Volatile Anesthetics – How We Got to Here

We are now moving to phase 2 of the course on Gases and Vapors – and this is principally directed to anesthesiologists.

General anesthesia is not simply unconsciousness; it requires hypnosis, amnesia, immobility, autonomic stability, and analgesia.
There is no universally agreed quantitative definition of anesthetic depth; practical clinical endpoints guide real-world anesthesia.
Ether ushered in modern anesthesia but was limited by high blood and tissue solubility and flammability, leading to slow induction and emergence.
Safety concerns, particularly flammability, led to the abandonment of agents such as cyclopropane despite favorable pharmacology.
Methoxyflurane represented a major advance but fell out of routine use due to extensive metabolism and fluoride-related toxicity.
Progressive halogenation of ether derivatives produced agents with greater stability, lower solubility, and reduced metabolism.
Isoflurane marked a major milestone due to its minimal metabolism and predictable pharmacology.
Desflurane offers extremely rapid onset and emergence but is limited by pungency and airway irritation.
Sevoflurane became dominant primarily because it is non-pungent and universally applicable, allowing inhalational induction and use across all patient groups.
Nitrous oxide historically reduced volatile requirements in high-flow systems but is less essential in modern low-flow anesthesia.
Understanding volatile anesthetics requires grasping blood–gas solubility, lipid solubility, tissue uptake, and their effects on onset, potency, and emergence.

These principles set the foundation for understanding MAC, its utility, and its limitations.

Fundamentals of Anesthesiology and Critical Care Series

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

A SHORT COURSE ON LOCAL ANESTHETICS

I published 3 tutorials on Local Anesthetics this Month. These are part of a new series of Anesthesiology Tutorials.

Tutorial 1 looks at the basic pharmacology of local anesthetics

Tutorial 2 looks at the various different drugs that we use, the volume and concentration. I discuss the maximum safe doses at the end of the tutorial.

Tutorial 3 looks at the history of, the diagnosis of and the treatment of Local Anesthetic Systemic Toxicity (LAST)

Metabolic Acidosis in 2025 – More Important than Ever!

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

Nutrition 3 – Timing and Route of Nutrition in ICU

This HI-Impact tutorial looks at the common questions relating to commencement and route of nutrition in critical care. Is TPN good, bad or indifferent. Is enteral feed better than parenteral? When should we start feeding? Is it useful to add parenteral feed to enteral if the patients’ caloric goals have not been met? When should patients achieve their isocaloric goals. I guarantee you’ll learn something.

Methanol Poisoning

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.

HYPOVOLEMIC SHOCK

Hypovolemic shock is one of the major problems we encounter in acute critical illness. This tutorial explains the mechanisms by which the body compensates for hemorrhage/hypovolemia, why the blood pressure and hemoglobin saturation are unhelpful and what tools may be useful at the bedside to assess the patient.

I also briefly discuss resuscitation of the bleeding patient and compartment syndromes.

HYPOTENSION AND SHOCK: Working the Problem

This tutorial looks at the problems of Hypotension and Shock. I define the difference between the concepts – not all hypotensive patients are shocked and not all shocked patients are hypotensive. I then go through a system for exploring the hypotensive or shocked patients’ status to determine the underlying problem – illustrated by a series of clinical scenarios.

Cardiovascular Assessment 1: The Heart Rate

This is the first tutorial in the cardiovascular assessment module. In the tutorial I discuss heart rate, how it originates and how it is controlled. This is principally a discussion about sinus bradycardia and sinus tachycardia. I go on to discuss the parasympathetic nervous system and the sympathetic nervous system, how they function physiologically and how they are impacted by drugs that we administer and disease processes. I provide a detailed discussion of adrenoceptor agonists and antagonists.