Ab gs

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ABG analysis & Acid-Base Disorders 2012

Transcript of Ab gs

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ABG analysis & Acid-Base Disorders

2012

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Outline1. Discuss simple steps in analyzing ABGs

2. Calculate the anion gap

3. Calculate the delta gap

4. Differentials for specific acid-base disorders

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Steps for ABG analysis1. What is the pH? Acidemia or Alkalemia?

2. What is the primary disorder present?

3. Is there appropriate compensation?

4. Is the compensation acute or chronic?

5. Is there an anion gap?

6. If there is a AG check the delta gap?

7. What is the differential for the clinical processes?

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Normal Values

Variable Normal Range

pH 7.35 - 7.45

pCO2 35-45

Bicarbonate 22-26

Anion gap 10-14

Albumin 4

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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 or HCO3

Respiratory Acidosis pH low pCO2 high

Metabolic Acidosis pH low HCO3 low

Respiratory Alkalosis pH high pCO2 low

Metabolic Alkalosis pH high HCO3 high

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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 will check to see if there is a mixed disoder.

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

Acute: for every 10 increase in pCO2 -> HCO3 increases by 1 and there is a decrease of 0.08 in pH MEMORIZE

Chronic: for every 10 increase in pCO2 -> HCO3 increases by 4 and there is a decrease of 0.03 in pH

Respiratory Alkalosis Acute: for every 10 decrease in pCO2 -> HCO3 decreases by 2 and

there is a increase of 0.08 in PH MEMORIZE Chronic: for every 10 decrease in pCO2 -> HCO3 decreases by 5

and there is a increase of 0.03 in PH

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

Winter’s formula: pCO2 = 1.5[HCO3] + 8 ± 2 MEMORIZE If serum pCO2 > expected pCO2 -> additional respiratory

acidosis Metabolic Alkalosis

For every 10 increase in HCO3 -> pCO2 increases by 6

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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 = 18.5 So correct compensation so there is only one

disorder Primary metabolic

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Step 5: Calculate the anion gap

AG = Na – Cl – HCO3 (normal 12 ± 2) AG corrected = AG + 2.5[4 – albumin] If there is an anion Gap then calculate the

Delta/delta gap (step 6). Only need to calculate delta gap (excess anion gap) when there is an anion gap to determine additional hidden metabolic disorders (nongap metabolic acidosis or metabolic alkalosis)

If there is no anion gap then start analyzing for non-anion acidosis

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EXAMPLE Calculate Anion gap

ABG 7.23/17/235 on 50% VM BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin 4.

AG = Na – Cl – HCO3 (normal 12 ± 2) 123 – 97 – 7 = 19

No need to correct for albumin as it is 4

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Step 6: Calculate the different needed formulas 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

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EXAMPLE : Delta Gap 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

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EXAMPLE: WHY ANION GAP? 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

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

For non-gap metabolic acidosis, calculate the urine anion gapUAG = UNA + UK – UCL

If UAG>0: renal problemIf UAG<0: nonrenal problem (most commonly GI)

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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 7/BUN 119/ Cr 5.1

Most likely due to the diarrhea

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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<10 Saline-resistant UCL >10

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

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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

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Respiratory Acidosis

Causes of respiratory acidosis

CNS depression – sedatives, narcotics, CVA

Neuromuscular disorders – acute or chronic

Acute airway obstruction – foreign body, tumor, reactive airway

Severe pneumonia, pulmonary edema, pleural effusion

Chest cavity problems – hemothorax, pneumothorax, flail chest

Chronic lung disease – obstructive or restrictive

Central hypoventilation, OSA

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Steps for ABG analysis1. What is the pH? Acidemic or Alkalemic?

2. What is the primary disorder present?

3. Is there appropriate compensation?

4. Is the compensation acute or chronic?

5. Is there an anion gap?

6. If there is a AG, what is the delta gap?

7. What is the differential for the clinical processes?