ABG[1].pptx BY DR BHAWNA ESI PGIMSR, BASAIDA

ABG FOR ANAESTHESIA

1. Acid Base Gas (ABG) DR BHAWNA GARG MODERATOR: DR SANTOSH

2. Outlines of talk What’s an ABG? Difference between ABG and VBG Blood gas sampling Acid/Base Physiology Compensation General approach to ABG Interpretation Case scenarios Take home message

3. What is an ABG? Blood Gas drawn from an artery to assess oxygen deficiencies from primary ventilatory disturbances and/or metabolic acid-base abnormalities

4. Why Order an ABG? Aids in diagnosis Provides clues about clinically unrecognized disorders Helps guide treatment plan Aids in ventilator management Assess response to an intervention/ progress of illness Acid/base status may alter electrolyte levels critical to patient status

5. Which artery to choose?

6. Universal precautions Positioning (hyper-extending wrist) Palpate the arterial pulse & do ALLEN’s test Infiltrate 2% xylocaine Line the needle up with the artery, bevel side up Enter the artery & allow spontaneous fill of syringe Withdraw the needle & hold pressure on the site. Remove any air bubbles Gently mix the specimen by rolling it b/w palms Place the specimen on ice & transport immediately. Performing the Procedure: Allen’s test vs modified Allen’s test

7. Allen’s test The Allen's test assesses collateral circulation in the hand, in 2 steps . First – suspected radial artery occluded at wrist for 3 min , hand colour compared with the other hand, if no change means sufficient collaterals present through ulnar artery. Second – ulnar artery occluded for 3 min, change in colour of hand is highly suspicious of radial artery occlusion. Positive test – presence of radial artery occlusion. Step 2 occludes the ulnar artery. A change in hand color means the potential for radial artery occlusion is high. That is a positive Allen's test, which contraindicates radial-artery puncture

8. Modified allen’s test To assess ulnar artery collateral flow First – patient is asked to make tightly closed fist Second- pressure applied at wrist to compress both radial & ulnar artery Remove obstructing pressure from ulnar artery while keeping radial artery obstructed Flushing of palm within 5-15 sec- ulnar artery is capable of supplying entire hand while radial artery is occluded. This normal flushing of the hand is considered to be a positive modified Allen's test . A negative modified Allen's test is one in which the hand does not flush within the specified time period. This indicates that ulnar circulation is inadequate or nonexistent

9. Collection Problems Use of heparin Dilution effect -  HCO 3- & PaCO2 Air bubbles Specimen transport Sample to be analysed as soon as possible Iced sample can be stored for 1 hr in glass syringe and 15 min in plastic syringe Blood is living tissue that continues to consume O2 and produce CO2 PO2 150 mmHg & PCO2 0 mm Hg in air bubble (room air) In vivo values Air contamination pH 7.40 7.45 pCO2 40 30 pO2 95 110

10. Plastic vs glass syringes

11. Effect of Temperature Increased temperature Decreased temperature pO2 Increase Decrease pCO2 Increase Decrease pH Decrease Increase In pts with hypo/hyperthermia, body temp usually changes with time (per se/effect of rewarming/cooling strategies) – hence if all calculations done at 37 C easier to compare Values other than pH & PCO2 do not change much with temp

12. WBC Larcency Rare phenomenon due to very high levels of WBC(>50000) WBCs are metabolically active and consume the oxygen leading to a fall in PaO2 Solution: Get the ABG done within 5 min Others: Keep sample in ice / Add Potassium cyanide

13. Effect of anticoagulation

14. ABG Vs. VBG ABG VBG pH 7.4 7.35 PCO2 40 46 HCO3 24 25 pO2 80-100 < 40 O2 saturation >95 60-85

15. Normal reference range

16. Principles of Acid-Base Acid base relationship is critical for homeostasis pH is maintained by 3 systems Physiologic buffers Lungs Kidneys Disorders in any of these systems leads to alterations in blood pH

17. Buffers: Buffers in ICF Buffers in ECF Intracellular Proteins Carbonate-Bicarbonate Buffer 53% H 2 PO 4 -HPO 4 - system Plasma (35%) Erythrocyte(18%) Hemoglobin Plasma Proteins Organic & Inorganic Phosphates Intracellular buffers are responsible for ~85% buffering in Metabolic acidosis and ~35% in Metabolic alkalosis and almost complete buffering in Respiratory acidosis and alkalosis.

18. Lungs Changes in pH sensed by chemoreceptors Peripherally (carotid bodies) Centrally (medulla oblongata) Drop in pH-metabolic acidosis ↑ minute ventilation → ↓ PaCO2 Increase in pH –metabolic alkalosis ↓ ventilatory effort → ↑ PaCO2

19. Kidneys Play no role in acute compensation 6-12hrs respiratory acidosis Active excretion of H+ Retention of HCO3- >6hrs of respiratory alkalosis Active excretion of HCO3- Retention of H+

20. Blood Gas Report Acid-Base Information pH PCO2 HCO3 Oxygenation Information PO2 [oxygen tension] SO2 [oxygen saturation]

21. Oxygenation Information PaO2 80 - 100 mm Hg SaO2 95 - 100 % is a normal saturation pO2 (mm Hg) SpO2 (%) Normal values on air >80 >95 Mild hypoxemia 60-79 90-94 Moderate hypoxemia 40-59 75-89 Severe hypoxemia <40 <75

22. Inspired O2 – PaO2 Relationship FiO2 (%) Predicted minimum PaO2 (mmHg) 30 150 40 200 50 250 80 400 100 500 If PaO2 < FiO2 x 5, hypoxemic at room air

23. pH Normal serum pH is maintained within a very narrow range of 7.36-7.44 Acidosis (pH<7.35) Alkalosis (pH>7.45) Mild 7.3-7.34 7.46-7.5 Moderate 7.2-7.29 7.51-7.54 Severe <7.2 >7.55 Incompatible with life <6.8 >7.8

24. pCO2 PaCO2: partial pressure of carbon dioxide dissolved in the arterial plasma Normal: 35 - 45 mm Hg Is regulated in the lungs > 45 mm Hg = respiratory acidosis < 35 mm Hg = respiratory alkalosis

25. Bicarbonate (HCO3-) Std HCO3- : HCO3- levels measured in lab after standardizing at PCO2 of 40 mm Hg, temperature 37 degree C and SpO2 of 100% Actual HCO3- : HCO3- levels calculated from pH & PCO2 directly Reflection of non respiratory (metabolic) acid-base status Normal: 22 -26 mEq/L Is regulated by the kidneys < 22 = metabolic acidosis > 26 = metabolic alkalosis Significance – in cases of respiratory acidosis, actual bicarb > std bicarb

26. Simple vs Mixed Simple/Primary acid–base disorders : w hen compensation is appropriate A respiratory change is called “acute” or “chronic” depending on whether a secondary change in the bicarbonate concentration Mixed acid–base disorders When compensation is inappropriate i.e. the secondary response differs from that which would be expected Uncompensated Partially compensated Fully compensated Abnormal pH Abnormal pH Normal pH, other values abnormal

27.  acid-base disorders Disorder Primary Responses Compensation Metabolic acidosis  [H + ]  PH  HCO 3 -  pCO2 Metabolic alkalosis  [H + ]  PH  HCO 3 -  pCO2 Respiratory acidosis  [H + ]  PH  pCO2  HCO 3 - Respiratory alkalosis  [H + ]  PH  pCO2  HCO 3 - Respiratory acidosis  metabolic alkalosis Respiratory alkalosis  metabolic acidosis Buffers (mins) Respiratory (mins-24 hours) Renal ( hrs-5days )

28. RESPIRATORY ACIDOSIS RESPIRATORY ALKALOSIS ACUTE 1 2 CHRONIC 4 4 For 10 mm Hg change in PCO2: Change in HCO3

29. Metabolic Compensation Compensation HCO3- : pCO2 Metabolic Acidosis 1 : 1.25 Metabolic Alkalosis 1 : 0.75

30. Steps to Solve Acid-Base Disorders

31. Step-wise approach to ABG Check ABG validity? Assess oxygenation Acidemic or Alkalemic? Primary ds -- Metabolic or Respiratory? For metab acidosis -- what is the Anion Gap? If high-AG metab acidosis -- dHCO3? Respiratory compensation for metab ds?

32. ABG Validity Calculate [H+] : modified Henderson – Haselbach equation [H+] = 24 x [PaCO2] / [HCO3-] Normal [H+] = 40 nmol /L (pH=7.4) 1nmol/l change in [H+] changes pH by 0.01 in a pH range of 7.1 – 7.5 OR Subtract the two digits after decimal point in pH from 80 E.g. pH = 7.23 , [H+] = 80-23 = 57 nmol /L Calculated pH must be close to the measured pH

33. Base Excess Normal value -2 to + 2 mEq /L HCO3 amount above or below normal content of buffer base Depends upon entered Hb value and measured pH and PCO2 values Negative BE also referred to as Base Deficit True reflection of non respiratory (metabolic) acid base status

34. ANION GAP AG = [Na+] - ([ Cl - ] + [HCO3 - ]) Normal anion gap is 12 ± 4 meq/l Unmeasured Anions Unmeasured Cations Proteins (Alb) 15 mEq/L   Calcium 5 mEq/L Organic acids 5 mEq/L   Potassium 4.5 mEq /L Phosphates 2 mEq/L  Magnesium 1.5 mEq/L Sulfates 1 mEq/L Totals: 23 mEq/L 11 mEq/L Anion Gap reflects the unmeasured anion and cations .

35. Na + Cl - HCO 3 - Albumin, PO 4 3- Acetate Mg 2+ Ca 2+ K + Unmeasured ions Anion Gap

36. Bicarbonate gap (dHCO3) Only necessary if there is an AG metabolic acidosis. Does the increase in AG completely explain the ABG? Bicarbonate ↓ → presence of unmeasured anions For one molecule of anion, one molecule bicarbonate lost. Bicarbonate level can be therefore be calculated by formula= (patient AG -12) – (24 – patient HCO3) + ve Bicarbonate gap : Met alkalosis Resp acidosis compensated by HCO3 retention - ve Bicarbonate gap: Non AG Met acidosis. HCO3 excretion to compensate for resp acidosis.

37. Case 1 A 66 year old man seen in emergency room. He has had 8 days of severe diarrhea, abdominal pain, & decreased intake, but adequate intake of liquids. His medical history is significant for diabetes & hypertension. Presently on enalapril, aspirin, atenolol, metformin.Physical examination: B.P 105/70, Pulse 72/min, R.R 32. Lab report: Na 136, K 3.9, Cl 114, Creatinine 1.2, Gluc:128 ABG: pH 7.27 ; PO2 90; PCO2 27 and HCO3 13 Which acid base disorder is present?

38. pH low & ↓ HCO3 Metabolic acidosis. Respiratory compensation : 1 mEq decrease in HCO3 compensated by 1.25 mmHg decrease in pCO2 Decrease in HCO3 = 24-13 =11 Decrease in pCO2 = 1.25 x 11 =13.75 Expected PCO2 = 40-14 = 26 (Adequate) Anion Gap = 136– (114 + 13) =9 Non-AG Metabolic Acidosis

39. Characterized by fall in plasma HCO 3 & fall in pH and compensatory decreased PaCO2 Metabolic acidosis Normal Anion Gap Increased Anion Gap 1. Loss of HCO 3 Diarrhoea , Ureterosigmoidostomy , Proximal RTA 1. Metabolic disorders: Lactic acidosis, DKA 2. Failure to excrete H + Distal RTA 2. Addition of exogenous acids Salicylate / methanol poisoning 3. Addition H + NH 4 CL infusion 3. Failure to excrete acid Acute/chronic renal failure

40. Clinical manifestations Respiratory Kussmaul’s breathing CVS Increased susceptibility to arrythmia Decreased response to inotropes and secondary hypotension CNS Headache Confusion Coma Kidney Renal failure

41. Treatment of Metabolic Acidosis Specific management of underlying disorder Alkali therapy Reserved only for selective patients with Severe Acidemia Indications : pH< 7.15-7.2 HCO 3 < 10meq/l Amount of HCO 3 required= (Desired HCO 3 – Actual HCO 3 ) X0.3 X Body weight Half of the correction is given followed by repeat ABG after 30 minutes

42. Case 2 ABG of a patient with CHF on furosemide pH 7.48 HCO3 34 mEq/l PaCO2 48 mmHg Which acid-base disorder is present?

43. pH  = alkalosis HCO3  = s/o metabolic alkalosis PaCO2  = s/o compensation Rise in PaCO2 = 0.75 x rise in HCO3 = 0.75 x (34-24) = 7.5 Expected compensation = 40+7.5= 47.5 mmHg ~ actual PaCO2 s/o simple acid base disorder So patient has primary metabolic alkalosis due to diuretics

44. Metabolic Alkalosis Characterized by ↑ HCO3 , ↑ pH ,& compensatory ↑ in PaCO2 Serum potassium & chloride low Urinary chloride estimation useful for diagnosis Clinical features: CNS- ↑ neuromuscular excitability leading to paraesthesia, headache. CVS- hypotension & arrhythmias Others- weakness, muscle cramps

45. : Causes Chloride sensitive (urine CL - <20meq/l) Chloride resistant (urine CL - > 40meq/L) GI Losses Nasogastric suction Vomiting Renovascular hypertension Hyperaldosteronism Renal acid losses Penicillins Post-diuretic, Post- hypercapneic Normotensive Administration of alkali

46. Treatment Chloride sensitive- IV normal saline volume expansion Discontinue diuretics Chloride resistant- Remove offending agent Replace potassium if deficit Extreme Alkalosis Hemodialysis

47. Case 3 Case scenario: Following sleeping pill ingestion, patient presented in drowsy state with sluggish respiration with rate of 4/min pH 7.1 HCO3 28 mEq/l PaCO2 80 mmHg PaO2 42 mmHg Which acid-base disorder is present?

48. Interpretation PaO2  = severe hypoxemia pH  = acidosis PaCO2  = s/o respiratory acidosis HCO3  = s/o compensation Rise in HCO3 = 0.1 x rise in PaCO2 = 0.1 x (80-40) = 4 mEq/l Expected compensation = 28 mEq/l ~ actual PaCO2 s/o simple acid base disorder So patient has primary respiratory acidosis due to respiratory failure (sleeping pills)

49. Causes CNS depression Sedatives, narcotics, CVA, brain trauma Neuromuscular disorders Myasthenia gravis, tetanus, guillain barre syndrome Acute airway obstruction Foreign body, tumor, reactive airway, obstructive sleep apnea, laryngospasm or bronchospasm Respiratory disorders Severe pneumonia, pulmonary edema, pleural effusion, ARDS Chest cavity problems Hemothorax , pneumothorax, flail chest Chronic lung disease Obstructive or restrictive Central hypoventilation OSA Respiratory Acidosis

50. Clinical presentation: Headache, confusion, irritability, delirium Treatment: Treat underlying cause Establish patent airway & restore oxygenation. Treatment of pulmonary infection, brochodilator therapy, removal of secretions. Oxygen therapy Mechanical ventilatory support

51. Case 4 A 15 year old boy brought from examination hall in apprehensive state with complain of tightness in chest. pH 7.54 PCO 2 21 HCO 3 21 Which acid-base disorder is present?

52. Interpretation pH ↑ = s/o alkalosis ↓ PCO 2 = s/o respiratory alkalosis ↓ HCO 3 = s/o compensation Expected compensation = 0.2 X (40- 21) = 4 Expected HCO 3 = 24-4= 20 meq/l ~ actual HCO 3 s/o simple acid-base disorder. so, the patient has primary respiratory alkalosis due to anxiety.

53. Respiratory Alkalosis Diagnosis: ↓ PaCO2 (<35mmHg) ↑ pH Compensatory ↓ HCO3 Clinical features: Headache Arrhythmias Tetany Seizures

54. Causes of Respiratory Alkalosis Anxiety, pain, fever Hypoxia, CHF Lung disease with or without hypoxia – pulmonary embolus, reactive airway, pneumonia CNS diseases Drug use – salicylates , catecholamines , progesterone Pregnancy Sepsis, hypotension Hepatic encephalopathy, liver failure Mechanical ventilation Hypothyroidism High altitude Respiratory Alkalosis

55. Treatment Reassurance Anxiolytic Sedation Pain control ↓ RR and TV when on mechanical ventilation Oxygen supplementation

56. Case 5 Known case of COPD develops severe vomiting pH 7.4 HCO3 36meq/l PCO2 60mmHg Which acid-base disorder is present?

57. CAN A PATIENT WITH NORMAL pH HAVE ACID BASE DISTURBANCES ? YES MIXED ACID BASE DISTURBANCES

58. Interpretation pH normal = s/o either no acid –base disorder or mixed ↑ PCO2 = s/o respiratory acidosis ( due to COPD) ↑ HCO3 = s/o metabolc alkalosis ( due to vomiting) the patient has mixed disorder , respiratory acidosis & metabolic alkalosis. Normal pH can be due to end result of opposite changes caused by primary disorder.

59. Case 6 35, woman, community acquired pneumonia, brought with confusion. TLC-24000 Na-138, K-3.4, Cl-107 Urea-15mg/dl, Cr-0.8 mg/dl ABG pH- 7.08 p CO2 -20mmHg paO2 86 HCO3- 5 mEq/l 1. Assess oxygenation: Adequate 2. Acidemic or Alkalemic ?:Acidaemia 3. Primary disoder ?: Metabolic 4. AG 26 5. If high-AG -- dHCO3? Excess anions= 26-12= 14 Hence, HCO3 should be 25-14 = 11 But HCO3 6 less than predicted Non AG Met acidosis. 6. Respiratory compensation for metab ds ? Expected PaCO2 = 1.5 (HCO3-) + 8 + 2 = 1.5 (5) + 8 + 2 = 15 + 2 = 13-17 Here PaCO2 is 20 Additional respiratory acidosis

60. Interpretation FINAL DIAGNOSIS Anion gap metabolic acidosis Non anion gap acidosis Respiratory acidosis Adequate oxygenation

61. CASE 7 History An 8-week-old child is brought to the emergency department, with weight loss and projectile vomiting. The parents report that he had an uncomplicated delivery with no postpartum complications. He initially fed well, appeared to be thriving and gave no cause for concern but has deteriorated markedly over the past 2 weeks, vomiting all of his meals and now losing weight. Examination The child is agitated, crying and malnourished. His mucous membranes are dry, and on examination of his abdomen, a small mass is found in the epigastrium.

62. H+ 29 nmol /L (35–45) pH 7.54 (7.35–7.45) PCO2 45.8 mmHg (35–45) PO2 80 mmHg (>80) Bicarb 37.5 mmol /L (22–28) BE +14 mmol /L (−2 to +2) SO2 99% (>96%) Lactate 1 mmol /L (0.4–1.5) K 2.5 mmol /L (3.5–5) Na 135 mmol /L (135–145) Cl 86 mmol /L (95–105) iCa + 1 mmol /L (1–1.25) Hb 18.0 g/ dL (13–18) Glucose 5.1 mmol /L (3.5–5.5) On room air

63. Answers 1.Gas exchange - Mild type 2 respiratory impairment (compensated response) 2. Acid–base status - Metabolic alkalosis with partial compensation 3. Other abnormalities - Cl - , K + 4. Treatment - Fluids and electrolyte replacement

64. CASE 8 Examination The patient is in evident distress and appears very unwell. He is tachycardic (120 beats/min) and hypotensive (75/60 mmHg). There is marked epigastric tenderness. A venous blood test taken on admission reveals a grossly elevated amylase (1890 U/ mL ) and C-reactive protein (274 mg/L). A chest X-ray on admission is shown below.

65. H+ 49 nmol /L (35–45) pH 7.33 (7.35–7.45) PCO2 24.3 mmHg (35–45) PO2 81 mmHg (>80) Bicarb 12.9 mmol /L (22–28) BE −11.8 mmol /L (−2 to +2) SO2 99% (>96%) Lactate 3.1 mmol /L (0.4–1.5) K 3.6 mmol /L (3.5–5) Na 141 mmol /L (135–145) Cl 96 mmol /L (95–105) iCa + 0.89 mmol /L (1–1.25) Hb 12.0 g/ dL (13–18) Glucose 16 mmol /L (3.5–5.5) 15L O2 by face mask

66. Answers 1.Gas exchange -Type 1 respiratory impairment (severe) PaO2 of 81 with FiO2 of 0.6-0.8 2.Acid–base status - severe metabolic acidosis with partial compensation 3. Anion gap - (141+3.6)-(96+12.9)= 35.7 4.Diagnosis - Acute pancreatitis (systemic inflammatory response)

67. Delta Gap

68. Key Takeaways Acid Base Homeostasis is all about maintenance of normal H+ concentration. Valuable information can be gained from an ABG as to the patient`s physiologic condition ABGs are frequently used to detect indices of oxygenation, ventilation and acid base balance All intensivist , anaesthesiologist and physician must know to analyze ABG report systematically ABG to be interpreted within 15 minutes of collection to prevent false results Anion gap must always be calculated to decipher the complex acid-base disorders in critically ill patients.

69. THANK YOU