The body keeps arterial pH in a narrow range (7.35–7.45) because enzymes, the heart, and the brain work poorly outside it. Acid is produced constantly by metabolism, and three systems defend pH:

Four primary disorders

• Respiratory acidosis — hypoventilation → CO₂ retention (↑PaCO₂)
• Respiratory alkalosis — hyperventilation → CO₂ loss (↓PaCO₂)
• Metabolic acidosis — acid gain or bicarbonate loss (↓HCO₃⁻)
• Metabolic alkalosis — acid loss or bicarbonate gain (↑HCO₃⁻)

Compensation. The system not causing the problem tries to move pH back toward normal: the kidneys compensate for respiratory disorders (slowly, over days), and the lungs compensate for metabolic disorders (quickly, by changing rate and depth). Compensation almost never overshoots, so the pH still points to the primary problem.

Potassium shifts. In acidosis, hydrogen ions move into cells and potassium moves out → hyperkalemia. In alkalosis, potassium moves into cells → hypokalemia. Correcting acidosis (for example, with insulin or bicarbonate) drives potassium back into cells, so serum potassium can fall quickly.

Common causes

Mixed disorders are common: severe liver disease commonly causes respiratory alkalosis and can add a metabolic acidosis (lactate); salicylate toxicity is the classic mixed respiratory alkalosis plus metabolic acidosis.

In respiratory acidosis, look for the cause: decreased level of consciousness, use of accessory muscles, cyanosis, and a history of sedatives or lung disease.

Arterial blood gas (ABG) reference ranges

Step-by-step interpretation

1. pH — acidosis or alkalosis?
2. PaCO₂ — does it move in the direction that explains the pH (high with acidosis, low with alkalosis)? If yes → respiratory primary.
3. HCO₃⁻ — does it explain the pH (low with acidosis, high with alkalosis)? If yes → metabolic primary.
4. Compensation — is the other value moving in the opposite-pH direction?
   • Other value normal → uncompensated
   • Other value abnormal, pH still abnormal → partially compensated
   • Other value abnormal, pH back in the normal range → fully compensated (the pH side of 7.40 it sits on shows the primary disorder)
5. Mixed disorder — if both PaCO₂ and HCO₃⁻ move toward the pH abnormality (e.g., pH 7.10, PaCO₂ 60, HCO₃⁻ 18), there is a combined respiratory and metabolic acidosis

A quick memory aid is ROME: Respiratory Opposite (pH and PaCO₂ move in opposite directions), Metabolic Equal (pH and HCO₃⁻ move in the same direction).

Worked examples

Supporting tests

• Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻); about 8–12 mEq/L normally (varies by laboratory). High gap → added acid (ketones, lactate, toxins, uremia); normal gap → bicarbonate loss. Low albumin lowers the gap and can hide a high-gap acidosis (add about 2.5 for each 1 g/dL (10 g/L) of albumin below 4 g/dL).
• Expected PaCO₂ in metabolic acidosis (Winter's formula) ≈ 1.5 × HCO₃⁻ + 8 (± 2). A PaCO₂ higher than predicted suggests a second, respiratory problem.
• Electrolytes (potassium, chloride), glucose, ketones, lactate, BUN/creatinine, toxicology as indicated.

ABG collection: check collateral circulation (e.g., a modified Allen test where policy requires it) before radial puncture; note the oxygen setting; remove air bubbles; send promptly; apply firm pressure for at least 5 minutes (longer if the client takes anticoagulants).

The key principle is to treat the underlying cause; the ABG then corrects.

Respiratory acidosis

• Improve ventilation: open the airway, bronchodilators, treat infection, reverse opioids with naloxone (watch for recurrent sedation because naloxone can wear off first, and for acute withdrawal)
• Noninvasive ventilation (BiPAP) for acute hypercapnic failure; intubation if it fails or consciousness falls
• In chronic CO₂ retainers, give controlled oxygen to SpO₂ 88–92% — but never withhold oxygen from a hypoxemic client
• Avoid sedatives and opioids that depress breathing unless the client is monitored

Respiratory alkalosis

• Treat the cause: anxiety, pain, fever, hypoxemia, pulmonary embolism, sepsis
• Coach slow breathing; reassure; adjust ventilator rate or tidal volume as ordered
• Paper-bag rebreathing is not recommended — it can cause dangerous hypoxemia, and hyperventilation may be hiding a serious illness

Metabolic acidosis

• DKA: IV fluids first; check potassium before insulin — if K⁺ is below 3.5 mEq/L (mmol/L), replace potassium and delay insulin (see Diabetes Mellitus topic); then IV insulin with ongoing potassium replacement guided by levels. Bicarbonate is not routine; current consensus reserves it for pH < 7.0
• Lactic acidosis: restore perfusion (fluids, vasopressors, treat sepsis)
• Kidney failure: dialysis; oral bicarbonate for chronic acidosis
• Sodium bicarbonate cautions: hypokalemia (potassium shifts into cells), sodium and fluid overload, low ionized calcium, and tissue damage if it infiltrates. Monitor potassium closely during therapy
• Drug-related causes: metformin (lactic acidosis — risk with kidney failure, contrast, hypoxia), sevelamer hydrochloride (can lower bicarbonate), carbonic anhydrase inhibitors (acetazolamide)

Metabolic alkalosis

• Replace volume with 0.9% NaCl and replace potassium chloride; most cases are chloride-responsive
• Stop or reduce diuretics; give antiemetics; use proton pump inhibitors to reduce acid loss during prolonged nasogastric suction if ordered
• Irrigate nasogastric tubes with 0.9% NaCl, not water (water washes out electrolytes)

Listed in priority order.

1. Airway and breathing
   • Assess rate, depth, effort, SpO₂, and level of consciousness; position upright
   • Respiratory acidosis: encourage deep breathing and coughing, suction as needed, prepare BiPAP or intubation; hold sedatives and report falling consciousness
   • Metabolic acidosis: recognize Kussmaul breathing as compensation — do not try to slow it; treat the cause
2. Cardiac monitoring
   • Continuous ECG; watch potassium closely, especially as acidosis is corrected
3. Neurologic safety
   • Seizure and fall precautions for confusion; alkalosis can cause tetany and seizures
4. Fluids and electrolytes
   • Intake and output, daily weight, IV fluids as ordered; measure and report nasogastric or fistula losses
   • Replace potassium only with adequate urine output
5. Anxiety — for hyperventilation, stay with the client, speak calmly, and coach slow breathing

• COPD: take bronchodilators as prescribed, seek care early for increasing breathlessness or drowsiness, use oxygen only at the prescribed flow
• Diabetes: follow sick-day rules; check ketones when glucose is high or when ill
• Avoid excessive use of baking soda or calcium carbonate antacids
• Replace fluids early during vomiting or diarrhea; report persistent vomiting
• Report numbness, tingling, muscle cramps, or confusion
• Anxiety-related hyperventilation: practice slow breathing techniques; see a clinician to rule out a medical cause

• Normal: pH 7.35–7.45, PaCO₂ 35–45 mmHg, HCO₃⁻ 22–26 mEq/L
• ROME: respiratory — pH and PaCO₂ move opposite; metabolic — pH and HCO₃⁻ move in the same direction
• pH abnormal + compensating value abnormal = partially compensated; pH normal = fully compensated
• COPD exacerbation → respiratory acidosis; oxygen target 88–92%
• Hyperventilation (anxiety, pain) → respiratory alkalosis → tingling, tetany
• Vomiting, NG suction → metabolic alkalosis; diarrhea → metabolic acidosis
• DKA → high anion gap metabolic acidosis with Kussmaul respirations; fluids first
• Acidosis → hyperkalemia; correcting acidosis or giving bicarbonate → potassium falls
• Respiratory acidosis → headache, drowsiness, confusion (CO₂ narcosis)
• Severe liver disease → respiratory alkalosis, sometimes with metabolic acidosis; salicylate toxicity → classic mixed pattern
• Bicarbonate in DKA is reserved for pH < 7.0