metabolic acidosis abg

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Metabolic Acidosis Dr. Nadia Mohsen Abdu Ibrahim Specialist of Nephrology. NMGH

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Page 1: Metabolic acidosis ABG

Appraoch to Metabolic Acidosis

Dr. Nadia Mohsen Abdu IbrahimSpecialist of Nephrology.

NMGH

Page 2: Metabolic acidosis ABG
Page 3: Metabolic acidosis ABG

Systematic ABG analysis

1. History taking and physical examination 2. Assess accuracy of data (validity).3. Identify the primary disturbance

1. Check arterial pH-------- acidosis or alkalosis2. HCO3

- & pCO2 analysis---primary disorder.4. Compensatory responses 5. Calculate AG 6. Assess delta ratio7. Urine anion gab8. Formulate acid-base diagnosis

Page 4: Metabolic acidosis ABG

• Step 1. History taking and physical examination

Comprehensive history taking and physical examination can often give clues as to the underlying acid-base disorder

Page 5: Metabolic acidosis ABG

Systematic ABG analysis

1. History taking and physical examination 2. Assess accuracy of data (validity).3. Identify the primary disturbance

1. Check arterial pH-------- acidosis or alkalosis2. HCO3

- & pCO2 analysis---primary disorder.4. Compensatory responses 5. Calculate AG 6. Assess delta ratio7. Urine anion gab8. Formulate acid-base diagnosis

Page 6: Metabolic acidosis ABG

Validity

H = (PCO2/ HCO3) ×24 =7.8 -PH ×100

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Systematic ABG analysis

1. History taking and physical examination 2. Assess accuracy of data (validity).3. Identify the primary disturbance

1. Check arterial pH-------- acidosis or alkalosis2. HCO3

- & pCO2 analysis---primary disorder.4. Compensatory responses 5. Calculate AG 6. Assess delta ratio7. Urine anion gab8. Formulate acid-base diagnosis

Page 8: Metabolic acidosis ABG

Determine whether the patient is : acidemic (pH < 7.35) or alkalemic (pH > 7.45) whether the primary process is : metabolic (initiated by a change in HCO3-) or

respiratory (initiated by a change in PaCO2).

Step 3. Identify the primary disturbance

Page 9: Metabolic acidosis ABG

PCO2 HCO3 PH

Acidosis

Acidosis

Alkalosis

Alkalosis

Metabolic

Metabolic

Respiratory

Respiratory

Page 10: Metabolic acidosis ABG

Systematic ABG analysis

1. History taking and physical examination 2. Assess accuracy of data (validity).3. Identify the primary disturbance

1. Check arterial pH-------- acidosis or alkalosis2. HCO3

- & pCO2 analysis---primary disorder.4. Compensatory responses 5. Calculate AG 6. Assess delta ratio7. Urine anion gab8. Formulate acid-base diagnosis

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Step 4. Compensatory responsesMetabolic

Metabolic acidosisExpected pCO2 = 1.5 x [HCO3] + 8 (range: +/- 2)

Metabolic alkalosisExpected pCO2 = 0.7 [HCO3] + 20 (range: +/- 5)

“If the actual pCO2 or [HCO3-]

is different from the predicted values,You must suspect a 2nd acid-base disorder”

Page 12: Metabolic acidosis ABG

Metabolic Acidosis

Page 13: Metabolic acidosis ABG

Systematic ABG analysis

1. History taking and physical examination 2. Assess accuracy of data (validity).3. Identify the primary disturbance

1. Check arterial pH-------- acidosis or alkalosis2. HCO3

- & pCO2 analysis---primary disorder.4. Compensatory responses 5. Calculate AG 6. Assess delta ratio7. Urine anion gab8. Formulate acid-base diagnosis

Page 14: Metabolic acidosis ABG

Basis of Metabolic Acidosis

H+ + HCO3- H2O + CO2

Added acids

Loss ofNaHCO3

New A- No New A-(rise in plasma AG) (no rise in plasma AG)

(Exhaled)

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Electrochemical Balance in Blood

CATIONS ANIONS0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

SulfatePhosphateMg- OAK - ProteinsCa-HCO3Na- Cl

UAUC

Na

Cl

HCO3

Page 16: Metabolic acidosis ABG

Step 5: calculating the anion Gap

• (Na + K) + UC = (Cl + HCO3) + UA• The anion gap is defined as the quantity of

anions not balanced by cations.• Anion Gap= measured cation- measured

anion.• AG = [Na + K] – (Cl + HCO3) = 12 ± 4 meq/L• Corrected AG (in Hypoalbuminemia):

4-alb*2.5

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High Anion Gap Normal anion gap

• 1. Ketoacidosis - Diabetic - Alcoholic - Starvation• 2. Lactic acidosis• 3. Toxicosis - Ethylene glycol - Methanol - Salicylates• 4. Advanced renal failure

• 1. GIT HCO3- loss

- Diarrhea - External fistulas• 2. Renal HCO3

- loss - Proximal RTA - Distal RTA - Hyperkalemic RTA

metabolic acidosis

( MUD PILES )MethanolUremia

Diabetic ketoacidosisPropylene glycolIsoniazid intoxicationLactic acidosisEthanol ethylene glycolSalicylates

Page 18: Metabolic acidosis ABG

Basis of Metabolic Acidosis

H+ + HCO3- H2O + CO2

Added acids

Loss ofNaHCO3

New A- No New A-(rise in plasma AG) (no rise in plasma AG)

(Exhaled)

Page 19: Metabolic acidosis ABG

Electrochemical Balance in Blood

CATIONS ANIONS0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

SulfatePhosphateMg- OAK - ProteinsCa-HCO3Na- Cl

UAUC

Na

Cl

HCO3

Page 20: Metabolic acidosis ABG

Systematic ABG analysis

1. History taking and physical examination 2. Assess accuracy of data (validity).3. Identify the primary disturbance

1. Check arterial pH-------- acidosis or alkalosis2. HCO3

- & pCO2 analysis---primary disorder.4. Compensatory responses 5. Calculate AG 6. Assess delta ratio7. Urine anion gab8. Formulate acid-base diagnosis

Page 21: Metabolic acidosis ABG

Step 6: Calculating the delta ratio

Delta ratio= ∆ Anion gap/∆ [HCO3-]∆ Anion gap = (AG-12)∆ [HCO3-] = (24 - [HCO3-])

Page 22: Metabolic acidosis ABG

Delta ratio Assessment Guidelines

< 0.4 Hyperchloremic normal anion gap acidosis < 1 High AG & normal AG acidosis

= 1 Pure Anion Gap Acidosis Lactic acidosis: average value 1.6DKA more likely to have a ratio closer to 1 due to urine ketone loss

> 1 High AG acidosis and a concurrent metabolic alkalosis

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s

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Ketoacidosis

• In patients with IDDM, alcoholics and pts undergoing fasting or starvation

• due to the overproduction of ketone bodies (Ketosis) leading to accumulation of ketones in plasma (Ketonemia) and urine (Ketonuria).

• In starvation states where plasma glucose levels are low or in states of low plasma insulin where uptake of glucose by cells is diminished, fatty acids will be mobilized and transported to tissues (brain, skeletal muscle, heart) for fatty acid oxidation and energy production.

• acetyl CoA from fatty acid oxidation can not be oxidized and is instead converted to the generation of ketone bodies. (acetoacetate and β-hydroxybutyrate) Which serve as a source of fuel

Page 26: Metabolic acidosis ABG

Treatment of KA

• Fluids: IVF• Insulin infusion• Potassium replacement• Bicarb replacement: If pH < 7.1 and/or cardiac instability

present

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Lactic Acidosis

• Dead-end product of glycolysis• Occurs when the body must regenerate ATP without oxygen• Normal lactic level is maintained at 0.7-1.3 mEq/L• Eliminated in liver (50%), kidneys (25%), heart and skeletal

muscles• Normal Lactate/Pyruvate ratio suggest that the cause is not related

to anaerobic metabolism or anoxia

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Treatment for Lactic Acidosis

1. Identification of the primary illness and correction of that disturbance.

2. Restoration of tissue oxygen delivery through hemodynamic and/or respiratory support is the key therapeutic goal in type A lactic acidosis.

3. the use of sodium bicarbonate in lactic acidosis is controversial, particularly in patients with circulatory and respiratory failure. Despite the controversy most physicians support administration of NaHCO3 for very severe acidemia and will give small amounts of NaHCO3 to maintain the arterial pH above 7.10, since a pH beyond this value will promote the development of arrhythmias and cardiac depression.

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Actual Bicarbonate LossNormal Plasma Anion Gap

• Direct loss of NaHCO3

• Gastrointestinal tract (diarrhea, ileus, fistula or T-tube drainage, villous adenoma)

• Urinary tract (RTA, use of carbonic anhydrase inhibitors)

Page 30: Metabolic acidosis ABG

Renal Tubular Acidosis

• Inability of the kidney to reabsorb the filtered HCO3

-

• Inability of the kidney to excrete NH4

+

Page 31: Metabolic acidosis ABG

Proximal RTA Distal RTA RTA IV

cause impairment of HCO3- reabsorption in the proximal tubules

Acidification defect

Hypoaldosteronism or Pseudohypoaldosteronism

Type of Acidosis

Hyperchloremic metabolic acidosis

Hyperchloremic metabolic acidosis

Hyperchloremic metabolic acidosis

S.Potassium

low low high

Urine pH < 5.5 >5.5 < 5.5

Urine HCO3 loss

+++ ++ ++

Page 32: Metabolic acidosis ABG

Metabolic Acidosis in Renal Failure

• Normal AG acidosis results from failure of the kidney to generate new HCO3

- from a reduced rate of synthesis and excretion of NH4

+

• Increased AG acidosis results from the reduced GFR, with accumulation of anions: HPO4

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MANAGEMENT OF METABOLIC ACIDOSISCause

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• Bicarbonate is probably not useful in most cases of high anion gap acidosis

• Bicarbonate therapy may be useful for correction of normal anion gap acidosis

Page 36: Metabolic acidosis ABG

THANK YOU