Category Archives: Critical Illness

TUTORIALS ON CAPNOMETRY AND CAPNOGRAPHY

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Here are three tutorials on inspiratory and expiratory CO2 gas analysis. Tutorial 1 looks at Capnometry and the process behind measuring CO2 in exhaled gas. I cover mainstream CO2 analysis and explain why the end tidal CO2 (EtCO2) may be high or low. Tutorial 2 addresses the Capnograph, the trace and anomalies of the Capnograph at the time of intubation. I also explain Sidestream and Microstream CO2 and gas analysis. The final tutorial will be very helpful to anesthesiologists, particularly those taking exams: I go through a series of abnormal Capnographs, explaining why they are abnormal. I guarantee that you will learn something.

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.

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.

Acute Coronary Syndromes and Cardiogenic Shock

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This is a trio or tutorials on Acute Myocardial Ischemia, Acute Coronary Syndromes and Cardiogenic Shock.

Critical Illness Nutrition 2 – Calories, Protein, Enteral Route, Gastric Residuals

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This is the second tutorial in the nutrition series. Previously I looked at metabolism in critical illness. In this tutorial I start to answer many of the questions that arise on rounds principally: how many calories does the patient need? How much protein? What are the routes of food administration? Is there a benefit to post pyloric feeding tubes? Should I feed the stomach continuously or by bolus? Should I check gastric residual volumes? I provide you with the answers to these questions using the best available evidence.

Critical Illness Cachexia (metabolism in acute and chronic critical illness)

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Patients who spend significant time in critical care may lose a staggering amount of weight, particularly lean body mass. In early critical illness glucose is used as the principle energy source in the stress response; glycogen is rapidly exhausted and glycogenic amino acids are mobilized from muscular protein to generate glucose via gluconeogenesis, to maintain plasma glucose levels to feed, principally red blood cells. This has a major impact on muscle mass and in particular muscular strength, that may take years, perhaps a decade to restore. The most effective mechanism of preventing the development of critical illness cachexia is to curtail the duration of the stress response, by rapid source control, deresuscitation and early mobilization. In general, patients should be receiving full nutrition and be mobilized by day 8 following injury.

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.