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
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.
I am now moving on to the “meat” of the mechanical ventilation course, starting with volume controlled ventilation. The first of these tutorials is on volume assist control. Even if you think you know a lot about this mode – stick with me, there is a lot of information packed in and I guarantee that you will learn something. Comments always welcome.
How does the ventilator know that it needs to deliver a breath? The term to describe this is “Triggering.” In this tutorial I will cover time triggering, pressure triggering and the relentlessly confusing concept of flow triggering. I guarantee that you will learn something in this 12.5 minute tutorial.
As promised – here is the first tutorial from Module 1 (“Setting Up a Mechanical Ventilator”) of the course on Mechanical Ventilation. I discuss the difference between Volume Control and Pressure Control and Dual Control – including the advantages and disadvantages associated with each mode.
Intravenous fluid, fluid management, the physiology of body fluids – all relentlessly controversial and complicated issues. I decided a couple of years ago to put together a course that covers the whole spectrum of fluids – from basic chemistry to basic and advanced physiology, applied physiology, fluid and electrolyte disorders and therapy and acid base chemistry. I will also cover diseases and disorders associated with fluids – either as therapies for, or iatrogenic causes of, disease. I am posting Part 1 on the fluids course in its entirety. Subsequent parts of the course will be posted ad-hoc depending on when each tutorial is completed (I will set aside pages on this website for the tutorials in order and as playlists on you-tube). I hope you find this useful. All of the tutorials on this set (plus a number that I have not posted yet) were road tested as Galway University Hospital in 2021-2022.
Pat Neligan Dec 22nd 2022
Introduction to the Course
This is a quick introduction to the course, explaining what I am proposing to cover over four parts.
This is some really basic chemistry that will allow you to understand the content of subsequent tutorials.
Tutorial 1 Water and Concentrations
This tutorial convers the physical properties of water, what a mole and mmol is and what is g%. I use dextrose as my major example and look at the different ways that glucose concentration is measured in the USA (mg/dl) versus the rest of the world (mmol/L). The end of the tutorial covers the alcohol and calorie content of drinks and drink driving limits.
PART 1 MODULE 1
I rather like caffeinated drinks and am frequently the subject of sanctimonious comments about my caffeine habit. This tutorial covers caffeine content. Subsequently I look at the issue of 1% versus 2% lidocaine and explain exactly what 1:200,000 epinephrine (adrenaline) is.
Tutorial 2 Salts
This tutorial explains how to calculate out the quantity of electrolytes released from salts as they are dissolved in intravenous fluids. I also take an early look at hypertonic saline solutions.
Tutorial 2 Supplement 1 – More Salt
This tutorial goes through a couple of conundrums where I look at intravenous fluid products and show you how to calculate out the electrolyte contents when you are only given the salts in g/L
Tutorial 2 Supplement 2
This is an early look at calcium supplement products that we typically use in critical care. What exactly is the difference between Calcium Chloride and Calcium Gluconate?
Tutorial 3 Osmosis
Fundamental to understanding how water behaves in body fluids is the concept of osmosis. It is also very important when we visit renal replacement therapies in Part 4 of the course. In this tutorial I use traumatic brain injury and mannitol as my main example.
Tutorial 4 Osmolality and Tonicity
What is the difference between osmolality and osmolarity? What are mOsm? How do you calculate Osmolarity? This tutorial looks at the concept of Osmolality and the Tonicity of intravenous fluids, and why understanding this concept is essential for practitioners of hospital medicine. The clinical scenario is of a patient with hypotonic hyponatremia. I will revisit hypertonic saline solutions and look at the concept of the Osmotic Co-efficient.
Tutorial 5 Electrolyte Distribution
This tutorial looks at the distribution of electrolytes in the body – between the intracellular and extracellular compartments. I look at the needs of a patient who is unable to take oral fluids and electrolytes. I emphasize the importance of maintenance fluids in this situation rather than resuscitation fluids. This tutorial also looks at the interstitial matrix and how it is vulnerable to hydraulic fracturing (“fracking”) caused by intravenous fluids.
This is the end of Module 1.
PART 1 MODULE 2
Tutorial 6 The Adaptive Perioperative Stress Response
Whether we are injured, assaulted or undergo surgery, our bodies respond with an inflammatory response that involves endocrine, metabolic and immune components. The “adaptive” stress response is predictable and its magnitude mirrors the degree of injury. To understand emergency and perioperative medicine and critical illness you must understand the stress response. Having explained the basic physiology, I then go on to discuss fluids and fluid balance and describe the conventional approach (that I do not necessarily subscribe to) to perioperative fluid therapy.
Tutorial 7 Critical Illness and Resuscitation
A patient presents with an “acute abdomen.” His bowel is obstructed and he is losing fluid and becoming both dehydrated and electrolyte depleted. This tutorial looks at the different types of body fluids that may be lost – how they all resemble extracellular fluid and suggests a type of fluid that can be used for resuscitation. I then progress to describing the maladaptive stress response of critical illness, and why it is associated with capillary leak syndrome. There follows a discussion of fluid overload and the need for de-resuscitation. Finally I introduce the topic of chronic critical illness and death.
Tutorial 8 The Macro Circulation
What happens to the body when there is major blood loss? This tutorial looks at the different components of the circulation and how blood flow is redistributed in shocked states. I also look at the assessment of hypovolemic shock, oxygen consumption versus delivery and the mixed venous oxygen saturation. Finally I address resuscitation strategies in acute blood loss.
This ends Part 1 Module 2.
PART 1 MODULE 3 ADVANCES
Tutorial 9 Venous Return
Since the 1970s the venous (and lymphatic) side of the circulation and the right side of the heart seem to have been ignored by doctors. At worst is the widely held belief that central venous pressure represents an appropriate measure of blood volume and resuscitation status. This tutorial looks at the concept of cardiac output versus venous return. I discuss the Guyton concept of mean systemic pressure, the stressed and unstressed blood volume and vascular compliance. I then go on to look at venous return during anesthesia, the impact of low and high dose vasopressors and the impact of fluid overload.
Tutorial 10 The Microcirculation & Capillaries
For the past 125 years or so, the vast majority of clinicians have based their understanding about transendothelial fluid flux on the work of Ernest Starling. Problem is that his hypothesis – the Starling Principle – is wrong. The presence of the capillary glycocalyx and enhanced understanding of fluid kinetics has changed our view of fluid therapy, in particular the role of colloids in treating critically ill patients. This tutorial looks at the capillary network, the traditional Starling method, the “Revised” Starling method, the glycocalyx, oncotic pressure gradients, the impact of fluid extravascation and the lymphatic system.
Tutorial 11 Albumin & Colloids
Colloids, whether they are hydroxyethyl starches, dextrans, gelatins or even albumin, were popular resuscitation fluids until the 2010s. Multiple studies failed to demonstrate the effectiveness of these agents. However, the use of hyperoncotic human albumin solution has gained popularity, based on no real evidence, in recent years. Given our knowledge of the microcirculation, is there any compelling reason to be treating a patient with human albumin solution in the 2020s?
Tutorial 12 Fluid Kinetics
In this last tutorial in Part 1 of this course, we are returning to the operating room. What happens to intravenous fluid once it is injected into the veins a) in normal volunteers, b) during anesthesia, c) during the stress response? This tutorial is all about fluid or volume kinetics and is based on the work of Robert Hahn, from Sweden. I discuss fast versus slow boluses, resuscitation with crystalloid in hypovolemic states, the urinary output during surgery and what happens during hypervolemia.
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