Blood Gas I

Abstract

Blood gas analysis is an important means to assess someone’s oxygenation, adequacy of ventilation, and also acid–base status. Blood gas analysis can be done with either arterial or venous blood, but it provides valuable information to make a diagnosis, to assess the severity of the condition, and also to assess the effectiveness of treatment. Anion gap is routinely measured which provides us with the information regarding “cations” and “anions” in the blood and also points toward the possible cause of acidosis. Winter’s formula is used to determine the compensatory mechanism of acid–base disorder, and delta (Δ) gap provides the information regarding mixed acid–base disorder.

A 36-year-old woman presents to the emergency room with severe abdominal pain, nausea, vomiting, anorexia, and somnolence.

ABG: pH 7.20, PCO₂ 35 mmHg, pO₂ 68 mmHg on room air

Laboratory values: Na 130 mEq/L, Cl 80 mEq/L, HCO₃ 10 mEq/L

• 1. How do you diagnose a simple acid–base disorder?

• 2. What blood gas abnormality does this patient have?

• 3. How do you calculate anion gap and corrected anion gap?

• 4. How do you diagnose a mixed acid–base disorder and does this patient have mixed acid–base disorder?

• 5. What is Winter’s formula?

• 6. Is there any compensation in this blood gas value?

• 7. What are the possible causes of metabolic acidosis?

• 8. What are the possible causes of respiratory acidosis?

Answers

• 1. Initially the pH is used to determine acidosis or alkalosis, and then the value of PaCO₂/HCO₃ is used to determine if the derangement is metabolic or respiratory. If it is of respiratory origin, then we will have to determine whether the process is acute or chronic. If it is due to a metabolic component, then respiratory compensation should be calculated using the appropriate formula.

• 2. Our patient has a pH less than 7.4, which signifies acidosis. The HCO₃ is less than 24 mEq/L; therefore the primary abnormality in this patient is metabolic acidosis. This chart (Fig. 36.1) shows the steps to follow in order to diagnose an acid–base disorder [1].

• 

  Fig. 36.1 Diagnosis of acid–base disorders (This figure was published in Miller textbook, Chap. 21 in 2011. Permission obtained from Elsevier to reproduce the image.)

• 3. Anion gap (AG) = Na − (Cl + HCO₃)

  • (a) AG is the difference in the ‘routinely measured’ cations (Na) and ‘routinely measured’ anions (Cl and HCO₃) in the blood and depends on serum phosphate and albumin concentrations [2]. Determination of AG is useful in determining the cause of acidosis [3, 4]. The normal value for serum AG is usually 8–12 mEq/L. In our patient, AG = 130 − (80 + 10) = 40 mEq/L. So, this patient has a high AG, most likely due to starvation or diabetic ketoacidosis.

  • (b) In a normal healthy patient, negatively charged albumin is the single largest contributor to the AG [5]. Hypoalbuminemia causes a decrease in AG; hence AG is corrected to albumin level using the equation of Figge as follows: corrected AG = AG + [0.25 × (44 – Albumin)] [6].

    • If corrected AG >16, there is high AG acidosis.

    • If corrected AG <16, non-AG acidosis.

• 4. Delta gap formula can be used to assess mixed acid–base disorder.

  • (a) Δ gap = AG − 12 + HCO₃ (12 is normal serum AG value)

    • If Δ gap <22 mEq/L, then concurrent non-gap metabolic acidosis exists.

    • If Δ gap >26 mEq/L, then concurrent metabolic alkalosis exists.

  • (b) In our patient, Δ gap = 40 − 12 + 10 = 38 mEq/L. So, there is a concurrent metabolic alkalosis probably from vomiting in addition to high AG metabolic acidosis in this patient.

    So, there is a concurrent metabolic alkalosis probably from vomiting in addition to high AG metabolic acidosis in this patient.

• 5. Winter’s formula is used to determine whether there is an appropriate respiratory compensation during metabolic acidosis [1].

  • (a) Winter’s formula: PCO₂ = (1.5 × HCO₃) + 8

    • If measured PCO₂ > calculated PCO₂, then concurrent respiratory acidosis is present.

    • If measured PCO₂ < calculated PCO₂, then concurrent respiratory alkalosis is present.

• 6. In our patient, calculated PCO₂ = (1.5 × 10) + 8 = 23 mmHg according to Winter’s formula.

  Our measured PCO₂ of 35 mmHg is higher than the calculated PCO₂ of 23 mmHg, so our patient also has concurrent respiratory acidosis. Usually, metabolic acidosis is compensated by respiratory alkalosis, but due to somnolence in this patient, concurrent respiratory acidosis exists.

• 7. Causes of anion gap metabolic acidosis are easily remembered by pneumonic MUDPILES [1].

  • M: methanol

  • U: uremia

  • D: diabetic ketoacidosis

  • P: paraldehyde

  • I: infection, INH therapy

  • L: lactic acidosis

  • E: ethanol, ethylene glycol

  • S: salicylates (aspirin)

  Causes of non-gap metabolic acidosis:

  • Excessive administration of 0.9% normal saline

  • GI losses: diarrhea, ileostomy, neobladder, pancreatic fistula

  • Renal losses: renal tubular acidosis

  • Drugs: acetazolamide

• 8. Respiratory acidosis which is from increased CO₂ is due either to increased production or decreased elimination [2].

  • (a) Increased production of CO₂:

    • Malignant hyperthermia

    • Hyperthyroidism

    • Sepsis

    • Overfeeding

  • (b) Decreased elimination of CO₂:

    • Intrinsic pulmonary disease (pneumonia, ARDS, fibrosis, edema)

    • Upper airway obstruction (laryngospasm, foreign body, OSA)

    • Lower airway obstruction (asthma, COPD)

    • Chest wall restriction (obesity, scoliosis, burns)

    • CNS depression (anesthetics, opioids, CNS lesions)

    • Decreased skeletal muscle strength (myopathy, neuropathy, residual effects of neuromuscular blocking drugs)

  Rarely, an exhausted soda–lime or incompetent one-way valve in an anesthesia delivery system can contribute to respiratory acidosis.