1. I.S. MD 5/18/01ABG Interpretation1 ABG INTERPRETATION

2. I.S. MD ABG (Astrup) opH - measured opCO 2 - measured oHCO 3 - - calculated opO 2 - measured oBE (BD) - calculated

3. I.S. MD ABG Interpretation oFirst, does the patient have an acidosis or an alkalosis oSecond, what is the primary problem – metabolic or respiratory oThird, is there any compensation by the patient – respiratory compensation is immediate while renal compensation takes time

4. I.S. MD ABG Interpretation oIt would be extremely unusual for either the respiratory or renal system to overcompensate oThe pH determines the primary problem oAfter determining the primary and compensatory acid/base balance, evaluate the effectiveness of oxygenation

5. I.S. MD Normal Values opH 7.35 to 7.45 opaCO 2 36 to 44 mm Hg oHCO 3 22 to 26 meq/L

6. I.S. MD Abnormal Values pH < 7.35 oAcidosis (metabolic and/or respiratory) paCO 2 > 44 mm Hg oRespiratory acidosis (alveolar hypoventilation) HCO 3 < 22 meq/L oMetabolic acidosis pH > 7.45 oAlkalosis (metabolic and/or respiratory) paCO 2 < 36 mm Hg oRespiratory alkalosis (alveolar hyperventilation) HCO 3 > 26 meq/L oMetabolic alkalosis

7. I.S. MD Putting It Together - Respiratory So paCO 2 > 44 with a pH < 7.35 represents a respiratory acidosis paCO 2 7.45 represents a respiratory alkalosis For a primary respiratory problem, pH and paCO 2 move in the opposite direction oFor each deviation in paCO 2 of 10 mm Hg in either direction, 0.08 pH units change in the opposite direction

8. I.S. MD Putting It Together - Metabolic And HCO 3 < 22 with a pH < 7.35 represents a metabolic acidosis HCO 3 > 26 with a pH > 7.45 represents a metabolic alkalosis For a primary metabolic problem, pH and HCO 3 are in the same direction

9. I.S. MD Metabolic Acidosis Increase in H + involves:  Extracellular buffering  Intracellular buffering  Respiratory compensation  Renal excretion of the H + load

10. I.S. MD Compensation ometabolic alkalosis orespiratory alkalosis ometabolic acidosis orespiratory acidosis The body’s attempt to return the acid/base status to normal (i.e. pH closer to 7.4) Primary Problem orespiratory acidosis ometabolic acidosis orespiratory alkalosis ometabolic alkalosis

11. I.S. MD Expected Compensation Respiratory acidosis oAcute – the pH decreases 0.08 units for every 10 mm Hg increase in paCO 2 ; (HCO 3  0.1-1 mEq/liter per  10 mm Hg paCO 2 ) oChronic – the pH decreases 0.03 units for every 10 mm Hg increase in paCO 2 ; (HCO 3  1.1-3.5 mEq/liter per  10 mm Hg paCO 2 )

12. I.S. MD Expected Compensation Respiratory alkalosis oAcute – the pH increases 0.08 units for every 10 mm Hg decrease in paCO 2 ; HCO 3  0-2 mEq/liter per  10 mm Hg paCO 2 oChronic - the pH increases 0. 17 units for every 10 mm Hg decrease in paCO 2 ; HCO 3  2.1-5 mEq/liter per  10 mm Hg paCO 2

13. I.S. MD Expected Compensation Metabolic acidosis opaCO 2  10-15 per  10 mEq/liter HCO 3 Metabolic alkalosis opaCO 2  5-10 per  10 mEq/liter HCO 3

14. I.S. MD Classification of primary acid-base disturbances and compensation oRespiratory acidosis (alveolar hypoventilation) - acute, chronic oRespiratory alkalosis (alveolar hyperventilation) - acute, chronic oMetabolic acidosis – uncompensated, compensated oMetabolic alkalosis – uncompensated, partially compensated

15. I.S. MD Acute Respiratory Acidosis opaCO 2 is elevated and pH is acidotic oThe decrease in pH is accounted for entirely by the increase in paCO 2 oBicarbonate and base excess will be in the normal range because the kidneys have not had adequate time to establish effective compensatory mechanisms

16. I.S. MD Acute Respiratory Acidosis oCauses oRespiratory pathophysiology - airway obstruction, severe pneumonia, chest trauma/pneumothorax oAcute drug intoxication (narcotics, sedatives) oResidual neuromuscular blockade oCNS disease (head trauma)

17. I.S. MD Chronic Respiratory Acidosis opaCO 2 is elevated with a pH in the acceptable range oRenal mechanisms increase the excretion of H + within 24 hours and may correct the resulting acidosis caused by chronic retention of CO 2 to a certain extent

18. I.S. MD Chronic Respiratory Acidosis oCauses oChronic lung disease (BPD, COPD) oNeuromuscular disease oExtreme obesity oChest wall deformity

19. I.S. MD Acute Respiratory Alkalosis opaCO 2 is low and the pH is alkalotic oThe increase in pH is accounted for entirely by the decrease in paCO 2 oBicarbonate and base excess will be in the normal range because the kidneys have not had sufficient time to establish effective compensatory mechanisms

20. I.S. MD Respiratory Alkalosis Causes oPain oAnxiety oHypoxemia oRestrictive lung disease oSevere congestive heart failure oPulmonary emboli oDrugs oSepsis oFever oThyrotoxicosis oPregnancy oOveraggressive mechanical ventilation oHepatic failure

21. I.S. MD Uncompensated Metabolic Acidosis oNormal paCO 2, low HCO 3, and a pH less than 7.30 oOccurs as a result of increased production of acids and/or failure to eliminate these acids oRespiratory system is not compensating by increasing alveolar ventilation (hyperventilation)

22. I.S. MD Compensated Metabolic Acidosis opaCO 2 less than 30, low HCO 3, with a pH of 7.3-7.4 oPatients with chronic metabolic acidosis are unable to hyperventilate sufficiently to lower paCO 2 for complete compensation to 7.4

23. I.S. MD Anion Gap and Acidosis (AG) represents the concentration of all the unmeasured anions in the plasma Anion gap = )[Na + ] +[K + ])- ([Cl - ] - [HCO3 - ]) Normal = 8-14

24. I.S. MD Anion Gap and Acidosis (AG) represents the concentration of all the unmeasured anions in the plasma 0 = )[Na + ] +[K + ] + [ ? + ]) - - ([Cl - ] + [HCO3 - ] + [ ? - ])

25. I.S. MD Anion Gap and Acidosis [? + ] – Ca +, Mg + [? - ] – plasma proteins, phosphate, sulfate, organ. anions

26. I.S. MD Anion Gap and Acidosis [? + ] – Ca +, Mg + and [? - ] – phosphate, sulfate, organ. anions Tend to balance out So plasma proteins [Pro - ] – account for most of the missing anions

27. I.S. MD Anion Gap and Acidosis [? - ] > [ ? + ] i.e. AG = [? - ] - [ ? + ]

28. I.S. MD Anion Gap and Acidosis AG = [? - ] - [ ? + ] i.e. AG if ? + - very small, 1-3 meq/l or

29. I.S. MD Anion Gap and Acidosis or AG if ? - may be significant

30. I.S. MD Anion Gap and Acidosis [? - ] may be induced by high Albumin concentration (i.e. hypovolemia) or [? - ] accumulation of different anions

31. I.S. MD Elevated AG Metabolic Acidosis Causes oKetoacidosis - diabetic, alcoholic, starvation oLactic acidosis - hypoxia, shock, sepsis, seizures oToxic ingestion - methanol, ethylene glycol, ethanol, isopropyl alcohol, paraldehyde, toluene oRenal failure - uremia

32. I.S. MD Normal AG Metabolic Acidosis - Causes oRenal tubular acidosis oHypoaldosteronism oDiarrhea oPotassium sparing diuretics

33. I.S. MD Effectiveness of Oxygenation oFurther evaluation of the arterial blood gas requires assessment of the effectiveness of oxygenation of the blood oHypoxemia – decreased oxygen content of blood - paO 2 less than 60 mm Hg and the saturation is less than 90% oHypoxia – inadequate amount of oxygen available to or used by tissues for metabolic needs

34. I.S. MD Mechanisms of Hypoxemia oInadequate inspiratory partial pressure of oxygen oHypoventilation oRight to left shunt oVentilation-perfusion mismatch oIncomplete diffusion equilibrium

35. I.S. MD Summary oFirst, does the patient have an acidosis or an alkalosis oLook at the pH oSecond, what is the primary problem – metabolic or respiratory oLook at the pCO 2 oIf the pCO 2 change is in the opposite direction of the pH change, the primary problem is respiratory

36. I.S. MD Summary oThird, is there any compensation by the patient - do the calculations oFor a primary respiratory problem, is the pH change completely accounted for by the change in pCO 2 oif yes, then there is no metabolic compensation oif not, then there is either partial compensation or concomitant metabolic problem

37. I.S. MD Summary oFor a metabolic problem, calculate the expected pCO 2 oif equal to calculated, then there is appropriate respiratory compensation oif higher than calculated, there is concomitant respiratory acidosis oif lower than calculated, there is concomitant respiratory alkalosis

38. I.S. MD Summary oNext, don’t forget to look at the effectiveness of oxygenation, (and look at the patient) oyour patient may have a significantly increased work of breathing in order to maintain a “normal” blood gas ometabolic acidosis with a concomitant respiratory acidosis is concerning

39. I.S. MD Case 1 Little Billy got into some of dad’s barbiturates. He suffers a significant depression of mental status and respiration. You see him in the ER 3 hours after ingestion with a respiratory rate of 4. A blood gas is obtained (after doing the ABC’s, of course). It shows pH = 7.16, pCO 2 = 70, HCO 3 = 22

40. I.S. MD Case 1 What is the acid/base abnormality? 1.Uncompensated metabolic acidosis 2.Compensated respiratory acidosis 3.Uncompensated respiratory acidosis 4.Compensated metabolic alkalosis

41. I.S. MD Case 1 Uncompensated respiratory acidosis oThere has not been time for metabolic compensation to occur. As the barbiturate toxicity took hold, this child slowed his respirations significantly, pCO 2 built up in the blood, and an acidosis ensued.

42. I.S. MD Case 2 Little Suzie has had vomiting and diarrhea for 3 days. In her mom’s words, “She can’t keep anything down and she’s running out.” She has had 1 wet diaper in the last 24 hours. She appears lethargic and cool to touch with a prolonged capillary refill time. After addressing her ABC’s, her blood gas reveals: pH=7.34, pCO 2 =26, HCO 3 =12

43. I.S. MD Case 2 What is the acid/base abnormality? 1.Uncompensated metabolic acidosis 2.Compensated respiratory alkalosis 3.Uncompensated respiratory acidosis 4.Compensated metabolic acidosis

44. I.S. MD Case 2 Compensated metabolic acidosis oThe prolong history of fluid loss through diarrhea has caused a metabolic acidosis. The mechanisms probably are twofold. First there is lactic acid production from the hypovolemia and tissue hypoperfusion. Second, there may be significant bicarbonate losses in the stool. The body has compensated by “blowing off” the CO 2 with increased respirations.

45. I.S. MD Case 3 You are evaluating a 15 year old female in the ER who was brought in by EMS from school because of abdominal pain and vomiting. Review of system is negative except for a 3.5 kg weight loss over the past 2 months and polyuria for the past 2 weeks. She denies any sexual activity or drug use. On exam, she is alert and oriented, HR 115, RR 26, BP 114/75, pulse ox 95% on RA, mild abdominal tenderness on palpation in the midepigastric region and capillary refill time of 3 seconds. The result of the blood gas: pH = 7.21 pCO 2 = 24 pO 2 = 45 HCO 3 = 10 BE = -10

46. I.S. MD Case 3 What is the blood gas interpretation? oUncompensated respiratory acidosis with severe hypoxia oUncompensated metabolic alkalosis oCombined metabolic acidosis and respiratory acidosis with severe hypoxia oMetabolic acidosis with respiratory compensation

47. I.S. MD Case 3 Metabolic acidosis with respiratory compensation oThis is a patient with new onset diabetes mellitus in ketoacidosis. Her pulse oximetry saturation and clinical examination do not reveal any respiratory problems except for tachypnea which is her compensatory mechanism for the metabolic acidosis. The nurse obtained the blood gas sample from the venous stick when she sent off the other labs.