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.
It is time to discuss Pressure Controlled Ventilation. In general if a patient has normal lungs or minimal disease, it really does not matter what mode of ventilation you use, pressure or volume controlled. However, there are some major advantages to using Pressure Control – principally in Acute Hypoxic Respiratory Failure. There are also many disadvantages. This is the first of two tutorials that cover the fundamentals of Pressure Control. I start with a discussion of the terminology that I will be using – the Pressure Limit (PL), the Inspiratory Pressure (IP), the Driving Pressure (DP)/Inspiratory Ramp, the Inspiratory Time (Ti) and the Expiratory Time (Texp). Pressure Controlled Ventilation (PCV) is pressure targeted/limited and volume variable. Breaths are time cycled – in inspiration, expiration or both. The flow pattern is always decelerating.
Following the introduction of a clinical scenario – a patient who is developing ARDS, I describe the process of PCV. I explain that tidal volumes are variable in all settings and all modes of PCV and later describe how changing patient position, chest wall elastance and airway resistance can all impact the tidal volume. I discuss why pressure control is the best option for mechanically ventilating children (particularly where there is no endotracheal tube cuff and a significant air leak) and why you need to pay attention to the rise time and respiratory rate. Finally I discuss the major disadvantages of using PCV. I guarantee you’ll learn something! @ccmtutorials
In the previous tutorials I explained how hypoxemia results from low lung volumes, resulting in low functional residual capacity, airway closure and atelectasis. We looked at the mechanisms by which CPAP reduces the work of breathing in obstructed airways and how, following lung recruitment, PEEP maintains FRC.
In this tutorial I elaborate on these themes. I look at the problem of phasic V/Q mismatch (shunt) during expiration and how it may cause dis-correlation between pulse oximeters and blood gasses. PEEP prevents this at the expense of increasing dead space and negatively impacting ventilation. Optimal PEEP should restore lung compliance – compliance is low with low and high lung volumes. Compliance may also appear poor in pressure control when there is clinically significant auto-PEEP: the ventilator cannot distinguish auto-PEEP from driving pressure and lower than expected tidal volumes may result.
I explain the concept of the “Waterfall” effect to overcome Auto-PEEP. Finally, in our first visit to ARDS, I introduce the problem of deciding on optimal PEEP in that setting. I guarantee that you will learn something. @ccmtutorials http://www.ccmtutorials.org
For most of us, the terms CPAP (continuous positive airway pressure) and PEEP (positive end expiratory pressure) have existed for all of our careers. But this was not always the case. Although mechanical ventilation, including the positive pressure variant, was a child of the 1950s – PEEP was not described until the late 1960s and even then was seen as a therapy for postoperative atelectasis in cardiac surgery patients. PEEP subsequently became the mainstay of therapy for hypoxic respiratory failure, but was always used in associated with positive pressure breaths. CPAP was developed in the early 1980s as a therapy for sleep disordered breathing. Over two decades the non invasive CPAP therapy and the invasive ventilation (pressure targeted breaths with PEEP) coalesced such that CPAP became a therapy for hypoxic respiratory failure and congestive heart failure, and pressure support (BiPAP or NIV) became a therapy for sleep apnea.
Strictly speaking PEEP and CPAP are different. It is possible to apply PEEP at end expiration and then commence the next breath from atmospheric pressure (try slapping your hand over your mouth mid expiration – then remove it and take a breath) – spontaneous PEEP. However this is almost never used in clinical practice. In CPAP the patients sinusoidal respiratory pattern persists – but starts and ends at an elevated baseline pressure. In PEEP the positive pressure breath starts and ends at that pressure (i.e. pre inspiration and end expiration). So, these days, in most scenarios PEEP and CPAP are indistinguishable. How they are delivered is, of course, different. Nevertheless they serve the same functions 1. To overcome airway resistance that causes disrupted or obstructed gas flow in expiration; 2. To reduce the work of breathing by reducing the magnitude of negative pleural pressure required to generate a tidal volume; 3. Most importantly – to restore functional residual capacity (FRC); 3. To prevent derecruitment of vulnerable lung units in the posterior dorsal segments of the lungs.
PEEP does not easily re-expand collapsed lung tissue – this is usually achieved by applying a recruitment maneuver (30cmH2O or more for 10 seconds during anesthesia, for 30 seconds in lung injury). The application of PEEP then prevents derecruitment. As such the majority of lung tissue may be re-expanded during anesthesia. This may not be the case in diseased lungs – the principle is to restore a functional residual capacity even if that effectively utilizes the inspiratory reserve volume.
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.
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).
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)
ORtoICU 