What causes a low pH on an Arterial Blood Gas (ABG)?

What Causes Low pH on an Arterial Blood Gas (ABG)

A low pH (<7.35) on an ABG indicates acidemia, which results from either respiratory acidosis (elevated PaCO2 >6.0 kPa or >45 mmHg) or metabolic acidosis (reduced bicarbonate <22 mmol/L), or a combination of both. 1

Primary Mechanisms of Low pH

Respiratory Acidosis

• Elevated PaCO2 (>6.0 kPa or >45 mmHg) combined with pH <7.35 defines respiratory acidosis, which occurs when alveolar hypoventilation prevents adequate CO2 elimination 1
• Common causes include:
  • Severe or moderate COPD, especially with previous respiratory failure or on long-term oxygen 1
  • Severe chest wall or spinal disease (e.g., kyphoscoliosis) 1
  • Neuromuscular disease affecting respiratory muscles 1
  • Severe obesity (obesity hypoventilation syndrome) 1
  • Cystic fibrosis and bronchiectasis 1
  • Narcotic or sedative overdose 1

Metabolic Acidosis

• Metabolic acidosis is characterized by primary reduction in serum bicarbonate (<22 mmol/L) with pH <7.35, and the body attempts respiratory compensation by increasing ventilation to eliminate CO2 2, 3
• The anion gap distinguishes the mechanism: elevated anion gap indicates acid accumulation (lactic acidosis, ketoacidosis, toxins), while normal anion gap indicates bicarbonate loss (diarrhea, renal tubular acidosis) or chloride salt ingestion 4, 3

High Anion Gap Metabolic Acidosis Causes:

• Lactic acidosis from tissue hypoperfusion in shock states (septic, cardiogenic, hemorrhagic shock), where inadequate oxygen delivery produces lactate as a byproduct 5
• Diabetic ketoacidosis (DKA), with bicarbonate 15-18 mmol/L indicating mild DKA and <15 mmol/L indicating moderate to severe DKA 2
• Drug toxicity (salicylates, methanol, ethylene glycol) 6
• Renal failure impairing hydrogen ion excretion and ammonia synthesis 2, 6

Normal Anion Gap Metabolic Acidosis Causes:

• Bicarbonate loss from diarrhea or renal tubular acidosis 4, 3
• Ingestion of acidifying chloride salts 4

Mixed Acid-Base Disorders

• When pH <7.35 with normal or low PaCO2, investigate for metabolic acidosis even if respiratory parameters appear normal 1
• In chronic kidney disease, a Western diet high in animal protein generates nonvolatile acids that accumulate when kidneys cannot excrete hydrogen ions adequately 2
• Septic shock exhibits complex metabolic acidosis with contributions from lactic acidosis, hyperchloremic acidosis, and increased strong ion gap 5

Clinical Assessment Algorithm

Step 1: Identify the Primary Disorder

• Check pH first: <7.35 = acidemia, >7.44 = alkalemia 2, 3
• If pH <7.35, examine PaCO2 and bicarbonate:
  • PaCO2 >6.0 kPa (45 mmHg) = respiratory acidosis 1
  • Bicarbonate <22 mmol/L = metabolic acidosis 2, 3
  • Both elevated PaCO2 and low bicarbonate = mixed disorder 3

Step 2: Assess Compensation

• In metabolic acidosis, expected compensatory PaCO2 drop indicates adequate respiratory compensation; if PaCO2 remains elevated, suspect concurrent respiratory acidosis 3
• In respiratory acidosis, chronic cases show elevated bicarbonate (>26 mmol/L) as renal compensation, while acute cases have minimal bicarbonate elevation 2, 4

Step 3: Calculate Anion Gap (if metabolic acidosis present)

• Anion gap = Na+ - (Cl- + HCO3-) 4, 3
• Normal anion gap (8-12 mEq/L) with low bicarbonate indicates bicarbonate loss or chloride salt ingestion 4
• Elevated anion gap indicates unmeasured anions from lactic acid, ketoacids, or toxins 4, 3

Critical Clinical Pitfalls

• In COPD exacerbations, approximately 20% of patients with initial respiratory acidosis normalize pH with optimal medical therapy and controlled oxygen (targeting SpO2 88-92%) within 60 minutes—avoid premature escalation to NIV 1
• Do not assume all low pH in shock requires bicarbonate therapy; sodium bicarbonate should not be used to treat metabolic acidosis from tissue hypoperfusion in sepsis, as restoring tissue perfusion with fluids and vasopressors is the primary treatment 2
• In diabetic ketoacidosis, bicarbonate therapy is generally NOT indicated unless pH falls below 6.9-7.0; insulin therapy and fluid resuscitation correct the underlying ketoacidosis 2
• Serial lactate, base deficit, and pH measurements provide more valuable information than single values for assessing shock severity and treatment response 5
• Hypothermia, hypocalcemia, and worsening acidosis during resuscitation can exacerbate coagulopathy—actively prevent these complications 5

Severity Thresholds for Intervention

• pH <7.35 with PaCO2 >6.5 kPa and respiratory rate >23 breaths/min persisting after 1 hour of optimal medical therapy warrants NIV initiation 1
• pH <7.25 with hypercapnia indicates severe respiratory acidosis requiring ICU-level monitoring and readiness for intubation 1
• Bicarbonate <18 mmol/L indicates severe metabolic acidosis requiring pharmacological treatment with sodium bicarbonate in chronic kidney disease patients 2
• Base deficit is an independent predictor of mortality in traumatic hemorrhagic shock, reflecting global tissue acidosis 5