Acid-Base Unit 2

Human Buffering Systems…

First line of defense → solution containing a weak acid and anion (base) to resist pH change upon addition of strong acid or base

3 Buffering Systems:

1. Extracellular/Intracellular - immediate action 

2. Respiratory regulation - fast onset (minutes)

3. Renal regulation - slower onset

ABG:

pH/paCO2/paO2/HCO3/O2

Normal pH:

7.4 

• pH < 7.35 = acidemia 

• pH > 7.45 alkalemia

Interpreting acid-base disorder steps

1. Asses pH

2. Determine if respiratory or metabolic

3. Check degree of compensation 

4. Calculate the anion gap for AGMA 

5. If AGMA, calculate delta anion gap 

Step 2) what is the primary process?

Evaluate the HCO3 and PCO2…

• Normal HCO3 is 24

• Normal PCO2 is 40

• HCO3 < 24: metabolic acidosis

• HCO3 > 24: metabolic alkalosis 

• PCO2 < 40: respiratory alkalosis

• PCO2 > 40: respiratory acidosis  

metabolic acidosis

HCO3 < 24

Metabolic Alkalosis

HCO3 > 24

Respiratory alkalosis

PCO2 < 40

Respiratory Acidosis

PCO2 > 40

Step 3) Interpreting Compensation - Metabolic Acidosis

• Winter’s formula

  • The calculated pCO2 should be within 2 points of actual pCO2

  • If pCO2 is HIGHER than calculated: respiratory acidosis is present

    • > 2 = respiratory acidosis (high CO2 high acid)

  • If pCO2 is LOWER than calculated: respiratory alkalosis is present

    • < 2 = respiratory alkalosis (LOW CO2, low acid, basic pH)

Metabolic Alkalosis Problem to Interpret Compensation

Worked example

A patient has:

• pH = 7.50

• HCO3- = 36 mEq/L

• Actual pCO2 = 48 mmHg

Step 1: Calculate how much bicarbonate increased.

36-24=12mEq/L

Step 2: Estimate the expected increase in CO₂.

0.4(12)=4.8

0.6(12)=7.2

So CO₂ should increase by approximately 4.8–7.2 mmHg.

Step 3: Add the increase to normal CO₂.

40+4.8=44.8

40+7.2=47.2

Expected pCO2 is approximately 45–47 mmHg using your slide's rule.

Step 4: Compare with the actual CO₂ of 48 mmHg.

Step 3) Interpreting Compensation Respiratory Acidosis 

• ACUTE respiratory acidosis: HCO3 increase by 0.1 times the change in PaCO2

• CHRONIC: HCO3 increases by 0.4 times the change in PaCO2

Step 3) Interpreting Compensation Respiratory Alkalosis 

• ACUTE: HCO3 decreases by 0.2 times the change in PaCO2

• CHRONIC: HCO3 decreases by 0.4 times the change in PaCO2 

ACUTE Respiratory Acidosis compensation problem

Step 1: Identify the disorder.

• pH 7.25 = acidosis.

• PaCO₂ 60 = elevated CO₂ causing the acidosis.

This is respiratory acidosis.

Step 2: Calculate expected compensation.

PaCO₂ increased from 40 to 60, a change of 20 mmHg.

In acute respiratory acidosis, HCO₃⁻ increases by approximately 1 mEq/L per 10 mmHg increase in PaCO₂.

24+(12)=26

Expected HCO₃⁻ = 26 mEq/L.

Conclusion: The actual HCO₃⁻ is 26, matching the expected acute compensation.

CHRONIC Respiratory Acidosis Compensation Problem

Step 1: Identify the disorder.

• pH 7.35 = at the lower limit of normal.

• PaCO₂ 60 = elevated CO₂, indicating a respiratory acidifying process.

This is consistent with chronic respiratory acidosis.

Step 2: Calculate expected compensation.

In chronic respiratory acidosis, HCO₃⁻ increases by approximately 4 mEq/L per 10 mmHg increase in PaCO₂.

24+(42)=32

Expected HCO₃⁻ = 32 mEq/L.

Conclusion: The actual HCO₃⁻ is 32, matching the expected chronic compensation.

ACUTE Respiratory Alkalosis Compensation Problem 

Step 1: Identify the primary disorder.

• pH is high → alkalosis.

• PaCO₂ is low → respiratory alkalosis.

Step 2: Calculate expected compensation.

PaCO₂ decreased from 40 to 20, a decrease of 20 mmHg.

In acute respiratory alkalosis, HCO₃⁻ decreases by 2 mEq/L for every 10-mmHg decrease in PaCO₂.

24-(22)=20mEq/L

Conclusion: Acute respiratory alkalosis with appropriate compensation. The kidneys have had little time to respond, so bicarbonate decreases only slightly.

CHRONIC Respiratory Alkalosis Compensation Problem 

Step 1: Identify the primary disorder.

• pH is high → alkalosis.

• PaCO₂ is low → respiratory alkalosis.

Step 2: Calculate expected compensation.

PaCO₂ decreased by 20 mmHg.

In chronic respiratory alkalosis, HCO₃⁻ decreases by approximately 4–5 mEq/L for every 10-mmHg decrease in PaCO₂.

Using 4 mEq/L:

24-(42)=16mEq/L

Conclusion: Chronic respiratory alkalosis with appropriate compensation. The kidneys have had several days to excrete more bicarbonate, bringing the pH closer to normal.

Step 4) Is it an anion gap metabolic acidosis?

Anion Gap = Na - (HCO3 + Cl)

• Normal anion gap ~ 12

  • IF AG > 12: indicates an anion gap metabolic acidosis (AGMA)

  • IF AG ≤ 12: NORMAL anion gap metabolic acidosis (NAGMA)

    • H+ is accompanied by Cl-, therefore no increase in anion gap

Step 5) if AGMA is there another metabolic disturbance?

DETERMINE DELTA GAP

Delta = (AG -12) - (24 - HCO3)

If between -6 and 6 = ONLY AGMA

• If < -6: Combined AGMA and normal anion gap metabolic acidosis (NAGMA)

• If > 6: Combined with AGMA and metabolic alkalosis 

ACID BASE STEPS: summary dw

1. Assess pH 

   1. Acidosis (pH < 7.35)

   2. Alkalosis (pH > 7.45)

2. Determine primary process (respiratory or metabolic) ((pCO2 and HCO3))

3. Check for degree of compensation 

   1. Metabolic acidosis +/- winter’s formula 

   2. Metabolic alkalosis PaCO2 should increase by 0.4 to 0.6 times the change in HCO3

   3. Acute respiratory acidosis: HCO3 should increase by 0.1 times the change in PaCO2

   4. Chronic respiratory alkalosis: HCO3 should increase by 0.4 times the change in PaCO2 

   5. Acute resp. Alkalosis: HCO3 should decrease by 0.2 times the change in PaCO2

   6. Chronic res. Alkalosis HCO3 should decrease by 0.4 times the change in PaCO2

4. Is there AGMA?

   1. If AG > 12 = anion gap metabolic (AGMA is present)

5. If AGMA, calculate delta anion gap (AG - 12) - (24 - HCO3)

   1. Between -6 and 6 = only AGMA 

   2. If < -6 = combined AGMA with normal anion gap metabolic acidosis (NAGMA)

   3. If > 6 = combined AGMA and metabolic alkalosis 

Causes of Anion Gap Acidosis: 

A CAT MUDPILES

A - analgesics (NSAIDS, Acetaminophen)

C - cyanide, carbon monoxide 

A - arsenic, alcoholic ketoacidosis 

T - toluene 

M - methanol, Metformin

U - uremia

D - diabetic ketoacidosis 

P - paraldehyde, phenformin 

I - iron, isoniazid 

L - lactic acidosis 

E - ethylene glycol 

S - salicylates 

Causes of Lactic Acidosis:

• Shock (decreased tissue oxygenation)

• Drugs/toxins

  • Ethanol

  • Metformin 

  • NRTIs

  • Propylene glycol toxicity 

  • Propofol infusion syndrome 

  • Sodium nitroprusside 

Pathophysiology of Non-Anion Gap Acidosis…

→ loss of plasma HCO3- replaced by Cl- = AG remains normal

Causes of DECREASED HCO3-

• GI tract waste 

  • Diarrhea 

  • Pancreatic fistulas/biliary drainage 

• Renal loss of HCO3-

  • Proximal renal tubular acidosis 

• Impaired renal acid excretion 

  • Distal renal tubular acidosis

Causes of Proximal Renal Tubular Acidosis?

• Toxins (Pb, Cd, Hg, or outdated tetracyclines) 

• Carbonic anhydrase inhibitors (Acetazolamide)

Distal Renal Tubular Acidosis…Type 1 Causes:

• Amphotericin B

• Lithrium 

• Toulene 

• Vitamin D intoxication

Distal Renal Tubular Acidosis…Type 2 Causes:

• ACEi

• ARBs

• Spironolactone 

Treatment for Metabolic Alkalosis:

High pH (>7.45), high serum HCO3 (> 30) and compensatory increased PaCO2

• Increase HCO3

  • Infusion of acetate, lactate, or citrate 

  • Administration of HCO3

• Excessive H+ losses 

  • GI loss of H+ via vomiting/NG suctioning 

  • Renal loss of H+