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**Blood Gas Analysis and it’s Clinical Interpretation**

Dr R.S.Gangwar MD, PDCC, FIPM Assistant Professor Geriatric ICU,DGMH

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**Outline Common Errors During ABG Sampling Components of ABG**

Discuss simple steps in analyzing ABGs Calculate the anion gap Calculate the delta gap Differentials for specific acid-base disorders

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Delayed Analysis Consumptiom of O2 & Production of CO2 continues after blood drawn Iced Sample maintains values for 1-2 hours Uniced sample quickly becomes invalid within minutes PaCO2 3-10 mmHg/hour PaO2 pH d/t lactic acidosis generated by glycolysis in R.B.C. Consumptiom of O2 & Production of CO2 continues after blood drawn into syringe Iced Sample maintains values for 1-2 hours Uniced sample quickly becomes invalid

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**Temp Effect On Change of ABG Values**

Parameter 37 C (Change every 10 min) 4 C (Change every 10 min) pH 0.01 0.001 PCO2 1 mm Hg 0.1 mm Hg PO2 0.1 vol % 0.01 vol %

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**FEVER OR HYPOTHERMIA Most ABG analyzers report data at N body temp**

If severe hyper/hypothermia, values of pH & PCO2 at 37 C can be significantly diff from pt’s actual values Changes in PO2 values with temp also predictable If Pt.’s temp < 37C Substract 5 mmHg Po2, 2 mmHg Pco2 and Add pH per 1C decrease of temperature No consensus regarding reporting of ABG values esp pH & PCO2 after doing ‘temp correction’ ? Interpret values measured at 37 C: Most clinicians do not remember normal values of pH & PCO2 at temp other than 37C In pts with hypo/hyperthermia, body temp usually changes with time (per se/effect of rewarming/cooling strategies) – hence if all calculations done at 37 C easier to compare Values other than pH & PCO2 do not change with temp ? Use Nomogram to convert values at 37C to pt’s temp Some analysers calculate values at both 37C and pt’s temp automatically if entered Pt’s temp should be mentioned while sending sample & lab should mention whether values being given in report at 37 C/pts actual temp Hansen JE, Clinics in Chest Med 10(2),

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**Steady state is achieved usually within 3-10 minutes**

AIR BUBBLES : PO2 150 mmHg & PCO2 0 mm Hg in air bubble(R.A.) Mixing with sample, lead to PaO2 & PaCO2 To avoid air bubble, sample drawn very slowly and preferabily in glass syringe Steady State: Sampling should done during steady state after change in oxygen therepy or ventilator parameter Steady state is achieved usually within 3-10 minutes

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**0.1 ml of O2 consumed/dL of blood in 10 min in pts with N TLC **

Leucocytosis : pH and Po2 ; and Pco2 0.1 ml of O2 consumed/dL of blood in 10 min in pts with N TLC Marked increase in pts with very high TLC/plt counts – hence imm chilling/analysis essential EXCESSIVE HEPARIN Dilutional effect on results HCO3- & PaCO2 Only .05 ml heperin required for 1 ml blood. 25% lower values if 1ml sample taken in 10 ml syringe (0.25 ml heparin in needle) Syringes must be > 50% full with blood sample So syringe be emptied of heparin after flushing or only dead space volume is sufficient or dry heperin should be used

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**Risk of alteration of results with:**

TYPE OF SYRINGE pH & PCO2 values unaffected PO2 values drop more rapidly in plastic syringes (ONLY if PO2 > 400 mm Hg) Differences usually not of clinical significance so plastic syringes can be and continue to be used Risk of alteration of results with: size of syringe/needle vol of sample HYPERVENTILATION OR BREATH HOLDING May lead to erroneous lab results Min friction of barrel with syringe wall Usually no need to ‘pull back’ barrel – less chance of air bubbles entering syringe Small air bubbles adhere to sides of plastic syringes – difficult to expel Though glass syringes preferred,

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COMPONENTS OF THE ABG pH: Measurement of acidity or alkalinity, based on the hydrogen (H+) – 7.45 Pao2 :The partial pressure oxygen that is dissolved in arterial blood mm Hg. PCO2: The amount of carbon dioxide dissolved in arterial blood – 45 mmHg HCO3 : The calculated value of the amount of bicarbonate in the blood – 26 mmol/L SaO2:The arterial oxygen saturation. >95% pH,PaO2 ,PaCO2 , Lactate and electrolytes are measured Variables HCO3 (Measured or calculated) Std HCO3-: HCO3- levels measured in lab after equilibration of blood PCO2 to 40 mm Hg ( routine measurement of other serum electrolytes) Actual HCO3-: HCO3- levels calculated from pH & PCO2 directly Reflection of non respiratory (metabolic) acid-base status. Does not quantify degree of abnormality of buffer base/actual buffering capacity of blood.

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**Contd… Buffer Base: Base Excess/Base Deficit:**

It is total quantity of buffers in blood including both volatile(Hco3) and nonvolatile (as Hgb,albumin,Po4) Base Excess/Base Deficit: Amount of strong acid or base needed to restore plasma pH to 7.40 at a PaCO2 of 40 mm Hg,at 37*C. Calculated from pH, PaCO2 and HCT Negative BE also referred to as Base Deficit True reflection of non respiratory (metabolic) acid base status Normal value: -2 to +2mEq/L

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**CENTRAL EQUATION OF ACID-BASE PHYSIOLOGY**

Henderson Hasselbach Equation: where [ H+] is related to pH by To maintain a constant pH, PCO2/HCO3- ratio should be constant When one component of the PCO2/[HCO3- ]ratio is altered, the compensatory response alters the other component in the same direction to keep the PCO2/[HCO3- ] ratio constant [H+] in nEq/L = 24 x (PCO2 / [HCO3 -] ) [ H+] in nEq/L = 10 (9-pH)

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**Compensatory response or regulation of pH**

By 3 mechanisms: Chemical buffers: React instantly to compensate for the addition or subtraction of H+ ions CO2 elimination: Controlled by the respiratory system Change in pH result in change in PCO2 within minutes HCO3- elimination: Controlled by the kidneys Change in pH result in change in HCO3- It takes hours to days and full compensation occurs in 2- 5 days

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**Normal Values Variable Normal Normal Range(2SD) pH 7.40 7.35 - 7.45**

pCO2 40 35-45 Bicarbonate 24 22-26 Anion gap 12 10-14 Albumin 4 Memorize these values . Just read off slides.

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**Steps for ABG analysis What is the pH? Acidemia or Alkalemia?**

What is the primary disorder present? Is there appropriate compensation? Is the compensation acute or chronic? Is there an anion gap? If there is a AG check the delta gap? What is the differential for the clinical processes? Just read the steps off the slides. Quick overview . Determine if you have acidemia or alkalemia based on the PH Here we determine primary disorder is it respiratory or metabolic Check to see if there is appropriate compensation for the primary disorder in order to figure if its simple or mixed disorder Then analyze if this is an acute event or chronic Always look to see if there is an anion gap Due the other calculation depending on the underlying primary source . Such as if AG acidosis check to see if there is also a Delta gap to see if there is also non-anion gap present And lastly then come up with a DDX

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Step 1: Look at the pH: is the blood acidemic or alkalemic? EXAMPLE : 65yo M with CKD presenting with nausea, diarrhea and acute respiratory distress ABG :ABG 7.23/17/235 on 50% VM BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1 ACIDMEIA OR ALKALEMIA ????

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EXAMPLE ONE ABG 7.23/17/235 on 50% VM BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1 Answer PH = 7.23 , HCO3 7 Acidemia

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**Step 2: What is the primary disorder?**

What disorder is present? pH pCO2 HCO3 Respiratory Acidosis pH low high Metabolic Acidosis low Respiratory Alkalosis pH high Metabolic Alkalosis Just go over the table Then point out the arrows :A quick trick is to determine respiratory versus metabolic is : If PH and PCO2 are going in the opposite direction : then its respiratory, If PH and PCO2 are going in same directions then its metabolic. - Be careful with the mixed disorders using the trick.

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**Contd…. Metabolic Conditions are suggested if**

pH changes in the same direction as pCO2 or pH is abnormal but pCO2 remains unchanged Respiratory Conditions are suggested if: pH changes in the opp direction as pCO2 or pH is abnormal but HCO3- remains unchanged

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EXAMPLE ABG 7.23/17/235 on 50% VM BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5. PH is low , CO2 is Low PH and PCO2 are going in same directions then its most likely primary metabolic

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**Primary Disorder Expected Changes**

EXPECTED CHANGES IN ACID-BASE DISORDERS Primary Disorder Expected Changes Metabolic acidosis PCO2 = 1.5 × HCO3 + (8 ± 2) Metabolic alkalosis PCO2 = 0.7 × HCO3 + (21 ± 2) Acute respiratory acidosis delta pH = × (PCO2 - 40) Chronic respiratory acidosis delta pH = × (PCO2 - 40) Acute respiratory alkalosis delta pH = × (40 - PCO2) Chronic respiratory alkalosis delta pH = × (40 - PCO2) From: THE ICU BOOK - 2nd Ed. (1998) [Corrected]

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**Step 3-4: Is there appropriate compensation? Is it chronic or acute?**

Respiratory Acidosis Acute (Uncompensated): for every 10 increase in pCO2 -> HCO3 increases by 1 and there is a decrease of 0.08 in pH Chronic (Compensated): for every 10 increase in pCO2 -> HCO3 increases by 4 and there is a decrease of 0.03 in pH Respiratory Alkalosis Acute (Uncompensated): for every 10 decrease in pCO2 -> HCO3 decreases by 2 and there is a increase of 0.08 in PH Chronic (Compensated): for every 10 decrease in pCO2 -> HCO3 decreases by 5 and there is a increase of 0.03 in PH You need to memorize these and know it by heart . Then quickly go over the changes Then summarize : The easiest one is that for acute situations for every change of 10 in the PCO2 there is should be a change of 0.08 in PH and in chronic situation there should be a change of If there is a different change then know that there is most likely a mixed disorder In ac resp alkalosis, imm response to fall in CO2 (& H2CO3) release of H+ by blood and tissue buffers react with HCO3- fall in HCO3- (usually not less than 18) and fall in pH Cellular uptake of HCO3- in exchange for Cl- Steady state in 15 min - persists for 6 hrs After 6 hrs kidneys increase excretion of HCO3- (usually not less than 12-14) Steady state reached in 11/2 to 3 days. Timing of onset of hypocapnia usually not known except for pts on MV. Hence progression to subac and ch resp alkalosis indistinct in clinical practice Imm response to rise in CO2 (& H2CO3) blood and tissue buffers take up H+ ions, H2CO3 dissociates and HCO3- increases with rise in pH. Steady state reached in 10 min & lasts for 8 hours. PCO2 of CSF changes rapidly to match PaCO2. Hypercapnia that persists > few hours induces an increase in CSF HCO3- that reaches max by 24 hr and partly restores the CSF pH. After 8 hrs, kidneys generate HCO3- Steady state reached in 3-5 d 10 1 4 2 5 Partial Compensated: Change in pH will be between 0.03 to 0.08 for every 10 mmHg change in PCO2

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**Step 3-4: Is there appropriate compensation?**

Metabolic Acidosis Winter’s formula: Expected pCO2 = 1.5[HCO3] + 8 ± 2 OR pCO2 = 1.2 ( HCO3) If serum pCO2 > expected pCO2 -> additional respiratory acidosis and vice versa Metabolic Alkalosis Expected PCO2 = 0.7 × HCO3 + (21 ± 2) pCO2 = 0.7 ( HCO3) If serum pCO2 < expected pCO2 - additional respiratory alkalosis and vice versa Metabolic acidosis is the disorder you will mostly encounter in the hospital. You must memorize Winter’s formula Winter’s formula calculates the expected pCO2 in the setting of metabolic acidosis. If the serum pCO2 > expected pCO2 then there is additional respiratory acidosis in which the etiology needs to also be determined.

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EXAMPLE ABG 7.23/17/235 on 50% VM BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5. Winter’s formula : 17= 1.5 (7) +8 ±2 = 18.5(16.5 – 20.5) So correct compensation so there is only one disorder Primary metabolic

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**Step 5: Calculate the anion gap**

AG used to assess acid-base status esp in D/D of met acidosis AG & HCO3- used to assess mixed acid-base disorders AG based on principle of electroneutrality: Total Serum Cations = Total Serum Anions Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO Protein + Organic Acids) Na + UC = HCO3 + Cl + UA Na – (HCO3 + Cl) = UA – UC Na – (HCO3 + Cl) = AG Normal =12 ± 2 Delta/Delta gap needs to be calculated to see if there is other underlying acidosis/alkolosis that are present Don’t forget to look at albumin and adjust the calculated gap. If albumin is less than 4 then add 2.5 to your gap for every decrease of 1 Always calculate the AG . (fyi most BMP ordered calculate the gap for you but need to memorize the formula)

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**Contd… AG corrected = AG + 2.5[4 – albumin]**

If there is an anion Gap then calculate the Delta/delta gap (step 6) to determine additional hidden nongap metabolic acidosis or metabolic alkalosis If there is no anion gap then start analyzing for non-anion gap acidosis

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**EXAMPLE AG = Na – Cl – HCO3 (normal 12 ± 2) Calculate Anion gap**

ABG 7.23/17/235 on 50% VM BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin 2. AG = Na – Cl – HCO3 (normal 12 ± 2) 123 – 97 – 7 = 19 AG corrected = AG + 2.5[4 – albumin] = [4 – 2] = = 24

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**Step 6: Calculate Delta Gap**

Delta gap = (actual AG – 12) + HCO3 Adjusted HCO3 should be 24 (+_ 6) {18-30} If delta gap > 30 -> additional metabolic alkalosis If delta gap < 18 -> additional non-gap metabolic acidosis If delta gap 18 – 30 -> no additional metabolic disorders Must memorize how to calculate the delta gap Just read off the slide

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**EXAMPLE : Delta Gap Delta gap = (actual AG – 12) + HCO3**

ABG 7.23/17/235 on 50% VM BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin 4. Delta gap = (actual AG – 12) + HCO3 (19-12) +7 = 14 Delta gap < 18 -> additional non-gap metabolic acidosis So Metabolic acidosis anion and non anion gap

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**Metobolic acidosis: Anion gap acidosis**

Go over the table One thing to watch out for is Toluene (initially high gap, subsequent excretion of metabolites normalizes gap) Calculate osmol gap to determine if osmotically active ingestions (methanol, paraldehyde) are the cause of the gap metabolic acidosis. Other ingestions are toluene, isopropyl alcohol.

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**EXAMPLE: WHY ANION GAP? ABG :ABG 7.23/17/235 on 50% VM**

65yo M with CKD presenting with nausea, diarrhea and acute respiratory distress ABG :ABG 7.23/17/235 on 50% VM BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1 So for our patient for anion gap portion its due to BUN of 119 UREMIA But would still check lactic acid

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**Nongap metabolic acidosis**

For non-gap metabolic acidosis, calculate the urine anion gap URINARY AG Total Urine Cations = Total Urine Anions Na + K + (NH4 and other UC) = Cl + UA (Na + K) + UC = Cl + UA (Na + K) – Cl = UA – UC (Na + K) – Cl = AG Distinguish GI from renal causes of loss of HCO3 by estimating Urinary NH4+ . Hence a -ve UAG (av -20 meq/L) seen in GI, while +ve value (av +23 meq/L) seen in renal problem. - Go over the table - Most common cause in the hospital is IV fluids and Diarrhea UAG = UNA + UK – UCL Kaehny WD. Manual of Nephrology 2000; 48-62

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**EXAMPLE : NON ANION GAP ACIDOSIS**

65yo M with CKD presenting with nausea, diarrhea and acute respiratory distress ABG :ABG 7.23/17/235 on 50% VM BMP Na 123/ Cl 97/ HCO3 14 AG = 123 – = 12 Most likely due to the diarrhea

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**Causes of nongap metabolic acidosis - DURHAM**

Diarrhea, ileostomy, colostomy, enteric fistulas Ureteral diversions or pancreatic fistulas RTA type I or IV, early renal failure Hyperailmentation, hydrochloric acid administration Acetazolamide, Addison’s Miscellaneous – post-hypocapnia, toulene, sevelamer, cholestyramine ingestion

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Metabolic alkalosis Calculate the urinary chloride to differentiate saline responsive vs saline resistant Must be off diuretics in order to interpret urine chloride Saline responsive UCL<25 Saline-resistant UCL >25 Vomiting If hypertensive: Cushings, Conn’s, RAS, renal failure with alkali administartion NG suction If not hypertensive: severe hypokalemia, hypomagnesemia, Bartter’s, Gittelman’s, licorice ingestion Over-diuresis Exogenous corticosteroid administration Post-hypercapnia For metabolic alkalosis , check urine cholride (must be off diuretics) Urine chloride < 10 implies responsivenss to saline : extracelluar fluid volume depletion Urine chloride >10 implies resistance to sailne : severe poatssium depletion , mineralcorticoid excees syndrome Etc

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**Respiratory Alkalosis**

Causes of Respiratory Alkalosis Anxiety, pain, fever Hypoxia, CHF Lung disease with or without hypoxia – pulmonary embolus, reactive airway, pneumonia CNS diseases Drug use – salicylates, catecholamines, progesterone Pregnancy Sepsis, hypotension Hepatic encephalopathy, liver failure Mechanical ventilation Hypothyroidism High altitude Read the chart then summarize Can divide into three categories 1. systemic : (sepsis , asa , liver failure , endocrine , chf) 2. Central causes (respiratory center, ischmia , CNS tumor ) 3. Lungs (pna, asthma , PE )

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**Case1. 7.27/58/60 on 5L, HCO3- 26, anion gap is 12, albumin is 4.0**

1. pH= Acidemia (pH < 7.4) 2.CO2= Acid (CO2>40) Opposite direction so Primary disturbance = Respiratory Acidosis 3 &4: Compensation : Acute or chronic? ACUTE CO2 has increased by (58-40)=18 If chronic the pH will decrease 0.05 (0.003 x 18 = 0.054) pH would be 7.35 If acute the pH will decrease 0.14 (0.008 x 18 = 0.144) pH would be 7.26.

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**Contd. Dx-ACUTE RESPIRATORY ACIDOSIS 5: Anion gap –N/A**

6: There is an acute respiratory acidosis, is there a metabolic problem too? ΔHCO3- = 1 mEq/L↑/10mmHg↑pCO2 The pCO2 is up by 18 so it is expected that the HCO3- will go up by 1.8. Expected HCO3- is 25.8, compared to the actual HCO3- of 26, so there is no additional metabolic disturbance. Dx-ACUTE RESPIRATORY ACIDOSIS

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Case.2 7.54/24/99 on room air, HCO3- 20, anion gap is 12, albumin is 4.0. 1: pH= Alkalemia (pH > 7.4) 2.CO2= Base (CO2<40) pH & pCO2 change in opposite Direction So Primary disturbance = Respiratory Alkalosis 3 &4: Compensation ? acute or chronic? ACUTE ΔCO2 =40-24=16 If chronic the pH will increase 0.05 (0.003 x 16 = 0.048) pH would be 7.45 If acute the pH will increase 0.13(0.008 x 16 = 0.128) pH would be 7.53

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Contd… 5:Anion gap – N/A 6: There is an acute respiratory alkalosis, is there a metabolic problem too? ΔHCO3- = 2 mEq/L↓/10mmHg↓pCO2 The pCO2 is down by 16 so it is expected that the HCO3- will go down by 3.2. Expected HCO3- is 20.8, compared to the actual HCO3- of 20, so there is no additional metabolic disturbance. Dx-ACUTE RESPIRATORY ALKALOSIS

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Case-3 7.58/55/80 on room air, HCO3- 46, anion gap is 12, albumin is 4.0. Ucl -20 1: pH= Alkalemia(pH > 7.4) 2:CO2= Acid (CO2>40) Same direction so Primary disturbance = Metabolic Alkalosis 3&4: Compensation: ∆ pCO2=0.7 x ∆ HCO3- The HCO3- is up by 22.CO2 will increase by 0.7x22 = Expected CO2 is 55.4, compared to the actual CO2 of 55, therefore there is no additional respiratory disturbance.

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contd 5: No anion gap is present; and no adjustment needs to be made for albumin. Metabolic Alkalosis Urinary chloride is 20 meq/l (< 25 meq/l)so chloride responsive, have to treat with Normal saline. Dx-METABOLIC ALKALOSIS

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**Case-4 7.46/20/80 on room air, HCO3- 16, anion gap = 12, albumin = 4.0**

1: pH = Alkalemia (pH > 7.4) 2:CO2 = Base (CO2<40) So Primary disturbance = Respiratory Alkalosis 3 &4: Compensation? acute or chronic? Chronic ΔCO2 =40-20= 20. If chronic the pH will increase 0.06 (0.003 x 20 = 0.06) pH would be 7.46. If acute the pH will increase 0.16 (0.008 x 20 = 0.16) pH would be 7.56.

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**Contd…. Dx-CHRONIC RESPIRATORY ALKALOSIS 5: Anion gap – N/A**

6: There is a chronic respiratory alkalosis, is there a metabolic problem also? Chronic: ΔHCO3- = 4 mEq/L↓/10mmHg↓pCO2 The pCO2 is down by 20 so it is expected that the HCO3- will go down by 8. Expected HCO3- is 16, therefore there is no additional metabolic disorder. Dx-CHRONIC RESPIRATORY ALKALOSIS

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**Case-5 7.19/35/60 on 7L, HCO3- 9, anion gap = 18, albumin = 4.0**

1: pH = Acidemia (pH < 7.4) 2:CO2= Base (CO2<40) So Primary disturbance: Metabolic Acidosis 3&4: Compensation ? ∆ pCO2=1.2 x ∆ HCO3- CO2 will decrease by 1.2 (∆HCO3-) 1.2 (24-9) – 18= 22 Actual CO2 is higher than expected Respiratory Acidosis 5: Anion Gap = 18 (alb normal so no correction necessary)

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**Contd….. Delta gap = (actual AG – 12) + HCO3 = (18-12) + 9**

= = 15 which is<18 Non-AG Met Acidosis Dx-ANION GAP METABOLIC ACIDOSIS with NON-ANION GAP METABOLIC ACIDOSIS with RESPIRATORY ACIDOSIS (Diabeticic ketoacidosis) (secondary tochronic kidney disease or type IV Renal Tubular Acidosis (RTA 4)secondary to diabetic nephropathy),\ This problem is very complicated. Since the diabetic ketoacidosis is the presenting problem, it is therefore the primary disturbance. Presumably the CKD or RTA is a chronic issue that has been present for some time and is therefore, secondary (secondary to a strep pneumoniaepneumonia – which probably triggered the DKA)

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Case-6 7.54/80/65 on 2L, HCO3- 54, anion gap 12,albumin = 4.0 , Ucl 40 meq/l 1: pH = Alkalemia (pH > 7.4) 2:CO2= Acid (CO2>40) So Primary disturbance: Metabolic Alkalosis 3&4: Compensation? ∆ pCO2=0.7 x ∆ HCO3- CO2 will increase by 0.7 (∆HCO3-) 0.7 (54-24) 21 = 61 Actual CO2 is higher than expected Respiratory Acidosis

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Contd…. 5: Anion Gap = 12 (alb normal so no correction necessary) Urinary chloride is 40 meq/l (> 25 meq/l)so chloride resistant. So treatment would be disease specific and repletion of potassium Dx-METABOLIC ALKALOSIS with RESPIRATORY ACIDOSIS (secondary to contraction alkalosis from the furosemide) (secondary to COPD)

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**Case-7 7.6/30/83 on room air, HCO3- 28, anion gap = 12, albumin = 4.0**

1: pH = Alkalemia (pH > 7.4) 2:CO2= Base (CO2<40) SoPrimary Disturbance: Metabolic Alkalosis 3&4: Compensation ? ∆ pCO2=0.7 x ∆ HCO3- CO2 will increase by 0.7 (∆HCO3-) 0.7 (28-24) 2.8 = 42.8 Actual CO2 is lower than expected Respiratory Alkalosis Anion Gap = 12 (alb normal so no correction necessary) See urinary chloride for further Dx. Dx-METABOLIC ALKALOSIS with RESPIRATORY ALKALOSIS (secondary to vomiting) (secondary to pregnancy)

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Case-8 A 50 yo male present with sudden onset of SOB with following ABG 7.25/46/78 on 2L, HCO3- 20, anion gap = 10, albumin = 4.0 1: pH = Acidemia (pH < 7.4) 2:CO2= Acid (CO2>40) So Primary disturbance: Respiratory Acidosis 3 &4: If respiratory disturbance is it acute or chronic? ACUTE ∆ CO2 = 46-40= 6 If chronic the pH will decrease 0.02 (0.003 x 6 = 0.018) pH would be 7.38 If acute the pH will decrease 0.05 (0.008 x 6 = 0.048) pH would be 7.35. (This makes sense given the history of sudden onset of shortness of breath. Since the pH is lower than expected and the HCO3- is low, there is clearly a secondary metabolic acidosis. See below for clarification.)

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**Contd… Dx-RESPIRATORY ACIDOSIS with NON-ANION GAP METABOLIC ACIDOSIS**

Anion Gap = 10 (alb normal so no correction necessary) 6: There is an acute respiratory acidosis, is there a metabolic problem too? ∆ HCO3- = 1 mEq/L↑/10mmHg↑pCO2 The HCO3- will go up 1mEq/L for every 10mmHg the pCO2goes up above 40 The pCO2 is up by 6 so it is expected that the HCO3- will go up by Expected HCO3- is 24.6, compared to the actual HCO3- of 20. Since the HCO3- is lower than expected Non-Anion Gap Metabolic Acidosis (which we suspected). Dx-RESPIRATORY ACIDOSIS with NON-ANION GAP METABOLIC ACIDOSIS (secondary to pulmonary edema) (secondary to chronic kidney disease)

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**Case-9 7.15/22/75 on room air, HCO3- 9, anion gap = 10, albumin = 2.0**

1: pH = Acidemia (pH < 7.4) 2:CO2= Base (CO2<40) So Primary disturbance: Metabolic Acidosis 3&4:∆ Compensation ? pCO2=1.2 x ∆ HCO3- Expected pCO2 = 1.2 x ∆ HCO3- 1.2 (24 -9) 1.2 (15) The expected pCO2is 22mmHg. The actual pCO2 is 22, which is expected, so there is no concomitant disorder.

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**Contd…. 6: Delta Gap: = (15-12) + 9**

5: Anion Gap = 10 AGc = (4-2) = 15 Anion Gap Metabolic Acidosis 6: Delta Gap: Delta gap = (actual AG – 12) + HCO3 = (15-12) + 9 = 3+ 9 = 12 which is<18 Non-AG Met Acidosis Dx-ANION GAP METABOLIC ACIDOSIS with NON-ANION GAP METABOLIC ACIDOSIS secondary to lactic acidosis from ischemic bowel) (secondary to a Type IV Renal Tubular Acidosis from her Diabetes Mellitus)

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Acid-Base Disorders Adapted from Haber, R.J.: “A practical Approach to Acid- Base Disorders.” West J. Med 1991 Aug; 155:156-151 Allison B. Ludwig, M.D.

Acid-Base Disorders Adapted from Haber, R.J.: “A practical Approach to Acid- Base Disorders.” West J. Med 1991 Aug; 155:156-151 Allison B. Ludwig, M.D.

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