
Lactic Acidosis
Types of Lactic acidosis | Notes |
Type A | ⢠Hypoperfusion / hypoxia Examples ⢠Shock ⢠Cardiac failure ⢠Severe anemia ⢠Carbon monoxide toxicity ⢠Cyanide toxicity |
Type B | ⢠metabolic causes with normal oxygenation Examples ⢠Malignancy ⢠Renal failure ⢠Hepatic failure ⢠Drugs: metformin, ethanol, ethylene glycol, methanol ⢠Diabetes mellitus ⢠Seizures ⢠Severe malaria / cholera |



- Ureterosigmoid anastomosis
- Obsolete due to increased cancer risk, recurrent UTI,
- Hyperchloremic hypokalemia metabolic acidosis (normal anion gap)
- CF
- Predisposed to Hyponatremic hypochloremic metabolic alkalosis.
- â in sweat Clâť test.
- Pyloric Stenosis
- Hypokalemic metabolic alkalosis with paradoxical aciduria.
Renal Tubular Acidosis (RTA)

Type | Defect | Urine pH & Ca & Nephrolithiasis | Serum Kâş | Associations |
Type 1 | Impaired Hâş secretion distal tubule â Îą Intercalated disc of CD (NOT DCT) More Urinary pH | > 5.5 | â | Autoimmune diseases (Sjogrone â 1, RA) Amphotericin B, Analgesic nephropathy |
Type 2 | Impaired HCOââť reabsorption in proximal tubule in PCT Both low | < 5.5 | â | Fanconi syndrome, Multiple myeloma, Carbonic anhydrase inhibitors Wilsons disease Ifosfomide Tenofovir Lead poisoning |
Type 4 | Aldosterone deficiency/ resistance impaired NHââş excretion Four More â More Potassium | < 5.5 | âââ | Diabetic nephropathy, Addisonâs, ACEi/ARB, Kâş-sparing diuretics |
NOTE: Different Fanconis
ă
¤ | ă
¤ |
Fanconi disease/syndrome | ⢠Proximal tubular reabsorption problem â Type 2 RTA ⢠Glycosuria, aminoaciduria |
Fanconi anemia (Not syndrome) | ⢠Pancytopenia + radial ray |
Fanconi Bickel syndrome | ⢠Mutation in GLUT-2  ⢠Bickel â Bi â 2 (GLUT 2) Defect in glucose sensing â â insulin release ⢠Postprandial Hyperglycemia. ⢠Fasting Hypoglycemia ⢠Glycogen accumulation disorder |


Holt - Oram (ASD + Radial Ray)
TAR (thrombocytopenia + absent radius)
Congenital torticollis â Cock robin position
Stranger things characters
- Dustin (Cleido cranial dysplasia)
- Robin (Cock robin position)
- Ray (Radial Ray) Hopper (Holt Oram ASD)
BLOOD GAS ABNORMALITY

ANS
Â
Anion Gap Correction in Hypoalbuminemia
- Normal AG: 10 mmol/L (with albumin 4.5 g/dL)
- Correction:
- For every â 1 g/dL albumin below 4.5 â add 2.5 mmol/L to AG
- Example: Albumin 2.5 g/dL (â2 g/dL), AG = 15
- Correction = 2 Ă 2.5 = 5
- Corrected AG = 15 + 5 = 20 mmol/L
All About ABG Interpretation
- MCQ Question: Identify the acid-base disorder in a patient with the given values.
- Blood pH: 7.2
- PO2: 90 mmHg
- pCO2: 80mmHg
- Plasma HCO3: 35mEq/L
- A. Respiratory acidosis,
- B. Respiratory alkalosis,
- C. Metabolic acidosis,
- D. Metabolic alkalosis.
ANS
A
Interpretation
- Normal ranges:
- Blood pH: 7.36-7.44.
- pCO2: 36-44 mmHg.
- HCO3: 21-27 mEq/L.
Formulae for Compensation

a. Metabolic disorders
- Metabolic acidosis
- Compensation: Reduce PCO2.
- Expected pCO2 = [ 1.5 x HCO3 ]+ 8 (Winters formula)
- Metabolic alkalosis
- Compensation: Increase PCO2.
- Expected pCO2 = [0.9 x HCO3 ] + 16
- Inference
- If actual pCO2 = expected pCO2,
- compensated.
- If actual pCO2 > expected pCO2
- uncompensated OR
- If actual pCO2 < expected pCO2
- hidden acid-base disorder.
- Important:
- Body never overcompensates.
b. Respiratory disorders

- Study the table
- Respiratory acidosis
- For every 10 mmHg rise in pCO2,
- HCO3 elevates by:
- Acute: 1 mEq/L.
- Chronic: 3.5 mEq/L.
- Respiratory alkalosis
- For every 10 mmHg decline in pCO2,
- HCO3 reduces by:
- Acute: 2 mEq/L.
- Chronic: 5 mEq/L.
MCQ Question:
- Interpret the ABG report
- Blood pH: 7.30
- pCO2: 29mmHg
- Plasma HCO3: 14 mEq/L
- Expected pCO2 = 1.5 x 14 + 8 = 29mmHg.
- Step 1: Acidosis (Low pH).
- Step 2: Primary metabolic disorder (low HCO3).
- Step 3: Compensation is present (actual pCO2 matches expected).
- Step 4: Calculate Anion gap for Metabolic acidosis.
Explanation:
Anion gap
- Interpret the ABG report with electrolytes
- Blood pH: 7.30
- pCO2: 29mmHg
- Plasma HCO3: 14 mEq/L
- Na+: 130mEq/L
- Cl-: 90mEq/L
- A. Compensated increased anion gap metabolic acidosis,
- B. Uncompensated increased anion gap metabolic acidosis,
- C. Compensated normal anion gap metabolic acidosis,
- D. Uncompensated normal anion gap metabolic acidosis.
ANS
Compensated increased anion gap metabolic acidosis
High Anion-Gap Metabolic Acidosis (MUD PILES) | Normal Anion-Gap Metabolic Acidosis (FUSED CAR) |
â Unmeasured anions | â Measured anions (specifically â Cl-) â Hyperchloremic metabolic acidosis |
Methanol | Fistula pancreatic |
Uremia (Renal failure - Acute or Chronic) | Ureterosigmoidostomy |
Diabetic ketoacidosis | Small bowel fistula |
Paraldehyde | Extra chloride (Hyperalimentation) |
Iron tablets, INH | Diarrhea |
Lactic acidosis | Carbonic anhydrase inhibitor (acetazolamide) |
Ethylene glycol | Addison's disease |
Salicylates | Renal tubular acidosis |
- Anion gap
- = Unmeasured anion - Unmeasured Cations
= [Na+] - [(Cl-) + (HCO3-)].
- Normal anion gap:
- 12 Âą 2 mEq/L.
- Reflects
- Laws of Electroneutrality.
- Unmeasured anions:
- Sulfate,
- Protein anions,
- Lactate,
- Salicylate.
- Metabolic acidosis is from:
- Increased utilization of HCO3
- Loss of HCO3.
1. Increased utilization of HCO3
- HAGMA
- Abnormal acids use up HCO3.
- Unmeasured anion (UMA) increases.
- Causes of increased anion gap (abnormal acids):
- Ketoacidosis
- DKA, Starvation
- Lactic acidosis.
- Uric acidosis.
- Alcohol poisoning
- Methanol,
- Ethanol,
- Ethylene glycol
- Kidney failure.
2. Loss of HCO3
- NAGMA.
- Loss is via GIT or kidney.
- GIT loss: Diarrhea.
- Renal loss: Renal tubular acidosis.
- Hyperchloremic Metabolic Acidosis.
- The body reclaims chloride anions to maintain balance.
MCQ Question:
- Interpret the ABG report (Final Calculation)
- Blood pH: 7.30,
- pCO2: 29mmHg,
- HCO3: 14 mEq/L,
- Na+: 130mEq/L,
- Cl-: 90mEq/L
- Anion gap = 130 - (90 + 14) = 26 mEq/L.
- 26 > 14, so it is an increased anion gap.
Explanation:
Question:
- Q. A 60-year-old diabetic patient with repeated vomiting following a recent dine-out. Her blood pressure was 90/60 mmHg
- pH: 7.3
- HCO3: 18mEq/L
- pCO2: 35mmHg
- Identify the acid-base disorder
- A. Metabolic Acidosis
- B. Metabolic Alkalosis
- C. Respiratory Alkalosis
- D. Respiratory Acidosis
- Vomiting causes metabolic alkalosis.
- pH indicates acidosis.
- A diabetic with stress can develop DKA (metabolic acidosis).
Explanation:
Question:
- Q. A 7-week-old baby was brought by the mother with complaints of repeated projectile vomiting and pellet stools. The probable metabolic disturbance is:
- A. Normal anion gap metabolic acidosis
- B. Hypochloremic hypokalemic metabolic alkalosis
- C. Hyperchloremic hypokalemic metabolic alkalosis
- D. Respiratory acidosis
- B. Hypochloremic hypokalemic metabolic alkalosis
ANS
Question:
- Q. The interpretation of the following ABG value is?
- pH-7.34
- Na-135meq/L
- Cl 93 meq/L
- HCO3 20meq/L
- C. Increased anion gap metabolic acidosis
- Anion gap = 135 - (93 + 20) = 21.
- This is a High anion gap.
Explanation:
Question:
- Q. The interpretation of the following ABG value is:
- pH: 7.5
- pCO2: 50mm Hg
- HCO3: 30meq/L
Answer:
B. Metabolic alkalosis + Respiratory Acidosis
Question:
- Q. A hyperventilating hysterical woman presents with carpopedal spasm. The cause is:
- A. High total calcium
- B. Low total calcium
- C. Alkalosis
- D. Acidosis
- Hyperventilation causes respiratory alkalosis (high pH).
- Plasma proteins become more negatively charged to buffer the pH.
- These proteins bind more calcium.
- Free calcium concentration is reduced.
- Neurons become hyperstimulated, causing carpopedal spasm.
Explanation:
Hypocalcemic tetany
- H+ and Ca2+ competitively bind to albumin.
- Mechanism:Â
- âH+ (e.g., in respiratory alkalosis) âÂ
- â Ca2+ binding to albumin â â free Ca2+Â
IMPORTANT NOTES
Limiting pH:
- pH at which PCT stops excretion of H+ = 4.5
- Never seen in PCT due to strict buffering.
- Seen in collecting duct, where urine is acidified.
Normal Values:
Parameter | Normal Range |
pH | 7.35 â 7.45 |
pCOâ | 35 â 45 mm Hg |
HCOââť | 22 â 26 mEq/L (Avg: 24) |