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Blood Gases David Creery, MD MSc FRCPC MHSc Pediatric Critical Care, CHEO Medical Director of Patient Safety, CHEO Investigating Coroner, Ottawa Associate Professor, Faculty of Medicine, Pediatrics Objectives List the independently measured values in arterial blood gases and outline the normal values of these variables. Describe the measurement of oxygenation: saturation vs partial pressure of the gases versus arterial oxygen content. Explain the inter‐relation between HCO3 and PCO2. Explain how compensation occurs in blood gas disorders, identify the importance of the normal compensation values, and describe how this can be used to determine whether relevant compensation has occurred. Objectives Define respiratory acidosis and alkalosis, and metabolic acidosis and alkalosis, and explain how respiratory and metabolic compensation occur. Define the following terms: acute respiratory acidosis, acute respiratory alkalosis, chronic respiratory acidosis, chronic respiratory alkalosis, metabolic acidosis and metabolic alkalosis. Develop an approach to identifying acute and chronic metabolic acidosis and alkalosis, including mixed disorders. Arterial Blood Gas: Normal Values pH = 7.35 - 7.45 PaCO2 = 35 - 45 mm Hg PaO2 = 70 - 100 mm Hg SaO2 = 93 – 98% HCO3- = 22 - 26 mEq/L Base Excess = – 2.0 to 2.0 mEq/L Describe the measurement of oxygenation: saturation vs partial pressure of oxygen vs arterial oxygen content. PaO2 = Partial pressure of O2 in the plasma phase of arterial blood Measured by an electrode that senses dissolved oxygen molecules Oxygen passes through the thin alveolarcapillary 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. PaO2 = Partial pressure of O2 in the plasma phase of arterial blood The more dissolved molecules there are, the more are available to bind to Hb. Depending on the PaO2 and other factors, some O2 molecules will be dissolved and some will be bound. SaO2 = 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 smart sponge that “chooses” when to soak up oxygen and when to give it up. PaO2 and SaO2: The Relationship PaO2 is determined by alveolar PO2 and the state of the alveolar-capillary interface. PaO2, in turn, determines the oxygen saturation of hemoglobin (along with other factors that affect the position of the O2-dissociation curve). Oxygen Content: Hb and its relationship to SaO2 and PaO2 The more hemoglobin available to bind the dissolved oxygen molecules, the greater total number of oxygen molecules the blood will contain. PaO2 is not a function of hemoglobin level PaO2 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 PAO2. Oxygen Content: How much oxygen is in the blood? Tissues need a threshold amount of O2 molecules for aerobic metabolism. CaO2 = directly reflects the total number of oxygen molecules in arterial blood, both bound and unbound to hemoglobin = (1.39 x Hb x Sat) + (PaO2 x 0.003) Oxygen bound to Hb is much more important than dissolved oxygen CO = HR x SV Oxygen Delivery = CO X CaO2 Oxygen Content: Hb and its relationship to SaO2 and PaO2 SaO2 is determined mainly by PaO2. The relationship between the two variables is the oxygen-dissociation curve. PaO2 is the most important (but not the only) determinant of SaO2. The oxygen-Hb dissociation curve tells us about Hb’s affinity for oxygen. Some conditions shift the position of the oxygen dissociation curve left or right. Oxygen-Hb Dissociation Curve Small changes in paO2 make BIG change in Sats Shape and position of the curve are the same irrespective of the hemoglobin content. Big changes in paO2 make ALMOST NO change in Sats But there’s more…the curve shifts LEFT SHIFT = HARDER TO RELEASE, EASIER TO BIND RIGHT SHIFT = EASIER TO RELEASE, HARD TO BIND…..need higher PaO2 to maintain same Sat Clinical Problem A 28 yr old woman has just delivered a baby. She has a PaO2 of 85 mm Hg, a SaO2 of 98%, and a hemoglobin of 140. She then has a severe postpartum hemorrhage. The blood is replaced acutely with normal saline, which leaves her with a hemoglobin of 70. What will be her new PaO2, SaO2, and CaO2? Clinical Problem A 40 yr old woman has a PaO2 of 85 mm Hg, a SaO2 of 98%, and a hemoglobin of 140. She then has a severe post-partum hemorrhage. The blood is replaced acutely with normal saline, which leaves her with a hemoglobin of 70. What will be her new PaO2, SaO2, and CaO2? * PaO2 unchanged, SaO2 unchanged, CaO2 reduced. Hemoglobin content is suddenly reduced by half, which will lower CaO2 by half. However, the PaO2 and SaO2 will be unaffected, since their values are independent of the content of hemoglobin present. Define respiratory acidosis and alkalosis, and metabolic acidosis and alkalosis, and explain how respiratory and metabolic compensation occur. Interpreting Blood Gases Not complicated if you ask questions sequentially Information about two distinct things: acid-base status and oxygenation (key fact: how was the blood drawn?) Acidosis is much more clinically important than alkalosis CO2 “creates” acidosis (more CO2 is bad); bicarb “creates” alkalosis (more bicarb is good) Lungs compensate quickly, kidneys compensate slowly Compensation starts immediately (key question: how much compensation has occurred?) We never overcompensate A blood gas is a snapshot of a dynamic process pH ≈ HCO3PaCO2 pH is life and death The system almost instantly reflects any disturbances The changes in degree and direction of bicarb and CO2 are the keys to interpreting acid-base disorders Bicarb is good, CO2 is bad 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 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 Definitions: Primary acid-base disorder: One of the four acid-base disturbances that is manifested by an initial change in HCO3- or PaCO2. If HCO3- changes first, the disorder is either a metabolic acidosis (reduced HCO3-) or metabolic alkalosis (elevated HCO3-). If PaCO2 changes first, the problem is either respiratory alkalosis (reduced PaCO2) or respiratory acidosis (elevated PaCO2). Definitions: Compensation: The change in HCO3- or PaCO2 that occurs as a reaction to the primary event. Two types: metabolic compensation or respiratory compensation Snapshot of a dynamic process Lungs fast, kidneys slow; CO2 bad, bicarb good The 4 Primary Acid-Base Disorders Primary Event DISORDER Compensatory Event ↓HCO3PaCO2 Metabolic acidosis ↓pH ↓PaCO2 ↑ HCO3PaCO2 Metabolic alkalosis ↑pH ↑ PaCO2 HCO3↑ PaCO2 Respiratory acidosis ↑pH ↑ HCO3- HCO3↓ PaCO2 Respiratory alkalosis ↑ pH ↓HCO3- But they’re not equal… Acidosis is +++ more important Three types of acidosis: Respiratory: too much CO2 Metabolic – Anion Gap: unmeasured anion (CAT-MUDPILES) Metabolic – Nonanion gap: loss of bicarb in gut or kidneys Alkalosis 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 Respiratory alkalosis Hyperventilation Blood Gas Nomenclature Could be ABG, CBG or VBG (art, cap, venous) Standard short form pH/pCO2/pO2/Bicarb in that order Bicarb sometimes written HCO3 For CBG and VBG, pO2 usually omitted So for ABG pH 7.35 pCO2 43 pO2 105 and Bicarb 23 it would be written 7.35/43/105/23 For VBG and CBG it would be written 7.35/43/-/23 Steps to Acid-Base Interpretation 1. 2. 3. 4. Look at the pH. What is the acid/base disturbance? Look at the bicarb and the pCO2. Which element is driving the pH? (Could be both) Is there compensation occurring? How much? pH-BicCO2-Comp pH-BicCO2-Comp An Example Patient with COPD pH = 7.33, CO2 = 60, Bicarb = 31 pH is acidotic (barely) CO2 is high (driving acidosis) Bicarb is high (meaning compensation has begun and working to restore normal pH Which values are inside vs. outside the box? Side with two (or three) X’s defines the condition If third X is inside the box, compensation just starting If outside opposite, compensation is underway If pH is back within box, compensation has worked If X’s outside same, it’s combined ©2011 by American Physiological Society Blood gas data for a patient with COPD pH = 7.33 CO2 = 60 Bicarb = 31 Dietz J R Advan in Physiol Edu 2011;35:454-455 ©2011 by American Physiological Society Side with two (or three) X’s defines the condition Side with two (or three) X’s defines the condition If third X is inside the the box, compensation just starting If third X is inside box, it’s uncompensated If outside opposite, compensation is underway If outside opposite, it’s compensated If pH is backIf within compensation outsidebox, same, it’s combined has worked If X’s outside same, it’s combined pH-BicCO2-Comp Another Example Patient with diabetic ketoacidosis pH = 7.05, CO2 = 15, Bicarb = 6 pH is acidotic Bicarb is low (driving the acidosis) CO2 is low (i.e. NOT driving acidosis) Compensation has begun, and is helping (What would pH be if the CO2 was normal?) but pH still very low Same patient using the box pH = 7.05 CO2 = 15 Bicarb = 6 Dietz J R Advan in Physiol Edu 2011;35:454-455 ©2011 by American Physiological Society Side with two (or three) X’s defines the condition If third X is inside the box, compensation just starting If outside opposite, compensation is underway If pH is back within box, compensation has worked If X’s outside same, it’s combined pH-BicCO2-Comp Another Example Patient post cardiac arrest pH = 7.02, CO2 = 80, Bicarb = 6 pH is acidotic Bicarb is low (driving the acidosis) CO2 is high (i.e. ALSO driving acidosis) Compensation has NOT begun, because the acidosis is a COMBINED respiratory and metabolic acidosis Blood gas data for a patient in cardiopulmonary arrest. pH = 7.02 CO2 = 80 Bicarb = 19 Dietz J R Advan in Physiol Edu 2011;35:454-455 ©2011 by American Physiological Society Side with two (or three) X’s defines the condition Side with two (or three) X’s defines the condition If third X is inside the box, compensation just starting If third X is inside the box, it’s uncompensated If outside opposite, compensation is underway If outside opposite, it’s compensated If pH is back within box, compensation If outside same, it’s combined has worked If X’s outside same, it’s combined Answer: Need more info. You need 2 out of 3 variables to obtain the 3rd. The pH could be acidemic or alkalotic. Answer: HCO3-: usual value is 22 to 26, so this rose 50% PCO2: usual value is 35 to 45, so this rose 50% ∆ Ratio = none pH = 7.4 Case #1: Sarah Smith You are the on-call medical student for orthopedics. You are called to see Sarah, a 16 yr. old who is post-op day #2 following spinal instrumentation for scoliosis. Her nurse called you because Sarah is difficult to rouse. Sarah has been receiving morphine for pain control. Her most recent vital signs are: HR 70 BP 110/50 RR 7 Sats 90% R/A Temp 37.3 ax Case #1: Sarah Smith On exam she has occasional upper airway sounds and no accessory muscle use. You hear decreased air entry at the bases with no crackles or wheeze. She is warm to touch and is pink. She is unresponsive. You perform an arterial blood gas, support her breathing with a bag and mask and ask the nurse to draw up a medication. The results of the blood gas are: 7.20/65/65/25 Your attending arrives on the ward and asks you what you think is going on. What you’re thinking… 7.20/65/65/25 You have information about two distinct things: acid-base and oxygenation You remember pH-BicCO2-Comp For acid-base, first look at pH (Acidosis!) Then look at pCO2 and Bicarb (CO2 is high so it’s a respiratory acidosis); bicarb is high so kidneys are trying to compensate For oxygenation, first question is how was blood drawn (arterial, so pO2 is low) What you’re thinking 2… 7.20/65/65/25 “What could cause a respiratory acidosis with partial compensation and low arterial oxygen levels?” “What could cause these findings in this patient?” You mull over the following Could this be primary lung disease (pneumonia, pulmonary embolus, fluid overload, pleural effusion, pneumothorax) Could this be reduced respiratory drive (stroke, medications) Could this be an airway obstruction? You decide to put the results into the box… Case #1: Sarah Smith 7.20/65/65/25 Side with two (or three) X’s defines the condition If third X is inside the box, it’s uncompensated If outside opposite, it’s compensated If outside same, it’s combined You’re Ready to Speak… PaCO2 is elevated and pH is acidotic This is an partially compensated respiratory acidosis (partially because the bicarb is moving in the right direction but is not outside the box yet and the pH is still low) The bicarbonate is in the normal range because the kidneys have not had adequate time to establish effective compensatory mechanisms Lungs are fast, kidneys are slow The PaO2 is low, but in keeping with her oxygen saturation She has received too much narcotic, and needs airway support +/naloxone Primary Respiratory Problems: Pathophysiology PaCO2= CO2 Production / Alveolar ventilation PaCO2 ~ CO2 production Minute ventilation – Dead Space Ventilation Primary Respiratory Problems: Pathophysiology PaCO2 ~ CO2 production Minute ventilation – Dead Space Ventilation CO2 EXCRETION Alveolar ventilation = MV (tidal volume x rate) – DS Alveolar ventilation regulated by: Dead space = all airways larger than alveoli Does not contribute to gas exchange More is bad (e.g. breathing through garden hose) Central respiratory centers (pons, medulla) Chemoreceptors for PaCO2, PaO2, and pH in the brainstem Neural impulses from lung-stretch receptors As long as the lungs excrete the volatile fraction (CO2) through ventilation there is no acid accumulation What can cause respiratory acidosis? PaCO2 ~ CO2 production Minute ventilation – Dead Space Ventilation CO2 production OR CO2 excretion If Alveolar Ventilation does not match CO2 production PaCO2 CNS impairment (head trauma, brainstem lesion, medications) Airway obstruction Mechanical impairment (chest trauma, pneumothorax, muscle weakness, residual neuromuscular blockade) Decreased perfusion (pulmonary embolus, cardiac arrest) Parenchymal disease (pneumonia, edema) Acute Respiratory Acidosis: Important Points NOT a diagnosis - represents a failure of the respiratory system in some aspect that requires investigation and urgent treatment As PaCO2 increases, PAO2 (and hence PaO2) will fall unless inspired oxygen is supplemented Alveolar Gas Law: “Limited space in the alveoli for gases; CO2 crowds out oxygen” Case #2: Nate Norman You are on-call for pediatrics and called to see Nate, an 8 month old ex-28 wk baby admitted 3 days ago with respiratory distress and RSV bronchiolitis. His nurse called you because Nate 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 88% R/A Temp 37.6 ax Case #2: Nate Norman 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 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. Your Attending arrives and asks you to interpret the blood gas and the clinical situation. The results of the blood gas are: 7.36/70/55/34 You Consider the Key Points Again pH-BicCO2-Comp Information about two distinct things: acid-base status and oxygenation (How was the blood drawn?) Acidosis much more clinically important than alkalosis CO2 “creates” acidosis (more CO2 is bad); bicarb “creates” alkalosis (more bicarb is good) Lungs compensate quickly, kidneys compensate slowly This is a static snapshot of a dynamic process Inside Your Brain… 7.36/70/55/34 You’re somewhat surprised to see that the pH is normal, but the CO2 is high. Them you realize that the CO2 is high, and the bicarb is high, so there are two things going on The pH is at the lower end of normal, so you decide that this is a primary respiratory acidosis with metabolic compensation You think, if I had done a blood gas 12 hours ago, I might have seen a partially compensated respiratory acidosis Attending is tapping her fingers on the desk and looking at her watch You put the results in the box… Case #2: Nate Norman (1) 7.36/70/55/34 Side with two (or three) X’s defines the condition If third X is inside the box, it’s uncompensated If outside opposite, it’s compensated If outside same, it’s combined You’re Ready to Speak… PaCO2 is elevated and pH in acceptable range Bicarbonate is elevated because the kidneys have had adequate time to establish effective compensatory mechanisms Remember that we never overcompensate (unless there are two distinct things going on) The PaO2 is in keeping with his saturations What could be causing these findings in this patient? You say “Acute on chronic lung disease (RSV bronchiolitis on top of lung changes of prematurity)” Attending appears satisfied and moves on to grilling another student Case #2: Nate Norman You suggest to Nate’s nurse to give him oxygen, increase the frequency of suctioning and ventolin and start physiotherapy. Four hours later you’re back to see him: he seems to be getting tired and working harder. His most recent vital signs are: HR 165 RR 80 BP 80/55 Sats 93% on 40% oxygen Temp 38 ax Case #2: Nate Norman On examination you find nasal flaring, grunting and moderate to severe subcostal indrawing. He has decreased a/e on the right side and ++wheezes on auscultation. He appears tired and lethargic. You ask the nurse to call for an x-ray and you perform an arterial blood gas. Your Attending arrives and asks you to interpret the blood gas and the clinical situation. The results of the blood gas are: 7.20/96/80/37 Inside Your Brain… 7.20/96/80/37 You You You The You You consider the key points again first look at the pH (acidotic!) see that the CO2 is much higher than before bicarb is higher (but is it “higher enough”?) see the PaO2 is higher (but Nate is now on O2) put the values into the box… Case #2: Nate Norman (2) 7.20/96/80/32 Side with two (or three) X’s defines the condition If third X is inside the box, it’s uncompensated If outside opposite, it’s compensated If outside same, it’s combined You’re Ready… The PaCO2 is elevated and pH is low, even though bicarb is high (But not high enough) Kidneys have not had adequate time to fully compensate You decide that Nate is getting quite a bit sicker and needs some respiratory support Nate is transferred to PICU and placed on BiPAP An Example of Respiratory Failure 12 yo girl pH pCO2 Bicarb 10:00 10:25 11:25 13:35 13:55 18:10 7.06 69 20 7.17 58 21 7.23 48 20 7.35 36 20 7.33 37 20 7.37 34 20 Metabolic Acidosis When you find a patient has a primary metabolic acidosis, you must do more work: The ANION GAP Anion Gap: Na+ – (Cl- + HCO3-) Normal Gap: 8-16 Can also calculate with the K. Normal range about 4 higher Causes of Anion-Gap Acidosis Increased acid production: Ketones Lactic acid DKA, starvation tissue hypoxia, sepsis, exercise, EtOH/MeOH/ethylene glycol ingestion, paraldehyde, Inborn Error of Metabolism (IEM) Everything else ASA, NSAID, Iron Other Mnemonics DR. MAPLES SLUMPED D-DKA, R-Renal, M-Methanol, A-Alcoholic Ketoacidosis, P-Paraldehyde, L-Lactate, E-Ethylene Glycol, S-Salicylates S-Salicylates, L-Lactate, U-Uremia, M-Methanol, PParaldehyde, E-Ethylene Glycol, D-Diabetes GOLD MARK G-Glycols, Oxoproline, L&D-L&D Lactate, M-Methanol, A-Aspirin, R-Renal Failure, K-Ketoacidosis Causes of NON-Anion Gap Acidosis Hyperchloremic metabolic acidosis GI loss of HCO3 Renal loss of HCO3 Diarrhea, Necrotizing enterocolitis, small bowel drainage/fistula RTA, early renal failure, CA inhibitors Administration of HCl or other chloridecontaining substances (i.e. NS) hyperalimentation Another Example: 8 year old girl, Susie, presents to ER with tachypnea, tachycardia, altered level of consciousness Calculate the anion gap Vital signs: HR 140 RR 46 BP 95/50 Gas: pH 7.05 PCO2 20 HCO3 7 Na+ - (Cl- + HCO3) Normal anion gap 12-16 More Labs: Anion gap = 30 Na: 132 Cl: 95 HCO3: 7 Glucose: 44 Acute Metabolic Acidosis Primary metabolic acidosis, with increased anion gap with respiratory compensation CAT-MUDPILES Lactate, Ketones, Everything else DKA Example… 14 yo boy pH pCO2 Bicarb 8:20 9:45 11:40 13:15 17:10 21:00 7.05 33 9 7.03 26 7 6.94 33 7 7.05 33 9 7.26 35 16 7.28 36 17 Case #3: Diane Donaldson You are working in the ER and see Diane, a 27 yr. old who is complaining of pleuritic chest pain of several hours duration. She also complains of upper respiratory tract symptoms that started 2 days earlier. She is otherwise healthy with no significant past medical history. She has no allergies and her only medication is the oral contraceptive pill. Last evening she returned from overseas by plane. She is a half pack per day smoker. Case #3: Diane Donaldson Her most recent vital signs are: HR 95 • Sats 94% in room air BP 110/70 • Temp 37.0 ax RR 28 On exam 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. You decide to order a chest x-ray and arterial blood gas. Your Attending arrives and asks you to interpret the blood gas and the clinical situation. The results of the blood gas are: 7.47/31/83/22 What you’re thinking… 7.47/31/83/22 pH is high (alkalosis) pCO2 is low, bicarb is low normal (primary respiratory alkalosis) with partial compensation It’s an arterial gas, so you can comment on oxygenation PaO2 in keeping with sats But seems to be a primary oxygenation problem (!!!) You put it in the box Case #3: Diane Donaldson 7.47/31/83/22 Side with two (or three) X’s defines the condition If third X is inside the box, it’s uncompensated If outside opposite, it’s compensated If outside same, it’s combined Respiratory Alkalosis PaCO2 is low and the pH is alkalotic The increase in pH is caused by the decrease in paCO2 Bicarbonate is normal range because the kidneys have just started to compensate (but do a gas in 2 hours and compensation is likely to be more complete) You mull over what could cause these findings (partially compensated respiratory alkalosis and hypoxia) in this clinical scenario First, What Could Be Causing the 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 What you’re thinking 2… But most of these conditions don’t have an impact on oxygenation (if anything, they tend to increase PaO2) So you go back to the list again… What Could Be Causing Respiratory Alkalosis AND Hypoxia? Central nervous system Trauma Hypoxia High altitude Severe anemia Right-to-left intracardiac shunt Endocrine Late pregnancy Pulmonary Pneumonia Pulmonary edema Pulmonary embolism Aspiration Interstitial lung disease Asthma Could this be a pulmonary embolism? Recent long travel, OCP, smoker Respiratory alkalosis with hypoxia would fit Others not c/w clinical exam Steps to Oxygen Interpretation 1. Ask “How was the blood drawn?” 2. 3. 4. Can only comment on oxygenation for arterial Consider the PaO2 relative to the patient’s oxygen saturations Calculate the alveolar-arterial (A-a) gradient Think about the oxyhemoglobin dissociation curve and where the values would fall Oxygenation Are the lungs transferring oxygen properly from the atmosphere to the pulmonary circulation? Use the Alveolar Gas Equation to calculate PAO2 then find the A-a O2 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 the answer is YES A-a O2 gradient = 28 (normal <10) Elevated indicating a state of V-Q imbalance and therefore some parenchymal lung disease or abnormality. Hyperventilation should cause high PaO2, therefore NO increased A-a O2 difference You’re Ready… Diane’s PaCO2 is low and the pH is alkalotic The increase in pH is caused by the decrease in paCO2 Bicarbonate is normal range because the kidneys have just started to compensate (but do a gas in 2 hours and compensation is likely to be more complete) Her A-a oxygen gradient is elevated (meaning that there is less oxygen in the arterial blood than there should be) You order a spiral CT and diagnose a PE Summary Information about two distinct things: acid-base status and oxygenation Acidosis is much more clinically important than alkalosis CO2 “creates” acidosis (more CO2 is bad); bicarb “creates” alkalosis (more bicarb is good) Lungs compensate quickly, kidneys compensate slowly Compensation starts immediately (key question: how much compensation has occurred?) We never overcompensate A blood gas is a snapshot of a dynamic process Summary: Steps in Acid-Base Interpretation 1. 2. 3. 4. 5. Look at the pH. What is the acid/base disturbance? Look at the bicarb and the pCO2. Which element is driving the pH? (Could be both) Is there compensation occurring? How much? pH-BicCO2-Comp Use the box if that helps you visualize Summary: Steps in Oxygen Interpretation 1. Ask “How was the blood drawn?” 1. 2. 3. 4. 5. Consider the PaO2 relative to the patient’s oxygen saturations Think about the oxyhemoglobin dissociation curve and where the values would fall Calculate the alveolar-arterial (A-a) gradient Oxygen Content=(1.39 x Hb x Sat) + (paO2 x 0.003) 1. 6. Only comment on oxygenation if it is arterial Big contribution from Sat and Hb, v little from paO2 Oxygen Delivery = CO x CaO2 Thank you Questions and Discussion [email protected]