Arterial Blood Gas (ABG) Interpretation

Abstract

This chapter reviews the fundamentals in acid-base interpretation and the differential diagnosis for each acid-base pattern. We also discuss oxygen transfer physiology and pathophysiology with a final case based illustration of the topic.

Introduction

• • If you are given this ABG: pH (7.38); PaCO₂ (41 mmHg); PaO₂ (95 mmHg); HCO₃ (23 mmol/L); Na⁺ (143 mg/dl); Cl⁻ (98 mg/dl), how would you interpret it?

• • These values are all normal but the patient has significant acid base disturbances that may be fatal, if untreated. This chapter tries to introduce a simple approach to help solving any acid-base problem including the hidden ones, such as the one given above.

• • The above ABG is discussed in case number 4, below.

Definitions [1]

• • Acidosis: is a disturbance that lowers the extra-cellular fluid pH.

• • Alkalosis: is a disturbance that raises the extra-cellular fluid pH.

• • Acidemia: is a reduction of the extra-cellular fluid pH of the blood. Accordingly an acidemia may result from a combination of different types of acidosis or a combination of acidosis and alkalosis.

• • Alkalemia: is an elevation of the extra-cellular fluid pH of the blood.

• • Base Excess (BE): is the amount of acid (+) or base (−) (in mEq/liter) required to restore the pH of a liter of blood to the normal range at a PaCO₂ of 40 mmHg. Table 8.1 shows the normal values of the ABG components.

Table 8.1 ABG normal values

Henderson Equation [2]

• • This equation represents the relationship between the components of the ABG and may be written in different ways:

  • – A simple way is:$\left[{\mathrm{H}}^{+}\right]=\mathrm{K}\times \frac{\left[{\mathrm{H}}_2{\mathrm{CO}}_3\right]}{\left[{\mathrm{H}\mathrm{CO}}_3\right]},\kern0.875em \mathrm{where}\kern0.875em \mathrm{K}=24$

  • – By substituting PaCO₂ for [H₂CO₃] that is measured from ABG, the equation can be written in a more practical way [2]:

    $\left[{\mathrm{H}}^{+}\right]=\mathrm{K}\times \frac{{\mathrm{PaCO}}_2}{\left[{\mathrm{H}\mathrm{CO}}_3\right]},\kern0.875em \mathrm{where}\kern0.875em \mathrm{K}=24$

    • – [H⁺] is the Hydrogen ion (proton) concentration, and it can be easily calculated from pH, see Table 8.2 .

    • – The rest of the variables can be acquired directly from the ABG.

• • The purpose of this equation is:

  • – To ensure that the ABG values are accurately recorded. Solving the equation should result in equalization of its two sides.

  • – If one of the ABG values is missing, the equation can be solved to determine that missing value. Indeed this is usually done for ABG results. The pH and PaCO₂ are actually measured in the blood sample and the HCO₃ is calculated using this equation.

    e.g.: pH 7.3 ([H⁺] = 50); PaCO₂ = 50 mmHg; HCO₃ = unknown

    • – By applying Henderson equation:

      [H⁺] = K × (P_aCO₂/[HCO₃])

      50 = 24 × (50/[HCO₃])

      Therefore: [HCO₃] = 24.

Table 8.2 Calculating [H⁺] from pH [2]

Metabolic Acidosis

Causes

Metabolic acidosis can be classified into anion gap (AG) and non-anion gap (NAG) metabolic acidosis [3, 4]. The NAG metabolic acidosis is also called hyperchloremic metabolic acidosis, because it is associated with high serum chloride. Table 8.3 summarizes these causes.

Table 8.3 Causes of metabolic acidosis

Approach to Metabolic Acidosis

• • In both types of metabolic acidosis, the primary disturbance is a drop in bicarbonate. Because the respiratory system is fast in its compensation, there is a rapid drop in PaCO₂ which should always accompany a pure metabolic acidosis (remember that PaCO₂ changes in the same direction as HCO₃ in a pure metabolic disturbance). Don’t forget that normal bicarbonate doesn’t exclude a metabolic disturbance as metabolic acidosis may coexist with metabolic alkalosis.

• • We suggest using one of the many available protocols in interpreting the ABG. Table 8.4 summarizes a usefull one.

• • The first step is to determine the type of disturbance (acidemia or alkalemia) by looking at the pH.

• • Then determine the most likely primary disturbance. So, if a reduction in HCO₃ is the predominant abnormality in the setting of acidemia, then the primary disturbance is a metabolic acidosis.

• • Determine the type of metabolic acidosis you are dealing with (AG or NAG) by calculating the AG [5]:

  AG = Na ⁺ − (Cl ⁻ + HCO ₃ ⁻ )

  • – If normal (≤12), then this is a non-anion gap metabolic acidosis (NAGMA). Go to the next step.

  • – If high (>12), then this is an anion gap metabolic acidosis (AGMA). In AGMA, you need to determine then whether another metabolic disturbance is present, by calculating the corrected HCO₃:

    Corrected HCO ₃ = ΔG + measured HCO ₃; as ΔG = AG−12

    • (a) If the corrected HCO₃ is within the normal range of HCO₃ (21–26), then there is no other metabolic disturbance, so go to the next step.

    • (b) If the corrected HCO₃ is higher than the normal range, then there is an additional metabolic alkalosis (corrected HCO₃ is higher than it should)

    • (c) If the corrected HCO₃ is lower than the range, then there is an additional NAG metabolic acidosis (NAGMA)

• • Determine whether there is a primary respiratory disturbance by initially looking at the PaCO₂

  • – If PaCO₂ is normal or high (opposite direction to HCO₃), then there is a primary respiratory acidosis. Go to the next step.

  • – If PaCO₂ is low (same direction as HCO₃), then calculate the expected PaCO₂ range [4, 6]:

    Expected PaCO ₂ Range = 1.5 × HCO ₃ + (8 ± 2)

    • (a) If the patient’s PaCO₂ is within this range, then the patient has no respiratory disturbance (this is an appropriate compensation)

    • (b) If patient’s PaCO₂ is above the range, then there is a primary respiratory acidosis (inadequate compensation).

    • (c) If patient’s PaCO₂ is below the range, then there is a primary respiratory alkalosis (overcompensation). The lowest level PaCO₂ can reach as a compensation for metabolic acidosis is 10–12 mmHg [7].

• • In non-anion gap metabolic acidosis, determine whether the cause is of renal or non-renal origin by calculating the urine anion gap (also called Urine Net Charge or UNC) [8]:

  Urine Gap = (U _Na + U _K ) − U _Cl

  • – If urine gap is negative, then the kidney is appropriately compensating by secreting H⁺ in the form of ammonia (NH₄ ⁺) which neutralizes this negative urine anion gap. An extra-renal cause of metabolic acidosis is the most likely.

  • – If urine gap is positive (or zero), then the kidneys are not secreting H⁺ appropriately, indicating a renal cause of the metabolic acidosis (Renal tubular acidosis, RTA).

• • These steps are summarized in Table 8.5 .

Table 8.4 Approach to ABG interpretation

Table 8.5 Approach to metabolic acidosis

Metabolic Alkalosis

Causes

• • Are classified into Cl ⁻ responsive and Cl ⁻ resistant alkaloses, which are summarized in Table 8.6.

Table 8.6 Causes of metabolic alkalosis

Approach to Metabolic Alkalosis

• • Opposite to metabolic acidosis, metabolic alkalosis presents as a high HCO₃ which is compensated for by an increase in PaCO₂ [9, 10] (which rarely exceeds a level of 60 mmHg [7]). A normal or a low PaCO₂ indicates a respiratory alkalosis, in this setting.

• • Determine the type of disturbance (acidemia or alkalemia) by looking at the pH.

• • Then determine the most likely primary disturbance. So if the increase in HCO₃ is the predominant abnormality rather than a decrease in PaCO₂, then the primary disturbance is metabolic alkalosis.

• • Determine whether a primary metabolic acidosis is present as well by calculating AG:

  • – If normal (~12), then there is no primary metabolic acidosis. Go to next step.

  • – If high (>12), then there is an addition primary anion gap metabolic acidosis (AGMA).

• • Determine whether there is a primary respiratory disturbance by initially looking at the PaCO₂

  • – If PaCO₂ is normal or low (opposite direction to HCO₃), then there is a primary respiratory alkalosis. Go to next step.

  • – If PaCO₂ is high (same direction as HCO₃), calculate the expected PaCO₂ range [11,12,13]:

    Expected PaCO ₂ Range = 0.9 × HCO ₃ + (9 to 16)

    • (a) If the patient’s PaCO₂ is within this range, then the patient has no additional respiratory disturbance (this is an appropriate compensation).

    • (b) If patient’s PaCO₂ is above the range, then there is a primary respiratory acidosis (overcompensation).

    • (c) If patient’s PaCO₂ is below the range, then there is a primary respiratory alkalosis (inadequate compensation).

• • Determine the type of metabolic alkalosis (Cl⁻ responsive or Cl⁻ resistant) by measuring the urinary Cl⁻ (U_Cl) [1]:

  • – If U_Cl is <20 mmol/L, then this is Cl⁻ responsive (depleted) metabolic alkalosis. Think of it as the body is trying to conserve Cl⁻.

  • – If U_Cl is >20 mmol/L, then this is Cl⁻ resistant (expanded) metabolic alkalosis.

• • Table 8.7 summarizes these steps.

Table 8.7 Approach to metabolic alkalosis

Respiratory Acidosis

Types of Respiratory Acidosis

• • Because the body compensates slowly for a primary respiratory disturbance, the later is then classified into acute and chronic forms. The following will highlight these forms.

• • In acute respiratory acidosis, for every 10 mmHg rise in PaCO₂ [14]:

  • – pH drops by 0.08; that is:

    $\mathrm{pH}=0.08\times \frac{{\mathrm{PaCO}}_2-40}{10}$

  • – HCO₃ increases by 1 mmol/L; maximum level of HCO₃ is ~32 mmol/L.

• • In chronic respiratory acidosis, for every 10 mmHg rise in PaCO₂ [15]:

  • – pH drops by 0.03; that is:

    $\mathrm{pH}=0.03\times \frac{{\mathrm{PaCO}}_2-40}{10}$

  • – HCO₃ increases by 3 mmol/L; maximum level of HCO₃ is ~45 mmol/L.

• • Tables 8.8 and 8.9 summarize the causes and steps of interpretation of respiratory acidosis, respectively.

Table 8.8 Causes of respiratory acidosis

Table 8.9 Approach to respiratory acidosis

Respiratory Alkalosis

Types of Respiratory Alkalosis

• • In acute respiratory alkalosis, for every 10 mmHg drop in PaCO₂ [16]:

  • – pH rises by 0.08; that is:

    $\mathrm{pH}=0.08\times \frac{40-{\mathrm{PaCO}}_2}{10}$

  • – HCO₃ drops by 2 mmol/L.

• • In chronic respiratory alkalosis, for every 10 mmHg drop in PaCO₂ [17, 18]:

  • – pH increases by 0.03; that is:

    $\mathrm{pH}=0.03\times \frac{40-{\mathrm{PaCO}}_2}{10}$

  • – HCO₃ drops by 5–7 mmol/L.

• • Tables 8.10 and 8.11 summarize the causes and steps of interpretation of respiratory alkalosis, respectively.

Table 8.10 Causes of respiratory alkalosis

Table 8.11 Approach to respiratory alkalosis

Effect of a Low Albumin Level on AG

• • Because albumin is one of the unmeasured anions in the blood, a drop in its level (e.g. secondary to a critical illness or liver disease) will influence the AG level. In this case, the calculated AG should be adjusted for albumin:

  Adjusted AG = Calculated AG + [2.5 × (4.5 – alb in g/dl)]

• • If this adjustment is ignored with a low albumin, the calculated anion gap will be underestimated and a significant AGMA may be missed.

Acid Base Nomogram

• • The nomogram shown in Figure 8.1 is one of many acid-base nomograms developed to assisst in solving difficult acid base disturbances and involves plotting pH, HCO₃ and PaCO₂ [19]. These are commonly referred to as Flenley’s acid base nomograms.

Figure 8.1

An acid–base nomogram, used to interpret ABG by directly plotting HCO₃, PaCO₂, and pH (With permission from Goldberg et al. [20])

The Alveolar—Arterial (A-a) Gradient and Alveolar Gas Equation [21]

Alveolar Gas Equation

• • This equation allows us to estimate the O₂ tension in the alveoli (P_AO₂):

  ${\mathrm{P}}_{\mathrm{A}}{\mathrm{O}}_2={\mathrm{P}}_{\mathrm{I}}{\mathrm{O}}_2\hbox{--} \frac{{\mathrm{P}}_{\mathrm{a}}{\mathrm{CO}}_2}{\mathrm{RQ}};\kern1.125em \mathrm{where}\kern0.875em {\mathrm{P}}_{\mathrm{I}}{\mathrm{O}}_2={\mathrm{F}}_{\mathrm{I}}{\mathrm{O}}_2\left({\mathrm{P}}_{\mathrm{a}\mathrm{tm}}\hbox{--} {\mathrm{P}}_{{\mathrm{H}}_2\mathrm{O}}\right)$

• • To understand this equation it is good to go through certain definitions:

  • – P _atm O ₂: is the atmospheric O₂ tension or partial pressure of O₂. It is calculated by multiplying the atmospheric pressure (760 mmHg at sea level) by the percentage of O₂ in the atmosphere (21%):

    P_atmO₂ = 0.21 × P_atm

    = 0.21 × 760 = 160 mmHg, (at sea level)

  • – P _I O ₂: is the O₂ tension of inspired air. Because the inspired air contains water vapor, it doesn’t equal P_atmO₂. The water vapor tension (P_H2O) should then be extracted from the atmospheric pressure before applying the above equation:

    P_IO₂ = F_IO₂ × (P_atm − P_H2O)

     = 0.21 × (760–47) = 0.21 × 713 = 150 mmHg

    (if breathing room air, at sea level)

  • – P _A O ₂: the alveolar O₂ tension. CO₂ diffuses from the circulation into the alveoli and hence reduces the P_AO₂. Accordingly, P_ACO₂ has to be subtracted from P_IO₂ to get P_AO₂. P_aCO₂ can be substituted for P_ACO₂ (when taking the Respiratory Quotient (RQ) into consideration, which is assumed to be 0.8 while at rest):

        ${\mathrm{P}}_{\mathrm{A}}{\mathrm{O}}_2={\mathrm{P}}_{\mathrm{I}}{\mathrm{O}}_2\hbox{--} \frac{{\mathrm{P}}_{\mathrm{a}}{\mathrm{CO}}_2}{\mathrm{RQ}};\kern0.875em \mathrm{as}\kern0.875em \mathrm{RQ}=0.8$

          $=150\hbox{--} \frac{{\mathrm{P}}_{\mathrm{a}}{\mathrm{CO}}_2}{0.8}\kern0.875em \mathrm{OR}\kern0.875em 150\hbox{--} \left({\mathrm{P}}_{\mathrm{a}}{\mathrm{CO}}_2\times 1.25\right)$

            = 150 – (40 × 1.25) = 100 mmHg

          (if breathing room air, at see level)

  • – PaO ₂ : is the arterial O₂ tension that is measured in the ABG.

  • – F _I O ₂: is the Fractional Inspired O ₂, i.e. the percentage of O₂ in the inspired air. If breathing room air at sea level, it equals 0.21. This value changes if the patient is breathing through a nasal cannula or a face mask.

  • – RQ: is the Respiratory Quotient and represents the amount of CO₂ produced for a given amount of O₂ consumed by our bodies. It equals 0.8 at rest, in a normal individual (because we produce 0.8 mole of CO₂ for each mole of O₂ we consume while at rest). The RQ increases with exercise however. Next chapter discusses this in more detail.

A-a Gradient (P_(A-a)O₂)

• • It is the difference between the alveolar and the arterial O₂ tension. Its calculation is now easy; see Figure 8.2:

     ${\mathrm{P}}_{\left(\mathrm{A}-\mathrm{a}\right)}{\mathrm{O}}_2={\mathrm{P}}_{\mathrm{A}}{\mathrm{O}}_2\hbox{--} {\mathrm{P}}_{\mathrm{a}}{\mathrm{O}}_2;\kern0.875em \mathrm{where}\kern0.875em {\mathrm{P}}_{\mathrm{A}}{\mathrm{O}}_2={\mathrm{P}}_{\mathrm{I}}{\mathrm{O}}_2\hbox{--} \frac{{\mathrm{P}}_{\mathrm{a}}{\mathrm{CO}}_2}{\mathrm{RQ}}$

        $\mathrm{OR}\kern1.125em {\mathrm{P}}_{\left(\mathrm{A}-\mathrm{a}\right)}{\mathrm{O}}_2=\left[{\mathrm{P}}_{\mathrm{I}}{\mathrm{O}}_2\hbox{--} \frac{{\mathrm{P}}_{\mathrm{a}}{\mathrm{CO}}_2}{\mathrm{RQ}}\right]-{\mathrm{P}}_{\mathrm{a}}{\mathrm{O}}_2$

  • If at see level and breathing room air (F_IO₂ of 0.21), then the equation can be simply written as follows:

      ${\mathrm{P}}_{\left(\mathrm{A}-\mathrm{a}\right)}{\mathrm{O}}_2=\left[150\hbox{--} \frac{{\mathrm{P}}_{\mathrm{a}}{\mathrm{CO}}_2}{0.8}\right]-{\mathrm{P}}_{\mathrm{a}}{\mathrm{O}}_2$

     OR P_(A − a)O₂ = [150 – (1.25 × P_aCO₂)] − P_aO₂

• • P_(A-a)O₂ is normally ≤15 mmHg and increases with age. Different formulas are used to determine the normal P_(A-a)O₂ in relation to age, the following is a popular one [20]:

  Normal P_(A-a)O₂ = 2.5 + (0.21 × age in years)

Figure 8.2

This diagram summarizes the alveolar gas principles. Breathing RA at sea level in a normal person

Mechanisms of Hypoxemia [21]

These mechanisms can be classified into hypoxemia with a wide A-a gradient and hypoxemia with a normal A-a gradient:

• • Hypoxemia with a wide A-a gradient (P_(A-a)O₂ > 15)

  • – Shunting, like intra-cardiac shunts or pulmonary AV malformation.

  • – VQ mismatch, as in atelectasis

  • – Decreased mixed venous O₂ tension $\left(\mathrm{P}\overline{\mathrm{v}}{\mathrm{O}}_2\right)$.

  • – Diffusion limitation (reduced gas tranfer) (seen in severe ILD).

• • Hypoxemia with a normal A-a gradient (P_(A-a)O₂ ≤ 15)

  • – Low inspired O₂ (↓ F_IO₂), as in case of high altitude.

  • – Hypoventilation, as in obesity hypoventilation syndrome.

    • (a) Hypoventilation causes primarily hypercapnia because of impaired washout of CO₂. As the alveolar CO₂ equals the arterial CO₂, both PaCO2 and P_ACO₂ will be equally elevated.

    • (b) Hypoventilation causes hypoxemia, as well, if the patient is breathing room air. In this case, the degree of hypoxemia can be predicted from the level of PaCO₂ using the alveolar gas equation. In general, if P_aCO₂ increases by 20 mmHg, P_AO₂ drops by 25 mmHg, even if the lungs are normal; Figure 8.3.

Figure 8.3

Effects of hypoventilation on alveolar and arterial O₂ and CO₂ tension: This patient is breathing room air at sea level and has a normal A − a gradient but still has a severe hypoxemia (P_aO₂ of 45). The reason for this hypoxemia is the elevated P_ACO₂ (secondary to hypoventilation). The P_ACO₂ has increased by 40 mmHg resulting in a reduction in P_AO₂ by 50 mmHg, which resulted in this degree of hypoxemia: P_AO₂ = 150 − (1.25 × 80) = 150–100 = 50 mmHg

Types of Respiratory Failure [21]

• • Type I respiratory failure (hypoxemic respiratory failure) is characterized by hypoxia and defined as an isolated reduction of PaO₂ to <60 mmHg (the point at which the SaO₂ drops steeply as shown in the O₂ dissociation curve); Figure 8.4. This type of respiratory failure is associated with an increased A-a gradient.

• • Type II respiratory failure (ventilatory failure) is characterized by hypoxia and hypercapnia and defined as a PaCO₂ of >50 mmHg. The A-a gradient is normal.

Figure 8.4

O₂ dissociation curve: when P_aO₂ > 60 mmHg, SaO₂ changes slightly with any given change in P_aO₂. When P_aO₂ < 60 mmHg, SaO₂ changes significantly with any given change in P_aO₂

Illustrative Cases

Case 1

• • A 63-year-old man presents with generalized malaise. His ABG shows: pH (7.32); PaCO ₂ (24); HCO ₃ (12); Na ⁺ (135); K ⁻ (5.4); Cl ⁻ (101). What type of acid base disturbance does this patient have?

• • Interpretation:

  • – Applying the Henderson equation:

    [H⁺] = K × (PaCO₂/ [HCO₃]) ↔ 48 = 24 × (24/12) = 48

    – So, the equation proves that the values are accurate.

  • – pH is ↓, so this is an acidemia.

  • – The predominant abnormality is the ↓ HCO₃ → so this is primary metabolic acidosis.

  • – By calculating the AG = Na⁺ − (Cl⁻ + HCO₃) = 22 (↑). It is >12 → so this is an anion gap metabolic acidosis (AGMA).

  • – Corrected HCO₃ = ΔG + measured HCO₃ (as ΔG = AG – 12 = 10).

      = 10 + 12 = 22; it is within the normal range of HCO₃ (21–26), so there is no other metabolic disturbance.

  • – PaCO₂: is low, so we should calculate the expected PaCO₂ range:

    – Expected PaCO₂ Range = 1.5 × HCO₃ + (8 ± 2)= 24–28; the patient’s PaCO₂ lies within this range, so there is no primary respiratory disturbance.

  • – Conclusion: This patient has a pure anion gap metabolic acidosis. This patient was found to have a creatinine of 500 mg/dl and so the unmeasured anions producing the gap were related to renal failure.

Case 2

• • Interpret the following ABG: pH (7.11); PaCO ₂ (16); HCO ₃ (5); Na ⁺ (133); Cl ⁻ (118).

• • Interpretation:

  • – Applying Henderson equation indicates accurate results.

  • – ↓ pH → so this is an acidemia.

  • – ↓ HCO₃ → so this is a primary metabolic acidosis.

  • – AG = Na⁺ − (Cl⁻ + HCO₃) = 10 (normal) → so this is a non-anion gap metabolic acidosis (NAGMA).

  • – Expected PaCO₂ Range = 1.5 × HCO₃ + (8 ± 2) = 13.5–17.5 → the patient’s PaCO₂ lies within this range, so there is no primary respiratory disturbance.

  • – Conclusion: the patient has a simple non-anion gap metabolic acidosis. This patient is a 74-year-old very anxious lady who presented with severe gastroenteritis (diarrhea).

Case 3

• • Interpret the following ABG: pH (6.88); PaCO ₂ (40); HCO ₃ (7); Na ⁺ (135); Cl ⁻ (118).

• • Interpretation:

  • – Applying Henderson equation indicates accurate results.

  • – ↓ pH → so this is acidemia.

  • – ↓ HCO₃ → so this is primary metabolic acidosis.

  • – AG = Na⁺ − (Cl⁻ + HCO₃) = 10 (normal) → so this is a non-anion gap metabolic acidosis (NAGMA).

  • – PaCO₂ is normal (it should be low in the face of a very low pH) → so, there is a primary respiratory acidosis. Although unnecessary, you can still apply the Expected PaCO₂ Range = 1.5 × HCO₃ + (8 ± 2) = 16.5–20.5 → the patient’s PaCO₂ is higher than this range so there is primary respiratory acidosis.

  • – Conclusion: A combined non-anion gap metabolic acidosis and respiratory acidosis. This is the same patient described in case 2 after she was sedated with a benzodiazepine that suppressed her respiratory centre. Sedation can be harmful in elderly patients.

Case 4

• • A 23-year-old man presented with generalized malaise and vomiting. His ABG showed: pH (7.38); PaCO ₂ (41);PaO ₂ (95); HCO ₃ (23); Na ⁺ (143); Cl ⁻ (98). What type of acid base disturbance this patient has?

• • Interpretation:

  • – Applying Henderson equation indicates accurate results.

  • – Normal pH → so no acidemia or alkalemia.

  • – Normal HCO₃ → so no obvious metabolic abnormality.

  • – AG = Na⁺ − (Cl⁻ + HCO₃) = 22 (↑) → so there is an anion gap metabolic acidosis.

  • – Corrected HCO₃ = ΔG + measured HCO₃ (ΔG = 22–12 = 10). = 10 + 23 = 33; So, the corrected HCO₃ = 33 → it is higher the normal range of HCO₃ (21–26) → so there is an additional metabolic alkalosis.

  • – PaCO₂ is normal (so does the pH and HCO₃, so this is appropriate. If in doubt, apply expected PaCO₂ range).

  • – Expected PaCO₂ Range = 1.5 × HCO₃ + (8 ± 2) = 41–45 → the patient’s PaCO₂ (41) lies within this range → so, there is no primary respiratory disturbance.

  • – Conclusion: Although this ABG looked normal, a combined disturbance is present, anion gap metabolic acidosis and metabolic alkalosis. This patient was found to have a blood sugar of 28 mmol/L and he had ketones in the urine. He had diabetic ketoacidosis causing his AGMA and vomiting caused his metabolic alkalosis.

Case 5

• • Interpret this ABG: pH (7.55); PaCO ₂ (49); HCO ₃ (42); Na ⁺ (148); Cl ⁻ (84).

• • Interpretation:

  • – Applying Henderson equation indicates accurate results.

  • – ↑ pH → so there is an alkalemia.

  • – ↑ HCO₃ → so there is a metabolic alkalosis.

  • – AG = Na⁺ − (Cl⁻ + HCO₃) = 22 (↑) → so there is an anion gap metabolic acidosis.

  • – ↑ PaCO₂ (same direction as HCO₃) → Expected PaCO₂ Range = 0.9 × HCO₃ + (9-to-16) = 47–54 → the patient’s PaCO₂ (49) lies within this range → so, there is no primary respiratory disturbance.

  • – Conclusion: a combined anion gap metabolic acidosis and metabolic alkalosis with an alkalemic pH.

Case 6

• • A 58-year-old man (heavy smoker) admitted to the ICU with sepsis. He is not intubated yet but has an NG tube. His ABG showed: pH (6.88); PaCO ₂ (40); HCO ₃ (7); Na ⁺ (142); Cl ⁻ (100). What type of acid base disturbance does this patient have?

• • Interpretation:

  • – Applying the Henderson equation indicates accurate results.

  • – ↓ pH → so this is an acidemia.

  • – ↓ HCO₃ → so this is a primary metabolic acidosis.

  • – AG = Na⁺ − (Cl⁻ + HCO₃) = 35 (↑) → so this is an anion gap metabolic acidosis.

  • – Corrected HCO₃ = 30; it is higher than the normal range of HCO₃ (21–26), so there is an additional primary metabolic alkalosis.

  • – PaCO₂ is normal (it should be low) → there is a primary respiratory acidosis.

  • – Conclusion: A combined anion gap metabolic acidosis, metabolic alkalosis and respiratory acidosis. This patient’s metabolic acidosis is most likely related to sepsis. His respiratory acidosis is likely due to respiratory failure (COPD) and the metabolic alkalosis due to gastric suction.

Case 7

• • Interpret the following ABG: pH (7.55); PaCO ₂ (44); HCO ₃ (45); Na ⁺ (144); Cl ⁻ (112).

• • Interpretation:

  • – Applying Henderson equation:

    [H⁺] = K × (PaCO₂/ [HCO₃]) ↔ 28 ≠ 24 × (44/45) = 21

    So, the equation indicates that the values are incorrect. Repeat ABG sampling is advised or check with the lab to ensure accurate calculation of HCO₃ and recording of results.

Case 8

• • A 68-year-old man known to have COPD presented to the emergency department with increasing cough. His ABG showed: pH (7.34); PaCO ₂ (60); PaO ₂ (60); HCO ₃ (31); AG (11). What is the acid base disturbance? What is the A-a gradient provided that the patient was on room air, at sea level?.

• • Interpretation:

  • – Applying Henderson equation indicates accurate results.

  • – pH is slightly low indicating a mild acidemia.

  • – ↑ PaCO₂, so this is a primary respiratory acidosis.

  • – Metabolic compensation indicates a chronic respiratory acidosis: PaCO₂ increased by 20 mmHg which corresponds to a drop in pH by ~ 0.6 (0.3/10 mmHg of PaCO₂) and an increase in HCO₃ by ~ 6 (3/10 mmHg of PaCO₂).

  • – AG is normal and HCO₃ is adequately increased, therefore no metabolic disturbances.

  • – The A-a gradient = (150 – PaCO₂ × 1.25) – PaO₂ = 11 (normal)

  • – Conclusion: Chronic primary respiratory acidosis related to COPD.

Case 9

• • The patient in case 8 became drowsy and unresponsive 4 hours after presentation. A repeated ABG showed: pH (7.15); PaCO ₂ (96); PaO ₂ (169) HCO ₃ (33); AG (10).

• • Interpretation:

  • – Applying Henderson equation indicates accurate results.

  • – ↓ pH → acidemia.

  • – ↑ PaCO₂ → so this is primary respiratory acidosis.

  • – Metabolic compensation indicates an acute respiratory acidosis in addition to the chronic respiratory acidosis.

  • – AG is normal and HCO₃ is adequately increased, therefore no metabolic disturbances.

  • – Conclusion: Acute primary respiratory acidosis and a chronic respiratory acidosis. This COPD patient was given a high flow O₂ (indicated by the high PaO₂) unnecessarily resulting in CO₂ elevation (the pathophysiology behind this is multifactorial) and severe acute respiratory acidosis. The acute increase in PaCO₂ resulted in mental deterioration and unresponsiveness.

Case 10

• • The patient in the previous case was intubated and mechanically ventilated to protect his airways. A repeat ABG showed: pH (7.55); PaCO ₂ (39); PaO ₂ (198); HCO3 (33); AG (10).

• • Interpretation:

  • – Applying the Henderson equation indicates accurate results.

  • – ↑ pH, therefore alkalemia.

  • – The elevated HCO₃ indicates a metabolic alkalosis resulting from overcorrecting the chronic respiratory acidosis. The elevated HCO₃ was primarily a compensatory mechanism for the respiratory acidosis. The resulting metabolic alkalosis is sometimes called “post-hypercapnic metabolic alkalosis”. The ventilator should have been set to target a normal pH rather than a normal HCO₃.