Emergence From Anesthesia – Tissue Blood Partition Co-Efficient and Other Factors (2 tutorials)

Part 1 – Tissue Blood Partition Co-Efficients

This tutorial explains why emergence from volatile anesthesia depends on more than simply turning off the vaporizer. It reviews how blood gas partition coefficients influence onset, how oil gas partition coefficients relate to potency and MAC, and then focuses on tissue blood partition coefficients as a key determinant of recovery. The tutorial describes anesthetic uptake into blood, muscle, and fat during short, intermediate, and long cases, showing how tissue storage increases with time and with agent solubility. It also explains tissue back diffusion, where anesthetic stored in tissues continues to return to the blood and brain after the vaporizer is turned off, delaying wake-up. Finally, it compares volatile agents such as nitrous oxide, desflurane, sevoflurane, isoflurane, halothane, and methoxyflurane, emphasizing how lower tissue solubility produces faster, more predictable emergence.

Part 2 – Other Factors that Impact Emergence from Anesthesia

This tutorial examines the additional factors that determine how quickly a patient wakes after volatile anesthesia. It covers the concentration-flow ramp, fresh gas flow, alveolar ventilation, and cardiac output, explaining how these influence washout of anesthetic from the lungs and circulation. It discusses the effects of poor gas exchange, atelectasis, duration of surgery, higher inspired concentrations, and obesity on tissue loading and delayed emergence. The tutorial also reviews hysteresis and MAC awake, showing why patients can remain asleep at concentrations lower than those required for induction. Other important contributors such as hypothermia, opioids, benzodiazepines, propofol, dexmedetomidine, clonidine, ketamine, and nitrous oxide are included, along with a discussion of spontaneous ventilation versus intermittent positive pressure ventilation. The overall message is that emergence depends on both how efficiently the lungs clear anesthetic and how much anesthetic the body gives back

The kPa Rules – Part 1: Oxygen

In the early 1970s much of the world adopted the System International (SI) approach to scientific measurement. Unfortunately, the remainder of the world ignored it. This means that, today, we have different units presented in the scientific literature depending on the location of the source of the publication.

The USA is the most notable non SI country and this presents a problem in that the majority of English language textbooks and journals in medicine as well as a lot of the international guidelines and clinical pathways are derived in the US. In critical care this is important – as blood gasses are reported in mmHg in the USA (and most of the literature) and in kPa elsewhere – notably in Europe.

In many of my tutorials I have reported clinical “rules” such as the PaO2/FiO2 ratio, the Alveolar Gas Equation and the majority of the calculations in acid base – in mmHg. This series of two tutorials serve to right the balance. However there is a twist.

In this first tutorial I am not just rehashing the approach to oxygenation by swapping out mmHg for kPa. In fact, the use of kPa to measure and monitor oxygenation provides us with a significant helping hand. Effectively, as atmospheric gas is effectively 100kPa and Oxygen exerts 21% of that – Dalton’s law – then it is clear that the partial pressure of inspired oxygen (PiO2) is 21kPa. Oxygen is poorly soluble in blood and water – the solubility co-efficient is 0.225 – meaning that the quantity of oxygen dissolved in blood is the PaO2 x 0.225 kPa. Oxygen follows Henry’s law – meaning that solubility is related to temperature (37 degrees C) and pressure – the PiO2. In the best case scenario the PaO2 – the partial pressure of oxygen in arterial blood is 13kPa. That means that the gradient between PiO2 and PaO2 is, at a minimal, 8kPa. The greater the stretch between the two the larger the lung injury or ventilation perfusion mismatch.

The oxygen content of blood is 1.34 x Hb x SaO2/100 + (PaO2 x 0.225). I explore the impact of different FiO2s and ambient pressure on the blood oxygen content. Although dissolved oxygen is very low breathing air – the use of supplemental oxygen may dramatically increase it – particularly in hyperbaric conditions.

Finally I address the issue of PaO2/FiO2 as a way of quantifying oxygenation. The PF ratio, as we call it, is a significant component of the ARDS definition. A PF ratio of 200 in mmHg is equivalent to 25 in kPa and a ratio of 100 in mmHg is equivalent to 12.5 in kPa. An easier way to look at this, though, is to divide the PiO2 by the PaO2 – the numbers look similar but you now have a proportion in kPa. That PF ratio of 25 in kPa resolves to 0.25 meaning that only 25% of inspired oxygen is reaching the pulmonary veins (PaO2). Likewise a PF ratio of 12.5 in kPa (100 in mmHg) resolves to 0.125 – which means that only 1/8th of the inspired oxygen is delivered to arterial blood. I think that this is a really good way of assessing oxygenation – and a way of clarifying hypoxemia in your brain.

Tutorial 14 Mechanisms of Hypoxemia Part 2

This tutorial explains ventilation perfusion mismatch. It will provide you with a platform for understanding oxygen therapy – which I introduce towards the end. I also deal with the concept of oxygen induced hypercarbia. I guarantee you will learn something.  

Contents of This Tutorials:

Ventilation-Perfusion Relationships

Gravity and Blood and Gas Distribution Through the Lungs

Gas and Blood Distribution Through Diseased Lungs

Simplistic Ventilation-Perfusion From Dead Space to Shunt

Stale Gas Within Alveoli

Ventilation Perfusion Relationships – Slimy, Soggy and Stick Alveolar Units

Supplemental Oxygen Therapy For Bronchopneumonia

“Targeted Oxygen Therapy”

When Does Oxygen Therapy Fail? [Shunt]

COPD Flair

Why Does Hyperoxia Cause Hypercarbia (VQ mismatch theory)

The Haldane Effect