All Unser Miranda

1. What is an Arterial Blood Gas (ABG)?

It is a test in which a sample of arterial blood is collected and analyzed to help determine the quality and extent of pulmonary gas exchange and acid-base balance.

Note

It can be collected by direct arterial puncture or through a cannulated arterial line (e.g., A-line — Invasive Arterial Blood Pressure).

2. Reference Table

To make it easier to memorize in the day-to-day routine of the ICU or ER, use the following parameters:

Order	Character	Parameter	Reference Range
1	Blood pH	pH	7.35 - 7.45
2	Plasma O₂	PaO₂	80 - 100 mmHg
3	O₂ Saturation	SaO₂	93 - 99 %
4	Respiratory Component	PaCO₂	35 - 45 mmHg
5	Metabolic Component	HCO₃⁻	22 - 26 mEq/L

Tip

Always analyze from top to bottom, and consider the pH as the compass for "Acidemia" or "Alkalemia", unless the last parameter (HCO₃⁻ - Bicarbonate) is out of the reference range.

3. Understanding the Parameters

PaO₂ refers to the partial pressure of O₂ in arterial blood (free O₂).
SaO₂ refers to the saturation of O₂ in arterial blood (O₂ bound to Hb).
pH refers to the concentration of free Hydrogen in the blood. It indicates acidity or alkalinity.

For a better reference of the values of each parameter, and also regarding their evaluative character, check the reference table above.

3.1. Acids and Bases

Acids are substances that can donate Hydrogen to a solution. In this context, the ones of interest are Volatile and Non-Volatile:

Volatile: H₂CO₃ → H₂O and CO₂ eliminated by the lungs.
Non-Volatile: Excreted only by the kidneys (metabolic process) → Lactic Acid and Ketoacids (e.g., ketone bodies).

PaCO₂ relates to the ventilatory function of the lungs (how effective gas exchange is).

Hypoventilation (PaCO₂ > 45mmHg) can lead to Respiratory Acidosis.
Hyperventilation (PaCO₂ < 35mmHg) can lead to Respiratory Alkalosis.

Bases are substances that can receive Hydrogen, removing it from the plasma. Bicarbonate (HCO₃⁻) is the base compound, and its regulation is done by the kidneys in a metabolic process that takes about 24h to 48h to fully establish AFTER the onset of a respiratory disorder.

HCO₃⁻ regulates blood pH due to its ability to receive a Hydrogen ion, being produced by the kidneys.

Metabolic Acidosis: Bicarbonate < 22mEq/L.
Metabolic Alkalosis: Bicarbonate > 26mEq/L.

4. Important Clinical Definitions

Caution

Understanding the underlying cause is vital for nursing conduct and the therapeutic plan.

Respiratory Acidosis (↑ in CO₂, > 45mmHg).
- Possible causes: CNS depression, Pneumothorax, Hypoventilation, Bronchial obstruction, Atelectasis, Pulmonary edema, Pneumonia, Bronchiolitis, Cystic fibrosis, and Heart failure.
Metabolic Acidosis (↓ HCO₃⁻, < 22mEq/L).
- Possible causes: Increased acids (Renal Failure, Ketoacidosis), Base loss (e.g., diarrhea).
Respiratory Alkalosis (↓ CO₂, < 35mmHg).
- Possible causes: Anxiety, Pain, Hyperventilation, Fever.
Metabolic Alkalosis (↑ HCO₃⁻, > 26mEq/L).
- Possible causes: Base gain (excessive use of bicarbonate or antacids — Omeprazole), Acid loss (vomiting), and Adrenal insufficiency.

See more about the definitions and the reasoning involved regarding the nomenclatures below.

5. How to Interpret Step by Step

Evaluate oxygenation (PaO₂): What is the value? Is it normal or in hypoxemia?
Evaluate the pH: Is it normal? Acidemia? Alkalemia?
- Discover the source of the pH alteration. Is it due to CO₂ or HCO₃⁻?
Evaluate PaCO₂: If altered, there is a respiratory disorder. Observe the relationship with the pH.
Evaluate HCO₃⁻: If altered, there is a metabolic-renal disorder. Observe the relationship with the pH.
Evaluate Compensation: Normal pH, but with altered parameters.
- If there are 2 alterations directly related to the pH, it is a Mixed Disorder (e.g., Mixed Acidosis).

Important

When the origin is respiratory, the kidneys will try to compensate (takes a few hours to days), leading to increased secretion of H+ and REABSORPTION of HCO₃⁻ (in acidosis) or vice versa.
When the origin is metabolic, the lungs will try to correct (in 5-15min), altering the respiratory PATTERN and FREQUENCY (e.g., Kussmaul respiration in acidosis).
Overcorrection does not occur (supercompensation), under any circumstances.

If there are active compensatory mechanisms, name according to the compensation (e.g., Fully Compensated Metabolic Acidosis). The activation of the system opposite to the primary disorder is what indicates compensation, which can be full or partial. This will tell if the activation of the opposite system reflected in the actual correction of the pH.

5.1. Uncompensated Disorders

These occur when there is an acid-base imbalance that has not yet been corrected by the compensation system, keeping the blood pH outside the normal range. In these cases, only the primary component will be altered, while the compensatory one will be within the reference range.

Examples include:

Uncompensated Respiratory Acidosis occurs when there is an increase in PaCO₂, resulting in a lower than normal pH, and the renal system has not yet begun to compensate, keeping HCO₃⁻ within the normal range.

Uncompensated Respiratory Alkalosis occurs when there is a reduction in PaCO₂, resulting in a higher than normal pH, and the renal system has not yet begun to compensate, keeping HCO₃⁻ within the normal range.
Uncompensated Metabolic Acidosis occurs when there is a reduction in HCO₃⁻, resulting in a lower than normal pH, and the respiratory system has not yet begun to compensate, keeping PaCO₂ within the normal range.
Uncompensated Metabolic Alkalosis occurs when there is an increase in HCO₃⁻, resulting in a higher than normal pH, and the respiratory system has not yet begun to compensate, keeping PaCO₂ within the normal range.

5.2. Compensated Disorders

These occur when there is an acid-base imbalance resulting in a blood pH within the normal range (full) or still altered but with a response from the opposite system (partial), with alterations in both parameters (PaCO₂, HCO₃⁻).

Examples include:

Fully Compensated Metabolic Acidosis occurs when the excess of acids or loss of bicarbonate reduces the blood pH (trending toward acidemia), and the respiratory system compensates for this by rapidly eliminating carbon dioxide (CO₂) through hyperventilation, which brings the pH back to the normal range. In this case, the pH would be normal (but trending downward, e.g., 7.36), HCO₃⁻ would be low, and PaCO₂ would also be low.

Fully Compensated Metabolic Alkalosis occurs when the excess of bicarbonate or loss of acids increases the blood pH (trending toward alkalemia), and the respiratory system compensates for this by retaining carbon dioxide (CO₂) through hypoventilation, which brings the pH back to the normal range. In this case, the pH would be normal (trending upward, e.g., 7.44), HCO₃⁻ would be high, and PaCO₂ would also be high.
Fully Compensated Respiratory Acidosis occurs when the lungs cannot eliminate enough carbon dioxide (CO₂) (due to hypoventilation), increasing its concentration in the blood and, consequently, reducing the pH (trending toward acidemia). As a compensatory mechanism, the renal system increases the retention of bicarbonate (HCO₃⁻), raising its concentration to neutralize hydrogen ions (H⁺). In this case, the pH would be normal, PaCO₂ would be high, and HCO₃⁻ would also be high.
Fully Compensated Respiratory Alkalosis occurs when the lungs eliminate excess carbon dioxide (CO₂) (due to hyperventilation), decreasing its concentration in the blood and, consequently, raising the pH (trending toward alkalemia). As a compensatory mechanism, the renal system increases the excretion of bicarbonate (HCO₃⁻), reducing its concentration to neutralize the alkalemia. In this case, the pH would be normal, PaCO₂ would be low, and HCO₃⁻ would also be low.

Partially Compensated Respiratory Alkalosis occurs when the lungs eliminate excess CO₂, decreasing its concentration in the blood and, consequently, raising the pH (trending toward alkalemia). To compensate, the renal system begins to excrete bicarbonate (HCO₃⁻), but has not yet managed to reduce the pH to the normal range. In this case, the pH would be altered (alkalemia), PaCO₂ would be low, and HCO₃⁻ would also be low.

Partially Compensated Metabolic Alkalosis occurs when there is an excess of bicarbonate in the blood, and the respiratory system tries to compensate by retaining carbon dioxide (CO₂) through hypoventilation. As a result, the pH would be altered (alkalemia), HCO₃⁻ would be high, and PaCO₂ would be high.
Partially Compensated Respiratory Acidosis occurs when the lungs cannot eliminate enough CO₂, increasing its concentration in the blood and reducing the pH (acidemia). To compensate, the renal system increases bicarbonate (HCO₃⁻) retention. In this case, the pH would be altered (acidemia), PaCO₂ would be high, and HCO₃⁻ would also be high.
Partially Compensated Metabolic Acidosis occurs when the excess of acids or loss of bicarbonate reduces the blood pH, and the respiratory system compensates for this by eliminating CO₂ through hyperventilation. In this case, the pH would be altered (acidemia), HCO₃⁻ would be low, and PaCO₂ would be low.

5.3. Mixed Disorders

This occurs when there is a combination of problems, such as a simultaneous respiratory alkalosis and metabolic alkalosis. In this scenario, the systems do not "oppose" each other to compensate, but rather move in the direction of worsening the pH alteration.

Tip

The pH is the sum result of the disorders. In mixed disorders, the pH can be highly altered or even masked, appearing "normal" when two opposing problems cancel each other out (e.g., metabolic acidosis + respiratory alkalosis).

6. Anion Gap (AG)

Calculating the AG is fundamental, as it helps in differentiating between causes of metabolic acidosis that involve the retention of acids and consumption of base (ketoacidosis, lactic acidosis) and those that involve primary loss of bicarbonate (diarrhea).

The formula to calculate the AG is: AG = [Na⁺] - (Cl⁻ + HCO₃⁻)

Where:

[Na⁺] is the sodium concentration in the blood
[Cl⁻] is the chloride concentration in the blood
[HCO₃⁻] is the bicarbonate concentration in the blood
The normal reference value for AG is generally 8 to 12 mEq/L (without potassium in the formula).

6.1. Variations of Metabolic Acidosis according to AG

Hyperchloremic Acidosis (Normal AG): Occurs when there is a primary loss of bicarbonate, resulting in a decrease in HCO₃⁻. To maintain plasma electroneutrality (since bicarbonate, an anion, was lost), the kidneys increase Chloride (Cl⁻) reabsorption. In this case, the AG will be normal, because the loss of HCO₃⁻ is perfectly compensated by the increase in Cl⁻ (Hyperchloremia).

Causes of metabolic acidosis with normal AG (hyperchloremic) include gastrointestinal bicarbonate loss, such as in Diarrhea and Pancreatic Fistula, as well as the administration of certain medications, such as Ammonium Chloride, or Renal Tubular Acidosis.

Normochloremic Acidosis (High AG): Occurs when there is a production or accumulation of unmeasured acids (such as lactate, ketoacids, or toxins). These acids consume HCO₃⁻, but the unmeasured anions increase. Since Chloride does not need to increase to maintain balance, chloremia usually remains normal, resulting in a larger Gap. In this case, the AG will be elevated, reflecting the "invisible anions" in the formula.

Causes of metabolic acidosis with high AG include Diabetic Ketoacidosis, Lactic Acidosis, Renal Failure (uremia), and ingestion of certain toxins, such as Salicylate.

Note

When evaluating the Anion Gap, it is important to correct its value if the patient has hypoalbuminemia, because albumin is the main unmeasured anion that makes up the baseline "Gap".