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Acidosis and Alkalosis

Chapter 58 | Part 2: Acid-Base Disorders

KEY CLINICAL POINTS

  • Acid-base disorders are classified by their primary disturbance (metabolic/respiratory) and compensatory mechanisms.
  • The Henderson-Hasselbalch equation and Winter's formula guide interpretation of arterial blood gas results.
  • Mixed acid-base disorders require evaluation of anion gap, delta values, and clinical context.
  • Treatment of metabolic acidosis depends on etiology (e.g., alkali for uremic acidosis, fluids for diarrhea).
  • Respiratory acidosis/alkalosis management focuses on addressing underlying lung disease or ventilatory support.

1. DEFINITION & OVERVIEW

Acidosis and alkalosis refer to disturbances in systemic acid-base balance. Acidosis is characterized by arterial pH <7.35, while alkalosis is pH >7.45. These disorders can be metabolic (due to HCO3 − changes) or respiratory (due to CO2 changes).

Table 58-1: Compensatory Responses to Simple Acid-Base Disturbances

DISORDER PREDICTION OF COMPENSATION RANGE OF VALUES
Metabolic Acidosis Paco = (1.5 × HCO3-) + 8 ± 2 Low Low Low
Metabolic Alkalosis Paco = [HCO3-] + 15 High High High
Respiratory Alkalosis HCO3- fl 0.2 mmol/L per mmHg fl Paco High Low Low
Respiratory Acidosis HCO3- › 0.4 mmol/L per mmHg › Paco Low High High

1.1 Normal Acid-Base Homeostasis

Systemic arterial pH is maintained between 7.35-7.45 by extracellular and intracellular buffering, respiratory regulation, and renal excretion of H+ and reabsorption of HCO3 − . CO2 levels are regulated by the central nervous system and respiratory system.

1.2 Henderson-Hasselbalch Equation

pH = pK ′ + log([HCO3 − ]/(0.03 × PaCO2)). This equation relates pH to bicarbonate and CO2 levels, with pK ′ = 6.1 for CO2.

2. EPIDEMIOLOGY

Metabolic acidosis is common in critical illness, diabetes, and renal failure. Respiratory acidosis is prevalent in COPD and neuromuscular disorders. Respiratory alkalosis is often seen in sepsis, anxiety, and pregnancy.

2.1 Risk Factors

Vitamin D deficiency, chronic kidney disease, diuretic use, and gastrointestinal losses (e.g., diarrhea) increase risk. Alcoholism and malnutrition contribute to metabolic alkalosis.

3. ETIOLOGY & PATHOPHYSIOLOGY

Metabolic acidosis arises from excess acid production (e.g., lactic acidosis), bicarbonate loss (e.g., diarrhea), or impaired renal acid excretion (e.g., RTA). Respiratory acidosis results from CO2 retention due to lung disease or ventilatory failure. Respiratory alkalosis is caused by hyperventilation from anxiety, sepsis, or CNS stimulation.

Table 58-4: Causes of High-Anion Gap Metabolic Acidosis

CAUSE
Lactic Acidosis
Ketoacidosis (Diabetic, Alcoholic)
Toxins (Ethylene Glycol, Methanol, Salicylates)
Pyroglutamic Acid (Acetaminophen Toxicity)
Kidney Failure (Acute/Chronic)

3.1 High-Anion Gap Acidosis

Caused by accumulation of unmeasured anions (e.g., ketoacids, lactic acid, salicylates). Common in DKA, alcoholic ketoacidosis, and toxin ingestion.

3.2 Non-Anion Gap Acidosis

Due to chloride retention and bicarbonate loss (e.g., diarrhea, renal tubular acidosis). Often associated with hyperchloremia.

4. CLINICAL FEATURES

Metabolic acidosis presents with fatigue, confusion, and Kussmaul breathing. Respiratory acidosis causes lethargy, confusion, and respiratory distress. Respiratory alkalosis may manifest as paresthesias, tetany, and hypokalemia.

4.1 Complications

Severe acidosis can cause arrhythmias, encephalopathy, and multiorgan failure. Respiratory alkalosis may lead to cerebral vasospasm and hypocalcemia.

5. DIFFERENTIAL DIAGNOSIS

Distinguish between metabolic and respiratory causes. Consider mixed disorders (e.g., metabolic acidosis + respiratory alkalosis). Evaluate for underlying conditions like renal failure, sepsis, or drug toxicity.

5.1 Key Differentiators

Anion gap, urine anion gap, and chloride levels help differentiate between acid-base types. Hyperchloremic acidosis vs. uremic acidosis require distinct management approaches.

6. INVESTIGATIONS & DIAGNOSIS

Arterial blood gas analysis is essential. Measure serum electrolytes, BUN, creatinine, and anion gap. Urine electrolytes and chloride levels help identify renal tubular acidosis.

Table 58-3: Steps in Accurate Diagnosis of Acid-Base Disorders

STEP ACTION
1 Obtain arterial blood gas (ABG) and venous electrolytes simultaneously
2 Compare calculated [HCO3-] on ABG with measured value
3 Assess anion gap (correct for albumin)
4 Identify known causes of high-AG or non-AG acidosis
5 Estimate predicted compensatory response

6.1 Diagnostic Algorithm

  1. Obtain ABG and venous electrolytes simultaneously. 2. Calculate anion gap. 3. Assess for hyperchloremia or hypokalemia. 4. Evaluate for renal or gastrointestinal losses.

7. MANAGEMENT & TREATMENT

Acute metabolic acidosis requires alkali (NaHCO3) for severe acidemia. Chronic cases use oral bicarbonate. Respiratory acidosis is managed with ventilatory support. Respiratory alkalosis often resolves with addressing underlying causes.

Table 53-5: Causes of Non-Anion Gap Acidosis

CATEGORY CAUSES
Gastrointestinal Loss Diarrhea, Vomiting, Pancreatic Fistula
Renal Causes Thiazide/Loop Diuretics, RTA, Hyperkalemia
Drug-Induced Trimethoprim, NSAIDs, ACE-Is/ARBs
Other Hypercalcemia, Hypoparathyroidism, Diuretic Abuse

7.1 Specific Treatments

Fomepizole for ethylene glycol/methanol poisoning. Acetazolamide for Bartter’s/Gitelman’s syndrome. Potassium supplementation for hypokalemia.

7.2 Fluid Resuscitation

Isotonic saline for volume depletion. Avoid rapid infusion in renal failure. Monitor for hyperchloremia and hypernatremia.

8. PROGNOSIS & COMPLICATIONS

Chronic acidosis worsens renal function and increases mortality. Severe respiratory acidosis can lead to respiratory failure and cardiac arrhythmias. Alkalosis may cause hypocalcemia, seizures, and cerebral vasospasm.

8.1 Long-Term Outcomes

Metabolic acidosis in CKD correlates with faster disease progression. Respiratory alkalosis in ICU patients may indicate poor prognosis if uncorrected.

9. SPECIAL CONSIDERATIONS

Pregnancy: Monitor for gestational hypertension and eclampsia. Pediatrics: Watch for respiratory alkalosis in infants. Elderly: Higher risk of drug-induced alkalosis from diuretics.

9.1 Renal Failure

Uremic acidosis requires alkali therapy. Avoid overcorrection to prevent metabolic alkalosis.

10. KEY POINTS & CLINICAL PEARLS

  1. Use the anion gap to differentiate acidosis types. 2. Correct hyperkalemia before alkali therapy. 3. Monitor for drug interactions (e.g., NSAIDs with diuretics). 4. Avoid rapid NaHCO3 infusion in renal failure. 5. Use fomepizole for ethylene glycol/methanol poisoning.