Arterial Blood pH Calculator
Enter the bicarbonate (HCO3) and arterial carbon dioxide partial pressure (PaCO2) measured on an arterial blood gas sample. This calculator applies the Henderson-Hasselbalch equation to compute the arterial pH, then classifies the primary acid-base disorder, identifies the compensation phase (acute, partially compensated, or fully compensated), and calculates the anion gap when sodium and chloride are provided. Results update as you type.
Formula
Worked example
A patient has HCO3 = 24 mEq/L and PaCO2 = 40 mmHg. Dissolved CO2 = 0.0308 x 40 = 1.232 mEq/L. Ratio = 24 / 1.232 = 19.48. log10(19.48) = 1.289. pH = 6.1 + 1.289 = 7.39, which is within the normal range of 7.35-7.45.
What is arterial blood pH?
Arterial blood pH is a measure of the hydrogen ion concentration in blood drawn directly from an artery, most commonly the radial artery at the wrist. Because pH is defined as the negative logarithm of the hydrogen ion concentration, a lower pH means more acid (more H+ ions) and a higher pH means more alkaline (fewer H+ ions). The human body tightly regulates arterial pH between 7.35 and 7.45 through three interlocking systems: the bicarbonate-carbonic acid buffer, respiratory control of carbon dioxide, and renal excretion of hydrogen ions and bicarbonate. Deviations from this narrow window, even by a few tenths of a unit, can impair enzyme function, alter oxygen delivery to tissues, and in severe cases become life-threatening.
The Henderson-Hasselbalch equation
This calculator uses the Henderson-Hasselbalch equation, which relates pH to the ratio of bicarbonate (HCO3) to dissolved carbon dioxide in plasma: pH = pKa + log10(HCO3 / (0.0308 x PaCO2)). The constant 0.0308 is the solubility coefficient of CO2 in plasma at body temperature (37 degrees C), and pKa = 6.1 is the dissociation constant of carbonic acid. Because dissolved CO2 and PaCO2 are directly proportional, clinicians can substitute the directly measured PaCO2 from an arterial blood gas into the formula. A result below 7.35 indicates acidosis; a result above 7.45 indicates alkalosis.
Classifying acid-base disorders
Four primary acid-base disorders are recognized. Respiratory acidosis occurs when the lungs cannot excrete CO2 fast enough, raising PaCO2 and dropping pH; causes include hypoventilation, COPD, and neuromuscular disease. Respiratory alkalosis occurs when ventilation is excessive, lowering PaCO2 and raising pH; causes include anxiety, pain, fever, and mechanical over-ventilation. Metabolic acidosis occurs when the body accumulates non-respiratory acid or loses bicarbonate; bicarbonate falls, pulling pH down; high-anion-gap causes include diabetic ketoacidosis, lactic acidosis, and toxin ingestion, while normal-anion-gap causes include diarrhea and renal tubular acidosis. Metabolic alkalosis occurs when bicarbonate rises, raising pH; common causes are vomiting, diuretic use, and volume contraction. Compensation is the physiological response that partially counteracts a primary disorder: the lungs compensate for metabolic disorders by adjusting PaCO2, while the kidneys compensate for respiratory disorders by retaining or excreting bicarbonate over hours to days.
The anion gap and why it matters
The anion gap (AG) is calculated as sodium minus the sum of chloride and bicarbonate: AG = Na - (Cl + HCO3). It represents the concentration of unmeasured anions such as albumin, phosphate, sulfate, and organic acids. The normal range is approximately 8-12 mEq/L (using the formula without potassium). An elevated anion gap points to the accumulation of an unmeasured acid, which is the hallmark of high-anion-gap metabolic acidosis. Because hypoalbuminemia lowers the anion gap by about 2.5 mEq/L for every 1 g/dL decrease in albumin below 4.4 g/dL, the corrected anion gap (AG + 2.5 x (4.4 - measured albumin)) should be used in critically ill patients where hypoalbuminemia is common.
Arterial blood gas normal reference ranges
| Parameter | Normal Range | Low (Acidosis/Alkalosis) | Clinical Significance |
|---|---|---|---|
| Arterial pH | 7.35 - 7.45 | < 7.35 acidosis, > 7.45 alkalosis | Overall acid-base balance |
| PaCO2 | 35 - 45 mmHg | < 35 respiratory alkalosis, > 45 respiratory acidosis | Respiratory component |
| HCO3 (bicarbonate) | 22 - 26 mEq/L | < 22 metabolic acidosis, > 26 metabolic alkalosis | Metabolic component |
| Anion gap | 8 - 12 mEq/L | > 12 high anion gap acidosis | Unmeasured anions |
| Base excess | -2 to +2 mEq/L | Outside range suggests metabolic disorder | Deviation from normal buffer base |
Standard reference values for adult arterial blood gas (ABG) analysis at sea level and 37 degrees C.
Frequently asked questions
What is a normal arterial blood pH?
The normal range for arterial blood pH in adults is 7.35 to 7.45. A pH below 7.35 indicates acidosis, meaning the blood is more acidic than normal. A pH above 7.45 indicates alkalosis, meaning the blood is more alkaline. Values outside 7.20 or above 7.60 are considered severe and require urgent clinical evaluation.
What is the Henderson-Hasselbalch equation?
The Henderson-Hasselbalch equation expresses blood pH as a function of the bicarbonate concentration and the partial pressure of carbon dioxide: pH = 6.1 + log10(HCO3 / (0.0308 x PaCO2)). The number 6.1 is the dissociation constant (pKa) of carbonic acid, and 0.0308 is the solubility coefficient of CO2 in plasma at 37 degrees C. This equation is the cornerstone of clinical acid-base physiology and allows any of the three variables to be calculated if the other two are known.
What is the difference between respiratory and metabolic acidosis?
In respiratory acidosis, the primary problem is CO2 retention. PaCO2 rises above 45 mmHg because the lungs cannot eliminate CO2 fast enough, and this drives pH down. The kidneys respond over hours to days by retaining bicarbonate to normalize pH. In metabolic acidosis, the primary problem is either gain of non-respiratory acid or loss of bicarbonate. HCO3 falls below 22 mEq/L, pulling pH down. The lungs respond within minutes to hours by increasing ventilation to blow off CO2. Both disorders lower pH, but they have opposite effects on PaCO2.
What causes a high anion gap?
A high anion gap (above 12 mEq/L) in the setting of metabolic acidosis indicates the accumulation of an unmeasured acid. The classic mnemonic MUDPILES captures the major causes: methanol, uremia, diabetic ketoacidosis, propylene glycol or other toxins, isoniazid or iron, lactic acidosis, ethylene glycol, and salicylate toxicity. A normal anion gap metabolic acidosis has different causes, including diarrhea, renal tubular acidosis, and early renal failure, and is sometimes called hyperchloremic acidosis because chloride rises as bicarbonate falls.
How does this calculator differ from a full ABG report?
This calculator computes arterial pH from your entered HCO3 and PaCO2 values using the Henderson-Hasselbalch equation, classifies the primary acid-base disorder, and calculates the anion gap. A full arterial blood gas (ABG) panel from a laboratory also reports the directly measured pH, PaO2 (oxygen partial pressure), oxygen saturation, base excess, and sometimes lactate. The calculated pH from this tool closely matches the measured pH when the inputs are accurate, but it does not replace a laboratory ABG report in clinical decision-making.
Why is correcting the anion gap for albumin important?
Albumin carries a large negative charge and is the main unmeasured anion in normal plasma. When albumin falls below 4.4 g/dL, which is very common in critically ill or malnourished patients, the uncorrected anion gap is falsely low. A high anion gap metabolic acidosis can be completely masked by hypoalbuminemia. The corrected anion gap, calculated as AG + 2.5 x (4.4 - albumin), adjusts for this and is more reliable in patients with abnormal albumin levels.
Sources
- Berend K, de Vries AP, Gans RO. Physiological approach to assessment of acid-base disturbances. N Engl J Med. 2014;371(15):1434-1445.
- American Thoracic Society. Interpretation of Arterial Blood Gases (ABGs). ATS Clinical Resources.
- Kellum JA. Determinants of blood pH in health and disease. Crit Care. 2000;4(1):6-14.