ABGs and Acid-Base

1. Deborah Cappell, MD ABGs and Acid-Base

2. ABG • The ABG contains pH, PCO2, PO2 as analyzed by three electrodes at 37C • The presence of air bubbles can falsely can alter PO2 and PCO2 closer to RA. Ice keeps the gases from escaping from the solution. • Leukocyte larceny can cause a false decrement in PO2 due to WBC consumption of oxygen.

3. ABG question #1 • A 72 yo male, 50 pk-yr smoker, p/w dyspnea and sx c/w chronic bronchitis. His SpO2 via pulse oximeter is 95%. However, an ABG via co-oximeter reveals PCO2 54, PO2 65, SpO2 86%. According to a standard Hgb dissociation curve the SpO2 should be >90%. Which explains the discrepancy btwn his PO2 and SpO2? • A. He has significant leukocytosis • B. He has carboxyhemoglobinemia • C. He has respiratory alkalosis • D. He has 2,3,-diphosphoglycerate deficiency • E. He is hypothermic

4. ABG question #1 • A 72 yo male, 50 pk-yr smoker, p/w dyspnea and sx c/w chronic bronchitis. His SpO2 via pulse oximeter is 95%. However, an ABG via co-oximeter reveals PCO2 54, PO2 65, SpO2 86%. According to a standard Hgb dissociation curve the SpO2 should be >90%. Which explains the discrepancy btwn his PO2 and SpO2? • A. He has significant leukocytosis • B. He has carboxyhemoglobinemia • C. He has respiratory alkalosis • D. He has 2,3,-diphosphoglycerate deficiency • E. He is hypothermic

5. Explanation of ABG question 1 • Pulse oxymeter does not distinguish oxygenated Hgb from carboxy or met hemoglobin. • However, the co-oximeter can differentiate hgb, carboxy-hgb and met-hgb. The carboxy-hgb was 10.7% in this pt likely from smoking. • Hence using only standard oximetery in the setting of smoke inhalation can give a false sense of security. An ABG by co-oximetry to r/o carboxy-hgb is necessary.

6. Explanation of ABG question 1 • Leukocyte larceny will falsely reduce PO2 and SpO2. • Resp Alkalosis will shift the Hgb dissociation curve to the left and give a higher SpO2 for the same PO2. • 2,3 diphosphoglycerate deficiency shifts the Hgb dissociation curve to the left as well. • Only the measured SpO2 would be less than then PO2 not the calculated SpO2 less than PO2. • As the temperature decreases, pH increases. • When blood flows to the cool periphery the pH increases as PCO2 and H+ falls, so SpO2 rises with cooling and the PO2 decreases.

7. Question • A 23 yo male admitted to ICU with resp failure from diffuse PNA. PMH IVDU and HIV. He is Rx with IV Bactrim and prednisone for presumptive PCP. His initial PaO2 was 55. • Within 24 hours he is intubated for hypoxemic resp failure. Initial post-intubation ABG on 100% was 7.45/32/82 94%. CXR diffuse infiltrates. The following day on 70% his ABG is 7.45/30/121 SpO2 of 97%. He is bronched and the BAL is positive for PCP. • On day 5 he is on 40% and a weaning trial is begun.

8. Question • After 60 min of CPAP with PS of 5 and 40% oxygen his ABG is 7.43/35/90 SPO2 77%. • What is the most appropriate next step in this patient's management? • A. Repeat the ABG • B. Extubate to nonrebreather • C. Administer amyl nitrate by inhalation then sodium thiosulfate IV • D. Switch the patients Abx from Bactrim to pentamidine and administer IV methylene blue

9. Question • After 60 min of CPAP with PS of 5 and 40% oxygen his ABG is 7.43/35/90 SPO2 77%. • What is the most appropriate next step in this patient's management? • A. Repeat the ABG • B. Extubate to nonrebreather • C. Administer amyl nitrate by inhalation then sodium thiosulfate IV • D. Switch the patients Abx from Bactrim to pentamidine and administer IV methylene blue

10. Answer Explained • This pt has clinically improved, however his SpO2 has declined despite an adequate PaO2. • A recognized complication of sulfonomides is methemoglobinemia. (Then Hgb cannot bind oxygen because of oxidation of fe.) • [Also can happen with nitrites, nitrates, phenacetin, aniline dyes, and lidocaine] • Rx methylene blue IV by reducing the Fe.

11. SEEK • A 33 yo female with p/w lower abdominal pain for 1 day, assoc with nausea and decreased appetite. PE VS anl, abd soft with lower abd diffuse tenderness and the patient vomited twice during the exam. Pelvic showed b/l adnexal tenderness. WBC 19K, with 90% PMN. • She received Metronidazole, Cipro, Morphine and metoclopramide and was sent for CT abd/pelvis.

12. SEEK • 2 hours later she had acute onset SOB and feeling of impending doom. She was cyanotic despite 100% Oxygen by NRB. HR 132, BP 160/100, RR 28, SpO2 85% and the ABG 7.36/35/240. Naloxone was given but cyanosis and dyspnea continued, and she became lethargic. • What is the best Rx for the disorder that caused the acute decompensation?

13. SEEK What is the best Rx for the disorder that caused the acute decompensation? • High dose corticosteroids • Broad spectrum Abx • Surgery • Sodium nitrite and sodium thiosulfate • Methylene Blue

14. SEEK What is the best Rx for the disorder that caused the acute decompensation? • High dose corticosteroids • Broad spectrum Abx • Surgery • Sodium nitrite and sodium thiosulfate • Methylene Blue

15. SEEK • The pt has methemoglobinemia due to administration of metoclopramide and Rx with Methylene blue will reduce the seum ferric iron. Metoclopramide is an oxidizing agent which can convert ferrous (++) iron in hgb to the ferric form (+++). When given in excessive doses or to pt with enzyme deficiencies to convert methgb to hgb toxic levels may develop. • MetHgb has a higher Oxygen affinity and reduces blood oxygen content shifting the curve to the left. Cyanosis develops at 15%, sx at 30% and Change in MS at 50%. Level >70% are usually fatal.

16. SEEK • Many drugs are oxidants and cause this: chloroquine, dapsone, local anesthetics (benzocaine, nitrates (nitroglycerin, nitroprusside, NO), and sulfonamides. • High levels of MetHgb turn blood brown and does not turn red when exposed to air. SpO2 is inaccurate. The SpO2 not correlating with abg is a clue that co-oximetry is needed.

17. SEEK • Rx for MetHgb >30% with methylene blue which is a cofactor for NADP-metHb reductase and increases that enzymes capacity to reduce ferric iron. Dose is 1-2 mg/kg over >5 minutes. • Higher doses may increase MetHgb levels in doses >15mg/kg and in pt with G6PD. • This pt has PID and abx are useful. • Sodium nitrite and sodium thiosulfate are used as antidotes to cyanide poisoning and work by increasing metHgb levels to facilitate transport of cyanide as cyanomethemoglobin from mitochondrial cytochromes to hepatocytes.

18. ABG • Interpreting an ABG requires first an appreciation for the alveolar gas equation. • Alveolar-arterial oxygen gradient: • Aa= PAO2- PaO2 • FIO2(PB-PH20)-PaCO2/R -PaO2 • Where FIO2 = 0.21 PB=760 PH2O = 47 • A normal Aa gradient is dependent on age, body position, and nutritional status. • (It is increased with age, obesity, fasting, supine position, heavy exercise and fasting)

19. ABG • An increased Aa gradient can be caused by • A. Hypoventilation • B. Hyperventilation • C. Pulmonary embolus • D. A and C • E. B and C

20. C. Pulmonary embolus ABG • An increased Aa gradient can be caused by • A. Hypoventilation • B. Hyperventilation • C. Pulmonary embolus • D. A and C • E. B and C • Hypoventilation will increase PCO2 and decrease PaO2 proportionally. • Hyperventilation will decrease PCO2 and increase PaO2 proportionally. • VQ mismatch will increase the Alveolar-arterial gradient.

21. Question Acid-Base • In a hemodynamically stable pt on RA with nl BP and CXR which of the following arterial and venous ABG come from the same pt? • (pH/PCO2/PHCO3 arterial;venous) • A. 7.4/40/24 ; 7.4/40/24 • B. 7.25/23/10 ; 7.29/20/9 • C. 7.3/55/28 ; 7.2/65/33 • D. 7.39/44/23 ; 7.35/50/24 • E. 7.4/24/24 ; 7.37/30/26

22. Question Acid-Base • In a hemodynamically stable pt on RA with nl BP and CXR which of the following arterial and venous ABG come from the same pt? • (pH/PCO2/PHCO3 arterial;venous) • A. 7.4/40/24 ; 7.4/40/24 • B. 7.25/23/10 ; 7.29/20/9 • C. 7.3/55/28 ; 7.2/65/33 • D. 7.39/44/23 ; 7.35/50/24 • E. 7.4/24/24 ; 7.37/30/26

23. Answer, explained • 7.39/44/23 and 7.35/50/24 • The mean difference btwn arterial and venous pH was 0.036, PCO2 6, HCO3 1.5 • Venous pH should be lower and PCO2 higher than arterial. Bicarb is slightly higher in venous than arterial blood. • If only a trend is what is being followed, eg in DKA, venous blood gases are likely adequate.

24. Answer, explained • (Option A has same values for venous and arterial, option B the direction of change art to venous is backward, option C the magnitude of change is too great, option E makes no physiologic sense.)

25. SEEK • A pregnant asthmatic is in the ER. She is 22 yo with asthma since early child with rare medication use until her pregnancy. She is 34 weeks pregnant and this is her 1st pregnancy. In her 2nd trimester she was seen in her OB’s office and was Rx with IV corticosteroids and then started on inhaled corticosteroids and a long-acting beta agonist. She did well until the last 2 days when DOE progressed to dyspnea at rest and over the prior evening used her rescue beta agonist many times.

26. SEEK • On PE she is in moderate distress, using accessory muscles to breath while sitting upright. She can speak only 2-3 words at a time and there is insp and exp wheezing with decreased air movement. ABG on RA is 7.36/38/78. In this patient the most likely acute acid-base disturbance is: • Metabolic Alkalosis • Metabolic Acidosis • Respiratory Acidosis • Respiratoy Alkalosis • No acute acid-base disturbance

27. SEEK • On PE she is in moderate distress, using accessory muscles to breath while sitting upright. She can speak only 2-3 words at a time and there is insp and exp wheezing with decreased air movement. ABG on RA is 7.36/38/78. In this patient the most likely acute acid-base disturbance is: • Metabolic Alkalosis • Metabolic Acidosis • Respiratory Acidosis • Respiratory Alkalosis • No acute acid-base disturbance

28. SEEK explained • This ABG is signaling ventilatory failure from acute asthma. There are changes in pregnancy which must be taken into account. During pg oxygen consumption rises to 40-100% above baseline. This is due to fetal/placental needs and increased CO and work of breathing. Increased oxygen consumption is associated with a 30-50% increase in CO2 production by the 3rd trimester requiring an increase in minute ventilation that starts in the 1st trimester and peaks at 20-40% above baseline at term.

29. SEEK explained • Alveolar ventilation is increased above the level needed to eliminate the increased CO2 production and hence PCO2 falls to 27-32 mm Hg in most of pregnancy. The augmented ventilation is attributed to respiratory stimulation from increased progesterone and results in a 30-35% increased in TV while RR remains the same/slightly increased. Renal compensation results in a pH of 7.4-7.45 and bicarb 18-21.

30. SEEK explained • The patient has an increased Aa gradient likely related to VQ mismatch from asthma. The pregnancy with the acute respiratory distress make the sequence of chronic resp alkalosis from pregnancy, with renal compensation by chronic metabolic acidosis, now complicated by acute respiratory acidosis. This example underscores the clinical context importance in interpreting abg.

31. How to approach an Acid-Base

32. Acid Base • 1.Determine if acidemia (pH<7.36) or alkalemia is present (pH>7.44). In mixed disorders the pH will be normal but the bicarb/pCO2/AG will be abnl. • 2. Is the primary disturbance met or resp? Does the change in PCO2 account for the direction of pH change? • 3. Is there appropriate compensation for the primary disturbance? (see table ahead) • 4. Is the AG elevated? If so is there a Δgap? If so is there an additional non-gap acidosis or a metabolic alkalosis?

33. Appropriate Compensation • Met acidosis: • PCO2 = 1.5XHCO3 +8 ±2 • Met Alkalosis • PCO2 = 0.7XHCO3 +21 ±1.5 • (If bicarb >40 PCO2=0.75xHCO3)+19 ±7.5) • Resp Acidosis • Acute HCO3 = [(PCO2-40)/10] +24 • Chronic HCO3 = [(PCO2-40)/3]+24 • Resp Alkalosis • Acute HCO3 = [(40-PCO2)/5]+24 • Chronic HCO3=[(40-PCO2)/2]+24

34. SEEK A 60 yo female is admitted with 2 day of cough productive of purulent sputum. She has a history of severe COPD on home 2L Oxygen NC. On admission the HR is 120, BP 140/95, RR 28. Labs reveal Na 135, K 3.5, Cl 92, Bicarb 33. ABG on RA is 7.2/80/45. What is the acid-base disorder? • Inconsistent and uninterpretable data • Acute respiratory acidosis • Chronic respiratory acidosis • Acute on chronic respiratory acidosis • Acute respiratory acidosis with anion gap metabolic acidosis

35. SEEK A 60 yo female is admitted with 2 day of cought productive of purulent sputum. She has a history of severe COPD on home 2L Oxygen NC. On admission the HR is 120, BP 140/95, RR 28. Labs reveal Na 135, K 3.5, Cl 92, Bicarb 33. ABG on RA is 7.2/80/45. What is the acid-base disorder? • Inconsistent and uninterpretable data • Acute respiratory acidosis • Chronic respiratory acidosis • Acute on chronic respiratory acidosis • Acute respiratory acidosis with anion gap metabolic acidosis

36. SEEK • The first step is to check the internal consistency with the Henderson-Hasselback equation. The [H+] = 24xPaCO2/[HCO3] or each change in pH of 0.01 represents a 1meq decreased in [H+] so that at a pH of 7.2 the [H+] is around 62. 62does not=24X80/33=58.

37. SEEK • Respiratory acidosis is when pH is less the 7.4 and CO2 is increased. • In acute resp acidosis the Ph declines 0.08 for each 10 rise in CO2. So if the baseline CO2 was 40, the CO2 of 80 should decrease pH by 0.32 to 7.08. • In chronic resp acidosis the pH decline 0.03 for each 10 increase in CO2. A patient with chronic resp acidosis with CO2 of 80 would have a pH of 7.28. • Rather a combination of acute respiratory acidosis superimposed on chronic resp acidosis with baseline CO2 of 60 is more consistent with these values.

38. SEEK • Finally any acid base problem should include anion gap calculation. The ag in the case is 10 and normal is 12+/- 4 so this pt does not have an AG met acidosis.

39. Respiratory Acidosis • Ineffective alveolar respiration or increased CO2 production • Etiologies include: airway obstruction, resp center depression, neuromuscular d/o, pulm d/o, high carb diet

40. Respiratory Alkalosis • Hyperventilation • Etiologies: • Hypoxemic drive (eg altitude, shunt), acute/chronic pulm dz, vent over-breathing, stimulation of resp center (eg pain, psychogenic, pregnancy)

41. Metabolic Alkalosis • Etiologies: • Cl depletion (hypovolemic) • Ucl <20 • Saline responsive • Cl expanded (Hypervolemic) • Ucl >20 • Saline resistant

42. Etiologies of metabolic alkalosis • Hypovolemic/Cl depleted • GI loss: vomit, gastric suction, Cl rich diarrhea, villous adenoma • Renal loss of H • Diuretic • Post-hypercapnia • High dose carbenicillin

43. Etiologies of metabolic alkalosis • Hypervolemic/Cl expanded • Renal H loss: primary hyperaldo, primary hypercortisolism, adrenocorticotropic hormone xs. • Pharm xs steroids • Renal A. stenosis with RV HTN • Renin secreting tumor • Hypokalemia • Bicarb overdose • Pharm • Milk-alkali syndrome • Massive blood transfusion

44. Metabolic Acidosis Δ • An increase in acid accumulation or decreased extracellular bicarb. • Compensate with increased ventilation and decreased PaCo2 and increased renal H excretion. • During prolonged acidosis the last two digits of pH =PaCO2 as long as pH>7.1 down to PaCO2 of 10. • PaCo2 = 1.5xHCO3 +8 ± 2 • Or ;Δ PaCO2 = 1.2 X Δ bicarb

45. Etiologies of Metabolic Acidosis Δ • Increase in endogenous acid production (ketoacidosis), exogenous acid input (poisons), xs bicarb loss (diarrhea) or decreased renal excretion of endogenous acid (chronic renal failure). • Divided into anion gap and non-anion gap acidosis.

46. Etiologies of Metabolic Acidosis Δ • AG = Na -(Cl+HCO3) = 10 ±4 • AG increases with decreased unmeasured cations or increased unmeasured anions. • (Unmeasured anions: proteins, phosphate, sulfates and organic acids vs unmeasured cations K,Ca, Mg) • Hypoalbuminemia will decrease the normal AG to 4-5. For every 1 decrease in Alb a decrease of 2.5-3 in AG is expected. Similarly parproteinemia will decrease the normal anion gap.

47. Etiologies of Metabolic Acidosis Δ • Increased anion gap: Methanol Uremia Diabetic ketoacidosis Paraldehyde INH/Iron Lactic acidosis (including metformin) Ethylene glycol, EtOH Salicylates, starvation ketosis (others: CO, CN, Sulfur, theophylline, toluene)

48. Etiologies of Metabolic Acidosis Δ • Normal anion gap: • Bicarb loss (kidney/gut) • diarrhea • urinary diversion • fistulas/drain from bile/small bowel etc • RTA • Acid addition (with Cl- as the anion) • Hcl • NH4Cl • Arginine HCL • Lysine HCL • CaCl2/MgCL2 (oral) • sulfur

49. The DELTA GAP • If there is an abnormal AG you can look for triple disorders by checking for the delta gap • In an uncomplicated AG met acidosis for every 1 increase in AG the HCO3 should decrease by 1. If this is not the case there is likely a mixed d/o. • Δgap=(AG-12) – (24-HCO3) • The normal Δgap should be zero ± 6. • A positive delta gap indicates either simultaneous metabolic alkalosis (eg vomitting) or resp acidosis. • A negative delta gap indicates then a concomitant normal AG hyperchloremic acidosis (eg diarrhea) or chronic resp alkalosis is present.

50. Acid Base 1.Determine if acidemia (pH<7.36) or alkalemia is present (pH>7.44). In mixed disorders the pH will be normal but the bicarb/pCO2/AG will be abnl. 2. Is the primary disturbance met or resp? Does the change in PCO2 account for the direction of pH change? 3. Is there appropriate compensation for the primary disturbance? 4. Is the AG elevated? If so is there a Δgap? If so is there an additional non-gap acidosis or a metabolic alkalosis?