Point of care Echocardiography- Core Principles

This is the first part of a multi-part series on the topic of point-of-care echocardiography. In this initial episode, we will focus on the core content that all resuscitative experts must know in order to look after critically ill patients. As with any presentation, you must take this with some grain of salt, and in particular you must understand that expertise and comfort with point-of-care ultrasound is arrived at only after doing hands-on training, and ideally significant hands-on supervision and mentoring. As mentioned, the objective of this presentation is to review the essential scope for point-of-care echocardiography that all providers of acute care should understand and obtain. Now what this will look like for you over the next 40 minutes will be a overview of gross left ventricular systolic function, how to assess gross right ventricular size and function, the assessment of pericardial effusion, and the IVC and volume status. Now this scope that I just outlined to you is a synthesis from these two key papers. One, at the top there, is the American College of Emergency Physicians' paper that they published with the American Society of Echocardiography outlining the scope of point-of-care echo that is ideal for emergency physicians. The second paper, on the bottom, is the position paper from the American College of Chest Physicians about the ideal scope for echocardiography for all intensive care providers. This paper was further endorsed by 13 separate critical care societies from around the world. So between these two papers, we have a pretty good idea of the topics that we should understand and know how to use at the bedside of sick patients, whether they appear in the emergency room or in the intensive care unit. 

And I would further submit that this can be extrapolated to any sick patient anywhere in the hospital. Now this tutorial will not focus particularly on image acquisition techniques, as these are covered in other sections of the SonoSite Institute, and they have separate modules to cover these particular views here. Now these six views that I emphasize, I believe, and many of my colleagues share this belief, are sufficient to be able to answer the common questions that you face with critically ill patients. These six views, the parasternal long and short axis, the apical four chamber, subcostal four chamber, the subcostal short axis, and the long axis view of the inferior vena cava, provide information that allows you to answer those four key areas that I've previously outlined. Now let's get into the topic of left ventricular function. Left ventricular function is commonly of interest to us at the bedside. When taking on the task of evaluating left ventricular function in a point-of-care fashion, one must confront an immediate discordance between what seems instinctive for us to do and what we have been raised with. By that I mean, the eyeball method seems instinctive but we've all been raised and steeped in the tradition of the ejection fraction. Now, there is good news. The eyeball method, which loosely stated is a gross evaluation using your eyeballs rather than calipers in the determination of how well a patient's heart is beating. There is literature from multiple specialties supporting that eyeball methodology is just as accurate as ejection fraction, and that practitioners who are non-cardiologists can use this method to very accurately categorize classes of left ventricular function. Looking at this parasternal long axis, for instance, one can readily synthesize with their naked eye that the walls of the left ventricle are moving towards the middle, are thickening, and the mitral valve opens well. These are the three tentative eyeball methods we will review in some detail shortly. By comparison, the ejection fraction method is cumbersome and quite involved. You need two orthogonal views, typically apical four chamber and an apical two chamber view, and these views then need to be captured at end systole and end diastole with the left ventricular volume measured using special calipers at each of these states. The machine is then able to do some heavy lifting of Simpson's biplane method of disks, as it's called, and generate a number for you. Now while it is appealing to have an exact number, as we will review, an exact number is actually not as helpful as a more broad classification system for the acutely ill patient. For instance, an ejection fraction of 53% is of little meaning to you compared to a ejection fraction of 48% or an ejection fraction of 57% when considering what therapeutic options to entertain in a patient in shock. So the degree of absolute quantity can be a little more than we're actually looking for. I hope to convince you of this as we continue forward. Now, with practice you will simply look at this echo and say that is a normal left ventricle in the parasternal long axis. However, when starting out or when you need some extra confidence, use these three steps to visually assess for myocardial thickening, is it present or absent? And to assess for this, look at the actual muscle. Is it getting thicker during the systolic phase of the cardiac cycle? Then assess for endocardial excursion. Now this concept refers to the notion that the heart's walls should generally move towards the center of the chamber. This red dot here provides you with a visual goal to look at, but the beginner is encouraged to sometimes just place their finger on the screen or imagine a similar red dot in place. Here we can see that the two walls pictured in the parasternal long are indeed moving towards the center point. Lastly, when the mitral valve is in view in a long axis portrayal, so that would either be the parasternal long axis or the apical four chamber view, one can evaluate for how closely the anterior mitral valve leaflet comes to the interventricular septum. In this case, we can see that during diastole that anterior mitral valve leaflet effectively comes up and touches the interventricular septum. This concept, long since known to the cardiologists and called E-point septal separation or EPSS for short, is well correlated with degrees of systolic function and when used appropriately can be an extremely helpful tool in helping assess left ventricular function with the eyeball approach. Now, rather than a continuous variable like ejection fraction, we encourage the point-of-care echocardiographer to consider four separate broad classifications, with their corresponding ejection fraction gold standard values in brackets here. Firstly, a hyperdynamic heart is one whose ejection fraction is considered to be greater than 70%. Here this can be seen in the long axis view. We can appreciate, using our eyeball method, there is vigorous thickening and excursion and that the mitral valve leaflet in fact touches the interventricular septum. Now the heart is tachycardic, and this may make it harder to appreciate the subtleties, but suffice it to say at the end of systole there appears to be no more black, or that is blood, in the ventricular chamber, suggesting that ejection fraction is indeed upwards of 80 or 90% and this heart is hyperdynamic. Now a normal left ventricle, by comparison, which we've already seen, is in the range of an ejection fraction of 50 to 70%. We have good thickening and good excursion, we have anterior mitral valve leaflet movement or EPSS that approximates the septum. All is good with this ventricle. Not as vigorous as hyperdynamic, but perfectly normal. Next we have the mild to moderate dysfunction stage. Now this is a heart that is impaired in some capacity, but obviously not severely dysfunctional as we will review in a moment, and we can see that though there is thickening and though there is excursion it is considerably less than in the normal scenario. Of note, we can appreciate the mitral valve leaflet is not approximating the septum with the same closeness. In fact, I can place my mouse cursor between that leaflet and the septum, suggesting that in this closed system that there's not as much blood moving through that mitral valve to push it open. So this is the mild to moderate category or an ejection fraction of 30 to 50%. Then last on this continuum, we have the severely dysfunctional heart. Again, all of these views have been captured and shown to you in the parasternal long axis for consistency's sake. And here we see a parasternal long axis view where yes, there is movement of the heart and yes, you can appreciate probably some thickening of the inferior wall here, especially at the base of the heart. The mitral valve barely opens, there's almost no thickening or excursion of this septal wall. And this is a heart that is severely dysfunctional and in the range of an ejection fraction of less than 30%. Now here are the four broad classifications side-by-side for you to once again look at and review for a moment, appreciating the differences in excursion, thickening, and mitral valve movement between them. Now, here are the same categories shown to you using the parasternal short axis view at the papillary muscle level. We can see in the upper-left, the hyperdynamic heart. At end systole the papillary muscles are nearly touching each other, and the volume in the ventricle is quite low, consistent with a hyperdynamic heart. Notice that a hyperdynamic heart does not need to be tachycardic, as is shown in this case. In the normal scenario, we have again good thickening and good excursion, and the mild to moderate dysfunction we can see comparatively less, and of course the severely dysfunctional heart is often easiest to recognize with little to no thickening or excursion taking place. Of note, we have four walls of each ventricle in the short axis view, often making this view the most intuitive to make global assessments of function. The absence of the mitral valve in a long axis to help us with the EPSS does make it an assessment based just on excursion and thickening, which may challenge the novice. However, with sufficient practice this is easily overcome. Now for acute care practitioners, the impact of understanding left ventricular function likely needs no introduction, however it is important to stress that the left ventricle will influence many decisions you make as a practitioner for those in shock or respiratory failure, including the titration or initiation of vasoactive medications such as inotropes or vasopressors, the administration of IV fluids, the choice to implement mechanical support such as a balloon pump or ECMO, as well as prognostic features in multi-system disease. For instance, the patient with previously unrecognized severe LV dysfunction who presents with multi-organ failure and shock related to an infection will obviously carry a worse prognosis than someone who can generate a vigorous cardiac response. Therefore, an accurate and timely assessment of the left ventricle will have an enormous impact on your practice when looking after these sick patients. Let's move on to the right ventricle now. Now the right ventricle has often suffered a less glamorous existence than the left ventricle. However, we now understand just how important right ventricular function is and how much it can influence clinical trajectory and outcome for patients. Now the right ventricle, rather than being a simple assessment of squeeze which the left ventricle offers, the right ventricle offers a few separate findings that you must piece together to support or refute the notion that the right ventricle is impaired. We will review some of these findings here, including the most basic and important which is the right ventricular to left ventricular size. The kinetics of the interventricular septum are equally or nearly equally important. The presence or absence of IVC engorgement to support right ventricular function is critical. Assessment for gross systolic function. As well, the point-of-care sonographer can easily assess for right ventricular systolic pressure, however this will not be covered in this tutorial but will be covered in a separate module as this invokes spectral doppler which is an advanced technique. Now as I mentioned, I think the most important feature when doing a point-of-care assessment of the right ventricle is to identify whether or not the right ventricle is dilated. As one of my friends and mentors, Antoine Vieillard-Baron says, "A failed right ventricle is a "dilated right ventricle." You cannot have right ventricular failure of hemodynamic importance unless it is dilated. Now the best view to assess for dilation is the apical four chamber view, as this positions the right ventricle immediately adjacent to the left ventricle and allows for the relative size comparison, which is the foundation of how we determine whether the right ventricle is dilated. Again, this is an eyeball approach, no need for calipers or measurements here. You simply need to identify whether or not the right ventricle is less than or equal to two-thirds of the size of the left ventricle, such as in a normal scenario here. Or is there moderate RV enlargement where the right ventricle is more than two-thirds the size of the left ventricle but is not yet the dominant chamber and is less than equal in size? Here in this moderate RV enlargement, where the ventricle is indeed dilated, we can appreciate that the apex of the apical four chamber is starting, starting to be encroached upon by that right ventricle, but the dominant chamber remains the left ventricle. Lastly, in severe RV enlargement as is shown here, the right ventricle is larger than the left ventricle and it is now the dominant chamber also at the apex where, when shooting through the apex so that the apex of the right ventricle, which is most dominant. We will come back to this shortly, however septal motion can be appreciated in each of these cases as either being normal or disturbed in both of the latter two examples, where the interventricular septum can be seen to be shifting away from the right ventricle during systole. So let us consider further the septal kinetics, so how the interventricular septum moves during systole. Now, the parasternal short axis often provides the best view for this determination of septal kinetics. Here on the left we see a normal parasternal short axis without right ventricular dysfunction, and we see that the septum thickens and moves towards the middle of the left ventricle during systole. In the middle pane, we can see that the septum looks odd, and even a novice can appreciate in looking at this that there's something off. You may not be able to identify what phase of the cardiac cycle it's taking place in, or even what is actually being seen, but you can appreciate there's a regional nature to the contraction of the heart, and that is even a novice's earliest instinct. With practice and time, you will appreciate that during systole this septum is actually moving paradoxically away from the center of the LV cavity and is instead being controlled by the right ventricle. Lastly, when there is pressure and volume overload through both phases of the cardiac cycle, the septum behaves largely as a flattened object that leaves the left ventricle appearing like a capital D where the septum is largely flat and leaving the rest of the circular nature of the LV to make a D shape. So we've now reviewed that a failed right ventricle is a dilated right ventricle, and that with progressive phases of right ventricular dysfunction the septum will become progressively disordered in its kinetics, eventually arriving at a D-shaped left ventricle when both pressure and volume overload have taken over the right ventricle. Now the recipient of much less attention than left ventricular function is right ventricular systolic function. I just want to raise your awareness of how the right ventricle contracts differently than the left ventricle. When you look at the right ventricle here on the left-sided image, we can see that very vigorous right ventricular contraction is taking place, but not so much in a concentric fashion like a squeeze towards the middle, but more I would draw your attention to this tricuspid valve annulus and how it moves towards its own apex during systole. This vertical movement is classic for how the right ventricle is systolically active, and is really what you should pay attention to with your eyeballs yet again when considering whether the right ventricle has impaired systolic function. By comparison, the view here on the right, we see the tricuspid annulus offers very little vertical or apically directed movement. And by comparison, we see that this image demonstrates severely depressed right ventricular systolic function. There are objective ways of applying numbers to this measurement, which will be reviewed later on called a tricuspid annular plane systolic excursion, or a TAPSE, but I'll tell you right now that doing so offers very little beyond the eyeballs and you can easily appreciate the difference between these two images here. So I've presented somewhat of a laundry list of features that the right ventricle exhibits when it's failed. This is a bit more confusing for some people, whereas the left ventricle offers simply a range of systolic dysfunction which is of most interest to us. So let us introduce the concept of cor pulmonale, and that is really a euphemism, a fancy way of saying total RV system failure. When you have the RV that has failed, it will be dilated, it will have some degree of altered septal kinetics to support the fact that it is encroaching on the left ventricle. And, as we will review in the IVC section, the IVC will also be dilated in keeping with an elevated filling pressure to that disordered right ventricle. Systolic function will likely also be reduced. But overall I would say that that is of less concern to us when entertaining the often binary consideration, is the right ventricle down or is it working which often arises both in the emergency room and the ICU as well as in the perioperative or ward-based care areas. So how does the RV assessment influence your management? Well, it should certainly alter the way you think about shock, and if the patient isn't previously known to have RV dysfunction and you find a state of cor pulmonale in a patient with newly-acquired shock, pulmonary embolism remains a high consideration on your list. This is an important concept as the diagnosis of pulmonary embolism remains difficult for us to carry out without extensive imaging and testing. Fluid management should certainly be altered by the right ventricle, and this is a controversial topic. However, more and more people are moving away from aggressive fluid management for dilated right ventricles as was commonly espoused 20 or 30 years ago. The choice of vasoactive medications may differ for people with right ventricular failure. The choice of ventilator settings, including diminishing mean airway pressures, so as to offload the right ventricle, may make this assessment very important for your practice. And prognosis, we know that similar to left ventricular dysfunction, that those who present with right ventricular dysfunction as a complicator or culprit of critical illness will face a more grave prognosis. Now let's move on to the assessment for pericardial effusion. A very common and early part of point-of-care echocardiography, the assessment for pericardial effusion made its way into the FAST exam protocols that were developed in the early 90s. So many providers have comfort or some experience in this assessment. In the assessment for pericardial effusion, of course, is identification of fluid in the pericardial space. Once identified, trying to determine the size and the hemodynamic influence is paramount. And in particular, novices must be mindful of false positives in the form of epicardial fat, or a left pleural effusion when viewed from the parasternal long axis view, or ascites when viewed in particular from the subxiphoid approach. We will review these pitfalls with some images shortly. So using the subcostal view as a standard here, we can see the difference in appearance between a small, moderate, or large pericardial effusion. In general, for non-surgical or non-traumatic effusions, the effusion will be hypo- or anechoic and will generally be circumferential if of any meaning. So we see a small effusion here that doesn't quite make its way around, we see a moderate effusion here that does have circumferential quality to it, and a large effusion which quite dramatic and is clearly encasing the entire heart. There are measurements associated with small, moderate, and large effusions. However, the important thing to identify as we will review shortly is that tamponade, that is the life-threatening version of a pericardial effusion, remains a clinical diagnosis. Without extensive training, one should not focus on the echocardiographic features of tamponade which few of us are trained to identify, and instead identify whether or not a important effusion is present or not. In the right clinical scenario, such as a penetrating chest injury, a small effusion can be just as important as a large effusion when a leukemic presents in their 70s. So context is everything, and just once again pericardial tamponade is a clinical diagnosis. I see many cases where novices are very tempted, and in fact cannot control their eagerness, to tell me that there is no echocardiographic features of tamponade. When I ask them what those features are, they say something about chamber collapse but typically reverse the cardiac cycles and really they're better off resting on their years of experience as a doctor rather than trying to masquerade as a expert echocardiographer. So please remember this and we will review an algorithm that I hope will be of use to you here. So the key consideration is, is the effusion to you, does it appear non-trivial? And that is, does it evoke some degree of concern, either emotionally or cognitively, that this could be a life-threatening pericardial effusion? Clinical context, size, rapidity of accumulation, these are all things to consider. Now if the patient is arrested or arresting in front of you and you have identified a pericardial effusion that you think could be the cause, your move is to perform a pericardial centesis. Now most of us are not the experts in the hospital at performing pericardiocentesis. So this is not the preferred approach for you or the patient. However, thankfully it is the minority of patients who present with effusion who present in cardiac arrest, and instead the great majority are actually quite stable and therefore we have time to clinically integrate the effusion with clinical features such as their overall appearance, vital sign derangements, lab tests such as lactate, oliguria, other things. And those patients, I'm going to show you shortly, will really benefit also from an IVC ultrasound. An IVC ultrasound is helpful as one cannot have pericardial tamponade without having a dilated IVC, it just simply can't happen unless it's a regional effusion in a post-cardiac surgical patient but we aren't talking about those patients. So if the IVC ultrasound shows a normal IVC that has respiratory variation, you can dismiss concerns of tamponade. If, however, you have a patient who has a dilated IVC and a non-trivial effusion, it's possible they have tamponade and at most centers that might be worth a phone call to your friendly cardiologist to get a second opinion. Lastly, the hypotensive patient who has a non-trivial effusion, the right move if you think it could be the culprit is to initiate IV fluids as to increase filling pressures which is often all that's needed urgently to reverse shock mediated by pericardial effusion, and also simultaneously placing a call to the experts in pericardial centesis at your hospital should that be required, and typically at most hospitals that's a cardiologist. This is my synthesis of years of doing both critical care and echocardiography at the point of care. You will have your own, or your institution may have their own protocol, but I think this captures the three general lines of thought and clinical presentations you may face with a non-trivial pericardial effusion. Now in looking at false positives, one I mentioned previously is the left pleural effusion. Now this is essential to rule in or out pericardial fluid here where we see a parasternal long axis, we see a large anechoic space in the far field, could this conceivably be continuous with the pericardial space? No, it cannot because the descending thoracic aorta is here, which is the boundary of the mediastinum. Anything outside of this is in the pleural cavity. If the fluid ran anterior to this aorta, we could consider this huge space a pericardial collection. Of note, this patient does have a small pericardial effusion in the anterior space, but by no means is this pericardial fluid here because it does not go anterior to the aorta. So the aorta is a critical landmark in the long axis when considering whether or not fluid is a pericardial versus left pleural effusion. Another classic false positive is the epicardial fat pad which, thankfully, typically is not large enough to generate clinical concern on its own. However, it's essential to be mindful that when you see stranding or almost a muscle density or isoechoic density to something filling the pericardial space typically adjacent to the RV free wall, often best seen in the subcostal view, you should be thinking this could be epicardial fat. It can also be seen in the parasternal long axis along the RVOT in the near field. However, this is the classic view where you may see this. And recognizing that sometimes fat pads and effusions may coexist, however, not mistaking this for an effusion and not escalating care on account of this may be a valuable piece of knowledge for you to have. Lastly, also from the subcostal position, ascites may mimic pericardial effusion for a novice. As you place the probe on the upper abdomen, you see an anechoic free space adjacent to the pericardium. Now the absence of a circumferential effusion should cue you to the fact this could be a false positive, as should the presence of the falciform ligament which is floating here in the ascites. However, once again, just be mindful that fluid adjacent to the heart is not always pericardial. Now what is the impact of assessing the pericardial space? Well of course the rapid exclusion of pericardial disease, a frequent what I call boogeyman diagnosis for us for patients in shock. We certainly don't want to miss a tamponade situation that could be recognized rapidly at the bedside. So the exclusion of this item that is frequently on a differential diagnosis represents the vast majority of victories that we find using this approach. 

In the traumatic situation, ruling out penetrating cardiac injury and/or the rapid identification of a penetrating cardiac injury has been shown to offer a outcome and mortality benefit in early literature. And lastly, and slightly more complicated, but identifying and triaging pericardial effusions along the tamponade spectrum is the other key advantage here. I hope the flow sheet I reviewed with you will resonate with you so you may look after your patients safely and comfortably. Lastly, let's talk about the IVC. Now, the IVC is used for many purposes, some more legitimately than others. We use the IVC frequently to look at its size and its respiratory variation, so as to inform us about whether a patient may be volume responsive. That is, if we gave them volume would their cardiac output go up? Also, we use it to gauge what their central venous pressure might be. And like many tests, this test has the greatest value at extremes. The majority of findings, however, are somewhere in the middle which makes it of unclear value. And there are a great number of physiologic considerations for using the IVC appropriately, which we'll review. So when talking about the inferior vena cava in the long axis, you have to understand the concept of loading conditions. How does the IVC change its size? Well, it changes its size based on respiratory pressures. The respiratory pressures and volumes that patients generate when they're spontaneously breathing vary from breath to breath. No two breaths are identical. Further, patients who are breathing vigorously versus those who are breathing more shallowly will bring about different loading conditions on an IVC. So with that logic, two patients with different breathing tendencies, but who have the same volume status, will bring about different appearances in their IVC, making this test of unclear value for those who are spontaneously breathing. Now those who are not spontaneously breathing, such as those who are on a ventilator, but not just those who are on a ventilator, those who are passive on a ventilator, that is not triggering the ventilator at all, they will have the best chances of having standardized laboratory-quality loading conditions of their IVC. The same breath is prescribed and the same breath is given from breath to breath. So those who are spontaneously breathing includes, unfortunately, most of your patients. Spontaneously breathing, of course, room air, nasal prongs, face mask, but also non-invasive ventilation such as CPAP or BiPAP as it's commercially known, pressure support ventilation in the ICU, any triggering at all of the ventilator is a spontaneously breathing group, making the IVC of unclear value. Like I said, those who are not spontaneously breathing, so the deeply sedated and/or paralyzed patient on a ventilator, the passive patient, this is the patient who, rare as they are, offers us the greatest understanding of how changes in ventilation will influence the size of their vena cava, which we use as a surrogate has been shown in a few good studies to determine whether a patient will increase their cardiac output when you give them intravenous volume. It's complicated. The IVC is easy to generate the image. It's perhaps the most complicated of everything I've spoken to you about yet to interpret accurately. There are lots of people who are very enthusiastic about this, but I would submit humbly that I believe the great majority of people have some confusion about how to clinically integrate their findings. So lets us look at the example of a passive patient on a ventilator. Here we see an IVC in long axis, and remember when patients are on positive pressure the IVC doesn't collapse as is commonly sought out in the spontaneously breathing patient, it distends. So here we see, as the diaphragm comes towards the feet we actually see the caliber of the IVC distend, it gets larger. And if you can see it with your naked eyes, it certainly meets the threshold that was demonstrated in the two studies at the bottom where it was 12% in one study and 18% in the other study. That if there's that much distention then the patient will be volume responsive in response to fluids. Now this is the rarer scenario, both because the patient's passive but also because of the clarity with which the IVC distends in my experience doing thousands of these. Now as I alluded to you before, the same patient with the same volume status, applying different breathing mechanics will show very different respiratory patterns. Now this is actually my IVC and I'm moments apart. As you can see on the left, the IVC is relatively static as I took shallow breaths. If I got excited or got into DKA or any of the above, you can see on the right my breathing pattern became more pronounced. And despite having the same filling pressures and volume status only moments later you can see that a misinformed clinician might wrongly assume that I am in need of intravenous volume to improve my cardiac output. So just a message of caution for you when interpreting IVC in spontaneously breathing patients. It's been very difficult to study definitively because each patient breathes differently. So it is difficult to be as confident when applying this at the bedside. There is likely a signal when you find IVCs that vary or you find IVCs of very small size or large size. However, we cannot teach you or tell you to subscribe to any universal findings confidently as, for instance, we can with patients who are passive on the ventilator. Now IVC has long been used by cardiologists as a surrogate of CVP. And CVP, regrettably, is not particularly valuable in predicting volume responsiveness. However, it is a useful surrogate when we talk about tamponade or cor pulmonale, which we'll get to in a second. This table has well been validated and subscribed to in the cardiology literature for over 30 years. As I alluded to, the CVP has enjoyed a rather significant fall from grace in the resuscitative literature over the previous 10 years or so, including this rather damning systematic review which alludes to the fact that CVP has never been shown in humans, but only in mares, to predict volume responsiveness. With this paper and many other experts pushing to remove CVP from standard resuscitative bundles such as the Surviving Sepsis Campaign Guidelines, it's safe to say that using the IVC as a surrogate of CVP is of little value for us in the whole battle of volume responsiveness. So I'm just gonna say that in my experience, the IVC is most often indeterminate. At the extremes, it may provide a signal. This is undoubtedly disappointing. We were hopeful that the IVC would be able to provide us with a single shot window into the body's volume status, and give us very accurate and safe information about how to load a patient with volume. We have just published a multi-system approach to addressing this disappointment. I'll leave this on the screen to consider and you can check out the reference, but ultimately considering IVCs at the extremes such as an underfilled one, less than 1.5 centimeters on positive pressure or less than one centimeter when spontaneously breathing, those patients are generally hypovolemic and may need volume loading. At the other extreme is a distended IVC which, in the absence of competing right heart problems is frequently a patient who is volume loaded. And assuming the patient is not passive on the ventilator and is triggering, or not intubated, then the use of lung ultrasounds to help the indeterminate IVC and determine whether or not a patient has wet lungs or dry lungs, will provide I think a better signal on balance than just the IVC alone, and help you determine about who to consider giving fluids to, and who to restrict giving fluids to. So, if I haven't confused you entirely or discouraged you entirely with the IVC, I hope I can save the IVC with these two very important uses. The first, as I alluded to in the effusion portion of this tutorial, is that we can actually triage pericardial effusion using IVC. It is impossible to have tamponade without a dilated IVC. We can use this simple physiology to our advantage. And the second feature, which I also mentioned, is that it's very difficult to justifiably have clinically important right heart failure without a dilated IVC, recognizing the IVC does tell us about CVP and, a catastrophic right heart failure scenario must, by definition, carry with it high filling pressures. So let's look at the scenario with tamponade. Imagining the effusion above, which is not clearly massive. It certainly gets your attention in the parasternal long axis up here. We can look at this IVC down here, we can see there's respiratory variation, a lot of play in that IVC. Because of the fact that tamponade must bring with it a dilated IVC, we can say with 100% certainty, without having to be an expert on the echocardiographic features of tamponade, we can say this patient simply does not have tamponade. If the pericardial space has a pressure that is exceeding the right heart's pressure, then the IVC has to become engorged, such as this IVC. Now, it's important to say that because this tool is sensitive but not specific, there will be many dilated IVCs, especially those who are on positive pressure, with this effusion that are not tamponade. So use the IVC as a rule out parameter. This is helpful of course, because the majority of effusions we identify will not be tamponade. But you potentially, as a novice, or potentially for a complex patient, will need help in building your confidence to make this clinical conclusion. The non-dilated varying IVC will be your help. The dilated IVC, if you're still worried, then it's fair to say the patient meets physiologic consideration for the diagnosis, and if you're clinically concerned it's totally fair to escalate this to your pericardial effusion experts, typically the cardiologists. Similarly, these same two IVCs with this right heart, if you think this right heart is chronic or is not particularly the culprit for a patient's shock state, then you might find this IVC. This would suggest that whatever's going on here is not likely acutely hemodynamically important. This IVC, however, would justify that hypothesis that the right heart is disordered, because by being dilated and not varying with respiration it said the CVP is somewhere around 15 to 20 at least and a CVP of 15 to 20 without right heart, it satisfies a hypothesis that the right heart may be failing. So in summary with the IVC, as I mentioned it's easy to generate, but there are many challenges in how we interpret the IVC, and that is very common. I hope you, listening, will commit yourself to understanding these challenges and will educate others in how to be a good steward of IVC ultrasound. It is not frequently useful or accurate for volume responsiveness determination in the resuscitative scenarios, except at the extremes. You may consider using lung ultrasound in addition to IVC to help you understand who can safely be trialed with volume, and who maybe you should hold off. If you're unfamiliar with A lines and B lines, please see those respective modules here at the institute. Lastly, the IVC is most useful as an adjunct when considering the diagnosis of either tamponade or acute cor pulmonale as we have reviewed. So we're just gonna shut down now with a few concluding thoughts. You've received a lot of information over the past 50 minutes, but I hope to leave you with some important lasting points. Basic echo, as I have outlined here, is really what we all use, no matter how well trained you are this is the scope that you're gonna use at least 90, and I'd say 95% of the time to answer your point-of-care cardiac questions. What's the LV like, is the RV enlarged, is there tamponade or a meaningful pericardial effusion I need to think about, and does the IVC tell me anything about the right heart, pericardial effusion, or rarely at the extremes about the patient's likelihood to be volume responsive? A qualitative approach is really what we need. Quantitative, calipers, Simpson's biplane method of disks, time consuming and cognitively overloading. Simplify your assessments using an eyeball approach and you'll be happiest. 

Lastly, you must have supervised practical experience in order to become safe and competent in using these applications. You can certainly self teach to some degree, however without quality assurance and oversight and people to bounce your studies off of, you can't reliably become competent. So I hope this has been helpful for you and if you're motivated, I encourage you to check out the upcoming modules that will focus on more advanced topics within echo. As mentioned here on this slide, however, these are lesser-often used but are of great interest to those of us with a real passion for echocardiography at the point of care. So I hope you'll join me for those. But for now, thank you for listening and I wish you well as you continue to learn ultrasound.