ABG Analysis

A brief presentation on ABG analysis, mainly sourced from The ICU Book by Paul Marino

1. ARTERIAL BLOOD GAS ANALYSIS C hairperson: Dr. Vandana G ogate Presenter s : Dr . Priyanka Gadvi Dr. Ashwin Haridas JNMC, Belagavi

2. Life is a struggle, not against sin, not against money, power... but against hydrogen ions. - H.L. Mencken

3. Outline What is an ABG? Why order one? How to take a sample? Basics of acid-base balance Compensation Steps to analyse an ABG report Individual disorders

4. What does an ABG report tell you? pH, PaCO 2 and HCO 3 - PaO 2 and SaO 2 BE Electrolytes like Na + , K + , Ca 2+ , Cl - RBS

5. Why Order A n A BG? Aids in establishing a diagnosis Helps to guide a treatment plan Aids in ventilator management Improvement in acid/base manage allows for optimal function of drugs

6. How to take an ABG sample? Consent & patient identification Equipment Heparinized syringe* with 23G hypodermic needle Cotton swabs Spirit Allen’s test

7. Not what you want to see

8. How to take an ABG sample? Radial artery is preferred Easily accessible Easily compressible Good collaterals Brachial, femoral and dorsalis pedis may be used May be harder to locate and have poor collaterals Higher risk of hematoma Supinate and extend the wrist, you can use an NS bottle

9. How to take an ABG sample? Palpate the radial artery and disinfect the puncture site Steady the patient’s hand Hold the heparinised syringe like a pen and go at a 45 degree angle Syringe should fill by itself 1-2 ml should suffice

10. How to take an ABG sample? Remove the needle and put pressure on the puncture site for five minutes or till the bleeding stops Remove air bubbles Cap and the send the syringe ASAP If there is a delay in sending the sample you may keep it in a cold box with ice packs Mention FiO 2 while sending the sample Dress the puncture site

11. BASICS

12. pH pH is the negative common logarithm of the hydrogen ion concentration ‘Power of hydrogen’ pH = -log[H + ]

13. Logarithm

14. Why is the pH important? Enzymes Proteins get denatured Cardiac conduction Neuronal conduction Drugs might not act

15. The Balance  

16. How is the balance maintained? Pulmonary regulation Changes in the tidal volume and minute ventilation pH sensed through arterial chemoreceptors Takes place in minutes to hours Renal regulation Adjusting the amount of HCO3 - that is excreted and reabsorbed HCO3 - reabsorption is equivalent to excreting an H + ion Mainly in the proximal collecting tubule Can also synthesise ammonia

17. Renal Regulation

18. How is the balance maintained? contd. Buffers React immediately Carbonate buffer Phosphate buffer Haemoglobin buffer Protein buffers

19. NORMAL VALUES

20. pH = 7.35 – 7.45 PaO 2 = 80 – 100 mmHg on room air HCO 3 = 22 – 26 mEq /L PaCO 2 = 35 – 45 mmHg BE = -2 to +2 mEq /L

21. DISORDERS

22. Compensation or the Secondary Responses

23. Responses to Metabolic Disorders Metabolic Acidosis PaCO 2 = 1.2 * HCO 3 Expected PaCO 2 = 40 – (1.2 * (24 – current HCO 3 ) Metabolic Alkalosis PaCO 2 = 0.7 * HCO 3 Expected PaCO 2 = 40 + (0.7 * (current HCO 3 – 24)

24. Responses to Respiratory Disorders Acute respiratory acidosis HCO 3 = 0.1 * PaCO 2 Acute respiratory alkalosis HCO 3 = 0.2 * PaCO 2 Neither of the above changes are significant For chronic respiratory disorders HCO 3 = 0.4 * PaCO 2 Expected HCO 3 = 24 + [0.4 * (current PaCO 2 – 40)] for acidosis Expected HCO 3 = 24 - [0.4 * (40 – current PaC0 2 )] for alkalosis

25. Rule of same direction In simple acid base disorder HCO 3 and PaCO 2 compensatory changes are in the same direction HCO 3 leads to PaCO 2 HCO 3 leads to PaCO 2 This will bring pH to wards normal although not to normal Change in o pposite direction or not equal to expected suggestive of mixed disorder

26. A Stepwise Approach to Acid-Base Interpretation T he first stages will allow to identify major acid-base abnormalities using only three variables: pH, PaCO 2 , and HCO 3 The last stage allows to further investigate cases of metabolic acidosis using commonly measured serum electrolytes.

27. Stage I: Identify the Primary Acid-Base Disorder In the first stage the PaCO 2 and pH are used to determine if an acid-base disturbance is present and, if so, to identify the primary acid-base disorder.

28. Stage I Rule 1: An acid-base abnormality is present if either the PaCO 2 or the pH is outside the normal range.

29. Stage I Rule 2: If the pH and PaCO 2 are both abnormal, compare the directional change. If both change in the same direction the primary disorde r is metabolic . If both change in opposite directions, the primary acid-base disorder is respiratory.

30. Stage I Rule 3: If either the pH or PaCO 2 is normal, there is a mixed metabolic and respiratory acid-base disorder . If the pH is normal, the direction of change in PaCO 2 identifies the respiratory disorder I f the PaCO 2 is normal, the direction of change in the pH identifies the metabolic disorder.

31. Stage II: Evaluate Compensatory Responses The second stage of the approach is for cases where a primary acid-base disorder has been identified in Stage I. If a mixed acid-base disorder was identified in Stage I, go directly to Stage III The goal in Stage II is to determine if the compensatory responses are adequate and if there are additional acid-base derangements.

32. Stage II Rule 4: If there is a primary metabolic acidosis or alkalosis, use the measured HCO 3 to identify the expected PaCO 2 . If the measured and expected PaCO 2 are equivalent, the condition is fully compensated. If the measured PaCO 2 is higher than the expected PaCO 2 , there is a superimposed respiratory acidosis. If the measured PCO 2 is less than the expected PCO 2 , there is a superimposed respiratory alkalosis.

33. Stage II Rule 5: For a primary respiratory disorder, a normal or near-normal HCO 3 indicates that the disorder is acute. Rule 6: For a primary respiratory disorder where the HCO 3 is abnormal, determine the expected HCO 3 for a chronic respiratory disorder.

34. Stage II: Rule 6 For a chronic respiratory acidosis, if the HCO 3 is lower than expected, there is an incomplete renal response, and if the HCO 3 is higher than expected, there is a secondary metabolic alkalosis. For a chronic respiratory alkalosis, if the HCO 3 is higher than expected, there is an incomplete renal response, and if the HCO 3 is lower than expected, there is a secondary metabolic acidosis.

35. Stage III: Use The Anion Gap to Evaluate Metabolic Acidosis The final stage of this approach is for patients with a metabolic acidosis, and it involves determination of the anion gap It is a n estimate of unmeasured anions that helps to identify the cause of a metabolic acidosis.

36. A 20 year old primipara with severe protracted vomiting presents to you in a confused and irritable state. ABG revealed pH – 7.6, PCO2 -

37. Metabolic A lkalosis C haracterized by hyperbicarbonatemia (>27 mEq/L) and by an alkalemic pH (>7.45) Factors that generate metabolic alkalosis include vomiting and diuretic use

38. Metabolic Alkalosis A ssociated with H ypokalemi a V entricular arrhythmias H ypercarbia , although compensation rarely results in Pa CO 2 >55 mm Hg.

39. Metabolic Alkalosis Causes Saline responsive (urine chloride <15mEq/L) Vomiting/Gastric suction Diuretics (K + ) Multiple transfusion Saline resistant (urine chloride>20mEq/L) Hyperaldosteronism Cushing syndrom e

40. Metabolic Alkalosis Clinical features CNS: Neuromuscular excitability, paresthesia, l ight headache CVS : Hypotension,cardiac arrhythmia s RS: Compensatory hypo - ventilation

41. Metabolic Alkalosi s Treatment Treat the underlying cause Saline responsive alkalosis Adequate correction of volume, IV isotonic saline H1 inhibitor or PPI to decrease gastric secrection Avoid exogenous sources of alkali such as NaHCO 3 infusion,

42. Metabolic Alkalosis If alkalosi s is due to diuretics, dose reduction may be required, KCL supplementation, spironolactone or carbonic anhydrase inhibitor. Saline resistant metabolic acidosis Needs specific treatment of underlying causes (surgical treatment of pitutary tumor or adrenal adenoma in cushing syndrome) Supportive treatment such as spiranolactone

43. Type 1 DM patient who missed his last three doses of insulin presents with vomiting, abdominal pain and deep sighing breathing. ABG revealed pH- 7.1, PaO 2 - 88mmHg, HCO 3 - 8 mEq /L, and PaCO 2 – 20 mmHg. Na – 140 mEq /L, Cl – 106 mEq /L and urine ketone bodies were positive.

44. Metabolic Acidosis Metabolic acidosis, characterized by hypobicarbonatemia (<21 mEq/L) and by an acidemic pH (<7.35). Metabolic acidosis occurs as a consequence of buffering by bicarbonate of endogenous or exogenous acid loads or as a consequence of abnormal external loss

45. Pathophysiology of Metabolic Acidosis Loss of base HCO 3 via GI tract Over production of metabolic acids in the body Ingestion or infusion of acid or potential acids Failure of H + excretion by kidney

46. Metabolic Acidosis Causes of high anion gap metabolic acidosis DKA Alcoholic ketoacidosis Lactic acidosis Methanol poisoning Salicylate poisoning Ethlylene glycol poisoning

47. Metabolic Acido sis Causes of normal anion gap acidosis Diarrhoea RTA Acetazolamide Pancreatic fistula

48. Metabolic Acidosi s Clinical features RS : Kussumal breathing CVS: A rrhythmia s , decrease in response to i n ot r opes, secondary hypotension CNS: Headache, confusion, lethargy

49. Metabolic Acidosis - Treatment Treat the underling cause Alkali therapy Correct volume status and electrolyte imbalance

50. Metabolic Acidosis - Treatment Alkali therapy Amount of HCO 3 required = (desired HCO 3 -actual HCO 3 ) ×0.5× body weight in kg Carbicarb - generates bicarbonate rather than CO 2

51. Patient with a history of overdosing on her sleeping pills presents in a drowsy state with sluggish respiration. ABG revealed pH – 7.1, HCO 3 – 28 mEq /L, PaCO 2 – 72 mmHg and PaO 2 of 78 mmHg.

52. Respiratory Acidosis Characterized by hypercarbia (Pa CO 2 ≥ 45 mm Hg) and low pH (<7.35), occurs because of a decrease in minute alveolar ventilation Respiratory acidosis may be either acute, without compensation by renal or chronic, with compensation
A reduction in minute ventilation may be due to an overall decrease an increase in production of carbon dioxide (V CO2 )

53. Respiratory Acidosis Decreases in minute ventilation may occur C entral ventilatory depression by drugs C entral nervous system injury I ncreased work of breathing A irway obstruction N euromuscular dysfunction.

54. Respiratory Acidosis Increases in dead space volume occur with COPD P ulmonary embolism Consolidations Mucus plugs or foreign body

55. Respiratory Acidosis Clinical features Hypercapnia causes neurological features - anxiety, headache, confusion, psychosis, hallucination & coma Mild to moderate chronic Hypercapnia may cause sleep disturbance, loss of memory, daytime somnolence, personality changes, impairment of coordination, tremors and myoclonic jerks

56. Treatment of Respiratory Acidosis Identify and treat the underlying cause Establish patent airway to restore OXYGENATION Oxygen therapy Mechanical ventilation - hyperventilate

57. A 26 year old male with septic shock is on volume control ventilation since the last 4 hours. ABG reveals pH – 7.8, HCO 3 – 14 mEq /L, PaCO 2 – 22 mmHg, PaO 2 – 250mmHg.

58. Respiratory Alkalosis Respiratory alkalosis, characterized by hypocarbia (PaCO 2 ≤ 35 mmHg) and an alkalaemic pH (>7.45) Results from an increase in minute ventilation that is greater than that required to excrete metabolic CO 2 production.

59. Respiratory Alkalosis Respiratory alkalosis may be a sign of pain, anxiety, hypoxemia, central nervous system disease or systemic sepsis Development of spontaneous respiratory alkalosis in a previously normo-carbic patient requires prompt evaluation.

60. Respiratory Alkalosis Most frequently encountered acid base disorder, since it occurs in normal pregnancy and high altitude Anxiety or pain induced hyperventilation Excessive mechanical ventilation

61. Respiratory Alkalosis Clinical features Light headache, tingling of the extremities, circumoral anaesthesia , headache, shortness of breath and chest wall tightness

62. Respiratory Alkalosis Treatment of respiratory alkalosis per se is often not required. The most important steps are recognition and treatment of the underlying cause.

63. Summary ABG analysis requires a thorough understanding of acid-base physiology There are no shortcuts Always correlate with the clinical scenario Just trying to correct any derangement from the normal values is not enough Correct the underlying cause

64. References Marino L. The ICU Book, Fourth Edition, Wolters Kluwer, New Delhi, 2016 Miller RD, Eriksson LI, Fleisher LA, Wiener- Kronish JP, Young WL, editors. Miller’s Anesthesia: 8 th edition. Philadelphia: Elsevier Saunders; 2015 Barash P, Cullen B, Stoelting R, Cahalan M, Stock M, editors. Clinical Anesthesia: 7 th edition. Lippincott Williams and Wilkins, 2013. Thomas EJ Healy, Paul RK, Editors. Wylie and Churchill- Davidson’s A practice of Anaesthesia : 7 th Edn, London: Arnold;2003

65. Thank you for listening