Abg analysis presentation for undergraduates and postgraduates

Abg

1. ABG ANALYSIS Presentor : Moderators: Dr. Santosh Hiremath Dr A Arya (MD) Dr K Deopujari (MD) Dr R R Barde (MD) Dr H Sharma (DM) Dr A Mittal (MD) Department of Internal Medicine Gandhi Medical College, Bhopal

2. ABG ARTERIAL BLOOD GAS ANALYSIS ACID BASE STATUS OXYGENATION GAS EXCHANGE VENTILATION PaO2 (A-a) gradient Haemoglobin PaCO2 pH Hco3 Base Excess

3. Why to order an ABG ? Asses adequacy of ventilation and oxygenation Aids in establishing a diagnosis and severity of respiratory failure Assess changes in acid- base homeostasis Helps to guide treatment plan Helps in management of ICU patients.

4. pH PaCO 2 PaO 2 HCO 3 O 2 saturation BE Haemoglobin / Hematocrit Electrolytes Lactate Glucose Components of an ABG

5. ABG machines routinely measure only 3 components: pH PaO2 PaCo2 Rest all the values are calculated using formulae by the machine

6. Normal Values - pH- 7.35- 7.45 PaCO 2 – 35-45 mmHg PaO 2 – 80- 100 mmHg HCO 3 – 22-26 O 2 sat – 95-100% Base Excess - +/- 2 m Eq / L

7. Base Excess : It indicates increase in the amount of buffer base. It is the number of mmol of strong acid needed to adjust pH to 7.4 at PCO2 40mm Hg. Base Deficit : It indicates decrease in the amount of buffer base.

8. Base Excess means the magnitude and direction of the metabolic contribution to the acid base disturbance It indicates if there was no respiratory component in the ABG and presuming everything being normal i.e Pco2- 40 and temp -37. then what would have been the metabolic component. Normal Value is -2 to +2 Ex: At pH 7.5, if BE is +3 ( metabolic alkalosis ) At pH 7.25, BE is -5 ( metabolic Acidosis ) – some people call this as Base Deficit, It indicates that the Metabolic Component of the Acidosis is -5

9. Standard Bicarb Vs Actual Bicarb Normal Bicarb will be in the range of 22-26. What if there is pure metabolic acidosis? It will decrease , lets say to 20 What if there was associated Co2 retention also, then it would further decrease to say 18 What machine gives us is called Actual Bicarb which is having both metabolic and respiratory component. Std Bicarb is the Bicarb, that would be, if C02, o2 and Temp was Normal Std Bicarb represents pure metabolic component

10. Standard bicarbonate It is the bicarbonate conc. In plasma in a completely oxygenated blood sample at Pco2 of 40 mm Hg at 37 o C. SBC >24 mmol /l indicates metabolic alkalosis SBC <24 mmol / l indicates metabolic acidosis

11. SITE SELECTION Radial Artery – 45 o insertion angle Brachial Artery – 60 o - 90 o insertion angle Femoral Artery – 90 o insertion angle Dorsalis Pedis Artery Posterior Tibial artery

12. Contraindications No absolute contraindications Dialysis shunt- choose another site Mastectomy – use opposite side Patient on anticoagulant/ aspirin therapy – may have to hold pressure on puncture site loner than normal

13. Post Puncture procedure Remove any air bubbles from sample and cap syringe Dispose of needle in sharps container Roll syringe to mix heparin with sample Immerse in ice On lab Slip indicate: A. FIO2 B. Patient temperature C. Ventilator parameters 5. Deliver to lab

14. ABG SPECIMEN COLLECTION/ HANDLING Transport specimen to laboratory in a biohazard container Analyze specimen on an instrument that has been recently calibrated Temperature correction specimen in analyzer Increase in patient temp: PO2 , PCO2 , pH Decrease in patient temp: PO2 , PCO2 , pH

15. ACID BASE PHYSIOLOGY pH is the negative logarithm to the base 10 of the hydrogen ion concentration in mmol /L pH = - log10 (H+) An increase in pH indicates a proportionate decrease in the (H+) and a decrease in the pH indicates a proportionate increase in the (H+).

16. Calculation of pH pH is calculated from Henderson – Hasselbalch equation. pH= pK + log acid/bas pH = 6.1 + log HCO 3 – H 2 CO 3 Kassirer and Bliech modified equation H+ = 24xPCO2 / HCO3 -

17. Regulation of pH pH is maintained in narrow range by In seconds: buffer systems In seconds: CO2 excretion by the lungs In hours to day: renal excretion of H+, reabsorption of HCO3

18. REGULATION OF ARTERIAL pH Buffers – Buffer systems minimize the change in pH resulting from production of acid. Main buffer system in humans include HCO3- ECF and protein and phosphate in ICF. 2. Role of the Respiratory System – Elimination of volatile acid CO2. a. Respiratory centres in te brain respond to changes in pH of CSF and blood to affect ventilatory rate. b. Ventilation directly controls the elimination of CO2.

19. ROLE OF KIDNEY It retains and regenerate HCO3 - thereby regenerating the body buffer with the net effect of eliminating the non violate acid load. H+ secretion Free urinary H+- minimal contribution Ammonia Phosphorus B. HCO3 - reabsorption Proximal tubule – 90 % Distal tubule – 10%

20. Carbon dioxide Transport In Dissolved form : Carbon dioxide is twenty times more soluble in water than oxygen. 100 ml of plasma with a PCO2 of 40 mmHg carries about 2.4 mlCO2 in solution. 5% of total CO2 carriage. As carbamino compounds : 5- 10% of CO2 carriage Bicarbonate : The remaining 85-90% of carbon dioxide is carried by blood in the form of bicarbonate ions.

21. Acid base disorders Acidemia – pH less than 7.35 Acidosis – A process that would cause academia, if not compensated. Alkalemia – pH greater than 7.45 Alkalosis – A process that would cause alkalemia if not compensated

22. SIMPLE VS. MIXED ACID-BASE DISORDER Simple acid base disorder- a single primary process of acidosis or alkalosis. Mixed acid- base disorder- presence of more than one acid base disorder simultaneously

23. Compensation In the presence of acidosis or alkalosis, regulatory mechanisms occur which try to maintain arterial pH. a. Renal compensation — kidneys adapt to alterations in pH by changing the amount of HCO3- generated/excreted. Full renal compensation takes 2-5 days b. Respiratory compensation — alteration in ventilation allow immediate compensation for metabolic acid-base disorders

24. Prediction of Compensation

25. Summary of metabolic compensation for respiratory acid-base disorders PCO 2 : HCO 3 Respiratory Acidosis Respiratory alkalosis Acute 10:1 10:2 Chronic 10:4 10:4 For every rise of 10 in the pCO 2 in the HCO 3 will rise by 1 or 4 For every fall of 10 in the pCO 2 in the HCO 3 will fall by 2 or 4

26. Anion Gap Anion Gap • Anion gap used to assess acid-base status in D/D of metabolic acidosis Anion gap based on principle of electro neutrality: • Total Serum Cations = Total Serum Anions • Na — ( HCO3 + CI) = Anion gap • Normal Anion gap — 10 +/- 2meq/L

27. • Albumin is the major unmeasured anion • The anion gap should be corrected if there are gross changes in serum albumin levels. EXPECTED ANION GAP = Normal AG + pH correction - Albumin correction pH correction : ( -2 if <7.35 ,, +4 if > 7.45) Albumin Correction: { (4.5 -[ALBUMIN]) x 2}

28. High Anion Gap : if the anion gap is +2 more than the expected anion Gap Normal Anion Gap: If the anion gap is within +2 of or within 50% of expected anion gap Low Anion Gap: If the anion Gap is less than 50% of the expected anion Gap

29. Delta Anion gap • It is the Difference between the Actual Anion Gap and the Expected Anion Gap DELTA ANION GAP = ( Actual – Expected)

30. If there is HAGMA, then we will compute Corrected Bicarbonate Corrected Bicarb = Delta AG + Bicarb value <22 >26 22-26 HAGMA+NAGMA ONLY HAGMA HAGMA+MET ALKALOSIS Corrected Bicarb

31. PLASMA OSMOLAR GAP Calculated Plasma Osmolarity = 2[Na+] + [ Gluc ]/18 + [BUN]/2.8 Normal Measured Plasma Osmolarity > Calculated Plasma Osmolarity ( upto 10 mOsm /L) Measured Plasma Osmolarity - Calculated Plasma Osmolarity > 10 mOsm /kg indicates presence of abnormal osmotically active substance Ethanol Methanol Ethylene glycol

32. URINARY ANION GAP Urinary NH4+ levels can be estimated by calculating the urinary anion gap (UAG) UAG = [Nat + K + ] u -[CI-] u [CI - ] u > [Na + + K + ], the urine gap is negative by definition Helps to distinguish GI from renal causes of loss of HCO3 by estimating Urinary NH4 + (elevated in GI HCO3 loss but low in distal RTA ). Hence a - ve UAG (av -20 meq /L) seen in GI causes while + ve value (av +23 meq /L) seen in Renal Causes.

33. Urine PH • Non AG metabolic acidosis: — If urine pH > 5.5 : Type 1 RTA — If urine pH < 5.5 : Type 2 or Type 4 RTA • Type 2 or Type 4 RTA can be later differentiated using serum K+ level

34. METABOLIC ACIDOSIS

35. Causes of High AG Met Acidosis 1 . Ketoacidosis : Diabetic Alcoholic Starvation 2. Lactic Acidosis: Type A (inadequate O2 delivery to Cells) as in Hypotension, Shock, Cardiac Failure Type B (Inability of Cells to utilise O2 ) Type D (Abnormal bowel anatomy where bacteria produce D-Lactic Acid) 3. Toxicity Salicylates Paraldehyde Methanol Toulene Ethylene Glycol 4. Renal Failure 5. Rhabdomylosis

36. Causes of Normal Anion Gap Metabolic Acidosis Due To HCO3 loss : GIT : Diarrhoea Pancreatic or biliary drainage Urinary diversions ( Ureterosigmoidostomy ) Renal: Proximal (type 2) RTA

37. 2. Impaired renal acid excretion : Distal (type 1) RTA Hyperkalemia (type 4 ) RTA Hypoaldosteronism 3. Misc. Acid Administration ( NH4Cl ) Hyperalimentation Cholestyramine CL HCl therapy (Rx of severe met alkalosis)

38. METABOLIC ALKALOSIS

39. CAUSES OF METABOLIC ALKALOSIS 1. EXOGENOUS HCO3 -LOADS Acute alkali administration Milk - alkali syndrome 2. Effective ECFV contraction, normotension, K+ deficiency and secondary Hyper- reninemic hyperaldosteronism. GI Loss : Vomitting Gastric Aspiration Villous adenoma

40. Renal Loss : Diuretics Post hypercapnic state Hypercalcaemia Recovery from LA/KA Mg2+deficiency Bartters / Gitelmans syndr Nonreabs anions - Penicill 3. ECFC expansion, hypertension, K+ deficiency, and mineralocorticoid excess A) HIGH RENIN Type: RAS Accelerated hypertension Renin sec tumor

41. B) Low Renin Type: PRIMARY Hyper ALDOSTERONISM - Adenoma, hyperplasia, carcinoma ADRENAL ENZYME DEFECTS 11b Hydroxylase, 17 Alfa-Hydroxylase deficiency CUSHINGS SYNDROME OR DIS. 4. Gain of function mutation of renal sodium channel with ECF expansion, hypertension, K+ deficiency and hyporeninemic hypoaldosteronism : LIDDLES SYNDROME

42. Management Of Metabolic Alkalosis: Goal of the therapy is to correct the underlying stimulus for bicarb generation Hypokalemia should always be treated Isotonic saline is recommended to reverse the alkalosis when ECFV contraction is present. If Heart Failure precludes use of Saline, then Acetazolamide can be given ( 125-250mg iv ) to accelerate renal loss of bicarb.

43. RESPIRATORY ACIDOSIS

44. Causes of Respiratory Acidosis 1. CENTRAL Drugs ( anaesthetics , morphine, sedatives) Stroke Infection 2. AIRWAY Obstruction Asthma 3. PARENCHYMA Emphysema Pneumoconiosis Bronchitis ARDS Barotrauma

45. 4. NEUROMASCULAR Poliomyelitis Kyphoscoliosis Myasthenia Muscular dystrophies 5. MISCELLANEOUS Obesity Hypoventilation Permissive Hypercapnia

46. Management Of Respiratory Acidosis: Restoration of adequate Alveolar Ventilation Paco2 should be corrected slowly since rapid corrections can cause ill effects of respiratory alkalosis such as seizures, arrythmias and reduced cerebral perfusion. Ventilatory Parameters: Increase I:E ration Decrease RR ( Ideally 10cycles/min) Increase flow

47. RESPIRATORY ALKALOSIS

48. Causes of Respiratory Alkalosis 1. CENTRAL NERVOUS SYSTEM STIMULATION Structural Causes Head Trauma Brain Tumor CVA Meningitis , encephalitis Psychosis Non Structural Causes Pain Anxiety Fever 2. HYPOXEMIA OR TISSUE HYPOXIA Pneumonia, pulm oedema Aspiration High Altitude

49. 3. STIMULATION OF CHEST RECEPTORS : Hemothorax Flail chest Cardiac failure Pulmonary embolism 4. MIXED/UNKNOWN MECHANISMS: Drugs - Salicylates Progesterone Catechoalmines Xanthines ( Aminophylline and related compounds) Nicotine Thyroid Hormone Cirrhosis Gram- ve Sepsis Pregnancy Heat Exposure Mechanical Ventilation

50. Management Of Respiratory Alkalosis: The management of respiratory alkalosis is directed mainly towards alleviation of the underlying disorder.

51. A Stepwise Approach to Solving Acid Base Disorders

52. Step - 1 : Check for ERRORS Have the required parameters been correctly fed…??? Patient's Temperature FiO2 : Specially if patient is on ventilator Hemoglobin : Some machines may not measure it Barometric pressure : Some machines may not measure it

53. FiO 2 Entering FiO 2 is very important Most common mistake - FiO 2 not entered while the sample is fed in the machine. - % FiO 2 written on the report later on manually. If FiO 2 not fed properly Interpretation of PaO 2 affected adversely. (A-a)DO 2 values are wrongly calculated ( PAO 2 calculated from PiO 2 ) Interpretation of adequacy of Oxygenation affected adversely if Hb not fed properly.

54. Sampling error..?? Arterial, veinous or mixed..??? Arterial Venous Ask the person who aspirated the sample Blood Pulsates Blood does not pulsate Syringe plunger may rise on its own Syringe plunger never rises on its own. PO 2 PO 2 > 40mm Hg PO 2 <40 (often < 30mmHg ) O 2 Saturation values SaO 2 >75% " SvO 2 " <75% No. of attempts - Single or Multiple punctures Single puncture, rapid filling Multiple, Lower PO 2 due to venous mixture PCO 2 Abnormal or normal, Not diagnostic Abnormal or normal, Not diagnostic

55. Assessment of validity of test results Relation b/w pH and H+ conc. 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

56. Assessment of validity of tests results H+ in nmol/L = 24xPCO2/HCO3 If there is a discripancy between the 2 results, the blood should be reanalyzed.

57. Look at PaO 2 and SaO 2 first Healthy Adult - Sea Level, Room Air, A-a O 2 = 4 mm Hg, PAO2 = 101 Analyse the adequacy of oxygenation Low PaO 2 = Surely something wrong in terms of Oxygenation Low PaO 2 = degree of hypoxemia Saturation of Hb (S aO 2 ) is dependent upon PaO 2 PaO 2 (mmHg) SaO 2 (%) Normal values (on air ) >80 >95 Mild hypoxemia 60-79 90-94 Moderate Hypoxemia 40-59 75-89 Severe hypoxemia <40 <75

58. Step - 2 : Comprehensive history and physical examination Step - 3 : Acidosis or alkalosis ..??? see the pH (<7.35 or >7.45) Step - 4 : Identify the primary disorder See the change in PCo2 and HCO3 Step - 5 : Calculate the compensatory response is adequately compensated???

59. Step - 6 : Calculate anion gap Step - 7 : Calculate delta gap (unmask hidden mixed disorders) Step - 8 : Calculate the osmolar gap (for high AG acidosis) Step - 9 : Calculate the urinary anion gap (Non AG metabolic acidosis) Step - 10 : Formulate differential diagnosis

60. LET'S TRY

61. Case - 1 A known case of Chronic Kidney Disease, discontinued MHD and presented to the emergency in an altered state of sensorium . Attendants gave history of repeated episodes of vomiting at home. ABG results pH 7.42 PCO 2 40 HCO 3 25 Na 140 K 3.0 Cl 95

62. • pH, PCO2, HCO3 all WNL • AG = 20 ( ) • Delta gap =20-12= 8 • Corrcted Hco3= 8+25= 33,, which is >26 • Hence, Mixed disorder with presence of both high AG metabolic acidosis and metabolic alkalosis.

63. 60 years old M, presents to the ED with rapid breathing and less responsive than usual. No other history available Case - 2 ABG Results pH 7.31 PCO 2 10 HCO 3 5 Na 123 K 5 Cl 99

64. Stepwise interpretation Stepwise interpretation 1. At pH 7.3 H+ conc. Should be = 5Onmol /L - Calculated H+ = 24 x 10/5 = 24 x 2 = 48 - Both values corroborate, hence result is valid. 2. pH is 7.3 i.e Acidosis 3. HCO3 value has gone down, primary process is metabolic 4. Respiratory compensation: - Calculated PCO2 = (1.5 x 5)+8 ± 2 = 13.5 to 17.5 - OR ( Paco2= Hco3+15) i.e Paco2 should have been 20 but its 10 - Over compensated ; mixed disorder - a/w respiratory alkalosis

65. 5. Expected Anion Gap: 12-2= 10 Actual Anion gap: (123) -(99 + 5) = 19 - Hence its an High anion gap metabolic acidosis 6. Delta gap= 9 -Corrected Bicarb= 9+5 = 14 which is <22 Hence,, Presence of non anion gap metabolic acidosis also.!! 7. Osmolar gap: data not provided.

66. Finally ... • Mixed acid base disorder, with presence of both high AG & normal AG metabolic acidosis and respiratory alkalosis.

67. Case - 3 A k/c/o COPD with cor pulmonale on treatment presented with progressive breathlessness. ABG results pH 7.42 PCO 2 67 HCO 3 42 Na 140 K 3.5 Cl 88

68. • pH is normal, so may be a chronic disorder but PCO2 & HCO3 both are increased. • Change in PCO2 is 67-40 = 27 • Expected rise in HCO3 should be approx 35 • Expected HCO3 = 24+2.7*4= 35 • Actual HCO3 = 42 • Expected Anion AG = 12 Actual Anion Gap = 10 Hence No Anion Gap • Mixed disorder, both respiratory acidosis & metabolic alkalosis.

69. Case - 4 65 years old Man with past h/o AMI on medication, presented with high grade fever, with cough and yellowish expectoration for 5 days. Acute increase in shortness of breath. ABG results pH 7.3 PCO 2 38 HCO 3 16 Na 136 K 4 Cl 102

70. • pH 7.3 = Acidosis • HCO3 is low ; primary disorder is metabolic acidosis • Expected PCO2 = Hco3+15 = 16+15 = 31 • Calculated PCO2 < Actual PCO2 • Expected Anion Gap =12-2 ( pH correction )= 10 Actual Anion Gap = 18 • Delta gap = 18-10 = 8 Corrected Hco3= delta gap + hco3 value = 8+16 =24,, Hence only HAGMA • Mixed disorder with HA Metabolic acidosis & respiratory acidosis

71. THANK YOU