Eating Batteries, Drinking Alien’s Blood – Part 1

Oh I’m alkaline, I’m always keeping to the basics.

Mouth of the River by Imagine Dragons

Welcome back, guys…

Let’s start immediately with a couple of clinical cases…

Case 1:

You are doing your usual ward round when the attending nurse calls you because the patient in bed 13 is not doing well.

The patient is a 67-year-old man who underwent 5 days before a right colectomy for intestinal obstruction secondary to a large colonic cancer of the ileocecal valve. The postoperative period was going fine, until this moment.

When you enter the room, the patient is tachypneic, tachycardic, and hypotensive, saturation is 88% in room air, body temp is 36.3°C, and glycemia is mildly increased. The patient has no abdominal drains and no urinary catheter.

What would you do?

Case 2:

You are on-call, and the EM Doctor in the ER calls you for an 82-year-old granny with an acute abdomen. The pt is on anticoagulant therapy for AF and she reported a history of falling at home 2 days earlier (no loss of consciousness).

On arrival, the pt is tachycardic and hypotensive, saturation is 93% in room air and body temp is 36.7°C. The abdomen is distended and painful all over without clear rebound tenderness.

What to do next?

These two cases are completely different from one another. However, they have something in common… There is a simple test that may help you in establishing which is the most probable cause of their distress, thus supporting your following step… This simple and quickly obtainable test is the blood gas analysis (BTW, point-of-care ultrasound would have been another correct answer).

Introduction

The blood gas analysis, either arterial or venous, is an exam that can give you a lot of information in just a minute or so… Usually, it is able to report more information than the sole acid-base data (e.g. glycemia, hemoglobin, etc…). However, in this post, we will focus on how to read and interpret the acid-base balance and how to deduce the respiratory and metabolic status of patients.

Everything starts with a simple formula (that maybe some of you still remember):

CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃^–

In this formula, we can see three fundamental elements: H⁺, CO_2, and HCO₃^–. The hydrogen ion (H⁺) concentration in the extracellular fluid is determined by the balance between the partial pressure of carbon dioxide (PCO₂) and the bicarbonate concentration (HCO₃^–). This balance can be summarized by the Henderson equation as:

[H⁺] = k * (PCO₂ / [HCO₃^–])

Where k is a constant and it is 24 (considering a normal pH of 7.4). In fact, at a pH 7.4, [H⁺] is 40 nmol/L, PCO₂ is 40 mmHg, and [HCO₃^–] is 24 mmol/L. This means:

40 = k * (40 / 24)

k = (40 / 40) * 24

The most famous, but more complex, formula used to determine the [HCO₃^–] once you know the pH and the PCO₂, is the Henderson-Hasselbach equation:

pH = pK + log ([HCO₃^–] / [H₂CO₃])

The correlation between pH values and [H⁺] can be summed up in the following image:

By the way, we can leave all this chemo-math hell behind, and focus on the real stuff…

What matters to us are 3 elements: pH, PCO₂, and [HCO₃^–]. In a physiological arterial blood gas (BG) analysis, the normal values are:

• pH = 7.35-7.45
• PaCO2 = 35-45 mmHg
• [HCO₃^–] = 22-26 mmol/L

These values are a little bit different in a venous BG. However, VBG gives you information about the metabolic status only, where the ABG shows the respiratory condition as well, this is why a VBG has very few indications. For this reason, in this post, we will talk about ABG.

Acid-Base Derangements

Well then… Derangements from the normal values can be seen, and they can alter the pH of the blood, giving back two conditions:

• pH <7.35 = acidosis
• pH >7.45 = alkalosis

Both conditions can be the consequence of derangements in PCO2 or [HCO₃^–], and these imbalances can be reported with a simple table:

So, the types of acid-base disorders can be categorized as follows:

• Respiratory acid-base disorders: a change in [H⁺] as a direct result of a change in PCO₂;
• Metabolic acid-base disorders: a change in [H+] as a direct result of a change in [HCO₃^–].

Compensatory Responses

However, things are not as simple as they may seem… The human body is a beautiful machine, and when an imbalance emerges, it starts immediately to counterbalance it in order to re-establish normality. All these modifications in the acid-base balance secondary to an acid-base imbalance are defined as “compensatory responses”. In simple words, this means you can have imbalances with a normal pH.

As we have seen before, there are two regulatory systems: the metabolic (represented by [HCO₃^–]) and the respiratory one (represented by PCO₂). Compensatory responses aim to limit the change in [H⁺] generated by the primary acid-base disorder. This is achieved by changing the second variable in the same “direction” as the first. In simple words:

These responses generate a similar result, but they act in completely different ways.

• The primary metabolic disorder is recorded by peripheral chemoreceptors located in the carotid body at the carotid bifurcation. These chemoreceptors can adjust the respiratory system in response to changes in hypoxemia, hypercapnia, and acidosis.
  • Metabolic acidosis: the chemoreceptors increase the minute ventilation (i.e. tidal volume and respiratory rate) in 30-120 minutes, meaning a decrease in PCO₂. It can take up to 12-24 hours to complete;
  • Metabolic alkalosis: they decrease the minute ventilation, meaning an increase in PCO₂. This response is weaker than the opposite, though.
• The primary respiratory disorder changes the [HCO₃^–] being filtered by the kidneys. Here, the HCO₃^– absorption in the proximal tubules is adjusted to produce the appropriate change in plasma concentration. This is slower compared to the respiratory response, and it may take up to 2-3 days to complete.
  • Acute respiratory disorders do not have time to change substantially the [HCO₃^–];
  • Chronic respiratory disorders can produce a significant change in [HCO₃^–].

Ok, now everything is clear… Now we can go to the difficult part… How to determine which is the primary derangement and which is the response?

Yeah, we know, if the pH is altered, that’s quite easy… But, what if the pH is normal?

In these cases, you need to calculate the expected response with the following formulas:

Another method to determine the compensatory response is:

Recap on Acid-Base Evaluation

• Identify the primary disorder
  • If PCO₂ and pH are both abnormal: primary disorder
    • Same direction: metabolic disorder
    • Opposite direction: respiratory disorder
  • If only one variable between PCO₂ or pH is abnormal: mixed metabolic and respiratory disorder
    • Abnormal PCO₂: the directional change identifies the type of respiratory disorder and the opposite metabolic disorder
    • Abnormal pH: the directional change identifies the type of metabolic disorder and the opposite respiratory disorder
• Identify the secondary disorder
  • Calculate the expected acid-base changes using the formulas reported above and compare the changes to the actual values. The discrepancies between the two values are used to identify secondary acid-base derangements.

The Base Excess & The Anion Gap

Two more variables play an important role in helping us to determine the acid-base imbalance ongoing: the base excess and the anion gap.

The Base Excess (or BE for friends) is the total number of strong acids (in mmol/L) that needs to be added in vitro to 1 L of fully oxygenated whole blood to return the sample to standard conditions (i.e. pH 7.40, PCO₂ 40 mmHg, Temp 37°C). Under these standard conditions, BE is 0 mmol/L by definition. The standard BE reflects the role of hemoglobin as a buffer in the extracellular fluid.

The Base Deficit is the opposite of the BE (i.e. BE x -1).

SBE = [HCO₃^–]_act – 24.8 + [16.2 x (pH – 7.40)]

BE normal range is between ±2 mmol/L.

Base Excess represents the metabolic status; so that if it is abnormal, the metabolic component is deranged (primary or compensatory):

• SBE > +2 mmol/L – metabolic alkalosis (it represents an excess of HCO₃^–)
• SBE < -2 mmol/L – metabolic acidosis

In the case of reduced SBE (i.e. < -2 mmol/L), you need to compare it to the Anion Gap.

The Anion Gap (AG) is a measure of the relative abundance of unmeasured anions in the extracellular fluid, and it can be useful in the evaluation of metabolic acidosis.

Just to be clear, anions are those elements with more electrons than protons, and they have a negative charge. The others are called cations.

Therefore:

Na⁺ + UC = Cl^– + HCO₃^– + UA

Na⁺ – (Cl^– + HCO₃^–) = UA – UC

UA – UC ≡ AG

(UC = unmeasured cations; UA = unmeasured anions)

The UC and UA are the ions in the extracellular fluid with low concentrations compared to “more important” elements (quantitatively speaking) such as Na⁺, Cl^–, and HCO₃^–.

The AG normal range is between 3-11 mEq/L.

Let’s Clear Our Minds

Let’s try with a couple of examples:

Example 1.

pH 7.15; PCO₂ 20 mmHg; HCO₃^– 8 mmol/L; BE -16

pH is low, which means acidosis. pCO₂ is low, which does not explain the acidosis, but its direction is towards alkalosis. HCO₃^– is low, explaining the acidosis.

This is a metabolic acidosis (confirmed by the low BE).

Since this is metabolic acidosis, we have to establish the expected PCO2 to determine if there is respiratory compensation.

The formula is: ΔPaCO₂ = 1.2 x ΔHCO₃ = 1.2 x (24 – 8) = 1.2 x 16 = 19.2

The actual ΔPaCO₂ here is = 40 – 20 = 20

As you can see, the two values are quite similar. This means there is an expected respiratory response to compensate for the reduced bicarb.

Example 2.

pH 7.25; PCO₂ 74 mmHg; HCO₃^– 33 mmol/L

pH is low, which means acidosis. pCO₂ is high, which may explain the acidosis. HCO₃^– is high, meaning a possible compensatory response.

Since this is a respiratory acidosis, we have to establish the expected HCO₃^– to determine if there is a metabolic compensation.

The formula for an acute disorder is: ΔHCO₃ = 0.1 x ΔPaCO₂ = 0.1 x (40 – 74) = -3.4 = 3.4

The actual ΔHCO₃ here is = 24 – 33 = -9 = 9. This may mean there is a synchronous metabolic alkalosis.

However, let’s consider it a chronic disorder. In this case, the formula is different:

ΔHCO₃ = 0.4 x ΔPaCO₂ = 0.4 x (-34) = -13.6 = 13.6.

Another method is to consider the expected compensation:

• In acute respiratory acidosis, we expect the bicarb to increase by 1 mmol/L for every 10 mmHg rise in CO₂ (above the upper limit of 45 mmHg). This means that if the CO2 had increased by about 30 mmHg (74 – 45 mmHg), we would have a rise in bicarb of 3 mmol/l (i.e. 24 + 3 = 27). However, the pt has 33 mmol/L.
• In chronic respiratory acidosis, we expect the bicarb to increase by 4 mmol/L for every 10 mmHg rise in CO₂. In this case, the rise in carbs should be 12 mmol/L (24 + 12 = 36).

This example shows how the clinical presentation and the medical history of a patient may influence the reading of blood gas. The interpretation of this ABG is completely different if the pt is a young man with no comorbidities or an old lady with a known history of COPD.

Ok guys… We can call it over…

Let’s wait ‘til all this stuff has settled down before going on…

See you next time…

References

1. Berend K, et al. Physiological approach to assessment of acid-base disturbances. NEJM 2014:371:1434-45.
2. Seifter JL, et al. Integration of acid-base and electrolyte disorders. NEJM 2014:371:1821-31.
3. Berend K, et al. Diagnostic use of base excess in acid-base disorders. NEJM 2018:378:1419-28.
4. Marino PL. The little ICU book. 2^nd Ed. Philadelphia, PA: Wolters Kluwer; 2017.

How to Cite This Post

Bellio G, Marrano E. Eating Batteries, Drinking Alien’s Blood – Part 1. Surgical Pizza. Published on March 13, 2022. Accessed on December 8, 2024. Available at [https://surgicalpizza.org/critical-care/eating-batteries-drinking-alien-blood-part-1/].