ABG Class power point and it's importance

Abg and it's importance

1. ARTERIAL BLOOD GAS ANALYSIS Dr.MUKUL SAINI

2. Taking an Arterial blood sample What to consider before sampling ? Arterial puncture sites ? Radial artery sampling and modified allen test? Heparin use and transit time? After sampling ?

3. pH pO 2 pCO 2 HCO 3 BE Lactates Na+ Cl -

4. pH: Measurement of acidity or alkalinity, based on the hydrogen (H+). 7.35 – 7.45

5. pH is the negative logarithm (base 10) of the hydrogen ion activity in a solution

6. H + = 40 nEq/L To maintain a constant pH, PCO2/HCO3- ratio should be constant When one component of the ratio is altered, the compensatory response alters the other component in the same direction

7. p a o 2 :The partial pressure oxygen that is dissolved in arterial blood. PaO2 = 104 – (0.43 age )

8. FiO2– PaO 2 /FiO 2 ratio

9. FiO2- 75% P/F = 91.7/0.75 =122

10. ALVEOLAR GAS EQUATION (pAO 2 )

11. Physiologic A-a gradient changes with age [A-a gradient = (Age + 10) / 4]

12. pCO 2 : The partial pressure of carbon dioxide dissolved in arterial blood . TCO 2: CO 2 content HCO3 (Measured or calculated ) - actual HCO3 - std HCO3 T he concentration of bicarbonate in the plasma which is equilibrated with a normal PaCO2 (40 mm Hg) and a normal pO2 at a normal temperature (37°C )

13. BE The "Base Excess" is the amount of acid or base required to titrate a blood sample (of whole blood) to a pH of 7.40, at standard temperature and pressure, with a standard PaCO2 of 40mmHg . acidosis ←-2 to +2→ alkalosis

14. Lactic acidosis Lactate , the anion that results from dissociation of lactic acid, is a product of glucose metabolism; specifically it is the end product of anaerobic glycolysis . Blood lactate concentration is maintained within the approximate range of 0.5-1.5 mmol /L The combination of hyperlactatemia and acidosis is called lactic acidosis-most common cause of metabolic acidosis . blood lactate >5.0 mmol /L in combination with pH <7.35

15. BUFFER SYSTEMS Ii ECF BLOOD ICF URINE Major buffer Bicarbonate Minor buffers Proteins Phosphates Major buffers Bicarbonate H aemoglobin Minor buffers Pl Proteins Phosphates Major buffers Proteins Phosphates Major buffers Ammonia Phosphates

16. Carbonic acid-Bicarbonate buffer

17. Approach to Acid Base disorders Boston approach (traditional) Copenhagen approach (base excess) Stewart (physiochemical approach)

18. Steps of ABG analysis What is the pH? Acidemia or Alkalemia ? What is the primary disorder present? Is there appropriate compensation? Is the compensation acute or chronic? Is there an anion gap? If there is a AG check the delta gap?

19. Validity of ABG Rule of 80 Subtract the last 2 digits of pH from 80 80-28=52 (H+ conc ) Calculate H + using the equation 24×(41/19.3) 24×2.12=51

20. pH is the negative logarithm (base 10) of the hydrogen ion activity in a solution

21. Acid-Base disorders Respiratory acidosis (acute/chronic) R espiratory alkalosis (acute/chronic) Metabolic acidosis Metabolic alkalosis

22. Respiratory compensation can begin within minutes and becomes maximal in 12 - 24 hours. Renal compensation has an acute and chronic phase, where the effect is smaller at first before reaching a peak in 2 - 5 days.

23. The Boston Method Six bicarbonate-based bedside rules to assess compensation Schwartz and Relman

24. Respiratory acidosis

25. Respiratory alkalosis

26. Acute respiratory acidosis C hronic respiratory acidosis Acute respiratory alkalosis Chronic respiratory alkalosis

27. EXPECTED CHANGES IN pH in RESPIRATORY ACID-BASE DISORDERS 10 mm Hg change in PaCO2 Primary Disorder Expected Changes Acute respiratory acidosis delta pH = 0.008 × (PCO2 - 40) Chronic respiratory acidosis delta pH = 0.003 × (PCO2 - 40) Acute respiratory alkalosis delta pH = 0.008 × (40 - PCO2) Chronic respiratory alkalosis delta pH = 0.003 × (40 - PCO2) 0.08 acute chronic pH 0.03

28. pH-7.2 PCO 2 -65 mm Hg Change in CO 2 -- 25 Change in pH--25×.008=0.2 pH---7.4-0.2= 7.2 Acute respiratory acidosis

29. pH-7. 5 PCO2--20 mm Hg Change in CO2 --20 Change in pH- -20×.008=0.16 pH--- 7.4+0.16= 7.56------acute resp alkalosis 20×.003=0.06= 7.46------chronic resp alkalosis Partially compensated

30. Metabolic acidosis and alkalosis Winter’s formula OR PaCO2 = HCO3- + 15

31. Anion gap=Na-(Cl+HCO3) Normal anion gap 6-12mEq/L

32. DELTA GAP Only necessary if there is an AG metabolic acidosis. Does the increase in AG completely explain the ABG ? PRINCIPLE Bicarbonate is decreased due to the presence of unmeasured anions For one molecule of anion, one molecule of bicarbonate is lost Bicarbonate level can therefore be predicted

33. Delta gap = HCO3- + (AG-12) If <24, pt. has an additional non-anion gap metabolic acidosis If >24, pt. has an additional metabolic alkalosis

34. pH 7.26 pO2 90 mmHg pCO2 45 mmHg Bicarbonate 18 mmol /L Base excess -7 mmol /L Sodium 134 mmol /L Potassium 5.0 mmol /L Chloride 98 mmol /L Lactate 2.2 mmol /L -There is acidaemia -The PaO2 is normal -The base excess is low - metabolic acidosis -The expected CO2 = (1.5×18 )+8 = 35 respiratory acidosis -The anion gap is elevated ( 134 - (98 + 18)) = 18 -The delta ratio is therefore ( 18-12)/(24-18) = 1.0 HAGMA Metabolic acidosis (HAGMA) with Respiratory acidosis

35. How much should HCO3- fall? If pH= 7.08, Na= 143, Cl = 100 and HCO3 = 10 AG = 143 – (100+10) = 35 ( Normal AG = 12) Excess AG= 23 Hence HCO3 should have fallen by 23 ( From 24 to 1) But it is 10( 9 more than predicted) COEXISTANT METABOLIC ALKALOSIS

36. Diabetic pt with diarrhoea and DKA – METABOLIC ACIDOSIS ABG showing : pH = 7.08, Na= 136, Cl = 110 and HCO3= 5 AG= 136- (110+5) = 21 Normal AG= 12, Excess AG= 9 Hence HCO3 should have fallen by 9 from 24 to 15. But it is 5 ( 10 less than predicted) COEXISTANT NON-AG METABOLIC ACIDOSIS

37. HAGMA Imp. Points Osmolal gap especially in cases of toxin ingestion. Osmolal gap = Measured Serum osmolality – Calculated serum osmolality Calculated serum osmolality = 2[Na+] + [BUN]/2.8 + [Glucose]/18 Normal value ~ 10 So, if anion gap and osmolal gap both has increased then we should think in terms of Toxins.

38. NAGMA Imp. Points Check urinary anion gap in non-AG metabolic acidosis ( U Na + U K – U Cl ). Normal- Zero or negative Non-renal loss of bicarbonate(diarrhoea)- negative Renal loss of bicarbonate or decrease H+ secretion (renal tubular acidosis) – Positive

39. Can Anion gap decrease?? YES In cases of Multiple myeloma and paraproteinemia where there is increased paraproteins in blood which act as cations .

40. Pt presents with h/o multiple episodes of vomiting

41. Metabolic alkalosis Reflects an increase in plasma HCO3-. It is either due to gain of HCO3- or extracellular volume contraction. It can be classified into saline responsive or non responsive. For this spot urinary chloride is checked. More than 20 meq /L urinary chloride is saline unresponsive and less than 20meq/L is saline responsive.

42. Urine Cl - more than 20 mEq /L Primary hyperaldosteronism Cushing’s syndrome, ectopic ACTH Exogenous steroids, licorice ingestion, tobacco chewing Adrenal 11 or 17 OH defects Liddle’s syndrome Bartter’s syndrome K+ and Mg+ deficiency Milk alkali syndrome Urine Cl - less than 20 mEq /L Vomiting, nasogastric suctioning Chloride-wasting syndrome Villous adenoma of colon Posthypercapnia Diuretic therapy

43. An elderly pt who was administered large dose of opioids for post-operative pain and was found to be very drowsy.

44. Respiratory acidosis

45. Post op burns pt planned for weaning and extubation Fentanyl infusion has been stopped Pt spont . breathing on CPAP mode

46. Respiratory Alkalosis

47. Corrected AG A 60 Yr old homeless man presents with nausea, vomiting and poor oral intake 2 days prior to admission. The patient reports a 3 day history of binge drinking prior to symptoms. Labs: Na 132, k 5.0, Cl 104, HCO3 16, BUN 25, Creatinine 1.3, Glucose 75 ABG: Ph 7.30, PCO2 29, HCO3 16, PO2 92 Serum albumin 1.0

48. Anion gap = 12 which is normal Corrected Anion gap= Calculated Anion gap + 2.5 (4.5- Albumin). Corrected AG = 21 Albumin is the principal unmeasured anion and the principal determinent of the anion gap. A low albumin level in plasma will lower the AG, and this could mask the presence of an unmeasured anion( eg . Lactate) that is contributing to metabolic acidosis.

49. 56 yr F with COPD exacerbation and hypotension and associated diarrhoea since 7 days presents with following ABG PaCO2 : 30 pH: 7.22 PaO2: 65 Na: 139 Cl : 110 HCO3 : 10

50. pH(7.22) = Acidemia Low HCO3 and low PCO2 = Metabolic acidosis Winters formula expected PCO2= 23, Respiratory acidosis AG= 19 Delta gap = 10 + (19-12) = 17 So less than 24, hence the patient has an additional non anion gap metabolic acidosis.

51. 40 yr M with pneumonia and low BP on dopamine. He has been having vomiting over the last three days. ABG picture is : pH = 7.26 PCO2 = 15 PaO2 = 65 Na = 130 Cl = 90 HCO3 = 10

52. pH = acidemia Low HCO3 and Low PCO2 = Met. Acidosis Expected PCO2 = 1.5(10) + 8 = 23, Respiratory alkalosis AG = 130 – (90 + 10) = 30 Delta gap = 10 + (30-12) = 28 Additional metabolic alkalosis

53. Errors…… Delayed analysis- ↑CO 2 , ↓O 2 , ↓pH due to glycolysis in RBC

54. Air bubbles-↑O 2 , ↓CO 2 Excessive heparin- Dilutional effect on results ↓ HCO 3 & PaCO 2 Only .05 ml heparin required for 1 ml blood. Leucocytosis : ↓ pH and PO 2 ; and ↑ P co 2 Temperature : In c/o Hyperthermia PaO2 and PaCO2 decreases (opposite changes occurs in hypothermia) Venous admixture

55. Treat the underlying cause and not the ABG