ARTERIAL BLOOD GAS in details about all the parameters

Abg in details

1. ARTERIAL BLOOD GAS DR SOMASUNDARAM PL GUIDE- DR HIMANSHU DUA

2. INTRODUCTION ABG helps in understanding acid base status of a patient. ABG analysis is an investigation which will measure partial pressure of artyerial oxygen(paO2) and partial pressure of arterial CO2 (paCO2), acidity/alkalosis (pH), oxygen saturation(saO2) and bicarbonate correction (HCO3-) in blood. Analysis will help in knowing the type of acid-base disorder, its magnitude, nature and compensatory response status in patient. It will also help in optimizing mechanical ventilation and other respiratory supports in critically ill patients.

3. INDICATIONS Patients with respiratory distress on oxygen therapy, non invasive/invasive ventilation to know oxygenation and ventilation status. Sick children with sepsis, shock, decreased cardiac output and PDA to assess end organ perfusion status. Metabolic disorders (perinatal asphyxia, renal failure and suspected or proven inborn errors of metabolism)

4. Important terminology PH – it is a negative algorithm of hydrogen ion concentration PH= -log {H+} Increase in H+ -PH decreases – acidosis(<7.35) Decrease in PH – PH increases – alkalosis (>7.45) Normal PH- 7.35 to 7.45.

5. paO2 It represents the oxygen dissolved within the plasma of blood and offers an assessment of oxygenation status. Normal oxygenation status- 80 to 100 Mild hypoxia- 60-80mm Hg Moderate hypoxia 40-60mmHG Severe hypoxia <40mm HG In neonates -60-80mmHG

6. Partial pressure of arterial carbon dioxide It is the single best indicator of respiratory insufficiency & indicator of respiratory contribution to acid base control. Carbon dioxide is over 20 times more soluble than oxygen in blood. PaCO2 represents the partial pressure of arterial carbon di oxide. Normal pacO2- 35 TO 45

7. HCO3- bicarbonate is a base, meaning that it is a acceptor of hydrogen. HCO3 + H = H2O + CO2 It is therefore “ consumed” when neutralizing acids, resulting in lower bicarbonate concentration in the setting of metabolic acidosis. Normal HCO3 = 22 to 28 meq/L

8. Oxygen saturation (saO2) Bllod gas machines that uitilize co-oximetry measure multiple hemoglobin species directly and therefore provide more accurate saO2.

9. Lactate It is the result of metabolism of glucose during tissue hypoxia. Normal blood lactate- <2mmol/L Samples should be analyzed within 15mins to prevent lactate levels from increasing.

10. Base excess it refers to amount of acid/base required to return the PH to 7.4 in a setting of normal pacO2 . Normal base excess = -2 to +2 Low BE – indicates metabolic acidosis High BE – indicates metabolic alkalosis Normal BE in affected PH – indicates respiratory component involved

11. Anion gap To be done in case of metabolic acidosis. Anion gap = Na – (cl- + HCO3-) Normal anion gap= <12 meq/l High anion gap =>12

12. Delta ratio To be done incase of HAGMA. To look for presence of any associated concomitant disorder. Delta ratio = measured AG – normal AG(12)/normal HCO3(24)- measured HCO3 Delta ratio <1 = mixed HAGMA + NAGMA Delta ratio 1-2 = HAGMA Delta ratio >2 = metabolic alkalosis + HAGMA.

13. TCO2 0.03*PaCO2+HCO3 Normal levels are 22 to 28mmol/L It tells about metabolic process activity If TCO2 increases – indicates metabolic alkalosis If TCO2 decreases – indicates metabolic acidosis It is helpful when PH is normal, to find out the primary process.

14. Factors affecting PH CO2+H2O H2CO3 H + HCO3 Whenever there is increase in CO2 – increase production of H – leading to acidosis and viceversa Henderson hessalbach formula PH = Pka + Log [HCO3/CO2] PH = HCO3/PCO2 CARBONIC ANHYDRASE

15. Respiratory acidosis There is increase in co2 PH= HCO3/CO2 (Denominator is increased) Hence PH decreases Respiratory alkalosis There is decrease in CO2 PH= HCO3/CO2 (Denominator is decreased) Hence PH increases

16. Metabolic acidosis There is increase in H+ ions and decrease in HCO3 PH= HCO3/PCO2 Numerator is decreased, hence PH also will be low Metabolic alkalosis There is decrease in H+ ions and increase in HCO3 PH= HCO3/PCO2 Numerator is increased, hence PH will be high

17. Complications of altered PH on CVS ACIDOSIS Decrease in contractility , hence stroke volume decreases, cardiac output decreases- low BP Causes peripheral vasodilation , decrease peripheral resistance Increase in HR due to re entry phenomenon leading to arrythmias. ALKALOSIS No effect on contractility Causes peripheral vasoconstriction Increase in HR , can lead to arrythmias.

18. Complications of altered PH on cellular level ACIDOSIS Acidosis – increase in H+ in circulation, when H+ enters into cell- K+ comes out [ hyperkalemia ] Increase in H+ ions in circulation leading to resistance, hence hyperglycemia Alkalosis Decrease in H+ ions in circulation , hence less K+ & Mg2+ goes outside the cell leading to hypokalemia and hypomagnesemia Normally H+ ions binds with albumin which is negatively charged, but as H+ ions are decreased, calcium will bind to albumin- hypocalcemia

19. Complications of altered PH on RS &CNS Acidosis On RS - tries to increase RR to decrease CO2 , but excessive fatigue can lead to respiratory failure. On CNS- increase in H+ ions leads to altered sensorium & coma Alkalosis On RS- tries to decrease RR to increase Co2, but it can lead to hypoxia . On CNS – can lead to altered sensorium which can lead to COMA. Along with presence of increased firing of neurons leading to seizures/tetany

20. All these complications can be prevented by treating the underlying cause. Initially , our body tries to prevent the complications by compensating the PH – i.e, PH homeostasis.

21. PH homeostasis Buffer system A buffer is a molecule that tends to either bind or release H+ions in order to maintain a particular PH. Eg, Bicarbonate buffer Hb buffer Protein buffer Phosphate buffer Respiratory system Renal system

22. How compensation occurs? Incase of change in PH due to metabolic cause- indicates disturbance in HCO3 – results in respiratory compensation . Respiratory compensation leads to alteration in ventilation allows immediate compensation for metabolic acid base disorders Change in PH due to respiratory cause- indicates disturbance in CO2 – results in renal compensation Renal compensation leads to alteration in PH by changing the amount of HCO3 generated/excreted . Respiratory compensation is immediate Renal compensation occur in days

23. Homeostasis in low PH Buffer system Carbonic acid and bicarbonate buffers along with other buffers causes absorption of H+ ions. Renal compensation H+ secretion and HCO3 generation Respiratory compensation Increase in RR which excretes CO2 H + HCO3 H2CO3 CO2+H2O

24. Homeostasis in high PH Buffer system Carbonic acid and bicarbonate buffers along with other buffers donates H+ ions. Renal compensation H+ generation and HCO3 secr Respiratory compensation Decrease in RR which leads to CO2 retention CO2 +H20 H2CO3 this leads to generation of H+ions

25. Respiratory acidosis For acutely, buffer system of CO2 & HCO3 tries to compensate initially ( not very effective) Compensation by KIDNEY (takes hours to days ) H+ Excretion HCO3 reabsorption PH increases

26. Respiratory alkalosis For acutely, buffer system tries to compensate initially ( not very effective) Compensation by KIDNEY (takes hours to days ) H+ secretion HCO3 excretion PH decreases

27. Metabolic alkalosis For acutely, buffer system tries to compensate initially ( not very effective) Inhibits resp center in medulla (occurs immediately) Decrease rate Decrease depth PH decreases (CO2 levels increased)

28. Metabolic acidosis For acutely, buffer system tries to compensate initially ( not very effective) stimulates resp center in medulla (occurs immediately) Increase rate Increase depth PH decreases (CO2 levels increased)

29. ABG INTERPRETATION Look for PH Can be acidosis/alkalosis/normal Check for primary process Respiratory process PH and PaCO2 will go in opposite direction Metabolic process PH and HCO3- will go in same direction ROME Respiratory-opposite Metabolic-equal

30. Simple acid base disorders- primary process + adequate compensatory response In simple acid base disorders, primary process & compensation will move together RESPIRATORY ACIDOSIS PH decreases PaCO2 increases HCO3 increases METABOLIC ACIDOSIS PH decreases PaCO2 decreases HCO3 decreases RESPIRATORY ALKALOSIS PH increases PaCO2 decreases HCO3 decreases METABOLIC ALKALOSIS PH increases PaCO2 increases HCO3 increases Respiratory opposite PH & PaCO2 in opposite direction Metabolic equal PH & HCO3 in same direction

31. PH ACIDOSIS <7.35 ALKALOSIS >7.45 Match PaCO2 or HCO3 High PaCO2-Resp Acidosis Low HCO3 - Metab acidosis Match PaCO2 or HCO3 Low PaCO2-Resp Alkalosis High HCO3 - Metab alkalosis Look for Relationship between PaCO2 & HCO3 SAME Simple metabolic or resp acidosis OPPOSITE Mixed metabolic or resp acidosis OPPOSITE Mixed metabolic or resp alkalosis SAME Simple metabolic or resp alkalosis Look for Compensation COMPENSATED Simple acid base disorder with adequate compensation UNCOMPENSATED Suggests presence of additional acid-base disorder or insignificant time for compensation Look for Compensation COMPENSATED Simple acid base disorder with adequate compensation UNCOMPENSATED Suggests presence of additional acid-base disorder or insignificant time for compensation

32. Compensation Respiratory acidosis Acute – for every 10mmHG increase in CO2, HCO3- increases by 1meq/l Chronic–for every 10mmhg increase in CO2, HCO3- increases by 4meq/l Respiratory alkalosis Acute –for every 10mmhg decrease in CO2, HCO3- decreases by 2meq/l Chronic-for every 10mmhg decrease in CO2,HCO3- decreases by4meq/l

33. Patient is c/o pneumonia , presented with fever since 2 days , increased work of breathing since morning, ABG reveals, PH-7.44 PCO2-20mmHG PO2-65mmHG HCO3-20meq/L Respiratory alkalosis with compensated metabolic acidosis

34. Compensation Metabolic acidosis Expected PaCO2- (1.5 *HCO3)+8+-2 Eg, PH-7.36 PaCO2-18 HCO3-6 Expected PaCO2- (1.5*6)+8=17+-2=15 to 19 Metabolic acidosis with compensatory respiratory alkalosis

35. Metabolic alkalosis expected PaCO2- HCO3 + 15

36. Mixed acid base disorders When to suspect mixed acid base disorders? No compensation Overcompensation Full compensation with metabolic component within mins to hours Partial compensation with respiratory component after hours

37. Metabolic acidosis Concept of anion gap in metabolic acidosis Anion gap = Na – ( cl + hco3) NAGMA - <12 HAGMA ->12 Measured part Unmeasured parts Na & k Cl & hco3

38. Incase of HAGMA Addition of H+ (main pathogenesis) H+ binds with HCO3- HCO3 Anion gap increases (HAGMA)

39. Incase of NAGMA Initiated by loss of HCO3- (main pathogenesis) Causes Cl- reabsorption by kidney AG not affected Anion gap Normal (NAGMA)

40. HAGMA ETIOLOGY ( KULT ) K etoacidosis U remia L actic acidosis T oxins

41. Ketoacidosis DKA Starvation Alcohol DKA Decreased insulin Increased glucose Unable to utilize this glucose leading to LIPOLYSIS (breakdown of TG’s) Too much increase in acetyl coA Acetyl coA enters into krebs cycle & causes production of ATP( beta oxidation ). But as too much acetyl coA is produced, all cannot enter into krebs cycle Acetyl coA forms ketone bodies . ( Beta hydroxybutyrate, acetoacetate- conjugate bases ) Conjugate bases gives H+, hence PH decreases

42. Ethanol Increase NADH production Inhibits gluconeogenesis Decrease glucose levels , which stimulates glucagon and norepinephrine Stimulates lipolysis Ketone body formation Conjugate bases which donates H+ STARVATION

43. Uremia (seen in end stage renal failure) Kidney unable to filters out sulphates, phosphates, urate They are conjugate bases which gets accumulated Conjugate bases donates H+, ph decreases

44. Glucose Pyruvate LACTATE LOW PH ABSENCE OF O2 ACETYL COA ATP formed by krebs cycle Presence of O2

45. Lactic acidosis type a,b Type A lactic acidosis ( due to decreased O2) Lung disease (pneumonia, pulm edema, pulm embolism, etc) Low hemoglobin (anemia) Low circulation (shock) Type B lactic acidosis ( due to defective clearance of LA) Liver failure (mainly) Renal failure

46. Type B another type – increases production of lactic acidosis Drugs which inhibits oxidative phosphorylation(pyruvate to acetyl CoA) Propofol Metformin Prophylene glycol NRTIs Linezolid b) Increased glycolysis conditions, Seizures Malignancy (multiple myeloma, leukemia, lymohoma, etc)

47. TOXINS Methanol Formic acid Ethylene glycol Oxalic acid & glycolic acid Prophylene glycol Lactic acidosis Salicyclates Lactic acidosis & stimulates resp center Decreases PH

48. NAGMA (USED CARS) Uterosigmoidostomy – Na & cl enters into intestine from kidney Cl- enters systemic circulation Hco3- enters intestine & gets excreted NAGMA

49. Saline infusion Too much of saline infusion Increase in Cl- Decrease in HCO3- Low PH

50. Early renal failure Decreased ability to generate HCO3 NAGMA

51. Diarrhea Intestinal secretion has more of HCO3- In diarrhea Loss of HCO3- Low PH Pancreatic fistula Acinar cells release HCO3 directly into GIT

52. Carbonic anhydrase inhibitors (acetazolamide) Acts on renal tubules Loss of HCO3- NAGMA

53. Addisons disease ( type 4 RTA ) Generalised distal tubular defect ( alpha intercalated cells & principal cells) Defective intercalated cells Defective H+ excretion PH decreases Defective principal cells Defect in aldosterone action Hyponatremia hyperkalemia

54. Renal tubular acidosis Type 1 RTA – classical distal tubular defect ( alpha intercalated cells ) Defective intercalated cells Defective H+ excretion PH decreases

55. Type 2 RTA- Defective proximal convoluted tubules Defect in reabsorption of HCO3- HCO3 excretion along with excretion of Na & H2O Low PH Low blood volume Stimulate JG cells Release renin – increase aldosterone Hypokalemia

56. supplementation Total parental nutrition – increases cl- and acetate – leads to increase in HCO3-levels – decrease in PH.

57. PH-7.28 Pco2-26mmHG HCO3- 11 PO2-90mmHG Na- 129, cl-100 Step 1 – look for PH Step 2- look for primary process (ROME) Step 3- look for simple/mixed, and look for compensation if simple. Step 4- if metabolic acidosis, do anion gap calculation Step 5 –do delta gap ratio, incase of HAGMA

58. Ph decreased Pco2 decreased Hco3 decreased Ph and HCO3 – moving together (ROME) – metabolic is primary process HCO3 and PCO2 is moving together – simple acid base disorder It is metabolic acidosis Next step- calculate anion gap AG = Na – (cl + Hco3) = 129-111 =18 (HAGMA) Delta ratio = 18-12/24-11 =6/13 =<1 indicates HAGMA + NAGMA.

59. Delta ratio <1 = mixed HAGMA + NAGMA(HCO3- is lower than it should be) Delta ratio 1-2 = HAGMA Delta ratio >2 = metabolic alkalosis + HAGMA.(HCO3- is higher than it should be)

60. Metabolic acidosis HAGMA NAGMA Urinary ketones DKA Alcohol Starvation positive negative Look for Arterial lactate KFT Tox screen d/d’s Lactic acidosis Poisoning Late renal failure Look for urinary AG RENAL INCREASED DECREASED EXTRA RENAL Raised urea & creat Early renal failure K+ levels Type 4 RTA increased Type 1,2 RTA decreased Uterosigmoidostomy Saline infusion Diarrhea Acetazolamide TPN

61. Urinary anion gap Incase of NAGMA, if urinary AG increases indicates amount of ammonia excreted is decreased – RENAL CAUSE If urinary AG normal – indicates ammonia excretion is maintained.- EXTRARENAL CAUSE

62. Treatment of Metabolic acidosis Treat the underlying cause

63. Metabolic alkalosis Metabolic alkalosis Saline responsive (urinary cl- <20meq/l) Saline unresponsive Urinary cl- <20meq/l Vomitting NG suction Diuretic use(H+ excretion & HCO3- retention) Chr resp acidosis (eg, COPD) With co existing HTN Genetic defect Hyperaldosteronism Cushings Renin secreting tumor Barters Gietelmann Liddle’s

64. Chronic resp acidosis Eg, COPD – there is increase CO2 retention CO2+H2O = H2CO3 = H+HCO3 Increase in H+ - PH falls As it is a chronic process, kidney will start compensating by Increase H+ excretion Increase HCO3- reabsorption This will increase PH – leading to metab alkalosis If you ventilate this patient, it resolves respiratory acidosis but metabolic alkalosis persists, k/a POST HYPERCAPNEA METAB ALKALOSIS

65. Hyperaldosteronism Aldosterone Na & H2O reabsorption K+ and H+ excretion HTN Hypokalemia High PH PRIMARY HYPERALDOSTERONISM Conns syndrome SECONDARY HYPERALDOSTERONISM Renal artery stenosis CHF PSEUDOHYPERALDOSTERONISM Cushing’s

66. Barters syndrome Similar to loop diuretics Barters Na , K , H2O & H+ excretion HCO3- reabsorption Hypokalemia Hyponatremia Shock Metab alkalosis Metab alkalosis

67. Gietelmann syndrome Similar to thiazide diuretics Gietelmamn synd K & H+ excretion HCO3- reabsorption Hypokalemia Metab alkalosis Metab alkalosis

68. Approach to metabolic alkalosis Mc cause of metabolic alkalosis is saline responsive Look for input & output NG Suction/vomitting INPUT OUTPUT VOLUME OF URINE INCREASED DIURETIC USE COPD

69. 2. Look for urinary cl- Urinary cl- Saline responsive Volume contraction NACL reabsorption Urinary cl- <20meq/l Saline resistant Urinary cl- >20meq/l

70. 3. Patient with metab alkalosis with relatively normal volume status, with urinary cl- >20meq/l Look for BP HTN Metab alkosis Hypernatremia Hypokalemia Urinary cl->20 Suspicion of hyperaldosteronism

71. How to approach hyperaldosteronism? Look for renin angiotensin ratio Primary hyperaldosteronism Blood flow to kidneys are normal, hence renin levels are N/low Ratio will be decreased Secondary hyperaldosteronism Blood flow to kidneys are decreased, hence renin levels are high Ratio will be increased Pseudohyperaldosteronism Check for cortisol levels, INCREASED CUSHINGS ACTH dependent ACTH independent Pituitary adenoma Ectopic ACTH Iatrogenic Adrenal gland issue

72. Respiratory acidosis Respiratory centre(medulla) Spinal cord Anterior horn cells Nerves Nm junction Muscles PH-7.29 PCO2-58mmHG HCO3 -26meq/L PO2- 50mmHG Indicates uncompensated resp acidosis with moderate hypoxia

73. Etiology Lesions / disease of medulla Tumor ( CT/MRI) Infection (LP) Traumatic brain injury (H/O trauma to head) Drugs (supress resp center) Opioids BZD Barbiturates

74. Hypothyroidism Anterior horn lesions – eg, polio Demyelination – eg, GBS NM junction – myasthenia Muscle – exhaustion d/t prolonged increased WOB – d/t pneumonia, pulm edema, embolism, etc Airway obstruction Low T3, T4 Decrease action potential Resp efforts

75. RESPIRATORY ALKALOSIS PH -7.48 PCO2-20mmHG HCO3 -25meq/L PO2-45mmHG Respiratory alkalosis partial compensation with metabolic acidosis with moderate hypoxia

76. Respiratory alkalosis - Causes Increase activity of resp center Drugs – salicyclates like aspirin,methylxanthines, nicotine Infections – toxins causes hyperstimulation of resp center Liver failure – ammonia increases which stimulates resp center. Pain /anxiety/fear- hypothalamus activated- activates resp center Fever – increase BMR- activates hypothalamus & resp center. Pulmonary pathology like pneumonia,pulm edema, pulm embolism,etc can lead to hypoxia – stimulates peripheral chemoreceptors- which stimulates resp center. Raised ICP (hyperventilation occurs as a compensation to decrease CO2 which leads to cerebral vasoconstriction-hence decreases ICP.

77. Patient brought to casualty with c/o weakness of lower limb since 3 days , unable to walk since 2 days. For above complaints patient was admitted in district hospital. As there was no improvement & patient developed breathing difficulty , patient was brought to our hospital for further management o/e – GCS-15/15 Pulse -118/min BP- 104/60mmHG RR- 40/min Spo2-95% on RA s/e – tone decreased in all 4 limbs, Power decreased 1/5 in lower limbs, 2/5 in upper limbs DTR absent, abdominal reflex -

78. ABG reveals, PH- 7.25 PC02-51mmHG HCO3-24meq/L PO2-80mmHG ABG interpretation?

79. Questions 7 year old patient came to casualty with H/O abdominal pain since 1 day with increased work of breathing since morning. On examination – GCS-12/15 Pulse- 130/min BP-94/60mmHG RR- 40/min Spo2- 95% Systemic examination- Air entry present B/L equal uptill bases with no adventitious sounds Other S/E- NAD

80. On probing history further, patient had h/O 3episodes of vomiting ABG reveals, PH-7.2 PaCO2- 28mmHG HCO3- 18meq/l Na-144 Cl-101 ABG interpretation Diagnosis ?

81. DKA Pneumonia with vomiting DKA with vomiting Cardiopulmonary arrest

82. RBS-410

83. 6 year old female child brought to casualty with c/o weakness since 2days, increased work of breathing since 2 hours. on examination – GCS 14/15 HR-126/min BP – 104/60mmHG (towards 90 th ) RR-48/min Spo2- 94% on RA Systemic examination – air entry present bilaterally uptill bases, basal crepts present on right side

84. Casualty resident put patient on oxygen and gave 1 stat dose of Lasix and hydrocortisone. Patient was shifted to ICU, ABG along with 1 st line investigations were sent along with CXR was done ABG – PH- 7.47 PCO2-20mmHG PO2- 66mmHG HCO3- 29meq/L Abg interpretation?

85. 29 week gestation baby delivered via LSCS i/v/o impending eclampsia, baby CIAB, Birth wt of 1.1 kg/ male child having respiratory distress, patient was shifted to NICU i/v/o resp distress and LBW care. RDS score-2/10 ABG was done PH-7.29 PCO2-48mmHG PO2-56 HCO3-20 Interpretation ?

86. Gestational age pH pO2 pCO2 HC03- BE Term 7.32 - 7.38 80 – 95 35 – 45 24 – 26 ±4 Preterm (30-36 weeks) 7.30 - 7.35 60 – 80 35 – 45 22 – 25 ±4 Preterm (<30 weeks) 7.27 – 7.32 40 – 60 38 – 50 19 – 22 ±4 Term umbilical artery 7.10 – 7.38 4.1 - 31.7 39.1 – 73.5 22 – 23 ±2 Term umbilical vein 7.20 – 7.44 30.4 - 57.2 14.1 – 43.3 -7.7 to 1.9 -

87. Abg of 8 year old, PH- 7.3 PCO2- 30mmHG HCO3- 16 Na -133 Cl-106 K -3.1 All of the following can be possible reason except?

88. TPN Diarrhea Sepsis RTA