Category Archives: bicarbonate

The Blood Gas Machine – Measuring Oxygen, pH, Carbon Dioxide, Tips and Tricks and Derived Variables

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To round out the year, here are three tutorials on the blood gas machine, blood gas analysis and the blood gas printout.

The first tutorial looks at how oxygen is measured using the Clark Electrode on the blood gas analyser and demonstrates the importance of co-oximetry in modern blood analysis. From that the fractional saturation of hemoglobin with oxygen is derived.

The second tutorial explains the Glass Electrode that measures pH and PCO2. Subsequently I cover problems you might encounter with blood gas sampling. If you don’t want to watch the technical stuff, I strongly recommend you scroll to the middle of the tutorial (12 minutes in) as it covers information that all healthcare practitioners must know.

The final tutorial looks at all of that other data that appears on blood gas printouts that you may never have understood – and it can be really confusing – DERIVED or calculated variables (bicarbonate, temperature correction, TCO2, O2 content, Base Excess, Standard Bicarbonate, Anion Gap etc.). I cover both the Radiometer ABL machines and the GEM 5000. I guarantee you’ll learn something.

Acid Base Calculations for the ASA

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Here are the calculations that I used in my presentation at ASA 2025.

pH versus  PaCO2 

An increase of 10 mmHg in PaCO2 results in a pH drop of about 0.08

Respiratory Acidosis PaCO2  vs HCO3–

In Acute Respiratory Acidosis (e.g. patient hypoventilating in the OR) the Bicarbonate Increases by 1mmol/L for every 10mmHg Increase in PaCO2

In Chronic Hypercarbia (COPD) the Bicarbonate ↑ by 4mmol/L for every 10mmHg Increase in PaCO2 and Cl– falls by an equivalent amount

Modern Anion Gap = [Na+ + K+] – [Cl– + HCO3– + La–+ βOH–] = Albumin– + PO42- + UMA– mEq/L

[Albumin−]= [Albumin g/L] × (0.123 × pH−0.631)

Albumin Charge is simplified to 2.5 (albumin in g/dl) = Alb in mEq/L

Change in Albumin is (44 – Albumin) / 4

To determine the effectiveness of respiratory compensation use the Winters formula:

(Bicarbonate Version) Expected PaCO2 in Acute Metabolic Acidosis is
1.5 x [HCO3–] + 8 (in mmHg)

(Base Deficit Version) Expected PaCO2 in Acute Metabolic Acidosis is
Normal PaCO2 – BD (in mmHg)

The Base Excess Gap (Fencl Story with my modification)

Identify the BE on the ABG

Calculate the SID for Na+-Cl–+H2O by [Na+ – Cl– – 35] BDNaCl

Calculate the SID for La– and β-OH– (1mmol = 1mEq) BDLβOH

Calculate the Impact of Albumin (44 – Alb– g/L)/4 BEALB

Add these together BENaCl BDLβOH BEALB

Subtract from BE on the Blood Gas

The result is UMA in mEq/L

Finally, the Strong Ion Gap (arguably the gold standard)

The calculation for the strong ion gap (SIG) is:

Strong Ion Gap (SIG) = SIDa-SIDe

SIDa (apparent SID) = ([Na+] + [K+] + [Mg2+] + [Ca2+]) – ([Cl–] + [Lactate–] + [βOH–])

SIDe (effective SID) = [HCO3–] + [charge on albumin] + [charge on Pi]

The degree of ionization for weak acids is pH dependent, so one must calculate for this:

[charge on albumin] = [albumin] (in g/L) x (0.123 x pH – 0.631)

[charge on Pi] = [Pi] (in mg/dL) /10 x pH – 0.47

The SIG quantifies UMA

Carbon Dioxide in Acid Base – Three Tutorials

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As part of my fundamentals of Anesthesiology and Critical Care Series I have posted 3 tutorials on the Role of CO2 /HCO3 in Acid Base Balance. These are entirely new tutorials (not part of the previous acid base series – that I have not finished yet! There is some overlap and updated facts and figures) and I have put a lot of work into getting the message of why the respiratory system is so important in acid base. Tutorial 1 is the basics of acid base. Tutorial 2 discusses respiratory acidosis, acute and chronic, and respiratory alkalosis. Tutorial 3 discusses respiratory compensation for acute metabolic acidosis.
Although I cover the respiratory component in great depth, I also explain what metabolic acidosis is, what causes it and briefly discuss the anion gap, expected bicarbonate, base deficit and base deficit gap. I guarantee that you will learn something.

Fundamentals of Anesthesiology and Critical Care Series

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Here are the first 9 Tutorials in the Series – the majority are useful for Anesthesiologists and Intensive Care practitioners. Every tutorial contains something that you may not have previously known: I guarantee, who ever you are, that you’ll learn something.

Tutorial 1: Saturated Vapor Pressure

Tutorial 2: The Gas Laws

Tutorial 3: Mixtures of Gases

Tutorial 4: The Alveolar Gas Equation

Tutorial 5: Henry’s Law

Tutorial 6: Carbon Dioxide Solubility

Tutorial 7: Oxygen Solubility

Tutorial 8: Oxygen Content of Blood

Tutorial 9: Oxyhemoglobin Dissociation

Metabolic Acidosis in 2025 – More Important than Ever!

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This is a longer version of the lecture that I delivered at the 2025 College of Anaesthesiologists of Ireland Annual Scientific Meeting.

Methanol Poisoning

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In November 2024 six tourists died of suspected Methanol Poisoning in Laos, and several more were hospitalized. Methanol, or methyl alcohol, is an industrial chemical used to thin paints, as a precursor for medley chemicals and for fuel cells. It is passed off as “vodka” (odorless, tasteless, clear) to unsuspecting victims.

Methanol is metaboized by the same pathways as ethanol, but to formaldehyde and formate. Although small amounts of methanol may be found in the body, due to gut bacterial fermentation, methanol poisoning is a life threatening problem. Formate causes a widened anion gap metabolic acidosis, blindness, brain damage and interferes with mitochondrial function resulting in cytotoxic hypoxia.

The treatment for methanol poisoning is fomipazole given 12 hourly intravenously, folate, intravenous fluids and, if necessary, renal replacement therapy. Fomipazole competitively antagonizes the metabolism of methanol by the enzyme alcohol dehyrogenase. If fomipazole is unavailable, ethanol can be given as an emergency measure, intravenously or orally.

Assessing the Patient’s Ventilation Status

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This tutorial looks at the assessment of PaCO2 on the blood gas and how it interfaces with the pH and the Bicarbonate (HCO3-). The control of PaCO2 is a major physiological mechanism for maintaining homeostasis. CO2 production by the body must be balanced by CO2 elimination. PaCO2 rises when there is hypoventilation, this results in a fall in pH and an rise in HCO3 and this is called “Acute Respiratory Acidosis.” If the patient hyperventilates, the PaCO2 and the HCO3 fall and the pH rises: this is “Acute Respiratory Alkalosis.” When there is chronic CO2 retention, the body adapts by wasting Chloride in the urine, the pH normalizes and the HCO3 rises substantially.

Any patient who is intubated, or who has a laryngeal mask in situ, must undergo end tidal (end of exhalation) CO2 monitoring. The capnography waveform is worth evaluating, particularly if airway obstruction or increased resistance is suspected.

Included in this tutorial are various rules of thumb that you can use to determine the Respiratory Acid Base Status of the Patient – including the “Rule of 40.”

HYPERCHLOREMIC ACIDOSIS

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Hyperchloremic Acidosis is a common problem. It is usually an iatrogenic problem. Unfortunately, the majority of doctors who cause a patient to have Hyperchloremic Acidosis (HCA) are either unaware of the problem or ambivalent to it. For the most part, HCA is caused by the intravenous administration of isotonic saline solution (NS – “normal saline – NaCl 0.9%). This problem has been known about for more than 100 years and led Alexis Hartmann, a pediatrician from St Louis, to construct a balanced intravenous fluids, that he called “Lactated Ringers” solution. Ironically, in clinical practice, HCA is induced as part of the local hospital “protocol” for management of Diabetic Ketoacidosis. Inevitably, as the ketones fall, the Chloride rises, and the acidosis persists.

HCA is the only cause of “normal” anion gap metabolic acidosis and is almost always caused, . In the tutorial I explain that HCA is caused by a reduction in the Na-Cl strong ion difference (SID). The acidosis associated with NaCl 0.9% is more complex that merely a rise in plasma Chloride. Other serum electrolytes, Albumin and Hemoglobin are diluted – and this has an alkalinizing effect. Other resuscitation fluids have different impacts on acid base. Hyperchloremia is also a feature of Renal Tubular Acidosis (RTA), various other nephropathies, the administration of acetazolamide and other drugs, and following surgical transplantation of the ureters into the small bowel, If renal function is normal, and the Chloride level is lower than 125mmol/L, then the patient’s kidneys will resolve the problem over 36 to 48 hours. If the Chloride is very high, acidosis will persist, particularly in patients with poor renal function, and Sodium Bicarbonate infusions may be warranted.

Alcoholic and Starvation KETOACIDOSIS

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This tutorial looks at the twin problems of Alcohol related and Starvation Ketoacidosis. These diagnoses are frequently missed by clinicians because 1. they attribute the metabolic acidosis to another cause e.g. lactate or acute kidney injury or 2. they do not routinely measure blood ketones. It is my view that, in any patient presenting with a plasma bicarbonate below 20mmol or mEq/L or a base deficit of -5 or greater, it is mandatory to measure blood ketones (beta-hydroxybutyrate).

I present two cases, the first is a patient who is admitted with abdominal pain and a likely upper GI bleed, with a history of an eating disorder, who has metabolic acidosis. The second patient is an alcoholicwho recently stopped both eating and consuming alcohol. She also has a metabolic acidosis. I discuss the biochemistry of alcohol metabolism and explain why alcoholics are at risk for ketoacidosis. I also explain why this is part of a paradigm of metabolic failure that, without significant attention to detail, may result in therapy that precipitates a variety of withdrawal syndromes: these include acute Wernicke’s Encephalopathy, Alcohol Withdrawal Syndrome, and acute aquaresis and Osmotic Demyelination. Alcoholic ketoacidosis almost always follows cessation of alcohol intake – and one is unlikely to make this diagnosis in a patient who, for example, presents drunk to the ED (this results in a host of other metabolic anomalies, for example hypoglycemia despite high plasma lactate).

Starvation ketoacidosis is seen in patients who are chronically malnourished or fasted for prolonged periods for surgery, in whom the pancreatic Islet cells have either atrophied or are hibernating. Careful attention must be applied to feeding and refeeding: it is imperative that the patient does not lose further lean body mass. On the other hand refeeding syndrome may result in rhabdomyolysis and death. I guarantee you’ll learn something.