Appraoch to Metabolic Acidosis

Dr. Nadia Mohsen Abdu IbrahimSpecialist of Nephrology.

NMGH

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

• Step 1. History taking and physical examination

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

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

Validity

H = (PCO2/ HCO3) ×24 =7.8 -PH ×100

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

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

PCO2 HCO3 PH

Acidosis

Acidosis

Alkalosis

Alkalosis

Metabolic

Metabolic

Respiratory

Respiratory

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

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”

Metabolic Acidosis

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

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)

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

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

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

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)

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

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

Step 6: Calculating the delta ratio

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

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

s

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

Treatment of KA

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

present

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

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.

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)

Renal Tubular Acidosis

• Inability of the kidney to reabsorb the filtered HCO3

-

• Inability of the kidney to excrete NH4

+

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

+++ ++ ++

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

MANAGEMENT OF METABOLIC ACIDOSISCause

• 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

THANK YOU