1. Blood Gases: A Respirologist’s Perspective Joe Reisman MD, FRCP(C), MBA Pediatric Respirologist, CHEO Professor, Faculty of Medicine University of Ottawa

2. Blood Gases Unfortunately for you, I am not Anna-Theresa Lobos, MD FRCPC Pediatric Critical Care Medical Director, CHEO Critical Care Response Team Pediatric Critical Care Program Director Assistant Professor, Faculty of Medicine, Pediatrics

3. OBJECTIVES List the independently measured values in arterial blood gases and outline the normal values of these variables. Describe the measurement of oxygenation Saturation Partial pressure of oxygen Arterial oxygen content Calculate the alveolar ‐ arterial oxygen gradient and assess its significance. Define: Respiratory acidosis and alkalosis Metabolic acidosis and alkalosis

4. OBJECTIVES Develop an approach to interpreting blood gases How to identify acidosis, alkalosis and mixed disorders How to identify acute vs chronic acidosis and alkalosis How to tell whether compensation has occurred

5. List the independently measured values in arterial blood gases and outline the normal values of these variables.

6. Arterial Blood Gas: Normal Values pH = 7.35 - 7.45 PaCO 2 = 35 - 45 mm Hg PaO 2 = 70 - 100 mm Hg SaO 2 = 93 – 98% HCO 3 - = 22 - 26 mEq/L Base Excess = – 2.0 to 2.0 mEq/L

7. Describe the measurement of oxygenation: saturation vs partial pressure of oxygen vs arterial oxygen content.

8. How much oxygen is in the blood? Tissues need a requisite amount of O 2 molecules for metabolism CaO 2 = Arterial Oxygen Content = (1.39 mls O 2 /g Hb x Hb x Sat) + (PaO 2 x 0.003)

9. PaO 2 = Partial pressure of O 2 in the plasma phase of arterial blood Measured by an electrode that senses randomly- moving, dissolved oxygen molecules Oxygen passes through the thin alveolar- capillary membrane and enters the plasma phase as dissolved molecules…then most of these molecules quickly enter the red blood cell and bind with hemoglobin. Once bound to Hb, the oxygen molecules no longer exert any pressure.

10. PaO 2 = Partial pressure of O 2 in the plasma phase of arterial blood The more dissolved molecules there are, the more will bind to available to Hb. Depending on the PaO 2 and other factors, a certain percentage of all O 2 molecules will be dissolved and a certain percentage will be bound.

12. SaO 2 = Oxygen Saturation 4 oxygen binding sites per Hemoglobin Hemoglobin oxygen saturation = the percentage of all the available heme binding sites saturated with oxygen Hemoglobin is like an efficient sponge that soaks up oxygen so more can enter the blood. Hemoglobin continues to soak up oxygen molecules until it becomes saturated with the maximum amount it can hold.

13. PaO 2 and SaO 2 : The Relationship PaO 2 is determined by alveolar PO 2 and the state of the alveolar-capillary interface. PaO 2, in turn, determines the oxygen saturation of hemoglobin (along with other factors that affect the position of the O 2 -dissociation curve).

14. Oxygen Content: Hb and it’s relationship to SaO 2 and PaO 2 The more hemoglobin available to bind the dissolved oxygen molecules, the greater total number of oxygen molecules the blood will contain. PaO 2 is not a function of hemoglobin but only of the alveolar PO 2 and the alveolar-capillary interface. PaO 2 gives us valuable information about adequacy of gas exchange within the lungs, when (and only when) it is subtracted from the calculated alveolar PO2 (big A). We use the Alveolar Gas Equation to calculate PAO 2.

16. Oxygen Content: How much oxygen is in the blood? Tissues need a requisite amount of O 2 molecules for metabolism. CaO 2 = directly reflects the total number of oxygen molecules in arterial blood, both bound and unbound to hemoglobin = (1.39 x Hb x Sat) + (PaO 2 x 0.003) CO = HR x SV Oxygen Delivery = CO X CaO 2

17. Oxygen Content: Hb and it’s relationship to SaO 2 and PaO 2 SaO 2 is determined mainly by PaO 2. The relationship between the two variables is the oxygen-dissociation curve. PaO 2 is the most important (but not the only) determinant of SaO 2. The oxygen-Hb dissociation curve tells us about Hb’s affinity for oxygen. Other determinants of SaO 2 for a given PaO 2 are conditions that shift the position of the oxygen dissociation curve left or right.

18. Oxygen-Hb Dissociation Curve *P50 is the PaO2 at which hemoglobin is 50% saturated with oxygen; normal value is 27 mm Hg. Shape and position of the curve are the same irrespective of the hemoglobin content. RIGHT SHIFT = EASIER TO RELEASE, HARD TO BIND…..need higher PaO 2 to maintain same Sat LEFT SHIFT = HARDER TO RELEASE, EASIER TO BIND Little bits of oxygen make BIG change in Sats

19. Clinical Problem A 40 yr old woman has a PaO 2 of 85 mm Hg, an SaO 2 of 98%, and a hemoglobin of 140. One hour later, she suffers a severe hemolytic reaction that suddenly leaves her with a hemoglobin of only 70. Assuming no lung disease occurs from the hemolytic reaction, what will be her new PaO 2, SaO 2, and CaO 2 ? * PaO 2 unchanged, SaO 2 unchanged, CaO 2 reduced. Hemoglobin content is suddenly reduced by half, which will lower CaO 2 by half. However, the PaO 2 and SaO 2 will be unaffected, since their values are independent of the content of hemoglobin present.

20. Calculate the alveolar ‐ arterial oxygen gradient from the arterial blood gases and assess its significance.

21. The A-a gradient Alveolar Gas Equation PAO 2 = PIO 2 – (PaCO 2 ÷ R) = (FiO 2 x [Patm - PH 2 O]) - (PaCO 2 ÷ R) where PH 2 0 = 47, R = 0.8 = 713(FiO 2 ) – 1.2(PaCO 2 ) (at sea level) A-a O 2 difference = PAO 2 – PaO 2 (usually <10)

22. The A-a gradient Are the lungs transferring oxygen properly from the atmosphere to the pulmonary circulation? Use the Alveolar Gas Equation to calculate PAO 2 then find the A-a O 2 difference If the A-a gradient is elevated, the answer is NO – there is mismatch of ventilation and perfusion If the A-a gradient is normal is YES PAO 2 = (FiO 2 x [Patm - 47]) – 1.2(PaCO 2 ) A-a O 2 difference = PAO 2 – PaO 2

24. Define respiratory acidosis and alkalosis, and metabolic acidosis and alkalosis, and explain how respiratory and metabolic compensation occur.

25. Interpretation of Arterial Blood Gases 3 Physiologic Processes 1. Alveolar ventilation 2. Oxygenation 3. Acid-Base Balance

26. Acid–Base Disturbances May arise from cardiopulmonary or GI and renal problems or from exogenous chemicals/toxins/medications

27. The Henderson – Hasselbalch Equation pH = pK + log HCO 3 - 0.03 (PaCO 2 ) HCO 3 - = 24 = 20 0.03 (PaCO 2 ) 0.03(40) log 20 = 1.3 pK (dissociation constant for carbonic acid) = 6.1 ∴ normal pH = 6.1 +1.3 = 7.4

28. pH ≈ HCO 3 - PaCO 2 pH is life and death The system almost instantly reflects any disturbances Do NOT need to memorize equation or work with logs If have 2, can “calculate” the 3 rd The CHANGE in DEGREE and DIRECTION of HCO 3 - and PaCO 2 is the key to interpreting acid-base disorders.

29. Acid-Base Disturbances 7.35 7.25 7.45 7.40 7.55 acidosis alkalosis normal

30. Definitions: Acidemia: Blood pH < 7.35 Acidosis: A primary physiologic process that, occurring alone, tends to cause acidemia Can be acute or chronic increased production of H+ by the body or the inability of the body to form HCO3- in the kidney e.g. metabolic acidosis from decreased perfusion (lactic acidosis) e.g. respiratory acidosis from hypoventilation

31. Definitions: Alkalemia: Blood pH > 7.45 Alkalosis: A primary physiologic process that, occurring alone, tends to cause alkalemia. Can be acute or chronic Decrease in H+ concentration e.g. metabolic alkalosis from prolonged vomiting e.g. respiratory alkalosis from acute hyperventilation

32. Definitions: Primary acid-base disorder: One of the four acid-base disturbances that is manifested by an initial change in HCO 3 - or PaCO 2. If HCO 3 - changes first, the disorder is either a metabolic acidosis (reduced HCO 3 - ) or metabolic alkalosis (elevated HCO 3 - ). If PaCO 2 changes first, the problem is either respiratory alkalosis (reduced PaCO 2 ) or respiratory acidosis (elevated PaCO 2 ).

33. Definitions: Compensation: The change in HCO 3 - or PaCO 2 that results from the primary event. Compensatory changes are not classified by the terms used for the four primary acid-base disturbances.

34. Question #1: What is the pH of a blood sample with HCO 3 - = 36 mEq/L and PaCO 2 = 60 mm Hg? a) 7.1 b) 7.3 c) 7.4 d) 7.5 e) Indeterminate without more data

35. Answer to Question #1: HCO 3 - : usual value is 22 to 26, so this rose 50% PCO 2 : usual value is 35 to 45, so this rose 50% ∆ Ratio = none pH = 7.4

36. From Henderson-Hasselbalch pH= 6.1 + log [HCO3-]/[CO2] pH= 6.1 + log(36)/(0.03 X 60) pH= 6.1 + log 20 pH= 7.4

37. Question #2: What is the pH of a sample with PCO 2 = 55? a) 7.15 b) 7.25 c) 7.35 d) 7.45 e) Indeterminate without more data

38. Answer to Question #2: e) Indeterminate without more data. You need 2 out of 3 variables to obtain the 3 rd. The pH could be acidemic or alkalotic.

39. Question #3: What is the pH of a sample with HCO 3 - = 24 and PCO 2 = 80? a) 7.1 b) 7.3 c) 7.4 d) 7.5 e) 7.6

40. From Henderson-Hasselbalch pH= 6.1 + log [HCO3-] / [CO2] pH= 6.1 + log (24)/(0.03 X 80) pH= 6.1 + log10 pH= 6.1 + 1 = 7.1

41. Answer to Question #3: The HCO 3 - is unchanged. The PCO 2 is double so the blood will become more acidic (by 100%!) A pH drop from 7.4 to 7.3 is only a 25% change in [H + ] ions, so the only reasonable answer is 7.1

42. The 4 Primary Acid-Base Disorders Primary EventDISORDERCompensatory Event ↓ HCO 3 - PaCO 2 Metabolic acidosis ↓ pH ↓ PaCO 2 ↑ HCO 3 - PaCO 2 Metabolic alkalosis ↑ pH ↑ PaCO 2 HCO 3 - ↑ PaCO 2 Respiratory acidosis ↓ pH ↑ HCO 3 - HCO 3 - ↓ PaCO 2 Respiratory alkalosis ↑ pH ↓ HCO 3 -

43. Question 4: For each of the following situations, indicate which of the four primary acid-base disorders is present and give the nature and direction of compensation (e.g. ↑ HCO 3 - ). ConditionsPrimary Disorder CompensationClinical Example a) ↓ pH ↓ HCO 3 - b) ↓ pH ↑ PaCO 2 c) ↑ pH ↓ PaCO 2 d) ↑ pH ↑ HCO 3 -

44. Answer to Question #4: ConditionsPrimary Disorder CompensationClinical Example a) ↓ pH ↓ HCO 3 - Metabolic Acidosis ↓ PCO 2 Diabetic Ketoacidosis b) ↓ pH ↑ PaCO 2 Respiratory Acidosis ↑ HCO 3 - COPD c) ↑ pH ↓ PaCO 2 Respiratory Alkalosis ↓ HCO 3 - Asthma d) ↑ pH ↑ HCO 3 - Metabolic Alkalosis ↑ PCO 2 Vomiting

45. Primary Respiratory Events and Metabolic Compensation ConditionExpected pHAcuteChronic Respiratory acidosis Change in pH = 0.008 X (40 − PCO 2 ) HCO 3 - up by 1 mEq/L for every 10 PCO 2 up HCO 3 - up by 3.5 mEq/L for every 10 PCO 2 up Respiratory alkalosis Change in pH = 0.003 X (40 − PCO 2 ) HCO 3 - down by 2 mEq/L for every 10 PCO 2 down HCO 3 - down by 4 mEq/L for every 10 PCO 2 down NOTE: Renal compensation takes minutes to hours acutely and 3-5 days for complete compensation  renal excretion of carbonic acid is increased and bicarbonate reabsorption is increased

46. Primary Metabolic Events and Respiratory Compensation Metabolic Acidosis: 1 PCO 2 down for every 1 HCO 3 down Expected PaCO 2 = (1.5 x bicarb) + (8) at maximal compensation Metabolic Alkalosis: Least predictable PCO 2 up 0.5-0.7 for every 1 HCO 3 up

47. Compensation of Primary Disturbance DisturbancePrimary Disturbance pHExpected response Metabolic acidosis ↓ HCO 3 ↓ pH ↓ PaCO 2 Metabolic alkalosis ↑ HCO 3 ↑ pH ↑ PaCO 2 Acute respiratory acidosis ↑ PaCO 2 ↓ pH ↑ HCO 3 Chronic respiratory acidosis ↑ PaCO 2 ↓ pH or N ↑ HCO 3 Acute respiratory alkalosis ↓ PaCO 2 ↑ pH ↓ HCO 3 Chronic respiratory alkalosis ↓ PaCO 2 ↑ pH or N ↓ HCO 3

48. Metabolic Acidosis: The Next Step When you find a patient has a primary metabolic acidosis, you must do more work: The ANION GAP Anion Gap: (Na + + K + ) – (Cl - + HCO 3 - ) Normal Gap: 12 mEq/L ± 2

49. Causes of Anion-Gap Acidosis Increased acid production: Ketones DKA, starvation Lactic acid tissue hypoxia, sepsis, exercise, EtOH/MeOH/ethylene glycol ingestion, paraldehyde, Inborn Error of Metabolism (IEM) Drugs ASA, NSAID, Iron

50. Causes of Anion-Gap Acidosis M ethanol U remia D iabetic ketoacidosis P araldehyde I ron, isoniazid L actate E thylene glycol S alicylates

51. Causes of Anion-Gap Acidosis The Lancet, vol 372, September 13, 2008 G lycols (ethylene, propylene) O xoproline (paracetamol use) L -lactate D -lactate M ethanol A spirin R enal Failure K etoacidosis

52. Causes of NON-Anion Gap Acidosis Hyperchloremic metabolic acidosis GI loss of HCO 3 Diarrhea, NEC, small bowel drainage/fistula Renal loss of HCO 3 RTA, early renal failure, CA inhibitors Administration of HCl or other chloride- containing substances (i.e. NS) hyperalimentation

53. Some Clinical Causes of the Four Primary Acid–Base Disorders Metabolic acidosis With increased anion gap - MUDPLIES, GOLDMARK With normal anion gap - Diarrhea, renal tubular acidosis, interstitial nephritis, excess NaCl administration acetazolamide administration

54. Some Clinical Causes of the Four Primary Acid–Base Disorders Metabolic alkalosis Chloride-responsive (responds to NaCl/KCl) - Diuretics, corticosteroids, gastric suctioning, vomiting Chloride-resistant - Any hyperaldosterone state (e.g., Cushing’s syndrome), severe K + depletion

55. Some Clinical Causes of the Four Primary Acid–Base Disorders Respiratory Acidosis = Respiratory failure Central nervous system depression Muscle dysfunction Disease of lungs and/or upper airway

56. Primary Respiratory Problems: Pathophysiology PACO 2 = VCO 2 / VA PACO 2 ~ CO 2 production Minute ventilation – Dead Space Ventilation

57. Primary Respiratory Problems: Pathophysiology CO 2 PRODUCTION Metabolism  large quantities of volatile acid (carbon dioxide) and nonvolatile acid (sulfuric acid derived from the metabolism of sulfur-containing amino acid) Metabolism of fats and carbohydrates  +++carbon dioxide PACO 2 ~ CO 2 production Minute ventilation – Dead Space Ventilation Dissolved CO 2 + H 2 O  H 2 CO 3  HCO 3 - + H +

58. Primary Respiratory Problems: Pathophysiology CO 2 EXCRETION Alveolar ventilation = MV (tidal volume x rate) – DS Dead space = all airways larger than alveoli + air entering alveoli in excess of that which can take part in gas exchange Alveolar ventilation regulated by: Central respiratory centers (pons, medulla) Chemoreceptors for PaCO2, PaO2, and pH in the brainstem Neural impulses from lung-stretch receptors Lungs excrete the volatile fraction through ventilation  NO acid accumulation PACO 2 ~ CO 2 production Minute ventilation – Dead Space Ventilation

59. Primary Respiratory Problems: Pathophysiology  CO 2 production  CO 2 excretion If VA is inadequate for CO 2 production   PaCO 2 CNS impairment (head trauma, brainstem lesion, medications) Airway obstruction Mechanical impairment (chest trauma, pneumothorax, muscle weakness, residual neuromuscular blockade) Decreased perfusion (PE, cardiac arrest) Parenchymal disease (pneumonia, edema) PaCO 2 ~ CO 2 production Minute ventilation – Dead Space Ventilation OR

60. Some Clinical Causes of the Four Primary Acid–Base Disorders Respiratory alkalosis Voluntary hyperventilation Hypoxemia (includes altitude) Liver failure Anxiety hyperventilation syndrome Any acute pulmonary problem Acute pulmonary embolism, pneumonia, mild asthma attack, mild pulmonary edema

61. Develop an approach to identifying acute vs chronic respiratory acidosis and alkalosis, and whether the relevant compensation has occurred.

62. Acid-Base Interpretation 1. Does the patient have an acidosis or an alkalosis? Look at the pH 2. What is the primary problem – metabolic or respiratory? Look at the pCO 2 If the pCO 2 change is in the opposite direction of the pH change, the primary problem is respiratory

63. Acid-Base Interpretation 3. Is there any compensation by the patient? Do the calculations. For a primary respiratory problem, is the pH change completely accounted for by the change in pCO 2 if yes, then there is no metabolic compensation if not, then there is either partial compensation or concomitant metabolic problem

64. Acid-Base Interpretation For a metabolic problem, calculate the expected pCO 2 if equal to calculated, then there is appropriate respiratory compensation if higher than calculated, there is concomitant respiratory acidosis if lower than calculated, there is concomitant respiratory alkalosis **If it is a metabolic acidosis, you need to do more work = ANION GAP

65. Acid-Base Interpretation: Don’t forget about oxygenation and to look at your patent! your patient may have a significantly increased work of breathing in order to maintain a “normal” blood gas metabolic acidosis with a concomitant respiratory acidosis is concerning

66. Case #1: You are on-call CC for orthopedics and called to see Molly, a 16 yr. old who is POD #2 spinal instrumentation for scoliosis. Her nurse called you because Molly is difficult to rouse. You are also told that she has been given a PCA (patient-controlled analgesia) pump. Her most recent vital signs are: HR 70 BP 110/50 RR 7 Sats 90% R/A Temp 37.3 ax

67. Case #1: You do an examination and find that she has occasional upper a/w sounds, no accessory muscle use and you hear decreased at the bases with no crackles or wheeze. She is warm to touch and is pink. You are unable to rouse her and she only moans when you examine her. You ask the nurse to apply oxygen and you perform an arterial blood gas. The results of the blood gas are: 7.20/65/65/25

68. Case #1: 7.20/65/65/25 What is the problem?

69. Interpret the Blood Gas: Acute Respiratory Acidosis PaCO 2 is elevated and pH is acidotic The decrease in pH is accounted for entirely by the increase in PaCO 2 Acute respiratory acidosis, the plasma bicarbonate concentration rises 1 meq/L for every 10 mmHg elevation in the PaCO 2 Bicarbonate will be in the normal range because the kidneys have not had adequate time to establish effective compensatory mechanisms

70. Case #2: You are on-call for pediatrics and called to see Bobby, an 8 month old ex-28 wk baby admitted 3 days ago with respiratory distress and RSV bronchiolitis. His nurse called you because he seems to be working harder to breathe. He is receiving the usual supportive care and ventolin q3-4hrs. His usual meds include flovent and lasix. His most recent vital signs are: HR 150 RR 65 BP 80/55 Sats 92% R/A Temp 37.6 ax

71. Case #2: You do an examination and find that he has a lot of secretions, occasional nasal flaring but no grunting. He has mild subcostal indrawing and decreased a/e in the right upper lobe and ++wheezes on auscultation. You don’t hear any murmurs and he is warm to touch with capillary refill time being less than 2 seconds. He is awake and alert. You ask the nurse to give him some ventolin and you perform an arterial blood gas and lytes. The results of the blood gas are: 7.36/70/55/34 Na 140, K 3.6, Cl 98

72. Case #2: 7.36/70/55/34 What is going on?

73. Interpret the Blood Gas: Compensated Chronic Respiratory Acidosis PaCO 2 is elevated and pH in acceptable range Bicarbonate is elevated because the kidneys have had adequate time to establish effective compensatory mechanisms Chronic respiratory acidosis: Bicarbonate increases 3.5 mEq/L for each 10-mm Hg rise in PaCO 2. If you were thinking Metabolic alkalosis: increase in CO 2 0.5 to 0.7 for every 1 rise in bicarbonate…..if rise in CO 2 more than 0.7x the rise in bicarbonate, then there must be a respiratory acidosis present.

74. What do you think is going on? Causes of Chronic Respiratory Acidosis COPD Emphysema Severe asthma Chronic bronchitis Neuromuscular diseases ALS Diaphragm dysfunction Guillain-Barré syndrome Myasthenia gravis Muscular dystrophy Chest wall disorders Severe kyphoscoliosis Status post thoracoplasty Obesity-hypoventilation syndrome Obstructive sleep apnea CNS depression Drugs Neurologic disorders - Encephalitis, brainstem disease, trauma Primary hypoventilation Other lung and airway diseases - Laryngeal and tracheal stenosis

75. Case #3: You are working in the ER and sent to see Diane, a 27 yr. old who is complaining of pleuritic chest pain of several hours duration. She also complains of URTI symptoms that started 2 days earlier. She is otherwise healthy with no significant PMHx. She has no allergies and her only medication is the oral contraceptive pill. She just returned last evening from visiting her grandparents in Portugal. She has smoked a 1/2pk/day since she was 21.

76. Case #3: Her most recent vital signs are: HR 95 BP 110/70 RR 28 You do an examination and find that she is congested but in no distress. She is tachypneic but has no accessory muscle use. You hear equal air entry bilaterally and her chest is clear on auscultation. She complains of discomfort when you ask her to take big breaths. She is warm to touch and has strong pulses. You decide to order a chest x-ray and arterial blood gas. The results of the blood gas are: 7.45/31/83/21 Sats 96% R/A Temp 37.0 ax

77. Case #3: 7.45/31/83/21 What is going on?

78. Interpret the Blood Gas: Acute Respiratory Alkalosis PaCO 2 is low and the pH is alkalotic The increase in pH is accounted for entirely by the decrease in paCO 2 In acute respiratory alkalosis, the plasma bicarbonate concentration falls by 2 meq/L for every 10 mmHg decline in the PCO 2 Bicarbonate and base excess will be in the normal range because the kidneys have not had sufficient time to establish effective compensatory mechanisms

79. What do you think is going on? Causes of Respiratory Alkalosis Central nervous system Pain, Anxiety, Psychosis Hyperventilation syndrome Fever Cerebrovascular accident Meningitis, Encephalitis Tumor Trauma Hypoxia High altitude Severe anemia Right-to-left shunts Drugs eg. Salicylates Endocrine Pregnancy Hyperthyroidism Pulmonary Pneumo/hemothorax Pneumonia Pulmonary edema Pulmonary embolism Aspiration Interstitial lung disease Asthma Emphysema Chronic Bronchitis Miscellaneous Sepsis Hepatic failure Mechanical ventilation Heat exhaustion CHF

80. Let’s talk about oxygenation… PaO 2 = 83 PAO 2 = (FiO 2 x [Patm - 47]) - (PaCO 2 /0.8) = (21% x [760-47]) – (31/0.8) = (149.73) – (38.75) = 110.98 A-a O 2 difference = 28 Elevated  indicating a state of V-Q imbalance and therefore some parenchymal lung disease or abnormality. Hyperventilation should cause high PaO 2, therefore NO increased A-a O 2 difference

81. Case #4: 8 year old girl, Susie, presents to ER with tachypnea, tachycardia, altered level of consciousness Vital signs: HR 140 RR 46 BP 95/50 Labs: pH 7.05 PCO 2 20 HCO 3 7 Interpret the Blood Gas: Acute Metabolic Acidosis with respiratory compensation

82. Case #4: Calculate the anion gap Anion gap = 30 Na + - (Cl - + HCO 3 ) Normal anion gap 12-16 Labs: Na: 132 Cl: 95 HCO 3 : 7

83. What do you think is going on? Acute Metabolic Acidosis Primary metabolic acidosis, with increased anion gap with respiratory compensation Expected PaCO 2 = (1.5 x bicarb) + (8 +/- 2) = (1.5 x 7) + (8) = 18.5 +/- 2 MUDPILES!

84. SUMMARY PaO 2 and Sats: PaO 2 is determined by alveolar PO 2 and the state of the alveolar-capillary interface MUST calculate A-a gradient to talk about Alveolar- capillary interface Sats = % of all the available heme binding sites saturated with oxygen O 2 -Hb Dissociation curve – tells you about Hb’s affinity for oxygen

85. SUMMARY Oxygen Content: CaO 2 = (1.39 x Hb x Sat) + (PaO 2 x 0.003) Oxygen Delivery: CO x CaO 2

86. SUMMARY: Acid-Base Interpretation 1. Does the patient have an acidosis or an alkalosis? Look at the pH 2. What is the primary problem – metabolic or respiratory? Look at the pCO 2 If the pCO 2 change is in the opposite direction of the pH change, the primary problem is respiratory

87. SUMMARY: Acid-Base Interpretation 3. Is there any compensation by the patient? Do the calculations. For a primary respiratory problem, is the pH change completely accounted for by the change in pCO 2 if yes, then there is no metabolic compensation if not, then there is either partial compensation or concomitant metabolic problem

88. SUMMARY: Acid-Base Interpretation For a metabolic problem, calculate the expected pCO 2 if equal to calculated, then there is appropriate respiratory compensation if higher than calculated, there is concomitant respiratory acidosis if lower than calculated, there is concomitant respiratory alkalosis **If it is a metabolic acidosis, you need to do more work = ANION GAP

89. SUMMARY: Acid-Base Interpretation Don’t forget about oxygenation and to look at your patent! your patient may have a significantly increased work of breathing in order to maintain a “normal” blood gas metabolic acidosis with a concomitant respiratory acidosis is concerning