Guide — Acid-Base
Metabolic Acidosis vs Alkalosis
Metabolic acid-base disorders originate in the kidneys and bicarbonate buffering system. Understanding the causes, ABG patterns, and clinical findings for each disorder is essential for NCLEX and bedside practice.
9 min read · Acid-Base
Educational use only. Metabolic acid-base disorders require clinical assessment, provider notification, and treatment per facility protocol. This guide supports learning and NCLEX preparation. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
Overview
Metabolic acid-base disorders are driven by changes in bicarbonate (HCO₃¹) — the primary metabolic buffer. They are distinguished from respiratory disorders by which component is the primary driver of the pH change:
- Metabolic acidosis: HCO₃¹ depleted or acid excess → pH falls below 7.35
- Metabolic alkalosis: HCO₃¹ excess or acid loss → pH rises above 7.45
The lungs compensate for metabolic disorders by adjusting ventilation — the respiratory response begins within minutes to hours, unlike the slower renal compensation for respiratory disorders.
ABG Findings at a Glance
| Parameter | Metabolic Acidosis | Metabolic Alkalosis |
|---|---|---|
| pH | < 7.35 (Low) | > 7.45 (High) |
| HCO₃¹ | < 22 mEq/L (Low) | > 26 mEq/L (High) |
| PaCO₂ (compensatory) | < 35 mmHg (lungs compensate by blowing off CO₂) | > 45 mmHg (lungs compensate by retaining CO₂) |
PaCO₂ values shown reflect compensated states. In uncompensated disorders, PaCO₂ remains within normal range.
Metabolic Acidosis
Causes
Acid excess (increased acid load):
- Diabetic ketoacidosis (DKA) — ketoacid accumulation
- Lactic acidosis — shock, sepsis, hypoxemia, liver failure
- Renal failure — inability to excrete H⁺ ions
- Ingestions — aspirin (salicylate), methanol, ethylene glycol
- Starvation ketoacidosis
Bicarbonate loss:
- Severe diarrhea — loss of HCO₃¹-rich intestinal fluid
- Renal tubular acidosis (RTA) — impaired HCO₃¹ reabsorption
- Small bowel fistulas
Clinical Manifestations
- Kussmaul respirations: Deep, rapid breathing — the lung's attempt to blow off CO₂ and raise pH
- Headache, confusion, lethargy, coma (severe)
- Nausea, vomiting, abdominal pain (especially in DKA)
- Hypotension and arrhythmias (severe acidosis impairs cardiac function)
- Hyperkalemia — acidosis causes K⁺ to shift out of cells
- Fruity breath odor in DKA (from ketones)
Nursing Priorities
- Identify and treat the underlying cause — DKA management vs sepsis-driven lactic acidosis vs diarrhea require different interventions
- Monitor potassium closely — hyperkalemia may accompany severe acidosis and can cause life-threatening arrhythmias
- Administer sodium bicarbonate per provider order (typically reserved for pH < 7.10 or severe hyperkalemia)
- Continuous cardiac monitoring for dysrhythmias
- Assess level of consciousness — neurological deterioration suggests worsening acidosis
- Monitor respiratory effort — patient may fatigue if relying heavily on Kussmaul respirations for compensation
Metabolic Alkalosis
Causes
Acid loss:
- Vomiting or NG suction — loss of HCl from the stomach
- Diuretic use (loop diuretics, thiazides) — urinary H⁺ and K⁺ loss
Bicarbonate excess:
- Excessive antacid ingestion (milk-alkali syndrome)
- Excessive sodium bicarbonate administration
- Hyperaldosteronism — aldosterone promotes H⁺ and K⁺ excretion with HCO₃¹ retention
- Corticosteroid excess
Clinical Manifestations
- Hypoventilation: Shallow, slow breathing — the lung retains CO₂ to compensate (opposite of acidosis)
- Muscle cramps, weakness, tetany — hypocalcemia effect of alkalosis (alkalosis reduces ionized calcium)
- Positive Trousseau's and Chvostek's signs (from reduced ionized calcium)
- Nausea, vomiting, confusion, irritability
- Hypokalemia — alkalosis causes K⁺ to shift into cells; often co-present with vomiting or diuretic use
- Cardiac arrhythmias — risk increases with concurrent hypokalemia
Nursing Priorities
- Identify and treat the underlying cause — stop vomiting trigger, hold diuretics, reassess medications
- Monitor and replace potassium — hypokalemia and alkalosis are frequently co-present and mutually perpetuating
- Monitor chloride — hypokalemic metabolic alkalosis is often chloride-responsive; IV normal saline corrects chloride depletion
- Assess for neuromuscular excitability (tetany, spasms) — treat as calcium deficit even if total calcium is normal
- Continuous cardiac monitoring if significant hypokalemia is present
- Monitor respiratory status — compensatory hypoventilation may worsen oxygenation
NCLEX Pearls
- Metabolic acidosis and hyperkalemia frequently co-occur — acidosis drives K⁺ out of cells, raising serum K⁺
- Metabolic alkalosis and hypokalemia frequently co-occur — both caused by vomiting and loop diuretics, and alkalosis drives K⁺ into cells
- Kussmaul respirations = deep and rapid = metabolic acidosis compensation (think of the body “blowing off” acid)
- Vomiting causes metabolic alkalosis (HCl loss); diarrhea causes metabolic acidosis (HCO₃¹ loss)
- DKA is the highest-yield metabolic acidosis cause on NCLEX — recognize the triad: hyperglycemia, ketones, metabolic acidosis
- Alkalosis increases neuromuscular irritability by reducing ionized calcium — tetany, Trousseau's, and Chvostek's signs can appear even with normal total calcium
Related Resources
Standards & sources
Fact-checked Jun 21, 2026This page is written to align with American Association for Respiratory Care (AARC) · Standard clinical chemistry / ABG references. It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →