Bicarbonate is low……… Metabolic acidosis + respiratory acidosis ∆ CO 2 = 49 - 40 = 9 Expected ∆ pH ( Acute ) = 9/10 x 0.08 = 0.072 Expected pH ( Acute ) = 7.40 - 0.072 = 7.328 Acute resp. acidosis Case 3 8-year-old male asthmatic with resp. distress

50. Case 4 8yr old diabetic with respi . distress fatigue and loss of appetite. Blood Gas Report Measured 37.0 o C pH 7.23 PaCO2 23 mm Hg PaO2 110.5 mm Hg Calculated Data HCO 3 act 14 mmol / L O2 Sat % PO2 (A - a) mm Hg D PO2 (a / A) Entered Data FiO2 21.0 % pH <7.35 ; acidemia HCO3 <22; metabolic acidemia Last two digits of pH Correspond with co 2 If Na = 130, Cl = 90 Anion Gap = 130 - (90 + 14) = 26 High Anion Gap Metabolic Acidosis - DKA

51. Blood Gas Report Measured 37.0 o C pH 7.46 PaCO2 28.1 mm Hg PaO2 55.3 mm Hg Calculated Data HCO 3 act 19.2 mmol / L O2 Sat % PO2 (A - a) mm Hg D PO2 (a / A) Entered Data FiO2 24.0 % Case 5 : 10 year old child with encephalitis pH almost within normal range Mild alkalosis PaCO 2 is low, respiratory alkalosis low by around 10 ( Acute ) by .08 (Chronic ) by .03 BICARBONATURIA Bicarb looks low ? Is it expected ?

52. These findings are most consistent with…. a) Metabolic acidosis with compensatory Hypocapnia. b) Primary metabolic acidosis with respiratory alkalosis. c) Acute respiratory alkalosis fully compensated. d) Chronic respiratory alkalosis fully compensated . pH 7.39 PCO 2 15mmHg HCO 3 8mmol/L PaO 2 90 mmHg Case 6…………. For metabolic acidosis: FULL COMPENSATION Expected PaCO 2 = (1.5 x [HCO3]) + 8 ) + 2 (Winter’s equation) PCO 2 ……SHOULD BE 20

53. Adolescent boy with appendicitis , posted for surgery , he is a known case of SLE. His pre-op ABG (Room air) shows: pH 7.39 pCO 2 l5mmHg paO 2 90 mmHg HCO 3 8mmol/L These findings are most consistent with…. a) Metabolic acidosis with compensatory Hypocapnia. b) Primary metabolic acidosis with respiratory alkalosis. c) Acute respiratory alkalosis fully compensated. d) Chronic respiratory alkalosis fully compensated. What is the probable cause for the above findings ? Are they OK as far as oxygenation is concerned ? Case 7……….

54. Patient was hypo volumic , received Normal Saline bolus... Corrected acidosis He was operated ….but post-op became drowsy His ABG…….. FiO 2 30% pH 7.38 PaCO 2 38 PaO 2 60 1) Why hypoxemia ? 2) Were the lungs bad to begin with? ( PreOp PaO 2 90 mmHg ) 3) Micro atelectesis during surgery ? Anesthetist goofed up the case 4) Pure and simple hypoventilation …..Sedation ?

55. Why hypoxemia ? Lungs were bad to begin with ? Micro atelectesis during surgery Pure and simple hypoventilation ? sedation PRE Op ….ABG on room air pH 7.39 PaCO 2 l5mmHg PaO 2 90 mmHg HCO 3 8mmol/L Pre Op .....A/a gradient p alv O 2 = P i O 2 – PaCO 2 / RQ = 150 – 15 / 0.8 = 150 – 18 = 132 mm Hg A – a =132 – 90= 42 (WIDE A/a gradient) Oxygenation status good …..?

56. Apparently the lungs looked good with PaO 2 of 90……. But have a good look at the ABG again With wash out of CO 2 ………. The expected PaO 2 should have been more than 90 . This coupled with correction of acidosis ( normalizing PaCO 2 ) Lowered the PaO 2 …post operatively. Conclusion …….. Lungs were not normal to begin with ( SLE )……..

57. Thank You