In the previous tutorial we looked at the problem of high airway pressures and addressed inspiratory airway resistance in two ways: peak to plateau pressure gradient and dynamic and static inspiratory resistance.
In this tutorial we will look at three more ways of assessing airflow resistance: the identification and measurement of Auto-PEEP, Flow-Volume Loops and capnography.
Subsequently I discuss high airway pressure due to low total respiratory system compliance. I explain that when “compliance” is low – this may be a problem with the lungs as well as the chest wall – including the abdomen. I finish with the introduction into this course of Abdominal Compartment Syndrome.
The introduction of the active expiratory valve was a disruptive technology in critical care mechanical ventilation. This valve flutters when the airway pressure rises above the targeted level – to vent off surplus gas, but maintain airway pressure. It led to the development of newer modes of ventilation (and adjustments to older modes) that allowed the patient to breathe spontaneously independent of the ventilator. As such this was a development of intermittent mandatory ventilation (IMV) – without the risk of breath stacking and expiratory dys-synchrony.
The major mode of ventilation that evolved from the active expiratory valve has several different aliases – BiLevel, BIPAP, BIVENT, DuoPAP etc. but they are all, essentially, pressure controlled intermittent mandatory ventilation modes – that allow the patient to breathe supported or unsupported at a high (Phigh) or low (Plow) airway pressure.
I have chosen the term “Bilevel Pressure Control (BL-PC)” to describe this mode. This tutorial introduces BL-PC, from the perspective of IMV, explains the technology and then discusses the setup and use of the mode. It is a mode of ventilation that is used widely as the “default mode” in many ICUs and can be used in any patient at any time. @ccmtutorials http://www.ccmtutorials.org
This tutorial is about Automatic Tube Compensation (ATC). ATC is a setting that has been included in most modern ventilators. Its aim is to reduce the work of breathing associated with the drop in pressure across the endotracheal tube. The ventilator senses pressure, flow and resistance and changes the pressure during the breath to ensure that the patient has the sensation that they are breathing through their own airway. There are two configurations of ATC – one is as an alternative to pressure support in patients who are essentially weaned from mechanical ventilation: essentially a spontaneous breathing trial. The second configuration is as an accessory to all pressure limited modes – such that the pressure waveform is crafted in inspiration and expiration to reduce the workload of breathing during both phases of respiration. @ccmtutorials http://www.ccmtutorials.org
In the previous tutorial I introduced some of the fundamental elements of pressure control ventilation – time cycling, decelerating flow, pressure ramps etc. This time I discuss, in detail, the concept of mean airway pressure (Pmaw) and describe why increasing Pmaw is an effective way of treating patients with extensive lung disease. In volume controlled ventilation this can be achieved by titrating PEEP upwards and increasing respiratory rate. Care must be taken to keep the plateau pressure below 30cmH2O in the majority of patients. In pressure control Pmaw is generally increased by increasing inspiratory time – extreme care must be taken, though, to avoid escalating Auto-PEEP as this corrodes tidal volume and actually reduces Pmaw.
If auto-PEEP is unavoidable, as it is with inverse ratio ventilation, then extrinsic PEEP should be reduced to ensure that tidal ventilation is maintained. Pmaw can be achieved in volume control by adding an inspiratory pause, and in pressure control by increasing respiratory rate – but these are less effective approaches – in volume control because of necessary flow limitation and in pressure control because of fixed inspiratory times, and Auto-PEEP. I guarantee you’ll learn something.
In previous tutorials I discussed the problem of ventilation perfusion mismatch, intrapulmonary shunt and physiologic dead space. I explained how different injuries to the lung (the 6 s approach – slimy, soggy, sticky etc.) resulted in poorly aerated airways and atelectasis. Before moving on to a discussion about CPAP/PEEP we need to explore the problem of low lung volumes. Although the lungs can hold up to 6L of air – in reality most of the time there is 2-2.5L in the alveoli. This is the resting lung volume that is found at end expiration and results when the tendency for the chest wall to spring outwards is balanced by the tendency for the lungs to collapse inwards. That resting lung volume is established by negative pleural pressure and it represents the expiratory reserve volume and residual volume – together the functional residual capacity (FRC).
FRC is the lung capacity in which most oxygenation takes place, in which lung compliance is highest, airway resistance lowest and pulmonary vascular resistance optimal. Loss of FRC (“low lung volumes”) – results in hypoxemia, increased work of breathing, autopeep and pulmonary hypertension.
During the tutorial I elaborate on lung volumes – how they are affected by position and age, how airway closure becomes a major issue as we get older – particularly in the supine position, and I introduce the volume pressure curve which is essential for understanding dynamic respiratory system compliance.
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.
ORtoICU 