5 Acid-Base Balance

How the Body Regulates pH

Blood pH reflects hydrogen-ion concentration and is normally kept within a narrow arterial range, usually $7.35\text{–}7.45$. Three mechanisms work together:

• Chemical buffers, especially bicarbonate, hemoglobin, and proteins, bind or release hydrogen ions rapidly.

• The lungs adjust carbon dioxide through ventilation. Increased ventilation lowers $\mathrm{PaCO_2}$ and tends to raise pH; decreased ventilation raises $\mathrm{PaCO_2}$ and tends to lower pH.

• The kidneys conserve or generate bicarbonate and excrete hydrogen ions. Renal regulation is slower, developing over hours to days.

Keep processes distinct from measured states. Acidosis and alkalosis are processes that tend to lower or raise pH. Acidemia means measured pH below $7.35$, while alkalemia means measured pH above $7.45$. A pH within the reference range does not rule out an acid-base disorder: compensation or opposing disorders can bring the measured pH into range.

Takeaway: Buffers act rapidly, the lungs respond through ventilation, and the kidneys provide slower regulation.

Blood Gas Measurements

An arterial blood gas (ABG) commonly includes pH, carbon dioxide pressure, and oxygen pressure; bicarbonate reported on the ABG is generally calculated. Compare it with serum chemistry bicarbonate, often reported as total carbon dioxide. If the values materially disagree, verify the results and consult the care team.

Typical adult arterial values are approximate; use the laboratory’s reference ranges and clinical context:

• pH: $7.35\text{–}7.45$, the overall acid-base state.

• $\mathrm{PaCO_2}$: $35\text{–}45$ mm Hg, the respiratory component and an indicator of ventilation.

• $\mathrm{HCO_3^-}$: $22\text{–}26$ mEq/L, the metabolic and renal component.

• $\mathrm{PaO_2}$: about $75\text{–}100$ mm Hg, an indicator of arterial oxygenation that varies with age and oxygen support.

Interpret oxygenation in light of inspired oxygen concentration or the delivery device. A blood gas helps identify the direction and severity of a disturbance, but does not by itself establish its cause.

A Systematic Interpretation

Use a consistent sequence so that each result helps answer a specific question:

1. Check pH. Below $7.35$ indicates acidemia; above $7.45$ indicates alkalemia. A value within range can still reflect compensation or a mixed disorder.

2. Identify the primary change. With acidemia, low $\mathrm{HCO_3^-}$ points toward Metabolic acidosis, while high $\mathrm{PaCO_2}$ points toward Respiratory acidosis. With alkalemia, high $\mathrm{HCO_3^-}$ points toward Metabolic alkalosis, while low $\mathrm{PaCO_2}$ points toward Respiratory alkalosis.

3. Check the direction of the values. In a primary metabolic disorder, $\mathrm{PaCO_2}$ and $\mathrm{HCO_3^-}$ usually move in the same direction. In a primary respiratory disorder, they usually move in opposite directions.

4. Assess Compensation. Compensation moves pH toward normal, but an unexpected value may point to an additional primary disorder.

5. If metabolic acidosis is present, calculate the Anion gap and consider whether more than one disorder is present.

6. Relate the pattern to the person’s condition. Consider breathing, circulation, mental status, history, medications, electrolytes, and trends.

Takeaway: Read pH first, identify the primary component, test compensation, then connect the pattern to the clinical picture.

The Four Primary Disorders

The four primary disorders are identified by which component changes first. Their causes are clues to investigate, not diagnostic lists; multiple causes or disorders can coexist.

• Metabolic acidosis: $\mathrm{HCO_3^-}$ decreases. Possible causes include diarrhea or other bicarbonate loss, kidney dysfunction, lactic acidosis, ketoacidosis, and selected toxins. Assess perfusion, breathing pattern, renal function, electrolytes, and glucose or ketones when indicated. Deep, rapid breathing may be compensatory.

• Metabolic alkalosis: $\mathrm{HCO_3^-}$ increases. Possible causes include vomiting, gastric suction, diuretic use, and mineralocorticoid effects. Assess volume status, losses, medications, potassium, and chloride; hypoventilation may occur as compensation.

• Respiratory acidosis: $\mathrm{PaCO_2}$ increases. Possible causes include respiratory failure, airway obstruction, reduced respiratory drive, or neuromuscular weakness. Assess respiratory effort, airway, oxygenation, mental status, and sedating medications; consider whether carbon dioxide retention is acute or chronic.

• Respiratory alkalosis: $\mathrm{PaCO_2}$ decreases. Possible causes include increased ventilation related to pain, anxiety, fever, hypoxemia, pregnancy, or other illness. Investigate the cause rather than assuming anxiety before considering potentially serious explanations.

A single pattern may have more than one contributor, so interpret likely causes alongside the person’s presentation and other results.

Compensation and the Anion Gap

Compensation estimates help determine whether a secondary response is within an expected range. They are clinical estimates, not substitutes for laboratory ranges or clinical judgment.

• For Metabolic acidosis, Winter’s formula estimates expected carbon dioxide pressure:

  $$\mathrm{Expected\ PaCO_2} \approx (1.5 \times \mathrm{HCO_3^-}) + 8 \;\pm 2\text{ mm Hg}$$

  A measured value above the expected range suggests concurrent respiratory acidosis; a value below it suggests concurrent respiratory alkalosis.

• For Metabolic alkalosis, expected $\mathrm{PaCO_2}$ rises by about $0.7$ mm Hg for each $1$ mEq/L increase in $\mathrm{HCO_3^-}$ above $24$. This relationship is approximate.

• For Respiratory acidosis, $\mathrm{HCO_3^-}$ rises by about $1$ mEq/L per $10$-mm Hg rise in $\mathrm{PaCO_2}$ during an acute disturbance, and about $3\text{–}4$ mEq/L per $10$ mm Hg during a chronic disturbance.

• For Respiratory alkalosis, $\mathrm{HCO_3^-}$ falls by about $2$ mEq/L per $10$-mm Hg decrease in $\mathrm{PaCO_2}$ acutely, and about $4\text{–}5$ mEq/L per $10$ mm Hg chronically.

For metabolic acidosis, calculate the Anion gap using serum chemistry values:

Potassium is usually omitted. Interpret the result against the laboratory’s reference range; a commonly used traditional range without potassium is about $8\text{–}12$ mEq/L. A high gap suggests unmeasured acids, such as lactate or ketoacids, or acids associated with kidney failure or certain toxic ingestions. A low bicarbonate with a normal gap and higher chloride is consistent with normal-anion-gap, or hyperchloremic, metabolic acidosis. Low albumin can lower the measured gap and mask an elevated-gap acidosis.

Worked example: With sodium $140$, chloride $104$, and bicarbonate $12$ mEq/L:

This is elevated under the traditional range. Winter’s formula predicts $\mathrm{PaCO_2} = 26 \pm 2$ mm Hg; a measured value outside that range suggests an additional respiratory disorder.

Clinical Assessment and Response

Interpret the numbers alongside the person’s condition. Assess respiratory rate, depth and effort; oxygenation and oxygen delivery; circulation and perfusion; and level of consciousness. Consider relevant losses, illnesses, and medications. Review trends in blood gases, electrolytes, and renal function, and use lactate, glucose, or ketones when indicated.

Verify unexpected results and report critical or rapidly changing values according to local protocol. A blood gas is one part of assessment: it does not replace evaluation of the underlying cause or urgent escalation when the person is deteriorating.

Final takeaway: A reliable interpretation combines pH, the primary change, expected compensation, and—when metabolic acidosis is present—the anion gap, while remaining alert to mixed disorders and the patient’s clinical condition.