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What is metabolic acidosis
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"metabolic acidosis"[MeSH Terms]
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Here is a thorough explanation of metabolic acidosis based on authoritative medical textbooks:
Metabolic Acidosis
Definition
Metabolic acidosis is a primary acid-base disorder characterized by a decrease in serum bicarbonate (HCO3-), leading to a fall in blood pH below 7.35. It results from either:
- Excess accumulation of acid (H+) in the body
- Abnormal loss of bicarbonate
- Impaired renal excretion of acid
The primary determinant of serum pH is the balance between plasma HCO3- concentration and PaCO2. In metabolic acidosis, HCO3- falls, shifting this balance toward acidemia.
- Barash, Cullen, and Stoelting's Clinical Anesthesia, 9e, p. 4249
- Harrison's Principles of Internal Medicine 22E, p. block6
Classification by Anion Gap
The most important step in evaluating metabolic acidosis is calculating the anion gap (AG):
AG = Na+ - (Cl- + HCO3-)
Normal AG = approximately 10-12 mmol/L
This divides metabolic acidosis into two major categories:
1. High Anion Gap (Wide AG) Metabolic Acidosis
- AG > 13-15 mEq/L
- Caused by accumulation of unmeasured anions (e.g., lactate, ketones, toxins)
- Remembered by the mnemonic MUDPILES:
| Letter | Cause |
|---|---|
| M | Methanol |
| U | Uremia (advanced CKD) |
| D | Diabetic/alcoholic/starvation ketoacidosis |
| P | Paraldehyde / Propylene glycol |
| I | Isoniazid / Iron |
| L | Lactic acidosis (most common cause - ~50% of cases) |
| E | Ethylene glycol |
| S | Salicylates |
- ROSEN's Emergency Medicine, p. block22
- Barash, Clinical Anesthesia 9e, Table 16-4
2. Normal Anion Gap (Hyperchloremic) Metabolic Acidosis
- AG is normal; bicarbonate loss is offset by a rise in chloride
- Remembered by the mnemonic HARDUP:
| Cause | Example |
|---|---|
| H | Hyperalimentation |
| A | Acetazolamide (carbonic anhydrase inhibitors) |
| R | Renal tubular acidosis (RTA) |
| D | Diarrhea (GI bicarbonate loss - very common) |
| U | Ureteral diversion |
| P | Pancreatic fistula / saline infusion |
- ROSEN's Emergency Medicine, p. block22
Respiratory Compensation
The immediate physiologic response to metabolic acidosis is hyperventilation (Kussmaul respiration) - deep, rapid breathing that lowers PaCO2 and partially corrects the pH.
The expected PaCO2 can be predicted using Winter's Formula:
PaCO2 = (1.5 × HCO3-) + 8 ± 2 mmHg
- If the measured PaCO2 is higher than predicted - there is a concurrent respiratory acidosis
- If the measured PaCO2 is lower than predicted - there is a concurrent respiratory alkalosis
The PaCO2 cannot fall below 8-12 mmHg regardless of severity. The kidneys ultimately correct metabolic acidosis over hours to days by generating new HCO3- and excreting H+.
- Brenner and Rector's The Kidney, p. block9
- Harrison's Principles of Internal Medicine 22E, p. block6
Clinical Features
| Feature | Detail |
|---|---|
| Kussmaul breathing | Deep, rapid respirations (respiratory compensation) |
| Tachycardia | Sympathetic activation |
| Hypotension | Impaired cardiac contractility at low pH |
| Altered mental status | Cerebral acidosis |
| Tachypnea | Driven by low pH stimulating the respiratory center |
In restrained or severely agitated patients, metabolic acidosis from lactic acid buildup can progress to cardiovascular collapse and cardiac arrest. Clues include persistent tachycardia, tachypnea, and hyperpyrexia.
- Roberts and Hedges' Clinical Procedures in Emergency, p. block15
Diagnosis (Stepwise Approach)
- Obtain ABG and electrolytes simultaneously
- Confirm low HCO3- on both panels
- Calculate the anion gap (correct for albumin if hypoalbuminemic: for every 1 g/dL fall in albumin below 4.5, add 2.5 to the AG)
- Identify if it is a high-AG or normal-AG acidosis
- Apply Winter's formula to check for a concurrent respiratory disturbance
- Calculate the delta-delta ratio (ΔAG / ΔHCO3-) to detect mixed disorders:
- Ratio ~1-2: pure high-AG metabolic acidosis
- Ratio >2: concurrent metabolic alkalosis
- Ratio <1: concurrent normal-AG metabolic acidosis
- Harrison's Principles of Internal Medicine 22E, Table 58-3
Treatment
-
The primary goal is treating the underlying cause (e.g., insulin for DKA, fluids/vasopressors for lactic acidosis from septic shock)
-
In mechanically ventilated patients, maintain respiratory compensation by ensuring adequate minute ventilation
-
Sodium bicarbonate is generally reserved for severe cases (pH < 7.0-7.1); the BICAR-ICU trial showed no mortality benefit in less severe cases
-
Aggressively hydrate and sedate patients with agitation-induced metabolic acidosis
-
Barash, Clinical Anesthesia 9e, p. 4249
-
Roberts and Hedges' Clinical Procedures in Emergency, p. block15
Summary Table
| Feature | High-AG Acidosis | Normal-AG Acidosis |
|---|---|---|
| Anion gap | Elevated (>13-15) | Normal (10-12) |
| Chloride | Normal | Elevated |
| Common causes | Lactic acidosis, DKA, toxins, uremia | Diarrhea, RTA, saline infusion |
| Urine AG | Positive | Negative (diarrhea) or positive (RTA) |
No recent systematic reviews or meta-analyses (last 2 years) were found on this topic that would alter these established principles.
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