Journal of Research and Innovation in Anesthesia
Volume 4 | Issue 2 | Year 2019

Analyzing the Arterial Blood Gases: A Comprehensive Approach

Maithili Thakur

Department of Anesthesiology, HinduHrudaySamrat Balasaheb Thackeray Medical College and Dr RN Cooper Municipal General Hospital, Mumbai, Maharashtra, India

Corresponding Author: Maithili Thakur, Department of Anesthesiology, HinduHrudaySamrat Balasaheb Thackeray Medical College and Dr RN Cooper Municipal General Hospital, Mumbai, Maharashtra, India, Phone: +91 8369233147, e-mail:

How to cite this article Thakur M. Analyzing the Arterial Blood Gases: A Comprehensive Approach. Res Inno in Anesth 2019;4(2):50–54.

Source of support: Nil

Conflict of interest: None


The arterial blood gas analysis provides extensive and crucial information to the intensivist. It indicates the state of alveolar ventilation, the oxygenation, as well as the acid–base balance. It is an invaluable tool in expert hands. This review attempts to clarify the concepts related to respiratory and metabolic acid–base disturbances with several examples.

Keywords: Anion gap, Metabolic acidosis, Metabolic alkalosis, Oxygenation, Respiratory acidosis, Respiratory alkalosis.


Understanding arterial blood gas (ABG) reports is a crucial task in determining the management of patients requiring intensive and continuous monitoring. They give us a deep insight to the oxygenation deficiencies to be differentiated from primary ventilatory deficiencies and primary metabolic acid–base abnormalities. Hence, learning to interpret them in a proper way becomes an essential agenda in any anesthesiologist’s learning diary.1

The aims of doing a blood gas analysis are to detect the existence and intensity of oxygen- and carbon dioxide-related abnormalities in the blood levels and the degree of compensation in maintaining the acid–base equilibrium, thereby diagnosing the condition and planning their management.

The maintenance of potential hydrogen (pH) equilibrium by the three physiological processes of alveolar ventilation, oxygenation, and acid–base balance is reflected through the ABG report. There is a strong interrelation of all these three processes.

1. Alveolar Ventilation

The maintenance of carbon dioxide (CO2) levels reflected by arterial CO2 pressure (PaCO2) depends on the production and excretion of CO2 via alveolar ventilation by the body. Thus, alveolar ventilation is best assessed by PaCO2. Normal PaCO2 is 35–45 mm Hg.

2. Assessment of Oxygenation Status

Pulse oximetry (SpO2) and ABG analysis (SaO2) are useful for measuring oxygen saturation and thereby evaluating the oxygenation status. They determine the arterial oxygen content better than the partial pressure of arterial oxygen (PaO2). If the saturation shown by a pulse oximeter is less than 90% and the PaO2 is less than 60 mm Hg, the patient is termed hypoxemic.2

Whether the hypoxia occurs due to hypoventilation (due to increase in PaCO2) or due to deficiency in oxygenation can be determined by calculating an alveolar-arterial (A-a) oxygen gradient (P(A-a)O2).3 The alveolar-arterial difference in partial pressure of O2 is P(A-a)O2. The partial pressure of alveolar oxygen (PAO2) can be computed using fractional inspired oxygen concentration (FiO2), partial pressure of arterial CO2 (PaCO2), and barometric pressure while PaO2 is measured by ABG.

PAO2 = FiO2 (P(baro) – P(wv)) − PaCO2/R = 0.21 (760 − 47) – 40/0.8 = 150–50 = 100 mm Hg

PaO2 = 90–100 mm Hg

P(A-a)O2 is used as an index for shunting and ventilation-perfusion (V/Q) mismatch and is normally about 5–25 mm Hg. It is however affected by age and FiO2. A-a gradient = Age/4 + 4. So, it increases with increase in the age. For every 10% rise in FiO2, the A-a gradient rises by 5–7 mm Hg.

The PaO2/PAO2 ratio (independent of FiO2) can also be calculated. Normal values are 90–99/92.6–100 = 0.8–1.0. Grading of this ratio is done as follows: %3C;0.25 is critical shunt, 0.25–0.5 is significant shunt, and 0.5–0.8 is moderate shunt.

The PaO2/FiO2 ratio is important since the PaO2 value should always be correlated with the amount of oxygen received by the patient. For example, FiO2 of 20% gives PaO2 of 100 mm Hg. FiO2 1.0 gives PaO2 of 500 mm Hg in normal individuals.

The stepwise evaluation of hypoxemia is shown in Flowchart 1.

3. Acid–Base Balance

Potential hydrogen is defined as negative logarithm to base 10 of hydrogen ions measured in nmol per liter. The pH equilibrium can be maintained by the buffer system of the kidneys, lungs, and blood and is computed by the Henderson-Hasselbalch equation: pH = 6.1 + log HCO3/0.3 × [PaCO2]. The Henderson equation has been simplified by Kassirer and Bliech as H+ = 24 × PCO2/HCO3.4 Thus, maintaining pH within range of 7.35–7.45 is the primary objective of regulating acid–base balance. Decrease in arterial pH (pH < 7.35) is acidemia whereas rise in arterial pH (pH %3E; 7.45) points toward alkalemia. Thus, acidosis is defined as process tending to decline the pH by increasing H+ or eliminating HCO3, whereas the process causing surge in the pH on account of decreasing H+ or rise of HCO3 is termed alkalosis.

Flowchart 1: Flow diagram showing approach to hypoxemic respiratory failure


Primary modifications in ventilation lead to respiratory acidosis or alkalosis due to excessive removal or accumulation of CO2. Metabolic conditions cause acidosis or alkalosis by alterations in the bicarbonate ions concentration.


Compensation of primary acid–base disorder is done either by the lungs or kidneys. The respiratory system compensates for the metabolic changes due to deviations in HCO3 (metabolic acidosis or alkalosis) while kidneys compensate for fluctuations in CO2 (respiratory acidosis/alkalosis), which take around 2–5 days.


Simple acid–base disorder consists of only a primary single process of either acidosis or alkalosis whereas mixed acid-base disorder may have more than one acid–base disorder coexisting together.

In metabolic conditions, movement of pH and HCO3 is in same direction whereas in respiratory conditions the movement of pH and PaCO2 is in opposite direction. In simple disorders, the movement of HCO3 and PaCO2 is in same direction while in mixed disorders, fluctuations of HCO3 and PaCO2 are in opposite directions (Table 1).5,6

While evaluating for the acid–base status, the pH values range between 7.35 and 7.45; PaCO2 ranges between 35 and 45 mm Hg and HCO3 values range between 22 and 26 mEq/L. For calculation purposes, the base is taken as 7.40 for pH, PaCO2 is taken as 40 mm Hg, and 24 mEq/L for HCO3.7,8

The stepwise approach to the ABG Analysis4 was given by Narins and Emmett and modified by Morganroth in 1991.9

Table 1: Features of primary acid–base disorders
DisorderPrimary responses
Compensatory responses
Metabolic acidosis↑ [H+]↓ pH↓ HCO3↓ PaCO2
Metabolic alkalosis↓ [H+]↑ pH↑ HCO3↑ PaCO2
Respiratory acidosis↑ [H+]↓ pH↑ HCO3↑ HCO3
Respiratory alkalosis↓ [H+]↑ pH↓ HCO3↓ HCO3

If compensation is as per calculation, it is a single acid–base disorder. If compensation is less than or greater than calculated expected value, then it is mixed acid–base problem.


The pathophysiological causes of metabolic acidosis11 include: (1) HCO3 loss either due to renal or gastrointestinal tract (GIT) causes; (2) greater formation of nonvolatile acids, exogenous acids, lactates, ketoacids, and poisons; and (3) fall in renal acid secretion.

Causes of HAGMA include: (1) lactic acidosis; (2) diabetic ketoacidosis, alcoholic ketoacidosis, and starvation; (3) chronic renal failure; (4) rhabdomyolysis; (5) salicylate toxicity, methanol toxicity, and ethylene glycol toxicity.

Causes of normal AG metabolic acidosis (NAGMA): (1) HCO3 loss due to GIT causes—biliary or pancreatic drainage, diarrhea, ketoacidosis during treatment, renal-proximal (type II) renal tubular acidosis (RTA), urinary diversions (ureterosigmoidostomy); (2) reduced renal acid excretion: renal failure, hyperkalemia (type IV) RTA, distal (type I) RTA; (3) miscellaneous: ammonium chloride (NH4Cl) therapy, HCl therapy (treatment of severe metabolic alkalosis), hyperalimentation, and cholestyramine ingestion.

Diagnosing cause of metabolic acidosis:

Plasma osmolality = 2[Na+] + [Gluc]/18 + [BUN]/2.8. Plasma osmolality gap is defined as the difference between the calculated and measured plasma osmolality.


If the plasma osmolality gap is more than 15–20 mOsm/kg, then it shows presence of high osmolar substances like alcohol in the blood.

Ketones and hyperglycemia indicate diabetic ketoacidosis while ketones with normal glucose point to alcoholism and starvation. Serum lactate levels more than 2 indicate lactic acidosis.


Urine AG (UAG) is calculated. If positive UAG, then it indicates RTA; urine pH > 5.5 indicates type I RTA. If pH %3C; 5.5 and high K+, it indicates type IV RTA; if pH < 5.5 and low potassium (K+), it indicates type II RTA.

If negative UAG, the urine osmolality gap is calculated. If increased it’s due to iatrogenic acid gain and if normal it’s due to GIT causes.

Example 1: Patient comes with diabetic ketoacidosis at 0 hours at presentation. pH 7.06, CO2 = 10.3, HCO3 = 6.1, Na+/Cl 142/106

Thus, patient has HAGMA with respiratory alkalosis.

Same patient after 6 hours of treatment with insulin and saline, pH 7.22, CO2 = 24, HCO3 = 10.2, Na+/Cl 140/120

With saline, hyperchloremic acidosis sets in. Thus, the patient now has NAGMA owing to the treatment. Ketoacids are being cleared (AG ↓), thus indicating a good response. Only HCO3 will not indicate adequacy of response.

Treatment of metabolic acidosis includes treating underlying cause, HCO3 therapy as per the formula 0.5 × weight (kg) × HCO3 deficit (mEq/L). The objective is to raise the pH to %3E;7.2 and HCO3 > 10 mEq/L.


Metabolic alkalosis is commonly (up to 50% of all disorders) associated with significant mortality.

Pathophysiological causes of metabolic alkalosis are the following:11

(1) HCO3 accumulation: massive blood transfusion, giving large amounts of HCO3, ingestion (milk-alkali syndrome); (2) H+ loss: GIT—loss of gastric secretions, chloride losing diarrheal diseases; renal: mineralocorticoid excess, diuretics (loop/thiazide), Bartter’s syndrome, high-dose intravenous penicillin, post-chronic hypercapnia, hypercalcemia; (3) H+ movement into cells—hypokalemia, refeeding. Most in ICU are Cl responsive (urinary Cl %3C; 15 mEq/L) due to vomiting, nasogastric suction, diuretics, laxative, and volume depletion. Cl resistant (urinary Cl %3E; 25 mEq/L) due to severe hypokalemia and high aldosterone.

Example 2: A 70-year-old male with history of poor oral intake associated with areflexia and weakness. pH 7.54↑, CO2 54↑, HCO3 44, Na+/K+/Cl 145/2.1/86

Treatment: Immediate goal of therapy is partial correction of the alkalosis. The objective is reducing pH less than 7.55 and decreasing HCO3 less than 40 mEq/L.

Cl responsive type metabolic alkalosis is the most severe form. Treating the causes responsible for chloride and volume depletion. Administration of 3–5 L of 150 mEq/L sodium chloride should be done in patients with established signs of volume contraction. In case of chloride-resistant metabolic alkalosis, chloride should be repleted as potassium chloride. For metabolic alkalosis due to mineralocorticoid excess, spironolactone, which is a K+-sparing diuretic, proves beneficial.


Acute respiratory acidosis is caused by obstruction in elimination of CO2: (1) ventilation-related causes, airway obstruction like aspiration, bronchospasm (severe), laryngospasm; pulmonary edema; (2) perfusion-related causes: cardiac arrest, pulmonary thromboembolism; (3) restricted chest wall: tension pneumothorax, hemothorax, flail chest; (4) musculoskeletal system: myasthenia gravis crisis, hypokalemia; (5) failure of mechanical ventilator and other problems like (a) central nervous system (CNS): trauma, stroke, drugs (anesthetics, sedatives); (b) peripheral nerves: neurotoxins (OPC, tetanus, botulism), cervical cord injury, skeletal muscle relaxants (succinyl choline, curare, pancuronium and allied drugs, aminoglycosides)

Causes of chronic respiratory acidosis are obstruction in elimination of CO2 like (1) ventilation: interstitial lung disease, chronic obstructive pulmonary disease; (2) restricted chest wall movement: muscular dystrophy, polymyositis, etc., and (1) CNS: chronic trauma, obesity hypoventilation syndrome, brain malignancies, myxoedema, (2) peripheral nerves: diaphragmatic paralysis, poliomyelitis, multiple Sclerosis.

Example 3: A 21-year-old female presented with history of dyspnea and wheezing for 5 days. She was tachypneic with central cyanosis and bilateral wheezing present. Chest X-ray showed tubular heart with hyperinflated lung fields. pH = 7.31, CO2 = 64, HCO3 = 30, PaO2 = 68 mm Hg, Na+/Cl = 136/98

The diagnosis is chronic respiratory acidosis.

Treatment of respiratory acidosis is correction of underlying cause, appropriate oxygenation preventing subduing of respiratory drive, and avoid rapid correction of increased PaCO2 to avoid post-hypercapnic metabolic alkalosis (seizures, arrhythmias).


Causes of respiratory alkalosis comprises of head trauma, brain tumor, cerebrovascular accidents and other causes like pain, anxiety, fever, and peripheral respiratory stimulation like pulmonary V/Q imbalance, pulmonary shunts, hypovolemia, heights, diffusion problems, and miscellaneous causes like drugs—NSAIDs, progesterone, thyroid hormone, catecholamines, gram–ve sepsis, pregnancy, heat exposure, mechanical ventilation.

Example 4: 15-year-old boy presented with complaints of difficulty in breathing and upper abdominal discomfort for 3 hours. On examination per abdomen and respiratory system are normal except for hyperventilation. pH = 7.5, PaCO2 = 26 mm Hg, HCO3 = 20 mEq, PaO2 = 100 mm Hg, Na+/Cl = 137/99.

Treatment of respiratory alkalosis consists of treatment of underlying cause, administration of O2. If pH > 7.55, the patient is sedated and paralyzed and put on ventilator.

In Mixed Acid–base Disorders

  1. Step 1. Determine the primary component as explained previously depending on the direction of pH, pCO2, HCO3.
  2. Step 2. Calculate AG = Na − (Cl + HCO3), n = 12 ± 4.
  3. Step 3A. Calculate expected CO2 if metabolic.

    Metabolic acidosis: CO2 = (1.5 × HCO3) + 8

    Metabolic alkalosis: ΔCO2 = 0.7 × Δ HCO3

  4. 3B. Calculate expected HCO3 if respiratory

    ΔHCO3 = 0.1 × ΔCO2 (respiratory acidosis)

    0.2 × ΔCO2 (if respiratory alkalosis)

    0.4 × ΔCO2 (if chronic respiratory acid/alkalosis)

  5. Step 4. Calculate delta ratio = (AG – 12)/(HCO3 – 24)

Examples of mixed acid–base disorders

Example 5: A 68-year-old male taking diuretics for congestive heart failure admitted for lobar pneumonia: pH 7.62↑, CO2 32↓, HCO3 = 34↑, Na+/K+ 142/96

  • pH = Primary alkalemia, metabolic alkalosis due to high HCO3
  • AG = 142 – 129 = 13 normal
  • Since metabolic is primary check for respiratory compensation
  • Expected CO2 = 0.7 × HCO3 + 21 = 0.7 × 9 + 21 ± 2 = 44.8 ± 2
  • But actual CO2 32 ≪ 44.8 indicates that there is also associated respiratory alkalosis (hyperventilation)
  • Diagnosis is metabolic alkalosis (loss of K+ and Cl due to diuretics) + respiratory alkalosis

Example 6: A 60-year-old male, known case of hypertension, underwent emergency abdominal exploration and he suffered intraoperative infarct and arrest pH 7.27 ↓, CO2 66↑, HCO3 = 20 Na+/K+ = 138/102

  • pH = acidemia along with increased CO2 levels indicating respiratory acidosis
  • AG = 138 – (102 + 20) = 16 normal. Since, it was emergency abdominal exploration, the changes were acute.
  • ΔHCO3 = 0.1 × Δ CO2 = 0.1 × 26 = 2.6

Expected HCO3 = 24 + 2.6 = 26.6 but actual 20 < 26 indicating metabolic acidosis developing due to poor circulation. Hence diagnosis is post-arrest respiratory acidosis and developing metabolic acidosis.

Example 7: A 75-year-old male with severe abdominal pain and shock, pH 7.35, CO2 22, HCO3 = 14↓↓, Na+/K+/Cl 137/4.9/107

  • pH tends to acidemia = metabolic acidosis due to low HCO3
  • AG = (137+5) − (107 + 13) = 12 (NAGMA)
  • Respiratory compensation Winter formula CO2 (1.5 × 14) + 8 = 29

but actual CO2 22 < 29, there is overcompensation of ventilation resulting in respiratory alkalosis.

  • Urine AG and Urine Osmolarity Gap needs to be calculated.

Thus, the diagnosis is non-anion gap metabolic acidosis secondary to shock + respiratory alkalosis secondary to hyperventilation due to pain.

Example 8: A 45-year-old male known case of chronic renal failure admitted to the intensive care unit with severe vomiting pH 7.40, PaCO2 = 42, HCO3 = 22, Na+/K+/Cl 150/3.8/99, serum creatinine 8.7

  • pH = normal
  • AG = 150 − (99 + 22) = 29↑↑ (HAGMA)
  • Respiratory compensation CO2 = (1.5 × 24) + 8 = 44, compensation is adequate

ΔRatio = (AG − 12)/(HCO3 − 24) = 15/2 >2—presence of metabolic alkalosis. Thus, the diagnosis is HAGMA (uremic) + M alkalosis (vomiting), thus normalizing the pH values.


Thus, we conclude that knowledge about the triad of oxygenation, ventilation, and acid–base status helps us in thorough analysis of ABG. However, ABG results are only meaningful when inferred taking into account patients’ symptomatology, pathophysiology, and treatment in details. Hence, emphasis is to treat the patient and not the ABG.


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