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You Can’t Learn Blood Gases from a Lecture! Lawrence Martin, M.D. Clinical Professor of Medicine Case Western Reserve University School of Medicine, Cleveland [email protected] April 1, 2010 5/9/2017 1 Blood Gas Interpretation means analyzing the data to determine patient’s state of: Ventilation Oxygenation Acid-Base You can’t learn this from a lecture! 5/9/2017 2 To interpret ABGs you need to look at all the relevant data To interpret ABGs you need to look at all the relevant data From the blood gas machine PaCO2 PaO2 pH HCO3 From the Co-oximeter SaO2 CoHb MetHb To interpret ABGs you need to look at all the relevant data From the blood gas machine PaCO2 PaO2 pH HCO3 From the Co-oximeter SaO2 CoHb MetHb From venous blood Na+ K+ ClHCO3BUN Creatinine Hgb To interpret ABGs you need to look at all the relevant data From the blood gas machine PaCO2 PaO2 pH HCO3 From the Co-oximeter SaO2 CoHb MetHb From venous blood From the environment Na+ K+ ClHCO3BUN Creatinine FIO2 Barometric pressure Hgb To interpret ABGs you need to look at all the relevant data From the blood gas machine PaCO2 PaO2 pH HCO3 From the Co-oximeter SaO2 CoHb MetHb And not least, the patient Mental status Resp. rate & effort Ventilator settings (if intubated) Pulmonary & ABG history From venous blood From the environment Na+ K+ ClHCO3BUN Creatinine FIO2 Barometric pressure Hgb To interpret ABGs you need to look at all the relevant data From the blood gas machine PaCO2 PaO2 pH HCO3 From the Co-oximeter SaO2 CoHb MetHb And not least, the patient Mental status Resp. rate & effort Ventilator settings (if intubated) Pulmonary & ABG history From venous blood From the environment Na+ K+ ClHCO3BUN Creatinine FIO2 Barometric pressure Hgb 7 arterial blood gas values 7 venous blood values 2 environmental values Several patient variables Lots of variables…how to figure it all out? Give a man a fish and you feed him for a day. Teach a man to fish and you feed him for a lifetime. Chinese Proverb What does this have to do with blood gas interpretation? 5/9/2017 9 Just this. You need a framework, a foundation to properly learn ABG interpretation. If I tell you how to interpret a given blood gas, you will understand that blood gas only, and not the next one you may encounter. Much better if I show you an approach to interpreting all blood gases, in all situations, so that you understand them. But… …like any other skill based on interpreting a large number of variables (EKG, chest x-ray, physical exam), You Can’t Learn Blood Gases from a Lecture. 5/9/2017 10 The best way to learn ABGs is to work on blood gas problems with some knowledge of basic physiology, then check your work for instant feedback. This ‘iterative process’ will teach you blood gas interpretation. Books Web sites You Can’t Learn Arterial Blood Gases from a Lecture You CAN learn ABGs from selected web sites. See list at: www.lakesidepress.com/ABGindex.htm 5/9/2017 11 The Key to Blood Gas Interpretation: 4 Equations, 3 Physiologic Processes These 4 equations, crucial to understanding and interpreting arterial blood gas data, provide the basic foundation for understanding blood gas interpretation. Equation Physiologic Process 1) Alveolar ventilation PaCO2 equation PaCO2 = 2) VCO2 x 0.863 --------------VA Alveolar gas equation Oxygenation PAO2 = PIO2 - 1.2 (PaCO2) where PIO2 = FIO2 (PB – 47 mm Hg) 3) Oxygen content equation Oxygenation CaO2 = quantity O2 bound to Hb + quantity O2 dissolved in plasma CaO2 = (Hb x 1.34 x SaO2) 3) + Henderson-Hasselbalch equation (.003 x PaO2) Acid-base balance HCO3pH ~ -------PaCO2 5/9/2017 12 Start with PaCO2. PaCO2 is the center of the blood gas universe. pH PaO2 PaCO2 HCO3 SaO2 PaCO2 equation: PaCO2 reflects ratio of metabolic CO2 production (VCO2) to alveolar ventilation (VA) -- there is nothing ‘clinical’ in the equation except respiratory rate (f) PaCO2 = VCO2 x 0.863 ----------VA VCO2 = CO2 production VA = VE – VD = f (tidal volume) – f (dead space volume) 0.863 converts units to mm Hg PaCO2 35 - 45 mm Hg Condition in blood (PaCO2) Eucapnia State of alveolar ventilation Normal ventilation 200 ml/min x 0.863 40 mmHg = ------------------------4.3 L/min >45 mm Hg Hypercapnia Hypoventilation 200 ml/min x 0.863 80 mmHg = ------------------------2.15 L/min <35 mm Hg Hypocapnia Hyperventilation 200 ml/min x 0.863 20 mmHg = -------------------------8.6 L/min 5/9/2017 14 Hypercapnia A serious respiratory problem VCO2 x 0.863 PaCO2 = ------------- VA where VA = VE – VD = f (tidal vol.) – f (dead space vol.) • The PaCO2 equation shows that the only physiologic reason for elevated PaCO2 is inadequate alveolar ventilation (VA) for the amount of CO2 production (VCO2). Since VA = VE – VD, hypercapnia can arise from insufficient VE (eg, drug overdose), increased VD (eg, COPD), or a combination. • The PaCO2 equation also shows why PaCO2 cannot reliably be assessed clinically. Since you never know the patient's VCO2 or VA, you cannot determine the VCO2/VA, which is what PaCO2 provides. (Even if tidal volume is measured, you can’t determine the amount of air going to dead space.) • There is no predictable correlation between PaCO2 and the clinical picture. In a patient with possible respiratory disease, respiratory rate, depth, and effort cannot be reliably used to predict even a directional change in PaCO2. A patient in respiratory distress can have a high, normal, or low PaCO2. A patient without respiratory distress can have a high, normal, or low PaCO2. 5/9/2017 15 PaCO2 and alveolar ventilation A 60 yo man with severe chronic obstructive pulmonary disease is seen in the ED, anxious and tachypneic with RR=30/minute. The intern (who didn’t attend this lecture) says “he’s hyperventilating” and wants to give him Xanax. You, being wiser (since you attended), know better and demand a blood gas. Blood gas shows: PaCO2 = 85 mm Hg (severe hypo ventilation) pH = 7.23 Explain tachypnea and hypoventilation in this patient. 5/9/2017 16 PaCO2 and alveolar ventilation 60 yo man PaCO2 = 85 mm Hg pH = 7.23 PaCO2 = VCO2 x 0.863 ------------VA where VA = VE – VD = f (tidal volume) – f (dead space volume) Clinically all you know is this patient’s resp. rate, the “f” in the PaCO2 equation. You don’t know his tidal volume, dead space volume or CO2 production, i.e., you don’t know the numerator or denominator of the equation. Thus by exam alone, you cannot know even if he’s hypo- or hyper- ventilating. The blood gas shows he’s hypoventilating. Though tachypneic, MOST OF EACH BREATH IS GOING TO DEAD SPACE, NOT TO FUNCTIONING ALVEOLI! There is no predictable correlation between PaCO2 and the clinical picture. In a patient with possible respiratory disease, respiratory rate, depth, and effort cannot be reliably used to predict even a directional change in PaCO2. A patient in respiratory distress can have a high, normal, or low PaCO2. A patient without respiratory distress can have a high, normal, or low PaCO2. 5/9/2017 17 Hyperventilating? Hypoventilating? Normal ventilation? PaCO2 = VCO2 x 0.863 ----------------VA where VA = VE – VD = f (tidal volume) – f (dead space volume) PaCO2 is the center of the blood gas universe. Understanding PaCO2 facilitates understanding oxygenation & acid-base balance. PaCO2 Oxygenation Acid-Base PAO2 = FIO2 (BP-47) – 1.2 (PCO2) HCO3- pH ~ -----------PaCO2 PaO2 PaCO2 = VCO2 x .863 -------------------VA where VA = VE – VD = f (tidal volume) – f (dead space volume) Note: PaCO2 is from ABGs. HCO3- is calculated from ABG measurement of pH and PaCO2 or is measured in venous blood (serum) as part of electrolytes. When measured in venous blood it is variously labeled ‘bicarbonate’, ‘HCO3- ’ or ‘CO2’ (the latter NOT to be confused with PaCO2). Arterial blood – blood gases Venous blood - electrolytes The Key to Blood Gas Interpretation: 4 Equations, 3 Physiologic Processes These 4 equations, crucial to understanding and interpreting arterial blood gas data, provide the basic foundation for understanding blood gas interpretation. Equation Physiologic Process 1) Alveolar ventilation PaCO2 equation PaCO2 = 2) VCO2 x 0.863 --------------VA Alveolar gas equation Oxygenation PAO2 = PIO2 - 1.2 (PaCO2) where PIO2 = FIO2 (PB – 47 mm Hg) 3) Oxygen content equation Oxygenation CaO2 = quantity O2 bound to Hb + quantity O2 dissolved in plasma CaO2 = (Hb x 1.34 x SaO2) 3) + Henderson-Hasselbalch equation (.003 x PaO2) Acid-base balance HCO3pH ~ -------PaCO2 5/9/2017 21 Alveolar Gas Equation PAO2 = PIO2 - 1.2 (PaCO2) PAO2 is the average alveolar PO2 PIO2 is the partial of) inspired oxygen in the trachea. PAO pressure = PIO - 1.2 (PaCO 2 2 2 PAO2 = PIO2 - 1.2 (PaCO2) PIO2 = FIO2 (PB – 47 mm Hg) = 0.21 (760-47) =PIO 150 mm Hg = FIO (P - 47). where 2 2 B Breathing room air at sea level, PAO2 = 150 – 1.2 (40) = 150 - 48 = 102 mm Hg Note: FIO2 is fraction of inspired oxygen and PB is the barometric pressure. 47 mm Hg is the water vapor pressure at normal body temperature. This is the ‘abbreviated version’ of the AG equation, suitable for clinical purposes. 5/9/2017 22 Alveolar Gas Equation PAO2 = FIO2 (PB – 47 mm Hg) – 1.2(PaCO2) In order to bring O2 into the blood, alveolar PO2 (PAO2) has to always exceed arterial PO2 (PaO2). Whenever PAO2 decreases, PaO2 decreases as well. Thus, from the AG equation: • If FIO2 and PB are constant (i.e., constant PIO2), then as PaCO2 increases both PAO2 and PaO2 will decrease: hypercapnia causes hypoxemia. • If FIO2 decreases and PB and PaCO2 are constant, both PAO2 and PaO2 will decrease: suffocation causes hypoxemia. • If PB decreases (e.g., with altitude), and PaCO2 and FIO2 are constant, both PAO2 and PaO2 will decrease: mountain climbing causes hypoxemia. 5/9/2017 See web site: “Blood Gases on Mt. Everest” www.lakesidepress.com/pulmonary/MtEverest/bloodgases.htm. 23 Alveolar Gas Equation PAO2 = FIO2 (PB – 47 mm Hg) – 1.2(PaCO2) What is the alveolar PO2 (PAO2) at sea level* in the following circumstances? a) FIO2 = .21, PaCO2 = 20 mm Hg ANSWER: PAO2 = .21(713) - 1.2(20) = 126 mm Hg b) FIO2 = .21, PaCO2 = 60 mm Hg ANSWER: PAO2 = .21(713) - 1.2(60) = 72 mm Hg c) FIO2 = .40, PaCO2 = 30 mm Hg ANSWER: PAO2 = .40(713) – (1.2)30 = 249 mm Hg *BP = 760 mm Hg 5/9/2017 24 P(A-a)O2 • • • • • P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen. It is commonly called the “A-a gradient,” though it does not actually result from an O2 pressure gradient in the lungs. Instead, it results normal ventilation-perfusion imbalance in the lungs (normal “venous admixture,” about 3% of cardiac output). PAO2 is always calculated, based on FIO2, PaCO2 and barometric pressure. PAO2 = FIO2 (PB – 47 mm Hg) – 1.2(PaCO2) PaO2 is always measured, on an arterial blood sample in the ‘blood gas machine’. Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg breathing room air (it increases with age and with FIO2). A higher than normal P(A-a)O2 means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries. Except for right to left cardiac shunts, an elevated P(A-a)O2 signifies some sort of problem within the lungs that has caused ventilationperfusion imbalance (increase over the normal venous admixture). Virtually all lung disease lowers PaO2 via the mechanism of increased V-Q imbalance, e.g., COPD, pneumonia, atelectasis, pulmonary edema. 5/9/2017 25 P(A-a)O2 Alveolar PO2 * PaO2* * P(A-a)O2* a) FIO2 = .21, PaCO2 = 20 mm Hg PAO2 = .21(713) - 1.2(20) = 126 mm Hg 112 mm Hg 14 mm Hg (nl.) b) FIO2 = .21, PaCO2 = 60 mm Hg PAO2 = .21(713) - 1.2(60) = 72 mm Hg 62 mm Hg 10 mm Hg (nl.) c) FIO2 = .40, PaCO2 = 30 mm Hg PAO2 = .40(713) – (1.2)30 = 249 mm Hg 129 mm Hg 120 mm Hg * Always a calculation ** Always a measurement 5/9/2017 26 P(A-a)O2: Test your understanding Calculate P(A-a)O2 using the alveolar gas equation (assume PB = 760 mm Hg). a) A 28 yo woman with PaCO2 30 mm Hg, PaO2 88 mm Hg, FIO2 0.21. PAO2 = .21 (760 - 47) - 1.2(30) = 150 - 36 = 114 mm Hg; P(A-a)O2 = 114 - 88 = 26 mm Hg The P(A-a)O is elevated. This means the PaO2 is lower than expected for this degree of hyperventilation, indicating a gas-exchange problem. The patient was diagnosed with pulmonary embolism. b) A 22 yo anxious man with PaCO2 15 mm Hg, PaO2 120 mm Hg, FIO2 0.21. PAO2 = .21(760 – 47) - 1.2(15) = 150 - 18 = 132 mm Hg; P(A-a)O2 = 132 - 120 = 12 mm Hg The patient had anxiety-hyperventilation syndrome. Hyperventilation can easily raise PaO2 > 100 mm Hg when the lungs are normal, as in this case. c) A 54 yo woman with PaCO2 75 mm Hg, PaO2 95 mm Hg, FIO2 0.28. PAO2 = .28(760 - 47) - 1.2(75) = 200 - 90 = 110 mm Hg; P(A-a)O2 = 110 - 95 = 15 mm Hg Despite severe hypoventilation, there is no evidence here for lung disease. Hypercapnia is most likely a result of disease elsewhere in the respiratory system, either the central nervous system or chest bellows. 5/9/2017 27 The Key to Blood Gas Interpretation: 4 Equations, 3 Physiologic Processes These 4 equations, crucial to understanding and interpreting arterial blood gas data, provide the basic foundation for understanding blood gas interpretation. Equation Physiologic Process 1) Alveolar ventilation PaCO2 equation PaCO2 = 2) VCO2 x 0.863 --------------VA Alveolar gas equation Oxygenation PAO2 = PIO2 - 1.2 (PaCO2) where PIO2 = FIO2 (PB – 47 mm Hg) 3) Oxygen content equation Oxygenation CaO2 = quantity O2 bound to Hb + quantity O2 dissolved in plasma CaO2 = (Hb x 1.34 x SaO2) 3) + Henderson-Hasselbalch equation (.003 x PaO2) Acid-base balance HCO3pH ~ -------PaCO2 5/9/2017 28 SaO2 and oxygen content • Tissues need a requisite amount of oxygen molecules for metabolism. Neither the PaO2 nor the SaO2 tells how much oxygen is in the blood. How much is provided by the oxygen content, CaO2 (units = ml O2/dl). CaO2 is calculated as: CaO2 = quantity O2 bound + to hemoglobin quantity O2 dissolved in plasma CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2) CaO2 = 15 x 1.34 x .98 CaO2 = 19.7 (.003 x 100) 0.3 + + = 20 ml O2/dl blood Hb = hemoglobin in gm%; 1.34 = ml O2 that can be bound to each gm of Hb; SaO2 is percent saturation of hemoglobin with oxygen; .003 is solubility coefficient of oxygen in plasma: .003 ml dissolved O2/mm Hg PO2. 5/9/2017 29 Oxygen dissociation curve: SaO2 vs. PaO2 Also shown are CaO2 vs. PaO2 for two different hemoglobin contents: 15 gm% and 10 gm%. CaO2 units are ml O2/dl. P50 is the PaO2 at which SaO2 = 50%. 5/9/2017 30 How much oxygen is in the blood? PaO2 vs. SaO2 vs. CaO2 OXYGEN PRESSURE: PaO2 • Since PaO2 reflects only free oxygen molecules dissolved in plasma and not those bound to hemoglobin, PaO2 cannot tell us “how much” oxygen is in the blood; for that you need to know how much oxygen is also bound to hemoglobin, information given by the SaO2 and hemoglobin content. OXYGEN SATURATION: SaO2 • The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen saturation (in arterial blood, the SaO2). Note that SaO2 alone doesn’t reveal how much oxygen is in the blood; for that we also need to know the hemoglobin content. OXYGEN CONTENT: CaO2 • Tissues need a requisite amount of O2 molecules for metabolism. Neither the PaO2 nor the SaO2 provide information on the number of oxygen molecules, i.e., how much oxygen is in the blood. (Neither PaO2 nor SaO2 have units that denote any quantity.) Only CaO2 (units ml O2/dl) tells how much oxygen is in the blood; this is because CaO2 is the only value that incorporates the hemoglobin content. Oxygen content can be measured directly or calculated by the oxygen content equation: CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2) 5/9/2017 See: “The Differences Between PaO2, SaO2 and Oxygen Content” www.lakesidepress.com/pulmonary/ABG/PO2.htm 31 SaO2 and CaO2 Which patient, (a) or (b), is more hypoxemic? (a) Hb 15 gm%, PaO2 65 mm Hg, SaO2=88% (b) Hb 10 gm %, PaO2 100 mm Hg, SaO2=98% 5/9/2017 32 SaO2 and CaO2 Which patient, (a) or (b), is more hypoxemic? (a) Hb 15 gm%, PaO2 65 mm Hg, SaO2=88% (b) Hb 10 gm %, PaO2 100 mm Hg, SaO2=98% ANSWER: (b) (a) CaO2 = .88 x 15 x 1.34 = 17.6 ml O2/dl + dissolved O2 (b) CaO2 = .98 x 10 x 1.34 = 13.1 ml O2/dl + dissolved O2 Oxygen content determines hypoxemia. Patient (b) has a much lower oxygen content and so is more hypoxemic than (a). Note that PaO2 is not a significant factor in determining oxygen content and (for this question) can be ignored. Note that the low PaO2 in patient (a) means there is an oxygen transfer problem from air to blood, but in terms of what the body really needs – OXYGEN CONTENT – patient (b) is definitely more hypoxemic. 5/9/2017 33 The Key to Blood Gas Interpretation: 4 Equations, 3 Physiologic Processes These 4 equations, crucial to understanding and interpreting arterial blood gas data, provide the basic foundation for understanding blood gas interpretation. Equation Physiologic Process 1) Alveolar ventilation PaCO2 equation PaCO2 = 2) VCO2 x 0.863 --------------VA Alveolar gas equation Oxygenation PAO2 = PIO2 - 1.2 (PaCO2) where PIO2 = FIO2 (PB – 47 mm Hg) 3) Oxygen content equation Oxygenation CaO2 = quantity O2 bound to Hb + quantity O2 dissolved in plasma CaO2 = (Hb x 1.34 x SaO2) 3) + Henderson-Hasselbalch equation (.003 x PaO2) Acid-base balance HCO3pH ~ -------PaCO2 5/9/2017 34 <> ACID-BASE: traditionally the most difficult of the 3 physiologic processes • • • • • • 5/9/2017 Acidemia: blood pH < 7.35 Acidosis: a primary physiologic process that, occurring alone, tends to cause acidemia, Alkalemia: blood pH > 7.45 Alkalosis: a primary physiologic process that, occurring alone, tends to cause alkalemia. Primary acid-base disorder: One of the four acidbase disturbances manifested by an initial change in HCO3- or PaCO2. They are: metabolic acidosis (MAc) metabolic alkalosis (MAlk) respiratory acidosis (RAc) respiratory alkalosis (Ralk) Compensation: The change in HCO3- or PaCO2 that results from the primary event. Compensatory changes are not classified by the terms used for the four primary acid-base disturbances. For example, a patient who hyperventilates (lowers PaCO2) solely as compensation for MAc does not have a RAlk, the latter being a primary disorder that, alone, would lead to alkalemia. In simple, uncomplicated MAc the patient will never develop alkalemia. 35 Primary acid-base disorders: Respiratory alkalosis • Respiratory alkalosis - A primary disorder where the first change is a lowering of PaCO2, resulting in an elevated pH. Compensation (bringing the pH back down toward normal) is a secondary lowering of bicarbonate (HCO3) by the kidneys; this reduction in HCO3- is not metabolic acidosis, since it is not a primary process. Primary Event HCO38pH ~ ))))) 9PaCO2 Compensatory Event 9HCO3- 8 pH ~ ))))) 9PaCO2 RESPIRATORY ALKALOSIS 9PaCO2 & 8 pH Hypoxemia (includes altitude) Anxiety Sepsis Any acute pulmonary insult, e.g., pneumonia, mild asthma attack, early pulmonary edema, pulmonary embolism 5/9/2017 36 Primary acid-base disorders: Respiratory acidosis • Respiratory acidosis - A primary disorder where the first change is an elevation of PaCO2, resulting in decreased pH. Compensation (bringing pH back up toward normal) is a secondary retention of bicarbonate by the kidneys; this elevation of HCO3- is not metabolic alkalosis, since it is not a primary process. Primary Event HCO39pH ~ ))))) 8PaCO2 Compensatory Event HCO39pH ~ ))))) 8PaCO2 8 RESPIRATORY ACIDOSIS 8PaCO2 & 9pH Central nervous system depression (e.g., drug overdose) Chest bellows dysfunction (e.g., Guillain-Barré syndrome, myasthenia gravis) Disease of lungs and/or upper airway (e.g., chronic obstructive lung disease, severe asthma attack, severe pulmonary edema) 5/9/2017 37 Primary acid-base disorders: Metabolic acidosis • Metabolic Acidosis - A primary acid-base disorder where the first change is a lowering of HCO3-, resulting in decreased pH. Compensation (bringing pH back up toward normal) is a secondary hyperventilation; this lowering of PaCO2 is not respiratory alkalosis, since it is not a primary process. Primary Event 9pH 5/9/2017 Compensatory Event 9HCO3))))) PaCO2 ))))) 9HCO39pH 9PaCO2 AG = Na+ - (Cl- + HCO3); nl = 12 +/- 4 METABOLIC ACIDOSIS 9HCO3- & 9pH Increased anion gap (>16 mEq/L) lactic acidosis; ketoacidosis; drug poisonings (e.g., aspirin, ethyelene glycol, methanol) Normal anion gap (<= 16 mEq/L) diarrhea; some kidney problems, e.g., renal tubular acidosis, intersititial nephritis 38 Primary acid-base disorders: Metabolic alkalosis • Metabolic alkalosis - A primary acid-base disorder where the first change is an elevation of HCO3-, resulting in increased pH. Compensation is a secondary hypoventilation (increased PaCO2) which is not respiratory acidosis, since it is not a primary process. Compensation for metabolic alkalosis (attempting to bring pH back down toward normal) is less predictable than for the other three acid-base disorders. Primary Event 8pH Compensatory Event 8HCO3- ))))) PaCO2 8HCO38pH ))))) 8PaCO2 METABOLIC ALKALOSIS 8HCO3- & 8pH • Chloride responsive (responds to NaCl or KCl therapy): contraction alkalosis, diuretics; corticosteroids; gastric suctioning; vomiting • Chloride resistant: any hyperaldosterone state, e.g., Cushings’s syndrome; Bartter’s syndrome; severe K+ depletion 5/9/2017 39 Mixed Acid-base disorders are common • In chronically ill respiratory patients, mixed disorders are probably more common than single disorders, e.g., RAc + MAlk, RAc + Mac, RAlk + MAlk. • In renal failure (and other conditions) combined MAlk + MAc is also encountered. pH 7.40, PaCO2=40 mm Hg, HCO3- = 24 mEq/L, AG=24 mEq/L • In sepsis patients, MAc + Ralk is common. pH 7.40, PCO2=20 mm Hg, HCO3- = 12 mEq/L • Always be on lookout for mixed acid-base disorders. They can be missed! 5/9/2017 40 Tips to diagnosing mixed acid-base disorders TIP 1. Don’t interpret any blood gas data for acid-base diagnosis without closely examining the venous electrolytes: Na+, K+, Cl- and HCO3-. • • • • A venous HCO3- out of the normal range always represents some type of acid-base disorder (barring lab or transcription error). High venous HCO3- indicates metabolic alkalosis &/or bicarbonate retention as compensation for respiratory acidosis Low venous HCO3- indicates metabolic acidosis &/or bicarbonate excretion as compensation for respiratory alkalosis Note that venous HCO3- may be normal in the presence of two or more acid-base disorders. 5/9/2017 41 Tips to diagnosing mixed acid-base disorders (cont.) TIP 2 . Single acid-base disorders do not lead to normal blood pH. Although pH can end up in the normal range (7.35 - 7.45) with a mild single disorder, a truly normal pH with distinctly abnormal HCO3- and PaCO2 invariably suggests two or more primary disorders. • Example: pH 7.40, PaCO2 20 mm Hg, HCO3- 12 mEq/L, in a patient with sepsis. Normal pH results from two co-existing and unstable acid-base disorders: acute respiratory alkalosis and metabolic acidosis. 5/9/2017 42 Tips to diagnosing mixed acid-base disorders (cont.) TIP 3. Simplified rules predict the pH and HCO3- for a given change in PaCO2. If the pH or HCO3- is higher or lower than expected for the change in PaCO2, the patient probably has a metabolic acid-base disorder as well. Below are expected changes in pH and HCO3- (in mEq/L) for a 10 mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis). ACUTE CHRONIC • Resp Acidosis – pH 9 by 0.07 pH 9 by 0.03 – HCO3- 8 by 1*HCO3- 8 by 3-4 • Resp Alkalosis – pH 8 by 0.08 pH 8 by 0.03 – HCO3- 9 by 2 HCO3- 9 by 5 *Units for HCO3- are mEq/L 5/9/2017 43 Predicted changes in HCO3- for a directional change in PaCO2 can help uncover mixed acid-base disorders. 5/9/2017 a) A normal or slightly low HCO3- in the presence of hypercapnia suggests a concomitant metabolic acidosis, e.g., pH 7.27, PaCO2 50 mm Hg, HCO3- 22 mEq/L. Based on the rule for increase in HCO3- with hypercapnia, it should be at least 25 mEq/L in this example; that it is only 22 mEq/L suggests a concomitant metabolic acidosis. b) A normal or slightly elevated HCO3- in the presence of hypocapnia suggests a concomitant metabolic alkalosis, e.g., pH 7.56, PaCO2 30 mm Hg, HCO3- 26 mEq/L. Based on the rule for decrease in HCO3 with hypocapnia, it should be at least 23 mEq/L in this example; that it is 26 mEq/L suggests a concomitant metabolic alkalosis. 44 Tips to diagnosing mixed acid-base disorders (cont.) TIP 4. In maximally-compensated metabolic acidosis, the numerical value of PaCO2 should be the same (or close to) the last two digits of arterial pH. This observation reflects the formula for expected respiratory compensation in metabolic acidosis: Expected PaCO2 = [1.5 x venous HCO3] + (8 ± 2) • In contrast, compensation for metabolic alkalosis (by increase in PaCO2) is highly variable, and in some cases there may be no or minimal compensation. 5/9/2017 45 Acid-base disorders: test your understanding A patient’s arterial blood gas shows pH of 7.14, PaCO2 of 70 mm Hg, and HCO3- of 23 mEq/L. How would you describe the likely acid-base disorder(s)? Acute elevation of PaCO2 leads to reduced pH, i.e., an acute respiratory acidosis. However, is the problem only acute respiratory acidosis or is there some additional process? For every 10 mm Hg rise in PaCO2 (before any renal compensation), pH falls about 0.07 units. Because this patient's pH is down 0.26, or 0.05 more than expected for a 30 mm Hg increase in PaCO2, there must be an additional, metabolic problem. Also, note that with acute CO2 retention of this degree, the HCO3- should be elevated 3 mEq/L. Thus a low-normal HCO3- with increased PaCO2 is another way to uncover an additional, metabolic disorder. Decreased perfusion leading to mild lactic acidosis would explain the metabolic component. 5/9/2017 46 Acid-base disorders: test your understanding A 45-year-old man comes to hospital complaining of dyspnea for three days. Arterial blood gas reveals pH 7.35, PaCO2 60 mm Hg, PaO2 57 mm Hg, HCO3- 31 mEq/L. How would you characterize his acid-base status? PaCO2 and HCO3- are elevated, but HCO3- is elevated more than would be expected from acute respiratory acidosis. Since the patient has been dyspneic for several days it is fair to assume a chronic acid-base disorder. Most likely this patient has a chronic or compensated respiratory acidosis. Without electrolyte data and more history, you cannot diagnose an accompanying metabolic disorder. 5/9/2017 47 Acid-base disorders: test your understanding State whether each of the following statements is true or false. a) Metabolic acidosis is always present when the measured serum CO2 changes acutely from 24 to 21 mEq/L. b) In acute respiratory acidosis, bicarbonate initially rises because of the reaction of CO2 with water and the resultant formation of H2CO3. c) If pH and PaCO2 are both above normal, the calculated bicarbonate must also be above normal. d) An abnormal serum CO2 value always indicates an acid-base disorder of some type. e) The compensation for chronic elevation of PaCO2 is renal excretion of bicarbonate. f) A normal pH with abnormal HCO3- or PaCO2 suggests the presence of two or more acid-base disorders. g) A normal venous HCO3- value indicates there is no acid-base disorder. h) Normal arterial blood gas values rule out the presence of an acid-base disorder. 5/9/2017 48 Acid-base disorders: test your understanding State whether each of the following statements is true or false. a) Metabolic acidosis is always present when the measured serum CO2 changes acutely from 24 to 21 mEq/L. b) In acute respiratory acidosis, bicarbonate initially rises because of the reaction of CO2 with water and the resultant formation of H2CO3. c) If pH and PaCO2 are both above normal, the calculated bicarbonate must also be above normal. a) false b) true c) true d) true d) An abnormal serum CO2 value always indicates an acid-base disorder of some type. e) false e) The compensation for chronic elevation of PaCO2 is renal excretion of bicarbonate. f) true f) A normal pH with abnormal HCO3- or PaCO2 suggests the presence of two or more acid-base disorders. g) false g) A normal venous HCO3- value indicates there is no acid-base disorder. h) false h) Normal arterial blood gas values rule out the presence of an acid-base disorder. 5/9/2017 49 Summary ) Clinical and laboratory approach to acid-base diagnosis • Determine existence of acid-base disorder from ABG and/or venous electrolytes. • Examine pH, PaCO2 and HCO3- for obvious primary acid-base disorder, and for deviations that indicate mixed acid-base disorders (TIPS 2 through 4). • Use a full clinical assessment (hx, phys exam, other lab data, previous ABGs) to explain each acid-base disorder. Co-existing clinical conditions may lead to opposing acid-disorders, so that pH can be high when there is an obvious acidosis, or low when there is an obvious alkalosis. • Treat the underlying clinical condition(s); this will usually suffice to correct most acid-base disorders. Clinical judgment should always apply. 5/9/2017 50 Arterial Blood Gases – test your overall understanding Case 1. A 55-year-old man is evaluated in the pulmonary lab for shortness of breath. His regular medications include a diuretic for hypertension and one aspirin a day. He smokes a pack of cigarettes a day. FIO2 pH PaCO2 PaO2 SaO2 .21 7.53 37 mm Hg 62 mm Hg 87% HCO3%COHb Hb CaO2 30 mEq/L 7.8% 14 gm% 16.5 ml O2 How would you characterize his state of ventilation, oxygenation and acid-base balance? 5/9/2017 51 Arterial Blood Gases – test your overall understanding Case 1 - Discussion VENTILATION: Adequate for the patient's level of CO2 production; the patient is neither hyper- nor hypo- ventilating. OXYGENATION: The PaO2 and SaO2 are both reduced on room air. Since P(A-a)O2 is elevated (approximately 43 mm Hg), the low PaO2 can be attributed to V-Q imbalance, i.e., a pulmonary problem. SaO2 is reduced, in part from the low PaO2 but mainly from elevated carboxyhemoglobin, which in turn can be attributed to cigarettes. The arterial oxygen content is adequate. ACID-BASE: Elevated pH and HCO3- suggest a state of metabolic alkalosis, most likely related to the patient's diuretic; his serum K+ should be checked for hypokalemia. 5/9/2017 52 Arterial Blood Gases – test your overall understanding Case 2. A 46-year-old man has been in the hospital two days, with pneumonia. He was recovering but has just become diaphoretic, dyspneic and hypotensive. He is breathing oxygen through a nasal cannula at 3 l/min. pH PaCO2 %COHb PaO2 SaO2 Hb HCO3CaO2 7.40 20 mm Hg 1.0% 80 mm Hg 95% 13.3 gm% 12 mEq/L 17.2 ml O2 How would you characterize his state of ventilation, oxygenation, and acid-base balance? 5/9/2017 53 Arterial Blood Gases – test your overall understanding Case 2 - Discussion VENTILATION: PaCO2 is half normal and indicates marked hyperventilation. OXYGENATION: The PaO2 is lower than expected for someone hyperventilating to this degree and receiving supplemental oxygen, and points to significant V-Q imbalance. The oxygen content is adequate. ACID-BASE: Normal pH with very low bicarbonate and PaCO2 indicates combined respiratory alkalosis and metabolic acidosis. If these changes are of sudden onset the diagnosis of sepsis should be strongly considered, especially in someone with a documented infection. 5/9/2017 54 Arterial Blood Gases – test your overall understanding Case 3. A 58-year-old woman is being evaluated in the emergency department for acute dyspnea. FIO2 pH PaCO2 %COHb PaO2 SaO2 Hb HCO3CaO2 .21 7.19 65 mm Hg 1.1% 45 mm Hg 90% 15.1 gm% 24 mEq/L 18.3 ml O2 How would you characterize her state of ventilation, oxygenation and acid-base balance? 5/9/2017 55 Arterial Blood Gases – test your overall understanding Case 3 - Discussion VENTILATION: The patient is hypoventilating. OXYGENATION: The patient's PaO2 is reduced for two reasons: hypercapnia and V-Q imbalance, the latter apparent from an elevated P(A-a)O2 (approximately 27 mm Hg). ACID-BASE: pH and PaCO2 are suggestive of acute respiratory acidosis plus metabolic acidosis; the calculated HCO3- is lower than expected from acute respiratory acidosis alone. . 5/9/2017 56 Arterial Blood Gases – test your overall understanding Case 4. A 23-year-old man is being evaluated in the emergency room for severe pneumonia. His respiratory rate is 38/min and he is using accessory breathing muscles. FIO2 pH PaCO2 PaO2 SaO2 HCO3%COHb Hb CaO2 .90 7.29 55 mm Hg 47 mm Hg 86% 23 mEq/L 2.1% 13 gm% 15.8 ml O2 Na+ K+ ClHCO3- 154 mEq/L 4.1 mEq/L 100 mEq/L 24 mEq/L How would you characterize his state of ventilation, oxygenation and acid-base balance? 5/9/2017 57 Arterial Blood Gases – test your overall understanding Case 4 - Discussion VENTILATION: The patient is hypoventilating despite the presence of tachypnea, indicating significant dead space ventilation. This is a dangerous situation that suggests the need for mechanical ventilation. OXYGENATION: The PaO2 and SaO2 are both markedly reduced on 90% inspired oxygen, indicating severe ventilation-perfusion imbalance. ACID-BASE: The low pH (7.29), high PaCO2 (55) and normal HCO3- all point to combined acute respiratory acidosis and metabolic acidosis. Anion gap is elevated to 30 mEq/L indicating a clinically significant anion gap (AG) acidosis, possibly from lactic acidosis. AG = Na - (Cl + HCO3-) = 154 - (100 + 24) = 30 mEq/L With an of AG of 30 mEq/L his venous HCO3- should be much lower, to reflect buffering of the increased acid. However, his venous HCO3- is normal, indicating a primary process that is increasing it, i.e., a metabolic alkalosis in addition to a metabolic acidosis. The cause of the alkalosis is as yet undetermined. In summary this patient has respiratory acidosis, metabolic acidosis and metabolic alkalosis. 5/9/2017 58 Blood Gas Interpretation means analyzing the data to determine patient’s state of: Ventilation Oxygenation Acid-Base Oh, did I mention you can’t learn this from a lecture? 5/9/2017 59 The best way to learn ABGs is to work on blood gas problems with some knowledge of basic physiology, then check your work for instant feedback. This ‘iterative process’ will teach you blood gas interpretation. Books Web sites You Can’t Learn Arterial Blood Gases from a Lecture You CAN learn ABGs from selected web sites. See list at: www.lakesidepress.com/ABGindex.htm 5/9/2017 60