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Quick Reference
  • Normal Range: 7.35-7.45
  • Normal Mean: 7.40
  • Acidemia: pH <7.35
  • Alkalemia: pH >7.45
  • Critical Low: pH <7.20 (severe acidemia)
  • Critical High: pH >7.60 (severe alkalemia)
  • Primary Use: Determining acid-base status and identifying primary disorder
  • Sample Type: Arterial blood (ABG)
  • Key Point: pH is the first value to assess in ABG interpretation

Test Description

Arterial blood pH measures the concentration of hydrogen ions (H+) in the blood, reflecting the body's acid-base balance. The pH scale is logarithmic, meaning small changes in pH represent large changes in hydrogen ion concentration. A pH of 7.40 is considered neutral for blood, with values below 7.35 indicating acidemia and values above 7.45 indicating alkalemia.

The body maintains pH within a narrow range through three main buffering systems: chemical buffers (bicarbonate, phosphate, protein), respiratory regulation (CO2 elimination), and renal regulation (H+ excretion and HCO3- reabsorption). pH is the most important single value in ABG analysis as it determines the overall acid-base status and guides clinical decision-making.

Physiological Role

  • Enzyme function: Most enzymes function optimally within narrow pH ranges
  • Protein structure: pH affects protein folding and function
  • Electrolyte balance: pH influences potassium distribution (K+ shifts with H+)
  • Oxygen delivery: pH affects hemoglobin-oxygen binding (Bohr effect)
  • Cardiac function: Severe acidemia or alkalemia impairs myocardial contractility
Normal Ranges

Arterial blood pH is tightly regulated and does not vary significantly by age, sex, or other demographic factors in healthy individuals.

Swipe to see more
Classification pH Range Clinical Interpretation
Severe Alkalemia >7.60 Life-threatening, requires immediate intervention
Alkalemia 7.46-7.60 Abnormal, investigate cause
Normal Range 7.35-7.45 Physiologic range (mean 7.40)
Acidemia 7.20-7.34 Abnormal, investigate cause
Severe Acidemia <7.20 Life-threatening, requires immediate intervention
Critical Considerations
  • pH <7.20: High mortality risk, consider bicarbonate therapy in metabolic acidosis
  • pH >7.60: Risk of seizures, arrhythmias, and tetany
  • Venous pH: Typically 0.03-0.04 lower than arterial pH (not interchangeable)
  • Temperature correction: Blood gas analyzers measure at 37°C; hypothermia increases pH, hyperthermia decreases pH
Clinical Significance

Acidemia (pH <7.35)

Acidemia indicates excess hydrogen ions or acid accumulation. The cause is determined by evaluating PaCO2 and HCO3- to classify as respiratory or metabolic acidosis.

Metabolic Acidosis (Low pH + Low HCO3-)

  • Diabetic ketoacidosis (DKA): Accumulation of ketoacids (beta-hydroxybutyrate, acetoacetate)
  • Lactic acidosis: Tissue hypoperfusion, sepsis, shock, Type B (metformin, liver failure)
  • Renal failure: Inability to excrete H+ and regenerate HCO3-
  • Diarrhea: Loss of HCO3- in stool
  • Renal tubular acidosis: Impaired renal acid handling
  • Toxins/poisoning: Methanol, ethylene glycol, salicylates, metformin
  • Rhabdomyolysis: Muscle breakdown releasing H+ and phosphate

Respiratory Acidosis (Low pH + High PaCO2)

  • Respiratory failure: COPD exacerbation, severe asthma, pneumonia
  • Central hypoventilation: Opioid overdose, stroke, CNS depression
  • Neuromuscular disorders: Myasthenia gravis, Guillain-Barré syndrome, ALS
  • Chest wall disorders: Kyphoscoliosis, obesity hypoventilation syndrome
  • Airway obstruction: Foreign body, laryngospasm, severe bronchospasm

Alkalemia (pH >7.45)

Alkalemia indicates hydrogen ion deficit or base excess. Classification depends on PaCO2 and HCO3- levels.

Metabolic Alkalosis (High pH + High HCO3-)

  • Vomiting/NG suction: Loss of gastric HCl
  • Diuretic therapy: Loop and thiazide diuretics causing contraction alkalosis
  • Hypokalemia: K+ depletion leads to H+ movement into cells
  • Mineralocorticoid excess: Primary hyperaldosteronism, Cushing's syndrome
  • Excessive bicarbonate administration: Iatrogenic from IV NaHCO3
  • Post-hypercapnic alkalosis: Rapid correction of chronic respiratory acidosis

Respiratory Alkalosis (High pH + Low PaCO2)

  • Hyperventilation: Anxiety, pain, panic attack
  • Hypoxemia: Pneumonia, pulmonary embolism, high altitude
  • Pulmonary disease: Interstitial lung disease, early pneumonia
  • CNS stimulation: Stroke, meningitis, encephalitis, fever
  • Pregnancy: Progesterone-mediated hyperventilation
  • Mechanical ventilation: Excessive minute ventilation settings
  • Salicylate toxicity: Direct stimulation of respiratory center (early phase)
Interpretation Guidelines

Four Primary Acid-Base Disorders

Every acid-base disturbance falls into one of four primary categories based on pH, PaCO2, and HCO3-:

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Disorder pH PaCO2 HCO3- Primary Problem
Metabolic Acidosis ↓ ↓ (compensated) ↓ Loss of HCO3- or gain of H+
Metabolic Alkalosis ↑ ↑ (compensated) ↑ Gain of HCO3- or loss of H+
Respiratory Acidosis ↓ ↑ ↑ (compensated) Hypoventilation, CO2 retention
Respiratory Alkalosis ↑ ↓ ↓ (compensated) Hyperventilation, CO2 loss

Compensation Mechanisms

The body attempts to normalize pH through compensation, but compensation never fully corrects pH to normal—it only minimizes the change. The system not primarily affected responds to help restore pH.

Respiratory Compensation (for Metabolic Disorders)
  • Onset: Minutes to hours (fast)
  • Metabolic acidosis: Hyperventilation to decrease PaCO2 (Kussmaul respirations in DKA)
  • Metabolic alkalosis: Hypoventilation to increase PaCO2 (limited by hypoxemia)
  • Expected PaCO2 in metabolic acidosis: Winter's formula: PaCO2 = 1.5 × [HCO3-] + 8 (±2)
Metabolic Compensation (for Respiratory Disorders)
  • Onset: 3-5 days (slow, requires renal adjustment)
  • Respiratory acidosis: Kidneys retain HCO3- and excrete H+
  • Respiratory alkalosis: Kidneys excrete HCO3- and retain H+
  • Acute vs Chronic: Chronic respiratory disorders show more metabolic compensation

Mixed Acid-Base Disorders

Mixed disorders occur when two or more primary acid-base disturbances coexist. Clues include:

  • pH near normal with abnormal PaCO2 and HCO3-: Offsetting disorders (e.g., metabolic acidosis + metabolic alkalosis)
  • Over-compensation: If pH crosses 7.40 in the opposite direction, suspect mixed disorder
  • Compensation out of expected range: Use Winter's formula or compensation rules to detect
  • Clinical context: Patient with COPD (chronic respiratory acidosis) developing sepsis (metabolic acidosis)
Approach to pH Interpretation

Step-by-step method (use all three values together):

  1. Check pH: Is it acidemic (<7.35), alkalemic (>7.45), or normal?
  2. Determine primary disorder: Look at PaCO2 and HCO3- to identify if metabolic or respiratory
  3. Check for compensation: Is the compensatory parameter moving in the expected direction?
  4. Assess degree of compensation: Partial, complete, or over-compensated (suggests mixed disorder)
  5. Calculate anion gap (if metabolic acidosis): Anion Gap = Na+ - (Cl- + HCO3-), normal 8-12
  6. Consider clinical context: Correlate with patient presentation, history, and physical exam
Interfering Factors

Pre-Analytical Factors

  • Air bubbles in sample: Equilibration with room air increases PaO2 and decreases PaCO2, falsely increasing pH
  • Delayed analysis: Cellular metabolism consumes O2 and produces CO2, decreasing pH over time
  • Temperature: Patient hypothermia increases actual pH; hyperthermia decreases pH (analyzers measure at 37°C)
  • Heparin contamination: Excessive heparin dilutes sample and lowers pH
  • Venous vs arterial: Venous pH is ~0.03-0.04 lower than arterial pH

Physiological Factors

  • Hyperventilation from anxiety: Can cause respiratory alkalosis during blood draw
  • Breath-holding: Transient CO2 retention and acidemia
  • Vigorous exercise: Lactic acid production and transient metabolic acidosis
  • Altitude: Chronic hypoxia causes compensatory hyperventilation and respiratory alkalosis

Medications Affecting pH

  • Increase pH (alkalemia): Loop diuretics, thiazides, excessive bicarbonate, antacids
  • Decrease pH (acidemia): Metformin (lactic acidosis), salicylates (mixed disorder), acetazolamide (metabolic acidosis), opioids (respiratory acidosis)

Technical Factors

  • Arterial spasm: Pain-induced hyperventilation during difficult arterial puncture
  • Sample handling: Ice bath required if analysis delayed >15 minutes
  • Machine calibration: Ensure blood gas analyzer properly calibrated with quality control
Clinical Pearls
"pH tells you the primary problem"

The pH direction indicates which disorder is primary. If pH is acidemic, the primary disorder is acidosis (even if both acidosis and alkalosis are present). The primary disorder is the one that explains the pH abnormality.

"7.40 is normal, but the range is 7.35-7.45"

A pH of 7.39 may seem "close to normal," but it still represents acidemia and requires investigation. Don't dismiss values at the edges of the normal range without clinical correlation.

"Compensation never overcorrects"

If the pH crosses 7.40 in the direction opposite to the primary disorder, you're dealing with a mixed acid-base disorder, not simple compensation. For example, pH 7.48 with low HCO3- suggests mixed respiratory alkalosis + metabolic acidosis, not compensated metabolic acidosis.

"Use the triad: pH + PaCO2 + HCO3-"

Never interpret pH in isolation. Always look at all three values together. PaCO2 tells you about ventilation (respiratory component), HCO3- tells you about metabolic component, and pH tells you the net result.

Common pitfall – Normal pH with abnormal components

A pH of 7.40 does NOT mean normal acid-base status. Check PaCO2 and HCO3-. A patient can have pH 7.40 with PaCO2 60 and HCO3- 36, indicating chronic respiratory acidosis with full metabolic compensation.

"Winter's formula for metabolic acidosis"

Expected PaCO2 = 1.5 × [HCO3-] + 8 (±2). If actual PaCO2 is higher than expected, there's concurrent respiratory acidosis. If lower than expected, there's concurrent respiratory alkalosis. This detects mixed disorders.

pH and potassium relationship

For every 0.1 decrease in pH, potassium increases by ~0.6 mEq/L (as H+ enters cells and K+ exits). Correct acidemia before aggressively treating hyperkalemia, as pH normalization will lower K+ naturally. Conversely, alkalemia can mask or worsen hypokalemia.

"Acute vs chronic respiratory disorders"

Acute respiratory acidosis (e.g., opioid overdose) shows minimal HCO3- elevation because renal compensation takes days. Chronic respiratory acidosis (e.g., COPD) shows significant HCO3- elevation (often >30 mEq/L) with pH closer to normal.

Life-threatening pH values

pH <7.20 or >7.60 requires immediate intervention. Severe acidemia impairs cardiac contractility and can cause refractory hypotension. Severe alkalemia increases risk of arrhythmias, seizures, and can cause tetany. Do not delay treatment waiting for underlying cause correction in these cases.

"Mixed disorders are common in ICU patients"

Critically ill patients frequently have multiple simultaneous processes. A patient with COPD (chronic respiratory acidosis) who develops sepsis (metabolic acidosis) has a mixed disorder. Always consider the clinical context and don't assume a single disorder.

Anion gap calculation

If pH shows metabolic acidosis (low pH, low HCO3-), always calculate anion gap: AG = Na+ - (Cl- + HCO3-). High anion gap (>12) suggests acid accumulation (MUDPILES mnemonic: Methanol, Uremia, DKA, Propylene glycol, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates). Normal anion gap suggests HCO3- loss (diarrhea, RTA).

References
  1. Kratz, A., Ferraro, M., Sluss, P. M., & Lewandrowski, K. B. (2004). Laboratory reference values. New England Journal of Medicine, 351, 1548-1564.
  2. Lee, M. (Ed.). (2009). Basic skills in interpreting laboratory data. Ashp.
  3. Farinde, A. (2021). Lab values, normal adult: Laboratory reference ranges in healthy adults. Medscape. https://emedicine.medscape.com/article/2172316-overview?form=fpf
  4. Nickson, C. (n.d.). Critical Care Compendium. Life in the Fast Lane • LITFL. https://litfl.com/ccc-critical-care-compendium/
  5. Farkas, Josh MD. (2015). Table of Contents - EMCrit Project. EMCrit Project. https://emcrit.org/ibcc/toc/
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