ARTERIAL BLOOD GAS ANALYSIS & INTERPRETATION

Arterial Blood Gas Analysis and Interpretation with corrective suggestions

1. ABG- analysis & interpretation with corrective suggestions Presenter: Dr. Chris Nishanth Moderator: Dr. rangalakshmi Dr. Karthik

2. pH – importance in medicine Precise regulation of pH in a narrow range of 7.35 to 7.45 is vital for normal cellular enzymatic reaction and for normal ionic concentration. Change in pH can cause Cardiac Arrythmias & other potential life threatening complications because of disruption of vital physiological processes. Acid bases disorders occur more commonly in very ill patients & may be the first marker of the underlying disease.

3. Outline What’s an ABG? Basic terminology Basic physiology Clinical diseases causing acid-base disturbances Basics of acid-base disorders and compensation Interpretation Step by step analysis Case scenarios Corrective suggestions Take home message

4. ABG – History

5. Søren P. L. Sørensen 1868-1939 Protein Chemist at the Carlsberg brewery. To save having to write that H + = 0.000000040M , he devised the scale of acid in terms of pH, as the negative log of H + ion activity. (1907) Scientist in the acid-base story

6. Lawrence J Henderson Prof Biochemistry and Physiology. Theory of buffering and of bicarbonate-hydrogen ion- PaCO2 relationship . The Henderson equation K = [H + ][HCO 3 - ]/[H 2 CO 3 ] K is the dissociation constant of carbonic acid, about 10 -3 M A constant 0.1% of dissolved CO 2 in water is hydrated to carbonic acid. Therefore it can be simplified to H 2 CO 3 = dissolved CO 2 Where K’ is the apparent dissociation constant K’ = 10 -6.1 Scientist in the acid-base story

7. Karl A Hasselbalch 1874-1962 Agricultural chemist, Denmark. Adapted Henderson’s equation to Sørensen’s logarithmic pH by replacing H 2 CO 3 with S.PaCO2 creating the Henderson-Hasselbalch equation : pH= pK ’ + log [ HCO 3 - / ( S . PaCO2 ) ] 7.40 = 6.10 + log[24/{0.31 . 40}] Where S (solubility) = 0.031 mM/liter/mmHg at 37 o C Scientist in the acid-base story

8. Donald D Van Slyke 1883-1971 Major developer of clinical chemistry in the 1910-50 period. His manometric blood gas apparatus (1924) was used to measure the content in blood of oxygen, carbon dioxide and many other variables. Laboratories calculated PaCO2 using the Henderson-Hasselbalch equation after measuring pH of blood and the total plasma CO 2 by the Van Slyke apparatus until the polio epidemics resulted in two new methods: Astrup’s equilibration scheme and Severinghaus modification of the Stow CO 2 electrode . Scientist in the acid-base story

9. Poul Astrup 1915-2000 Prof of Clinical Chemistry Univ. of Copenhagen New method for PaCO2 To avoid need for the VanSlyke and Henderson-Hasselbalch method, he devised a method for graphically calculating PaCO2 by measuring pH before and again after equilibration of the blood to a known PaCO2 Scientist in the acid-base story

10. Leland C. Clark Jr. 1918–2005 American biochemist born in Rochester, New York Inventor of the Clark electrode , a device used for measuring oxygen in blood. Clark is considered the "father of biosensors", and the modern-day glucose sensor used daily by millions of diabetics is based on his research. Scientist in the acid-base story

11. John W Severinghaus 1922 Prof of Anesthesia University of California San Francisco Major developer of blood gas measurements since 1950. His modification (invention) of the CO2 electrode , the first blood gas apparatus (1958), the blood gas ruler, transcutaneous blood gas measurement and pulse oximetry, as well as important work in high altitude respiratory physiology Scientist in the acid-base story

12. ABG ABG provides us with rapid information on three physiologic processes. Alveolar ventilation Oxygenation Acid-base Balance

13. Alveolar ventilation The maintenance of CO2 level reflected by arterial CO2 tension (PaCO2) at any given moment depends on the quantity of CO2 produced in body and its excretion through alveolar ventilation (VA) This can be expressed by the equation, PaCO2 ∝ CO2/VA. The alveolar ventilation is that portion of total ventilation that participates in gas exchange with pulmonary blood. Thus PaCO2 is the best index for assessment of alveolar ventilation. High PaCO2 (> 45 mmHg) indicates alveolar hypoventilation. Low PaCO2 (< 35 mmHg) implies alveolar hyperventilation.

14. Oxygenation Ultimate aim of oxygenation → provide adequate delivery of oxygen to tissues . Depends on cardiopulmonary system arterial oxygen tension (PaO2), haemoglobin content and saturation with oxygen (SaO2), and cardiac output. The PaO2 and SaO2 are primarily used for assessment of oxygenation status. Approximately 98% of oxygen is carried in blood in the combined state with haemoglobin.

15. Oxygenation Hypoxemia - PaO2 of <80 mmHg at sea level in an adult patient breathing room air, the similar decrease in cells/tissues is known as hypoxia. Tissue hypoxia is unlikely in mild hypoxemia (PaO2=60-79 mmHg), and is almost always associated with severe hypoxemia (PaO2 < 45 mmHg). PaO2 must always be interpreted in relation to concentration of inspired oxygen FiO2 and age. Normal PaO2 on room air with FiO2 of 0.2 is 80 to 100 mmHg, the normal values for PaO2/FiO2 ratio or oxygenation ratio are 400-500 mmHg or 4.0 to 5.0 respectively. PaO2/FiO2 ratio of less than 200 most often indicates a shunt greater than 20%.

16. Basic terminology

17. What is pH? pH = - log 10 [ H+] It is inversely proportional to concentration of hydrogen ions Acid H+ pH Acid: A substance that can "donate" H+ ion or when added to solution raises H+ ion (i.e. lowers pH). Base: A substance that can accept H+ ion or when added to solution lowers H+ ion (i.e. raises pH) A n ion: An ion with negative charge is anion (i.e. Cl - , HCO3 - ) Ca t ion: An ion with positive charge is cation (i.e. Na + , K + , Mg + )

18. Basic physiology The body maintains pH within a normal range in spite of variation in dietary intake of acid and alkali, and endogenous acid production. Endogenous acid production Normally when food is metabolized, two types of acids are added to ECF. Volatile acid in the form of carbonic acid (H 2 CO 3 ), which determines level of CO2 in blood (PaCO2 ) and is excreted by lung . About 22,000 mEq volatile acid is produced daily. Nonvolatile(fixed) acids (like sulfuric and phosphoric acids) are produced by dietary and endogenous protein catabolism. Roughly at the rate of 1mEq/kg. They are excreted by the kidney .

19. Basic physiology

20. Basic physiology Regulation of acid base The regulation of the pH in a narrow range is the function of buffers, lungs and kidneys. The Henderson-Hasselbalch Equation describes the correlation of metabolic and respiratory regulations, which maintains pH. = pK a + Kidney/Lung

21. Henderson-Hasselbalch Equation The pH resulting from the solution of CO2 in blood and the consequent dissociation of carbonic acid is given by the Henderson-Hasselbalch Equation. The law of mass conservation gives the dissociation constant of carbonic acid as K a Now, since the concentration of carbonic acid is proportional to the concentration to the concentration of dissolved carbon dioxide, we can change to CO 2 + H 2 O ↔

22. Basic physiology Buffers - very rapid(seconds), incomplete Respiratory regulation - rapid (minutes), incomplete Renal regulation - slow (hours to days), complete

23. Buffers Buffers are chemical systems, which either release or accept H + . So buffers minimize change in pH induced by an acid or base load and provide immediate defense. Buffers act fastest but has lease buffering power .

24. Swan & Pitts Experiment Infusion of 14 mmols /L H + Drop in pH from 7.44 ([H + ] = 36 nmoles /l) to a pH of 7.14 ([H + ] = 72 nmoles /l). That is, a rise in [H + ] of only 36 nmoles /l.

25. Respiratory regulation By excreting volatile acids, lung regulates PaCO 2 . Normally CO 2 production and excretion are balanced, which maintains PaCO 2 at 40 mm of Hg. Respiratory regulation acts rapidly (in seconds to minutes) and has double buffering power as compared to the chemical buffers.

26. Respiratory regulation In case of failure of Respiratory regulation Hypoventilation → CO2 retention → Hypercapnia → Respiratory acidosis Hyperventilation → CO2 washout → Hypocapnia → Respiratory alkalosis

27. Renal regulation The role of kidney is to maintain plasma HCO 3 concentration and thereby pH regulation. It has the most powerful buffering system , which starts within hours, and takes 5-6 days for peak effect. The kidney regulates HCO3 by excreting non-volatile fixed acids by following three main mechanisms : Excretion of H + ions by tubular secretion. Reabsorption of filtered bicarbonate ions. Production of new HCO 3 ions.

28. Renal regulation Renal response to metabolic acid base disorders: In response to acid load , normal kidneys can increase net acid excretion greatly(more than 10 times). Increased excretion of H+ ions along with regeneration of bicarbonate will correct plasma HCO 3 to normal range.

29. Renal regulation When there is primary increase in plasma HCO 3 or when PaCO 2 increases there will be increased renal HCO 3 excretion in the urine.

30. Renal regulation

31. Gas Exchange

32. Gas Exchange

33. Gas Exchange

34. Gas Exchange

35. Basics of acid-base disorders and compensation Primary Acid-base disorders If initial disturbance affects PaCO 2 1. Respiratory acidosis (↑ in PaCO 2 ) 2. Respiratory alkalosis (↓ in PaCO 2 ) If initial disturbance affects HCO 3 3. Metabolic acidosis (↓ in HCO 3 ) 4. Metabolic alkalosis (↑ in HCO 3 ) Metabolic – HCO 3 Respiratory – PaCO2 R O M E Rule

36. Simple acid-base disorders Disorder Primary Responses Compensation Metabolic acidosis  [H + ]  PH  HCO 3 -  PaCO2 Metabolic alkalosis  [H + ]  PH  HCO 3 -  PaCO2 Respiratory acidosis  [H + ]  PH  PaCO2  HCO 3 - Respiratory alkalosis  [H + ]  PH  PaCO2  HCO 3 - Respiratory acidosis  metabolic alkalosis Respiratory alkalosis  metabolic acidosis Buffers (mins) Respiratory (mins-24 hours) Renal ( hrs-5days )

37. Compensation The body’s response to neutralise the effect of the Initial insult on pH homeostasis is called compensation. Remember pH is maintained by ratio of HCO 3 /PaCO2(Henderson-Hasselbalch equation) To maintain normal pH primary metabolic/respiratory disorders lead to compensatory vice versa responses.

38. Compensation Same direction Rule Disorder Primary Responses Compensation Metabolic acidosis  [H + ]  PH  HCO 3 -  PaCO2 Metabolic alkalosis  [H + ]  PH  HCO 3 -  PaCO2 Respiratory acidosis  [H + ]  PH  PaCO2  HCO 3 - Respiratory alkalosis  [H + ]  PH  PaCO2  HCO 3 -

39. Expected Compensation Importance of calculation and checking compensation in acid base disorders: Useful in differentiating simple from mixed disorder. If expected change = actual change , disorder is simple . If actual change is more or less than predicted, disorder is mixed . Compensation follows "same direction rule". If changes are in opposite direction, think of mixed disorder .

40. Expected Compensation Disorder Expected Compensation Metabolic Acidosis PaCO2 = (1.5 x HCO3) + 8   PaCO2 = HCO3 + 15 Metabolic Alkalosis PaCO2 = (0.75 x HCO3) + 21   Rise in PaCO2 = 0.75 x Rise in HCO3 Respiratory Acidosis   ACUTE (6-24hrs) HCO3 = 24 + 0.1 x (CO2 - 40)   Fall in pH = 0.01 x Rise in PaCO2 CHRONIC (>24hrs) HCO3 = 24 + 0.4 x (CO2 - 40)   Fall in pH = 0.003 x Rise in PaCO2 Respiratory Alkalosis   ACUTE (6-24hrs) HCO3 = 24 - 0.2 x (40 - CO2)   Rise in pH = 0.01 x Fall in PaCO2 CHRONIC (>24hrs) HCO3 = 24 - 0.5 x (40 - CO2)   Rise in pH = 0.002 x Fall in PaCO2

41. Expected Compensation Disorder Expected Compensation Metabolic Acidosis PaCO2 = (1.5 x HCO3) + 8   Metabolic Alkalosis PaCO2 = (0.75 x HCO3) + 21   Respiratory Acidosis   ACUTE (6-24hrs) HCO3 = 24 + 0.1 x (CO2 - 40)   CHRONIC (>24hrs) HCO3 = 24 + 0.4 x (CO2 - 40)   Respiratory Alkalosis   ACUTE (6-24hrs) HCO3 = 24 - 0.2 x (40 - CO2)   CHRONIC (>24hrs) HCO3 = 24 - 0.5 x (40 - CO2)    

42. Expected Compensation Disorder Expected Compensation Metabolic Acidosis PaCO2 = (1.5 x HCO3) + 8   Metabolic Alkalosis PaCO2 = (0.75 x HCO3) + 21   Respiratory Acidosis   ACUTE (6-24hrs) HCO3 = 24 + 0.1 x (CO2 - 40)   CHRONIC (>24hrs) HCO3 = 24 + 0.4 x (CO2 - 40)   Respiratory Alkalosis   ACUTE (6-24hrs) HCO3 = 24 - 0.2 x (40 - CO2)   CHRONIC (>24hrs) HCO3 = 24 - 0.5 x (40 - CO2)    

43. Mixed acid-base disorders Mixed acid base disorder is defined as independent coexistence of more than one primary acid base disorder. The most common mixed disorder is a mixed metabolic and respiratory acidosis. Respiratory Acidosis and Respiratory Alkalosis cannot co-exist.

44. Mixed acid-base disorders Disorder Common causes Metabolic Acidosis and Respiratory Acidosis a. Cardiac Arrest (hypoventilation + lactic acidosis) Low ph , ↓HCO3 , ↑PaCO2 b. Shock with respiratory failure   c. DKA with resp. diseases Metabolic Acidosis and Respiratory Alkalosis a. Salicylate intoxication N. ph , ↓HCO3 , ↓PaCO2 b. Sepsis   c. Liver failure Metabolic Alkalosis and Respiratory Acidosis a. COPD on diuretics N. ph , ↑HCO3 , ↑PaCO2 b. Metabolic alkalosis with severe hypokalaemia and respiratory weakness -> Hypoventilation Metabolic Alkalosis and Respiratory Alkalosis a. Liver failure with vomitting ↑ ph , ↑HCO3 , ↓PaCO2 b. Patient on ventilator with continuous NG aspiration Metabolic Acidosis and Metabolic Alkalosis a. DKA with vomitting Near N. ph and HCO3 b. Vomitting with severe volume depletion causing lactic acidosis Respiratory Acidosis and Respiratory Alkalosis Do not co-exist

45. Interpretation ABG and serum electrolytes should be performed simultaneously for correct interpretation of acid base disorders. 1. pH Normal Value: 7.4 -> suggests either absence if disorders or presence of mixed disorders( eg : Metabolic acidosis with compensated respiratory alkalosis) <7.35 -> Acidosis/acidaemia >7.45 -> Alkalosis/alkalaemia pH ∝ 1/H + H+ falls by 20% for each 0.1 pH unit increment

46. Interpretation 2. HCO3( mEq /L) Normal Value: 22-26mEq/L <22mEq/L -> Metabolic Acidosis(primary change) or Resp. Alkalosis(secondary change) >26mEq/L -> Metabolic Alkalosis(primary change) or Resp. Acidosis(secondary change) Normal HCO3 -> Does not exclude acid base disorder Acute respiratoy d/o or mixed d/o can give normal HCO3. 3. PaCO2(mm of Hg) Normal Value: 35-45mm of hg >45 -> Respiratory Acidosis(primary change) or Metabolic Alkalosis(secondary change) <35 -> Respiratory Alkalosis(primary change) or Metabolic Acidosis(secondary change)

47. Interpretation 4. Anion Gap Anion Gap(AG) = Na – (Cl + HCO3) = 12 ± 2 mEq /L (Normal Value) Importance of Anion Gap: AG in Metabolic Acidosis: Most useful to establish etiological diagnosis of Metabolic acidosis.

48. Interpretation Albumin normally compromises most of the AG. For every 1gm/dl decline in serum albumin a 2mEq/L decrease in anion gap will occur.

49. Interpretation 5. Serum Potassium Normal Value: 3.5 to 5.5mEq/L Low K+: Metabolic or respiratory alkalosis, diarrhoea, proximal RTA High K+: Metabolic acidosis due to renal failure, Type-4 RTA, DKA or Respiratory acidosis 6. Pulse Oximetry Measures O2 saturation of arterial haemoglobin. Normal Value: 96-100%. Less than 90% saturation suggests marked tissue hypoxia(less than 60mmHg PaO2). Useful for hypoxaemia screening but tells nothing about PaCO2 – hypercapnia can occur with 100% O2 saturation also.

50. Step by step analysis Step-1: Is there an acid base disorder? Check PaCO2 and HCO3 values and determine whether they are in normal range. If abnormal -> Step 2 If Normal -> either there is no acid base disorder or in Critically ill patients rule out mixed acid base disorders -> Step 5 Step-2: Is there Acidosis or Alkalosis Look at pH Step-3: What is the Primary acid base disorder? pH is low(<7.35) – Acidaemia d/t -> i .) Metabolic Acidosis – low HCO3 ii.) Resp Acidosis – high PaCO2 pH is high(7.45) – Alkalemia d/t -> i .) Metabolic Alkalosis –high HCO3 ii.) Resp Alkalosis – low PaCO2

51. Step by step analysis Step-4: Calculate the expected Compensation Determine whether the actual value matches with the expected compensation. Matching of both confirms diagnosis of primary disorder. Disorder Expected Compensation Metabolic Acidosis PaCO2 = (1.5 x HCO3) + 8   Metabolic Alkalosis PaCO2 = (0.75 x HCO3) + 21   Respiratory Acidosis   ACUTE (6-24hrs) HCO3 = 24 + 0.1 x (CO2 - 40)   CHRONIC (>24hrs) HCO3 = 24 + 0.4 x (CO2 - 40)   Respiratory Alkalosis   ACUTE (6-24hrs) HCO3 = 24 - 0.2 x (40 - CO2)   CHRONIC (>24hrs) HCO3 = 24 - 0.5 x (40 - CO2)  

52. Step by step analysis Step-5: Determine the presence of mixed acid base disorder Check direction of changes RULE OF SAME DIRECTION Compare expected compensation with actual value Check anion gap Compare fall in HCO3 with increase in plasma anion gap Disorder Primary Responses Compensation Metabolic acidosis  [H + ]  PH  HCO 3 -  PaCO2 Metabolic alkalosis  [H + ]  PH  HCO 3 -  PaCO2 Respiratory acidosis  [H + ]  PH  PaCO2  HCO 3 - Respiratory alkalosis  [H + ]  PH  PaCO2  HCO 3 -

53. Step by step analysis Step-5: Determine the presence of mixed acid base disorder Check direction of changes RULE OF SAME DIRECTION – if in opp direction s/o Mixed disorder Compare expected compensation with actual value Check anion gap Compare fall in HCO3 with increase in plasma anion gap Disorder Primary Responses Compensation Metabolic acidosis  [H + ]  PH  HCO 3 -  PaCO2 Metabolic alkalosis  [H + ]  PH  HCO 3 -  PaCO2 Respiratory acidosis  [H + ]  PH  PaCO2  HCO 3 - Respiratory alkalosis  [H + ]  PH  PaCO2  HCO 3 - Anion Gap(AG) = Na – (Cl + HCO3) = 12 ± 2 mEq /L (Normal Value) Disorder Expected Compensation Metabolic Acidosis PaCO2 = (1.5 x HCO3) + 8   Metabolic Alkalosis PaCO2 = (0.75 x HCO3) + 21   Respiratory Acidosis   ACUTE (6-24hrs) HCO3 = 24 + 0.1 x (CO2 - 40)   CHRONIC (>24hrs) HCO3 = 24 + 0.4 x (CO2 - 40)   Respiratory Alkalosis   ACUTE (6-24hrs) HCO3 = 24 - 0.2 x (40 - CO2)   CHRONIC (>24hrs) HCO3 = 24 - 0.5 x (40 - CO2)  

54. Step by step analysis Step-5: Determine the presence of mixed acid base disorder Check direction of changes RULE OF SAME DIRECTION – if in opp direction s/o Mixed disorder Compare expected compensation with actual value If actual value more or less as compared to compensation s/o Mixed Disorder Check anion gap In certain mixed d/o pH, PaCO2 and HCO3 are normal and the only clue might be an increased anion gap Compare fall in HCO3 with increase in plasma anion gap Disorder Primary Responses Compensation Metabolic acidosis  [H + ]  PH  HCO 3 -  PaCO2 Metabolic alkalosis  [H + ]  PH  HCO 3 -  PaCO2 Respiratory acidosis  [H + ]  PH  PaCO2  HCO 3 - Respiratory alkalosis  [H + ]  PH  PaCO2  HCO 3 - Disorder Expected Compensation Metabolic Acidosis PaCO2 = (1.5 x HCO3) + 8   Metabolic Alkalosis PaCO2 = (0.75 x HCO3) + 21   Respiratory Acidosis   ACUTE (6-24hrs) HCO3 = 24 + 0.1 x (CO2 - 40)   CHRONIC (>24hrs) HCO3 = 24 + 0.4 x (CO2 - 40)   Respiratory Alkalosis   ACUTE (6-24hrs) HCO3 = 24 - 0.2 x (40 - CO2)   CHRONIC (>24hrs) HCO3 = 24 - 0.5 x (40 - CO2)   Anion Gap(AG) = Na – (Cl + HCO3) = 12 ± 2 mEq /L (Normal Value)

55. Step by step analysis Step-5: Determine the presence of mixed acid base disorder Check direction of changes RULE OF SAME DIRECTION – if in opp direction s/o Mixed disorder Compare expected compensation with actual value If actual value more or less as compared to compensation s/o Mixed Disorder Check anion gap In certain mixed d/o pH, PaCO2 and HCO3 are normal and the only clue might be an increased anion gap Compare fall in HCO3 with increase in plasma anion gap Disorder Primary Responses Compensation Metabolic acidosis  [H + ]  PH  HCO 3 -  PaCO2 Metabolic alkalosis  [H + ]  PH  HCO 3 -  PaCO2 Respiratory acidosis  [H + ]  PH  PaCO2  HCO 3 - Respiratory alkalosis  [H + ]  PH  PaCO2  HCO 3 - Anion Gap(AG) = Na – (Cl + HCO3) = 12 ± 2 mEq /L (Normal Value)

56. Step by step analysis Step-5: Determine the presence of mixed acid base disorder Check direction of changes RULE OF SAME DIRECTION – if in opp direction s/o Mixed disorder Compare expected compensation with actual value If actual value more or less as compared to compensation s/o Mixed Disorder Check anion gap In certain mixed d/o pH, PaCO2 and HCO3 are normal and the only clue might be an increased anion gap Compare fall in HCO3 with increase in plasma anion gap In HAGMA Rise in AG = Fall in HCO3 If Rise in AG > Fall in HCO3 -> S/o co-existing metabolic alkalosis If Rise in AG < Fall in HCO3 -> S/o loss of HCO3(diarrhoea) causing Normal-AG Metabolic acidosis Step-6: Clinical correlation and to establish etiological diagnosis Disorder Primary Responses Compensation Metabolic acidosis  [H + ]  PH  HCO 3 -  PaCO2 Metabolic alkalosis  [H + ]  PH  HCO 3 -  PaCO2 Respiratory acidosis  [H + ]  PH  PaCO2  HCO 3 - Respiratory alkalosis  [H + ]  PH  PaCO2  HCO 3 -

57. The “Gap-Gap” ratio aka Delta Ratio Delta ratio = (Increase in AG/Decrease in HCO3)

58. The “Gap-Gap” ratio aka Delta Ratio Delta ratio = (Increase in AG/Decrease in HCO3)

59. Methods of analysing acid base disorders There are 4 methods of evaluation of acid base disorders- Carbon dioxide bicarbonate Bostan approach Base Deficit Excess Copenhegan approach Stewart Fencl Strong Ion Difference approach Traditional anion gap approach

60. Case scenarios Case 1: A 15-year-old boy is brought from examination Hall. In apprehensive state with complaint of tightness of chest. pH  7.54 HCO3  21 mEq /L PaCO2  21 mmhg

61. Case scenarios Case 2: A patient with poorly controlled IDDM missed his insulin for three days. pH 7.1 Na+ 140 mEq/L HCO3 8 mEq/L Cl- 106 mEq/L PaCO2 20 mmhg Urinary Ketones +++

62. Case scenarios Case 3: A patient with severe diarrhoea complaints of difficulty in breathing. pH 7.1 K+ 2.0 mEq /L HCO3 14 mEq /L PaCO2 44 mmhg

63. Case scenarios Case 4: ABG of patient with CHF on Frusemide is as follows: pH  7.48 HCO3  34 mEq /L PaCO2  48 mmhg

64. Case scenarios Case 5: Following sleeping pills ingestion patient presented in drowsy state with sluggish respiration with respiratory rate 4/min. pH 7.1 PaO2 42 mmhg HCO3 28 mEq /L PaCO2 80 mmhg

65. Case scenarios Case 6: ABG of patient with shock on ventilatory support since last four hours is pH  7.48 HCO3  14 mEq /L PaCO2  22 mmhg

66. Case scenarios Case 7: Known case of COPD developed severe vomiting. pH  7. 4 HCO3  36 mEq /L PaCO2  60 mmhg

67. Case scenarios Case 8: A case of hepatic failure has persistent vomiting. pH  7.54 HCO3  38 mEq /L PaCO2  44 mmhg

68. Corrective suggestions

69. Metabolic Acidosis Treatment of metabolic acidosis includes Specific management of underlying disorder As a rule treat underlying disorder meticulously. It is the most important measure and maybe the only require treatment for mild to moderate acidosis Alkali therapy Bicarbonate administration should be reserved only for selected patients with severe acidaemia. Treatment of all acidemia with NaHCO3 is not only unnecessary but can also be detrimental. Correct volume and electrolyte deficits

70. Alkali therapy - Metabolic Acidosis NaHCO3 should be administered judiciously Why to treat metabolic acidosis? Exogenous alkali is often required for prompt reduction of severe acidaemia and associated detrimental effects: Kussumaul’s Breathing, Cardiac arrhythmias, hypotension, impaired response to vasopressors, hyperkalaemia, etc. are the life-threatening complications

71. Alkali therapy - Metabolic Acidosis Why alkali therapy is given in selected patients and aimed for only partial correction?

72. Alkali therapy - Metabolic Acidosis

73. Alkali therapy - Metabolic Acidosis What should be the goal of treatment? NaHCO3 should be administered judiciously with an aim to return blood pH to a safer level of about 7.2 and bicarbonate must be increased to 8-10mEq/L . Patient with acute normal AG acidosis (i.e. diarrhoea) needs early bicarbonate therapy and goal of therapy is to maintain HCO3 at 15mEq/L. In lactic acidosis bicarbonate should be started late and discontinued early .

74. Alkali therapy - Metabolic Acidosis How much HCO3 is needed to achieve the goal? There is no simple prescription as several factors affect the acid-base status( i.e rate of acid production and bicarbonate loss, respiratory compensation, ECF volume status, and treatment of aetiology). Except in cases of extreme acidaemia NaHCO3 should be administered as an infusion over a period of several minutes to a few hours rather than a bolus. Amount of HCO3 required = (Desired HCO3 – ACTUAL HCO3) x 0.5 x body weight in kg

75. Alkali therapy - Metabolic Acidosis

76. Metabolic Alkalosis

77. Respiratory Acidosis Treatment varies as per the severity, rate of onset and underlying aetiology. A. General Measures The major goal of therapy is to identify and treat the underlying cause promptly. Establish patent airway and restore adequate oxygenation. If a patient with chronic hypercapnia develops sudden increase in PaC02, search for the aggravating factor. Vigorous treatment of pulmonary infection, bronchodilator therapy and removal of secretions can offer considerable benefits in such patients.

78. Respiratory Acidosis B. Oxygen Therapy Role of oxygen therapy in respiratory acidosis is like a "Double edged sword" and therefore needs careful titration. In acute respiratory acidosis , major threat to life is hypoxia and not hypercapnia or acidosis, so oxygen supplementation is needed. In chronic hypercapnia , O2 therapy should be instituted cautiously and in the lowest possible concentration , since hypoxemia may be the primary and only stimulus to respiration , injudicious therapy can lead to further reduction in alveolar ventilation and aggravate hypercapnia drastically.

79. Respiratory Acidosis C. Mechanical Ventilatory (MV) Support

80. Respiratory Acidosis C. Mechanical Ventilatory (MV) Support

81. Respiratory Acidosis C. Mechanical Ventilatory (MV) Support

82. Respiratory Acidosis C. Mechanical Ventilatory (MV) Support

83. Respiratory Acidosis C. Mechanical Ventilatory (MV) Support

84. Respiratory Acidosis D. Alkali Therapy Avoid alkali therapy except in patients with associated metabolic acidosis, severe acidaemia (pH < 7.15) or severe bronchospasm (as alkali therapy restores the responsiveness of the bronchial musculature to beta-adrenergic agonists).

85. Respiratory Alkalosis

86. Take home message 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 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.

87. References Paul L. Marino – The ICU Book, 3rd Edition Morgan & Mikhail's Clinical Anaesthesiology – 6e Harrison’s Principles of Internal Medicine, 17th edition, Chap 48 – Acidosis and Alkalosis Handbook of Blood Gas/Acid–Base Interpretation, 2e UpToDate articles on Simple and mixed acid-base disorders by Michael Emmett, MD; Biff F Palmer, MD Practical Guidelines on Fluid Therapy, 2e 'Acid-base pHysiology ' by Kerry Brandis

88. THANK YOU