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About Pat Neligan

Pat Neligan lives and works in Galway, Ireland

Oxygen Therapy: Variable vs Fixed Performance Devices

Oxygen is probably the most used and misused drug in a hospital. The purpose of oxygen therapy is to restore the PaO2 or SpO2 to a safe level for that patient. One of the major issues with targeted oxygen therapy is the problem of peak inspiratory flow.

During peak inspiration the FiO2 must be constant. That means that flow delivery must meet flow demand. Oxygen therapy can be delivered with variable or fixed performance devices. Variable performance devices include nasal cannula and simple (“Hudson”) facemasks. In both cases oxygen and air are blended in or near the airway. Nasal cannula are remarkably efficient and can deliver low inspired oxygen concentrations. Due to issues with dead space and rebreathing, simple facemasks are unreliable below 35% (5L). Both devices struggle where there is rapid breathing, particularly with large tidal volumes.

Venturi devices, which are really jets use a narrow injection port to entrain and blend oxygen and air proximal to the facemask. They are more precise but less efficient (in terms of total flow) than variable performance devices. Performance is remarkably robust between 24% and 40% inspired oxygen. They perform less well with rapid deep breathing particularly at high FiO2 levels. Non rebreather facemasks use a reservoir to store fresh gas during expiration and facilitate the delivery of FiO2 of approximately 80% with 10 to 15 liters of flow. As such they are highly efficient, although unreliable and non titratable. These devices can be used with modest oxygen flows for transporting hypoxic patients, but are short term remedies. @ccmtutorials http://www.ccmtutorials.org

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

Mechanisms of Hypoxemia – Part 1

If you treat patient with hypoxic respiratory failure you really need to understand what is going on in their lungs. These two tutorials look at diseases of the lung parenchyma and how blood flow and gas flow interact. The first tutorial focuses on alveolar oxygen content and how it is impacted by disease. I explain the concept of airway closure (which will will revisit in detail several times during this series), stale alveolar gas, the various causes of atelectasis and the six S approach to figuring out what is going on in the airways (Slimy, Soggy, Sticky, Stiff, Squished, Shunty).

Identifying and Quantifying Hypoxemia

The next part of the course is all about hypoxic respiratory failure. To treat hypoxemia you must understand it. The purpose of this sequence of tutorials is to lead up to discussions on CPAP and PEEP and provide a platform for understanding Pressure Controlled Modes of Ventilation. The first tutorial looks at oxyhemoglobin saturation, why the oxyhemoglobin dissociation curve is essential knowledge for the practicing clinician, how pulse oximeters work and how to quantify hypoxemia (A-aO2 gradient and PaO2/FiO2 ratio).

Pressure Support 4 – Expiratory Cycling

This is likely the most important of the four tutorials on Pressure Support Ventilation. As you may recall, PS is an unusual mode of ventilation because it is flow cycled – that is – the ventilator cycles to expiration as specific, user set, percentage of peak flow. The default expiratory sensitivity is usually around 25%. Expiratory dys-synchrony is frequently missed by bedside clinicians who have not been schooled in waveform analysis. This tutorial covers everything you need to know. @ccmtutorials http://www.ccmtutorials.org

Next time I am going to commence a series of tutorials on hypoxia-hypoxemia. This will start with a discussion about how we measure hypoxemia – in particular oxyhemoglobin saturation (Tutorial 12). I will then go on to discuss atelectasis, shunt, ventilation-perfusion mismatch and introduce oxygen therapy (Tutorial 13).

Pressure Support 3 – Setting the Level

This is the third tutorial on Pressure Support Ventilation. This tutorial discusses the thoracic pump – the inspiratory drive and transpulmonary pressure. It looks at when one can use Pressure Support and how to adjust the settings. I introduce the Rapid Shallow Breathing Index and provide a series of steps in adjusting the PS level. Finally I introduce an alternative version of PS known as Volume Support.
@ccmtutorials
Abu Dhabi 11/4/13

Inspiratory Rise Time

When a pressure limited breath is triggered there is a slight delay between that point and the airway pressure target being reached. This is controlled by a setting on the ventilator known as the “inspiratory ramp” or “inspiratory rise time.”

Although I am covering this topic under the banner of “Pressure Support,” all pressure limited modes include this function, although it may be hidden from sight and each ventilator has a different system for adjustment. Most of the time you will get away with not having to adjust the rise time beyond the factory setting. Nevertheless – having an understanding of the inspiratory ramp is useful for fine tuning breaths in patients who have a tendency to be dys-synchronous. I guarantee you will learn something.

Japan April 5th 2023.

Pressure Support Ventilation – Part 1

If you go into most ICUs today, the most commonly used mode of ventilation is Pressure Support. There are many reasons for this: it is widely believed that supporting spontaneous breathing results in less muscular – and in particular diaphragmatic – atrophy; patients require minimum sedation and can be gradually weaned and, because it is a pressure targeted mode, there is biologically variable ventilation. Although not every ICU uses Pressure Support as part of its invasive ventilation strategy, virtually all units use it for non invasive ventilation. If you work in ICU you MUST understand Pressure Support. In my view it is the MOST important mode of ventilation. It is also the easiest mode to get started with and one of the most difficult to master.

These are four tutorials on Pressure Support Ventilation – starting with Triggering, then Breath Initiation, then Setting the Level and, finally, Expiration. The first tutorial introduces the concept of Assisted Spontaneous Breathing and Pressure Support and revisits Triggering – Flow and Pressure Triggering. Although I covered this in the introductory tutorials, I go into much greater detail here. In particular I cover Undertriggering and Overtriggering. I guarantee you will learn something.

Everything You Need to Know About End Tidal CO2

I decided to do a tutorial on end tidal CO2 as there has been a lot of discussion about it’s merits and limitations in our practice. It is fairly long and can be broken into sections at 20 minutes and 37 minutes if you have a short attention span (I will split it up into smaller segments at some stage in the future).

The content is absolutely essential for doctors and nurses working in anesthesiology and intensive care. In my opinion measuring expiratory CO2 from the ventilator circuit is the most useful clinical measurement tool that we have. It gives us information about cellular metabolic activity, blood flow, venous return, lung unit perfusion, gas exchange and alveolar ventilation. The tutorial commences with a discussion of CO2 as a gas and discusses Henry’s and Daltons’ laws. I then discuss the various different CO2 moieties, particularly bicarbonate. Subsequently I go on to discuss the impact of alveolar ventilation on PaCO2. After 20 minutes I move on to discuss capnometry – the measurement of the presence and quantity of CO2 emerging from the lung at end expiration. I discuss why the etCO2 may rise of fall. I then look at a specific clinical scenario where the etCO2 falls precipitously. After 37 minutes I discuss capnography – initially the normal capnograph and then a series of different capnography traces that you should be able to recognize. As a final thought I mention that CO2 is not the only waste produce or metabolic intermediary that we measure, routinely, in clinical practice.

Tutorial 7: Understanding Ventilatory Failure, Alveolar Gas, Lung Volumes and Dead Space.

Clinicians who work in anesthesiology, intensive care or emergency medicine who are involved in the management of respiratory failure must understand the problem of failure to ventilate: “can’t breathe, won’t breathe.” This long tutorial covers a lot of ground and could be viewed in split sessions.

My principle goal is to give you the tools to work the problem of respiratory failure. Along the way I introduce the alveolar gas equation, ventilation perfusion matching and lung volumes; particularly functional residual capacity. In the second half (from 28:20 onwards), I discuss anatomical and physiological dead space, calculate out the dead space to tidal volume ratio and show how you can be inadvertently increasing physiologic dead space by applying PEEP or neglecting auto-PEEP.

Even if you think you know a lot about this subject, I guarantee that you will learn something.

As always, I welcome feedback.

Don’t Be Scared of Respiratory Physiology – it makes sense (well, most of it anyway!)