Episode 1 - Acute Respiratory Failure I: Mechanisms & Pathophysiology

And whether you primarily work in the ER, wards, Pac U, or ICU, it's really critical that you have an organized approach to the recognition and management of this common and potentially life threatening condition. There's a lot of reasons we're starting rounds with this particular topic. You know, acute respiratory failure is one of these final common pathways for a diverse range of clinical disease processes, and as such, it's frequently encountered both in the trauma bay and ICU.

Second, and this is really important, having a strong grasp on the core physiologic concepts underlying both oxygenation and ventilation as well as their relationships to one another, provides the foundation for understanding other core topics in trauma and critical care, including hemorrhagic shock, mechanical ventilation, resuscitation endpoints, just to name a few.

But before we delve into the clinical management side of things, I wanted to spend the next thirty five minutes reviewing the mechanisms of both acute hypoxemia and hypercarbia. So there are four key objectives for today's episode, and by the end of rounds you should be able to number one, discuss the key equations and concepts used to describe oxygenation and ventilation. This includes the DO two or oxygen delivery equation.

You should also understand the relationship between the partial pressure of oxygen and oxygen saturation, or the oxygen hemoglobin dissociation curve, the AAO two difference as well as the determinants of alveolar ventilation. Number two. You should be able to describe the differences between hypoxia on the one hand and hypoxemia on the other.

Number three, you should understand the six pathophysiologic causes of hypoxemia, with the two most relevant and commonly encountered mechanisms being VQ mismatch and shunt. Finally, we're going to apply an anatomic approach to understanding causes of hypercapnic respiratory failure.

Now when I talk about an anatomic approach, what I mean by this is that as surgeons, we rely heavily on an intimate knowledge of anatomy and the inner relationship between vital structures in order to safely and proficiently operate and cure disease. But we can also take this approach and apply it to the differential in management of critically ill and injured patients.

Time and time again on rounds, we're going to apply this anatomic approach to help us problem solve and at the same time avoid fixation error, particularly when time is of the essence and data is, well, either minimal or unavailable.

So what does it mean when we say that a patient is in or experiencing acute respiratory failure? Well, in your mind's eye, and please don't close your eyes if you're driving, I want you to picture the last patient you managed with acute respiratory failure. Uh for me, just the other day I encountered an elderly patient who was just transferred into our unit with SATS in the low eighties. He was takypnic with a resp rate of thirty-four, and an obvious distress manifested by accessory muscle use.

Paradoxical breathing. On the opposite end of the spectrum, however, maybe you came across a patient in the immediate post operative setting who, after receiving a little bit of or a little too much parental analgesia develops a depressed LOC or GCS with pinpoint pupils and a super slow respiratory rate.

In both scenarios which are quite divergent in presentation, I think we can all agree that the potential for further respiratory decompensation is present and that immediate institution of life saving therapies is indicated. In the ideal world, we would recognize patients way before they deteriorate to the point where we would need to urgently or emergently secure definitive airway.

With that said, there are a number of life saving interventions that can and should be performed prior to intubation. But let's get back to the question at hand. What is acute respiratory failure? And Put simply, acute respiratory failure is any impairment of oxygen uptake or carbon dioxide elimination, or both, which is typically the case, that's severe enough to threaten life.

Acute respiratory failure is typically classified into a primary failure to oxygenate, also known as hypoxemic respiratory failure. or a primary failure to ventilate, also known as hypercapnic or hypocarbic respiratory failure. Not to make things more confusing, but sometimes it helps to think of hypoxemic respiratory failure as pulmonary or lung failure. And hypercapnic respiratory failure as pump failure, which may be central or peripheral, more on that later.

Common causes of hypoxemic respiratory failure include pneumonia, ARDS, as well as pulmonary edema. Causes of hypercapnic respiratory failure can be divided into what I call can't breathe or won't breathe causes. Now whereas oxygenation is the process by which oxygen is added to the blood, Ventilation is the process whereby air moves from the atmosphere into the lungs so that gas exchange can occur.

The time over which respiratory failure develops is also important, and this is typically described as either acute, chronic, or acute on chronic. For the purposes of today's rounds, we're going to just limit the discussion to acute respiratory failure or respiratory failure that develops within minutes to hours.

I think a key point to mention before moving on to core equations and concepts is that in the majority of situations, I would say that there are problems with both forms of gas exchange. I think the whole idea behind classifying respiratory failure into acute hypoxemic and hypercarbic respiratory failure

is that it's helpful, or at least it helps me, really kind of narrow down the differential when I'm approaching or managing a patient with respiratory failure. And that really does help facilitate both the workup as well as management of these patients. So having to find acute respiratory failure is an impairment of oxygenation and carbon dioxide elimination that's a threat to life.

I guess the next logical question one might ask is what are the determinants of oxygen and carbon dioxide levels in the body? So let's start by focusing our attention on oxygenation. One of the fundamental equations that we're gonna come back to time and time again until it's simply etched into your beautiful brain is the oxygen delivery or DO2 equation equal to your cardiac output. times one point three four times your hemoglobin concentration.

times your O two saturation plus point zero zero three one times your P litol A or arterial oxygen. So oxygen delivery describes the rate at which oxygen is transported from the pulmonary vasculature through the left ventricle where it's pumped out to the systemic arteries and peripheral tissues. Now when you think about that equation and really kind of just break it down and simplify it, there's really two parts to it.

First, we have a pump, better known as cardiac output, which drives that oxygen rich blood out into the tissues where it's consumed to support activities of cellular respiration and metabolism. Second, we have what's being delivered, namely oxygen.

Now we'll come back to the cardiac output a little later, specifically with regards to how a depressed cardiac output or imbalance in oxygen delivery and oxygen consumption can lead to hypoxia, but for now Let's just focus on arterial oxygen content, which is comprised of either number one, oxygen bound to hemoglobin, or number two, oxygen dissolved in the plasma. Now, thinking about that equation and the arterial content of oxygen, so 1.34 times the hemoglobin times the percent saturation.

I mean ultimately from an overall content standpoint, the amount of oxygen bound to hemoglobin is huge compared to the dissolved component, which is point zero zero three one times your P little AO two. Now, assuming we're at sea level with an atmospheric pressure of seven hundred and sixty millimeters mercury, with normal or relatively healthy lungs, ultimately that PAO two is gonna be a hundred.

Whether your PaO2 is 50, 60, 100, or 500, ultimately, the dissolved oxygen content contributes very little to overall arterial oxygen content, probably about 1.5%. of the total arterial oxygen content in the blood. And this explains why the arterial oxyhemoglobin saturation or its surrogate, the SPO2, provides us with more meaningful data points. This has implications in terms of which value the PaO2 or SPO2 we should follow in titrate oxygen therapy to at the bedside.

But the bigger, more important question, at least in my mind is

What's the relationship between the arterial pressure of oxygen and oxygen saturation? And in order to answer that question, we need to briefly review the oxygen hemoglobin dissociation curve. So you may recollect that arterial oxygen saturation is determined by the arterial PO two. as well as the tendency of hemoglobin to bind oxygen, and this can be displayed graphically. Along the vertical or y axis we have our percent saturation of oxygen, and along the x-axis we have the PaO2.

So there's a few key observations or things to remember regarding the sigmoidal or S shape of the oxygen hemoglobin dissociation curve. First The PAO two is normally on the upper flat part of the curve, meaning that Even if there is a large drop in your PaO2, only a minor change in the oxygen saturation is going to occur. The environment in the lungs is really well suited for oxygen loading where the PaO2 is fairly high.

Second, the venous and capillary blood, or the PVO2 venous pressure of oxygen, is on the steep portion of the curve, which ultimately promotes the exchange of oxygen both in the systemic and pulmonary capillary beds. phenomenon of oxygen unloading in the peripheral tissues or systemic capillaries occurs via passive diffusion of oxygen down its concentration gradient in an environment where the PAO two is fairly low.

The mixed venous PO two, for example, is around forty millimeters of mercury. That's blood returning to the right side of the heart, which essentially corresponds to an S VO two of approximately seventy five percent. Now between the upper and lower flat portions of the curve is the steep portion or the so-called slippery slope. where even small or minute changes or decreases in the PAO two may dramatically reduce the oxygen saturation and overall arterial content.

Once the PAO two reaches sixty millimeters of mercury, which corresponds with a sat of about ninety percent, that's where we're approaching the slippery slope and In a future episode we'll take a closer look at oxygen and carbon dioxide kinetics.

So when it comes to monitoring or following the PAO two versus the SPO two, what are the advantages and disadvantages of one over the other? Well, some of this is pretty obvious. I mean, in order to obtain a partial pressure of arterial oxygen that's really contingent upon drawing an A B G or arterial blood gas and

depending on the unit that you practice in as well as local habits and customs, that may or may not be something that's done frequently. The big advantage of the pulse oximeter or spO2 is that it's continuous. It's non-invasive. And provided that the conditions for reliable reading are met, this is a really nice real-time way of gathering data on a patient's overall oxygenation status.

The one important point to bear in mind, and this may seem obvious, is that the SAO two and the SPO two really tell us nothing about the adequacy of alveolar ventilation. So before moving on to our second learning objective, there's a couple of more concepts that we need to examine and one of them is the AAO2 difference and the other one is the PF or P to F ratio. So the AAO2 difference, or the alveolar arterial O2 gradient, is a measure of efficiency of gas exchange. Let's face it.

It's cumbersome, it has to be interpreted with caution as normal values are unknown. when a patient's receiving supplemental O two, and as most patients with acute respiratory failure are receiving some form of oxygen therapy, and sometimes even hyperoxic therapy for that matter. I think it's safe to say that the widespread applicability of this formula in daily clinical care is questionable, which is why it's not one of those things that you need to memorize. Unlike the DO two equation.

Now again I would refer you to the show notes for the exact formula, but key variables considered in determining the alveolar PO two include barometric and water vapor pressures and not surprisingly the FiO2. Other factors include the concentration of the PACO2 as well as the respiratory quotient. So when you subtract the arterial PO2 from the alveolar PO2, the difference should be somewhere between 5 to 10 millimeters of mercury, and this value increases with age.

But in general, uh increases in the size of the AAO2 difference usually signify underlying problems with gas exchange, whereas a normal gradient implies fairly healthy lungs. Hypoxemia in the presence of a normal AAO two gradient is usually consistent with alveolar hypoventilation as the etiology. Perhaps a simpler and more pragmatic way of looking at the adequacy of oxygenation that's also not overly complicated, is simply just to calculate the P to F ratio or the PAO2 over FIO two ratio.

Normally that ratio is about five hundred, just thinking that the normal arterial pressure of oxygen should be a hundred. divided by point two one and anything less than three hundred would be suggestive of the presence of ARDS. Again, that's only one of the criteria that are used to define the acute respiratory distress syndrome. Unlike the AAO2 difference, the PF ratio is a nice simple equation and can be easily remembered provided of course that you have the results of an ABG on hand.

Now before we get into the different mechanisms underlying hypoxemia or hypercapnia, I'd like to take a few minutes to first discuss hypoxia. Specifically, what do we mean by hypoxia and what are the core causes for this potentially life-threatening condition, as we'll discuss

Although hypoxemia is a potential source for hypoxia, the two states are actually different and quite distinct from one another. So when we talk about hypoxia, what we're really saying is a lack of oxygen at the cellular level. How does this differ from hypoxemia? Well, given the suffix emia in the term hypoxemia it becomes pretty apparent that what we're talking about has something to do with the blood

or amount of something in the blood. So hypoxemia means a low arterial pressure of oxygen or PaO2, and this is typically defined as less than sixty millimeters of mercury. As we mentioned earlier, That's the point on the oxygen hemoglobin dissociation curve where we're about to transition from that upper flat portion of the curve to the steep portion or slippery slope.

So what's so bad about hypoxia? Well, that's pretty self-evident in the sense that in the absence of oxygen, our cellular machinery has to transition from aerobic to anaerobic lycolysis. And that's a much more than a less efficient means of energy production, specifically ATP, which is our body's energy currency. Along with that, we're going to have an accumulation of metabolic waste products, which ultimately need to be expelled from the body.

Why would there be a lack of oxygen at the tissue or cellular level? Well, a simple way of approaching causes of hypoxia is to think about those variables that comprise the DO2 equation. Together with factors affecting oxygen consumption. So, for example, if someone has a pump or cardiac output problem, that may result in circulatory hypoxia. If a patient's bleeding, they'll have reduced hemoglobin concentrations, resulting in anemic hypoxia.

For patients uh coming in with a severe community acquired or hospital acquired pneumonia who develop significant VQ mismatch and shunt physiology, these patients may develop a hypoxemic hypoxia. And another cause or etiology is known as histotoxic hypoxia.

And this is something that may be more commonly seen in victims or carbon monoxide poisoning. We know that carbon monoxide has an affinity for hemoglobin about 240 times that of oxygen. And so these patients may develop hypoxia as a result of that. Other causes of histotoxic hypoxia that we'll encounter both in the ER or ICU include things like methemoglobinemia as well as cyanide poisoning.

So now we finally get to the different causes of hypoxemia, of which there are six. Number one, alveolar hypoventilation. Number two, a low partial pressure of inspired oxygen. Three, uh diffusion abnormality. Number four and five are the two most common reasons that patients will develop hypoxemia, and that is VQ mismatch, the most common, and shunting.

Welling number six is a low mixed Venus O two saturation, also known as Venus Admixture. Now Given the first three causes of hypoxemia are fairly straightforward, let's just quickly hammer through those. Uh alveolar hypoventilation, uh this may result in both hypoxemia as well as hypercapnia. As was mentioned earlier, the AAO two gradient is not widened with this mechanism and there's no VQ imbalance in the lungs.

It may be obvious already, but the degree of hypoventilation is best measured not by examining the PAO two, but examining the PACO two. So again, alveolar hypoventilation is one of these causes of hypoxemia with a normal AAO2 gradient. A decreased partial pressure of inspired oxygen may also result in hypoxemia, usually as a result of altitude, or in the case of a vented patient disconnected O two tubing.

Uh regarding altitude, a lot of folks mistakenly refer to this as uh decreased FIO2, but the example I always like to give is that whether you're at sea level here in Los Angeles or at the top of Mount Everest, The FIO2 is the same, it's 21%. What differs is the barometric pressure. Diffusion defect, we may see this in a whole host of clinical conditions. I think the most common example of this, or the prototypical example of this.

would be a patient with uh, let's say idiopathic pulmonary fibrosis. whereby the interface between the alveolus and the pulmonary capillary is thickened. There's a variety of factors that are ultimately going to defect diffusion of gases, like oxygen and carbon dioxide across a permeable membrane, And these include the solubility coefficient, the surface area for gas exchange, the thickness of the membranes being transverse.

As well as the partial pressure of these gases and the pressure differential uh across those membranes.

Now we do want to spend a bit of time discussing VQ mismatch and shunt, and the reason for this is that they're going to be the two most common reasons that critically ill patients either develop or present with hypoxemia. So having a clear or a crystal clear understanding of these two mechanisms will ultimately guide us in our differential and clinical management, which we'll get into in a follow-up episode.

So across the lungs and alveolar capillary units, the VQ ratio, the ventilation perfusion ratio, is gonna vary such that in the standing position the apices of the lungs, or West Zone one, are gonna receive more ventilation relative to perfusion, whereas the lung bases, or West Zone three, by virtue of gravity, are gonna receive more pulmonary blood flow or perfusion versus ventilation. And an important point to bear in mind is that the VQ ratio isn't one, it's more on the order of about 0.8.

Now two extreme examples of VQ mismatch are dead space ventilation and shunt, and I'm sure these terms are familiar to you. Now in order to fully appreciate what dead space and shunt are, it'll help to picture things at the level of the individual alveolus and pulmonary capillary blood vessel. Dead space ventilation refers to an alveolar capillary unit whereby there is no flow through the capillary, yet ventilation of the alveolus is maintained. In this case, the VQ ratio approaches infinity.

Lots of ventilation, no perfusion. On the opposite end of the spectrum is a shunt, so again picturing the individual alveolar capillary unit, this is a situation where there's no ventilation, yet perfusion or blood flow is intact. And so the VQ ratio in this scenario approaches zero. But most cases of VQ mismatch aren't at these extremes. In other words, due to a variety of conditions including pneumonia, an asthma or COPD exacerbation, PE or pulmonary edema.

There may be alveolar capillary units across the pulmonary system that have a relatively high VQ. and others where there is a low VQ. So ventilation and perfusion mismatch is the most common cause of hypoxemia and definitely is associated with a widened AAO2 gradient. which can be differentiated from shunt on the basis of a response to the administration of supplemental or a hundred percent O two. VQ responds, shunt will not.

As we stated, a shunt is an extreme form of EQ mismatch whereby there is no ventilation happening at the level of the alveolus. And blood is essentially traveling from the right side or systemic venous circulation to the left side of the heart to be pumped out into the systemic circulation with no participation in gas exchange. Shunts can be either physiologic or anatomic.

And in the normal state, we typically have a physiologic shunt fraction of less than ten percent of our total cardiac output. As that shunt fraction increases to say 30%, and definitely by the time we have a shunt fraction of 50%, the administration of supplemental O2 in the form of 100% will not result in an increase in the O2 saturation.

Now, regarding anatomic shunts, these can be classified based on the location of the shunt, be it intracardiac or pulmonary, as well as on the direction of flow, either left to right or right to left. PFO or Peyton Frame Minal Valley is a classic example. of an intracardiac right to left shunt that we occasionally counter in the ICU. In fact among patients with acute pulmonary hypertension, say in the setting of severe ARDs or ARDS, for example.

It's the reason why we prefer a so called bubble test on Echo when we're trying to rule this out as a potential contributor or cause for severe refractory hypoxemia in patients with ARDS. So now to put this all together and understand why supplemental O2 is not gonna improve someone's O2 sats in the setting of a shunt. It might help to visualize a terminal bronchiole. And that terminal bronchiole is going to branch off into two alveoli.

And each alveola is going to be perfused by its own pulmonary capillary. And those two pulmonary capillaries are going to then converge to form a pulmonary venule and eventually vein to return to the left side of the heart. So let's say that one of those alveoli is completely collapsed to either atelectasis or it's filled with edema or mucus.

Blood essentially is going to pass or be shunted from the right to the left side of the heart, and it's going to have a PAO2 of 40 millimeters mercury and a PACO2 of 46. In other words, there's absolutely no gas exchange happening in this alveolar capillary unit. Now, in the healthy alveolar capillary unit, gas exchange occurs as it's supposed to. such that blood enters with the PAO two and PACO two of forty and forty six, similar to the previous scenario.

But that blood is gonna leave fully ventilated and have a PaO2 of 100 and a PACO2 of 40 millimeters mercury. Assuming that each of these alveolar capillary units are receiving an equal amount of blood, when you calculate the average or mean PaO2 of blood in that pulmonary venule, that's A hundred plus forty divided by two, you get a PaO two of seventy millimeters of mercury. And so why is this significant and why am I belaboring this point?

Well, if you're to increase the FiO two and bear in mind the relationship between PAO two and O two saturations on the basis of the oxygen hemoglobin dissociation curve we discussed earlier. What you'll very quickly realize is that any increase in FIO two, which is only going to be seen by that healthy alveolar capillary unit, will not result in a significant increase in the patient's O2 saturation. And why is that?

Well, even at a PaO2 of 70, if our O2 saturation is already in the high 90s, if we were to provide the patient with an FIO2 of 100%. Even if the increased overall PAO two increased to five or six hundred, well There is not going to be much of an increase in the O2 saturation because we're already beyond that upper inflection point and along the flat portion of the oxygen hemoglobin dissociation curve.

So, what are the clinical implications of this? Well, quite simply, in patients who have, let's say, severe ARDS. or significant refractory hypoxemia, keeping these patients on an FIO two of a hundred percent may actually be potentially detrimental and harmful

due to the generation of oxygen free radical species which are essentially gonna wreak havoc not just locally, but systemically. And this is what we mean by bio trauma. As we'll hear in a future episode specifically dedicated to ARDS, Biotrauma is ultimately what ends up killing patients with ARDS, not primary acute respiratory failure or ability to oxygenate. The other implication is that for patients with severe ARDS with refractory hypoxemia.

We need to think about ways that we can increase their mean airway pressures, recruit, derecruited, or add electatic segments, and not get so hung up on the FIO2. But we'll discuss this further in a future episode.

The sixth and final cause of hypoxemia, which people don't talk about as much as the other five causes, is a low-mixed venous O2 sat, aka Venus admixture. which can occur as a result of an imbalance in oxygen delivery and oxygen uptake or consumption. Later we'll do a deeper dive into oxygen and carbon dioxide kinetics We'll also explore the concept of a critical DO2 in the shock talk.

The one thing that I will say here before we move on is that there really does need to be a significant impairment in gas exchange above and beyond a low-mix Venus O2 sap. In other words, venous admixture in and of itself is usually not sufficient to result in hypoxemia. So that brings us to our final objective, in which we'll apply an anatomic approach to understanding causes of acute hypercapnic respiratory failure.

which is variably defined as an abrupt or acute increase in the PACO2, typically greater than fifty millimeters of mercury. That doesn't represent compensation for a metabolic uh alkalosis. In terms of the determinants of PACO two.

Arterial carbon dioxide tension is directly proportional to the rate of CO two production and and inversely related to alveolar ventilation, bearing in mind that alveolar ventilation is just the minute ventilation or your resp rate times your tidal volume minus dead space ventilation. So to sum that up, three sources of hypercapnia, one increased CO2 production, two increased dead space ventilation, and three hypoventilation.

Regarding conditions that may increase CO2 production in critically ill patients, there are several. Common etiologies include things like pain, anxiety, sepsis, fevers, seizures, and shivering, whereas conditions such as thyrotoxicosis,

High output cardiac failure, overfeeding, and in the OR, malignant hyperthermia are much less commonly encountered or rare. In the majority of cases, The increased CO two production is related to oxidative metabolism and in the absence of an impairment in CO two excretion, excess CO two production doesn't normally cause hypercapnia.

Now earlier we discussed physiologic dead space in the setting of VQ mismatch, but it's important to remember that in addition to physiologic dead space, we also have anatomic dead space. Or those segments of the ventilator circuit, airway, and tracheobronchial tree that do not participate in gas exchange. For any given breath, about thirty percent of the tidal volume is what we would call dead space or wasted ventilation.

And this is again is gas confined to the large conducting airways like the trachea and bronchi. In the average adult, anatomic dead space typically works out to about one C C per pound. In terms of hypoventilation as a cause for hypercapnia, you will recall at the beginning of the show that the other way of thinking about hypercapnic respiratory failure was as pump failure. So

What would result in pump or bellows dysfunction? I like to break this down into two major categories. Patients either won't breathe. Or they can't breathe. And here's where that anatomic approach is helpful in terms of both visualizing the various components of the respiratory pump and working through the differential diagnosis for hypercapnic respiratory failure.

So when we say that someone won't breathe, I think classic examples of this are patients who come in with an opioid overdose or a narcotic overdose. Essentially their central drive to breathe is suppressed, and because they won't breathe, They have ineffective ventilation and alveolar hypoventilation. And increasing CO2s will ultimately affect the patient's ability to oxygenate. Other won't breathe problems include patients with, for example, uh medullary CVA or stroke.

Patients with obstructive sleep apnea, and patients presenting with a variety of metabolic or endocrine conditions, for example, hypothyroidism or a severe metabolic alkalosis. And then in addition to the won't breathe problems, which are really in effect uh CNS brain or brainstem problems, we also have the can't breathe problems, and these refer to causes or failures of one or more components of the respiratory pump at or below the level of the brain and brainstem.

So, what are potential etiologies here? Again, this is where that anatomic approach is helpful. So, starting at the level of the spinal cord. Specifically the cervical spinal cord and anterior horn cells, we can think about things like a cervical spine injury.

So if a patient comes in with an injury at the level of C three four five, which involves the phrenic nerve or higher, you can imagine that due to phrenic nerve palsy, there's gonna be ineffective firing or activation of the diaphragm, which is the major muscle of respiration. Now as we move down or out into the periphery, we have the spinal cord as well as anterior horn cells. And so a classic example of a patient coming in with tetraplegia.

and maybe injury at the level of C three four five with phrenic nerve involvement. These patients, due to their absence of phrenic nerve firing, will have uh dysfunctional ventilation because the diaphragm is the major muscle of respiration. Beyond the anterior horn cell, the next anatomic step we have or level is the motor nerve.

a whole host of different conditions can affect the motor nerve, including demyelinating processes like GBS or Guillain Baret syndrome. More and more these days, in fact, we're seeing patients with critical illness polyneuromyopathies. And so there's a big push to ensure that we're lightning sedation, getting patients off the ventilator, and making sure that they're not delirious and getting up and moving as soon as possible to prevent this complication.

Beyond the motor nerve we have the NMJ or neuromuscular junction and a classic disease process affecting the NMJ is myasthenia gravis. There's also toxins such as botulism and organophosphate poisoning that may result in NNJ dysfunction. Muscles and myopathies, there is a number of reasons why the musculature may be ineffective in terms of adequacy of ventilation. And it's also important to think about the airways in alveoli as well.

Finally, excessive work of breathing can occur due to a whole host of abnormalities. Uh, when it comes to chest wall disorders and scoliosis, these are certainly anatomic variants which may increase the work of breathing, resulting in failure. of the respiratory pump. Obesity may do the same thing. In the postoperative setting, particularly in patients, let's say, who have undergone a damage control operation for major abdominal bleeding.

Uh these patients may develop an abdominal compartment syndrome. Uh from the EGS standpoint, patients can come in with tentacites and so there's a whole host of different processes that may result in failure of the respiratory pump and just having this sort of anatomic approach in mind may be helpful to you.

So with that, I think that pretty much concludes our first episode. Once again, I'd like to thank you for joining me on Trauma ICU Rounds. If you like what you listened to today, please do subscribe to the series wherever you normally download your podcast. And don't forget to visit the website, which should be up and running by the time you've listened to this episode. That's uh trauma ICU Rounds dot ca. Please stay safe and we'll talk soon.