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.
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:
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 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).
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!)
Most bedside practitioners pay little attention to ventilator waveforms – usually just the tidal volume and, occasionally, the pressure waveform. However, mechanical ventilation is all about flow – if there is no flow there is no breath. In this tutorial I will look at flow patterns in patients attached to a ventilator. Patients who breathe spontaneously, without assistance, draw flow from the ventilator, the positive flow in inspiration is hemispheric in appearance, exhalation is a v shape – reflecting elastic recoil. Volume controlled ventilation may be delivered by either constant or decelerating flow, with or without an inspiratory hold (also known as a pause). The flow pattern in pressure control is always decelerating – as airway pressure rises, flow falls. Tidal volumes are variable in pressure control, as the negative pressure deflection during inspiration increases the inspiratory ramp and and hence the tidal volume.
I guarantee you will learn something from this tutorial and will never look at a ventilator the same way again.
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.
Introduction to the Course
This is a quick introduction to the course, explaining what I am proposing to cover over four parts.
Preliminary Material
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
1 Supplement
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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ORtoICU 