This tutorial is best experience with a pencil and paper. Before I get into a discussion about high flow oxygen therapy you really need to understand flow. Conventional facemasks, Venturis and nasal cannula deliver modest flows of oxygen to the patient, but to ensure a correct FiO2, oxygen must be blended with air – in the airway or in the device. That air is drawn into the system by entrainment either from the room via the mask or mouth or injected in the case of Venturis into the breathing system. In any case – the inward flow of gas is determined, principally by the patient’s inspiratory effort and the concentration of oxygen during peak inspiratory flow is, hopefully, kept constant. In general, to keep FiO2 constant – a gas flow of at least 30L/min is required. Most devices deliver 40 liters or more, but only at lower FiO2 levels. It is essential to understand that, in this case, the 30 to 40L is NOT high flow – because it is “draw over” flow generated by the patient. High flow, as we will see in the next tutorial is delivered to the patient. For example – when delivering 24% and 28% oxygen to a patient – the total flow may be 44L but the fresh gas flow is only 2 to 4L. The remainder is entrained. This tutorial explains the concept of gas entrainment and how to calculate entrainment ratios and flow rates. If you have never encountered this concept before, I guarantee that you will learn something!
Equations Used In This Tutorial:
The FiO2 vs Flow Equation FiO2 = (Air Flow x 0.21) + (O2 Flow) / Total Flow
The Air:Oxygen Equation: Air/Oxygen = (100% -FiO2)/(FiO2 – 21%)
Oxygen Flow Equation: (Total Flow x (FiO2 -21))/79
I have been a “fanboy” for high flow oxygen therapy (HFOT) for a couple of decades, particularly once high flow nasal canula (HFNC) became available. While this was a bit of a cottage industry, coveted by those of us in critical care (and to a lesser extent in anesthesiology), once the COVID 19 pandemic took hold, high flow was everywhere. And everyone, it seemed, had an (ill informed) opinion about this therapy. So, before I introduce this tutorial, about which I procastinated for years, I have to register a disclaimer: the evidence to support a lot of the “beliefs” about high flow oxygen is scant. Most of the claimed “benefits” beyond treating hypoxemia are industry generated hypotheses without rigorous scientific data. Nevertheless, this put me in a difficult predicament when constructing the tutorial – if I limit the discussion to just the facts that I am certain about – it would be very short. Conversely, by describing alternative “benefits” I take the risk of hyping hypotheses (e.g. CO2 clearance) that may be incorrect…..
High Flow Oxygen Therapy (HFOT), particularly when delivered by nasal cannula (HFNC) has revolutionized the management of the patient with hypoxic respiratory failure – in particular in those patients whose lung pathology has plateaued or those resposive to medical treatment (antibiotics, steroids etc). High flow systems have been available for decades – they involve the use of a high pressure oxygen source, and oxygen air blender (air can be entrained into this device), a high flow flowmeter, a humidifier, a heated delivery tube and a delivery device: CPAP mask, T-Piece with PEEP valve, Tracheostomy or specially designed nasal cannula.
In this tutorial I describe the various devices configurations that are available – ranging from very straightforward standalone machines, to full mechanical ventilators. Regardless of device the major goal is to deliver sufficient flow to meet patient demand – resolving the problem of peak flow and separating out the FiO2 from the flow rate. I postulate that, at flows in excess of 30L per minute, and depending on the diameter of the nasal cannula, the patient’s anatomy and whether the mouth is open (and by how much!) – the patient likely receives a couple of cmH2O of pressure support and 3-5cmH2O of PEEP. So it represents mild CPAP (certainly a CPAP device delivering high flow at 5cmH2O will outperform HFNC). There is a dearth of non industry funded data on how HFOT may benefit the patient. Certainly these devices are very effective at targeting SpO2 and reducing the work of breathing. Certainly they increase non hypoxic apneic duration. Conversely – purported impacts on dead space washout, alveolar ventilation and CO2 clearance are currently unproven. I describe how this may work in the tutorial, but point out that this is principally a belief not a fact. HFNO may also improve mucociliary clearance – due to the high flow of humidified gas passing into the airways. However no-one, to my knowledge, has addressed whether constant flow of heated humidified gas for prolonged periods damages the lung mucosa.
In the second part of the tutorial I talk about how HFOT should be used in clinical practice and the scenarios in which it is beneficial (hypoxemia, weaning and liberation) and when it is not (hypercarbic respiratory failure, post op respiratory failure secondary to atelectasis).
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. @ccmtutorialshttp://www.ccmtutorials.org
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:
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]
Why Does Hyperoxia Cause Hypercarbia (VQ mismatch theory)
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. @ccmtutorialshttp://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).
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.
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.
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.
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.
This is the second tutorial on Volume Controlled Ventilation. I discuss the evolution of ventilators from pure controlled mechanical ventilation, to intermittent mandatory ventilation – with spontaneous breathing to synchronized IMV with Pressure Support. This mode remains robustly popular around the world and critical care practitioners and anesthesiologists should be familiar with the mode, along with its advantages and disadvantages. I guarantee you will learn something. @ccmtutorials