2 Acid–Base Disorders and Compensation

ABG essentials and core patterns

An arterial blood gas (ABG) helps assess acid–base status and oxygenation. Common adult reference ranges are pH $7.35$–$7.45$, PaCO₂ $35$–$45$ mm Hg, and HCO₃⁻ $22$–$26$ mEq/L, although ranges can vary by laboratory. Interpret results alongside the patient’s condition, electrolytes, and laboratory reference ranges, not in isolation.

PaCO₂ represents the respiratory component, while bicarbonate represents the metabolic component. ABG bicarbonate is generally calculated from pH and PaCO₂. Acidemia means blood pH is below $7.35$; alkalemia means it is above $7.45$. Acidosis and alkalosis describe processes that tend to lower or raise pH, respectively, so a patient may have an acid–base disorder even when pH is within its reference range.

In a primary respiratory disorder, pH and PaCO₂ move in opposite directions. In a primary metabolic disorder, pH and HCO₃⁻ move in the same direction.

A systematic interpretation method

Use a consistent sequence to interpret results:

1. Assess pH and classify it as acidemia, alkalemia, or within the reference range.

2. Identify which primary change fits the pH: PaCO₂ for a respiratory process or HCO₃⁻ for a metabolic process.

3. Check whether compensation is appropriate for the disorder and its duration. Compensation moves pH toward normal, but does not by itself explain a value outside the expected range.

4. If metabolic acidosis is present, calculate the anion gap:

A high gap may indicate unmeasured acids; consider albumin when interpreting the gap.
5. Compare the results with the clinical picture. Unexpected compensation or markedly abnormal PaCO₂ and HCO₃⁻ that do not fit one simple process suggest a mixed disorder.

The four primary disorders

Respiratory disorders

Respiratory acidosis has low pH and high PaCO₂; HCO₃⁻ rises with compensation. Causes include hypoventilation from airway or lung disease, central nervous system (CNS)-depressing drugs, impaired respiratory muscles, or chest-wall restriction. Manifestations may reflect the cause and include dyspnea, wheezing, headache, confusion, or reduced alertness. Severe hypercapnia can cause neurologic deterioration.

Respiratory alkalosis has high pH and low PaCO₂; HCO₃⁻ falls with compensation. It can result from hyperventilation associated with hypoxemia, pulmonary disease including pulmonary embolism, fever, pain, sepsis, pregnancy, or anxiety. Acute hypocapnia may cause light-headedness, confusion, tingling around the mouth or in the limbs, cramps, or carpopedal spasm. Do not automatically attribute respiratory alkalosis to anxiety; assess for serious causes such as hypoxemia, sepsis, and pulmonary embolism.

Metabolic disorders

Metabolic acidosis has low pH and low HCO₃⁻; PaCO₂ falls with respiratory compensation. Causes include acid accumulation, such as ketoacidosis or lactic acidosis, reduced renal acid excretion, toxins, or bicarbonate loss from the gastrointestinal (GI) tract or kidneys. Findings depend on the cause. Severe acidemia may cause nausea, vomiting, malaise, deep breathing, hypotension, arrhythmias, or altered mental status.

Metabolic alkalosis has high pH and high HCO₃⁻; PaCO₂ rises with respiratory compensation. Causes include vomiting or gastric suction, diuretics, volume or chloride depletion, hypokalemia, or excess alkali. Severe alkalemia may cause headache, lethargy, weakness, tingling, muscle cramps, tetany, seizures, or arrhythmias.

Causes and clinical effects vary with severity, speed of onset, and underlying illness.

Expected compensation

Expected compensation is estimated using reference values PaCO₂ $40$ mm Hg and HCO₃⁻ $24$ mEq/L. These bedside rules of thumb estimate the expected response; small differences may reflect rounding or clinical context. An observed value outside the expected range raises concern for another primary disorder.

• Metabolic acidosis: Winter’s formula predicts expected PaCO₂:

  $$\text{Expected PaCO₂} = (1.5 \times \mathrm{HCO_3^-}) + 8 \pm 2\ \text{mm Hg}$$

• Metabolic alkalosis: PaCO₂ rises about $0.6$–$0.75$ mm Hg for each $1$ mEq/L rise in HCO₃⁻ above $24$ mEq/L. Compensation usually does not raise PaCO₂ above about $55$ mm Hg.

• Acute respiratory acidosis: HCO₃⁻ rises about $1$–$2$ mEq/L for each $10$ mm Hg rise in PaCO₂ above $40$ mm Hg.

• Chronic respiratory acidosis: HCO₃⁻ rises about $3$–$4$ mEq/L for each $10$ mm Hg rise in PaCO₂ above $40$ mm Hg. Renal compensation develops over days.

• Acute respiratory alkalosis: HCO₃⁻ falls about $1$–$2$ mEq/L for each $10$ mm Hg fall in PaCO₂ below $40$ mm Hg.

• Chronic respiratory alkalosis: HCO₃⁻ falls about $4$–$5$ mEq/L for each $10$ mm Hg fall in PaCO₂ below $40$ mm Hg. Renal compensation develops over days.

For example, when HCO₃⁻ is $12$ mEq/L, Winter’s formula gives expected PaCO₂ of $(1.5 \times 12) + 8 = 26 \pm 2$ mm Hg. A measured PaCO₂ of $25$ mm Hg is within the expected range. A substantially higher value suggests additional respiratory acidosis; a substantially lower value suggests additional respiratory alkalosis.

Metabolic disorders are compensated mainly by changes in ventilation. Respiratory disorders are compensated mainly by the kidneys, and chronic respiratory compensation takes days.

Recognizing mixed disorders

A mixed disorder means that two or more primary acid–base processes are present. Do not label a change as compensation if it exceeds the expected response. For example, metabolic acidosis should lower PaCO₂ only to the range predicted by Winter’s formula; a PaCO₂ well below that range indicates an additional respiratory alkalosis.

Two processes can move pH in opposite directions and produce a near-normal pH, masking the severity of the underlying abnormalities. Useful clues include:

• PaCO₂ higher than Winter’s predicted range in metabolic acidosis suggests metabolic acidosis plus respiratory acidosis.

• PaCO₂ lower than Winter’s predicted range in metabolic acidosis suggests metabolic acidosis plus respiratory alkalosis.

• An HCO₃⁻ change greater than expected for an acute respiratory disorder suggests considering a second metabolic process or a chronic respiratory disorder.

• Near-normal pH with abnormal PaCO₂ and HCO₃⁻ calls for checking the direction of change and expected compensation; opposing primary disorders may be present.

• In high-anion-gap metabolic acidosis, comparing the rise in anion gap with the fall in HCO₃⁻ can reveal an additional metabolic process.

Nursing assessment and interventions

Nursing care supports rapid recognition, patient safety, and treatment of the underlying cause. Follow local protocols and prescribed orders; interventions depend on the patient’s condition.

• Assess first: Evaluate airway, respiratory effort and rate, oxygenation, circulation, mental status, vital signs, and relevant history, including vomiting, diarrhea, medications, diabetes, lung disease, or possible toxin exposure. Escalate promptly for respiratory distress, worsening consciousness, hemodynamic instability, or a critically abnormal ABG.

• Trend and communicate: Review ABGs alongside electrolytes, renal function, glucose, lactate, and other relevant results. Note oxygen delivery and ventilator settings when applicable. Report changes and communicate the suspected disorder and clinical findings to the care team.

• Support breathing and oxygenation as indicated: Position the patient, maintain prescribed oxygen or ventilatory support, monitor response, and collaborate with respiratory therapy. Do not independently change ventilator settings or rapidly alter a chronic CO₂ level.

• Address the cause under the care plan: Examples include supporting evaluation of hypoventilation or infection, monitoring for GI fluid losses, and administering prescribed fluids or electrolyte replacement. Treatment is cause-specific; bicarbonate and other corrective therapies require clinical assessment and orders.

• Use safety precautions: Monitor for arrhythmias, weakness, seizures, or neuromuscular irritability when indicated. Do not use paper-bag rebreathing for suspected hyperventilation; it can worsen hypoxia or interfere with compensation for an unrecognized metabolic acidosis.

Worked interpretation examples

Metabolic acidosis with expected compensation

For pH $7.29$, PaCO₂ $25$ mm Hg, and HCO₃⁻ $12$ mEq/L, the primary disorder is metabolic acidosis: pH and HCO₃⁻ are low. Winter’s formula predicts PaCO₂ of $(1.5 \times 12) + 8 \pm 2 = 26 \pm 2$ mm Hg. The measured PaCO₂ of $25$ mm Hg is within range, indicating appropriate respiratory compensation.

Acute respiratory acidosis

After hypoventilation following a CNS-depressing medication, an ABG shows pH $7.27$, PaCO₂ $60$ mm Hg, and HCO₃⁻ $26$ mEq/L. The high PaCO₂ explains the acidemia. PaCO₂ is $20$ mm Hg above $40$; an acute rise predicts an HCO₃⁻ increase of about $2$ mEq/L from $24$ to approximately $26$ mEq/L, consistent with expected early compensation. Assess ventilation and escalate care according to patient status and protocol.

Metabolic acidosis plus respiratory alkalosis

For pH $7.46$, PaCO₂ $20$ mm Hg, and HCO₃⁻ $14$ mEq/L, low HCO₃⁻ indicates metabolic acidosis. Winter’s formula predicts PaCO₂ of $(1.5 \times 14) + 8 \pm 2 = 29 \pm 2$ mm Hg. The measured PaCO₂ of $20$ mm Hg is lower than expected, indicating a second primary process, respiratory alkalosis. The low PaCO₂ explains why pH is alkalemic despite low bicarbonate.

Metabolic alkalosis with expected compensation

For pH $7.49$, PaCO₂ $49$ mm Hg, and HCO₃⁻ $36$ mEq/L, elevated pH and HCO₃⁻ indicate metabolic alkalosis. HCO₃⁻ is $12$ mEq/L above $24$; expected PaCO₂ rises roughly $0.6$–$0.75 \times 12$, giving about $47$–$49$ mm Hg. The measured PaCO₂ of $49$ mm Hg is consistent with that estimate.

Near-normal pH with a mixed disorder

For pH $7.40$, PaCO₂ $20$ mm Hg, and HCO₃⁻ $12$ mEq/L, low HCO₃⁻ is consistent with metabolic acidosis. Winter’s formula predicts PaCO₂ of $26 \pm 2$ mm Hg, but the measured value of $20$ mm Hg is lower than expected, showing an additional respiratory alkalosis. The opposing processes bring pH into the reference range; a normal pH does not rule out a serious mixed disorder.