Thank you for joining us for the session, Game On, Stomp the Intensivist with Critical Care Ultrasound Controversies. In the following session, we'll have a didactic overview of the clinical applications of critical care ultrasound in the evaluation of shock by Dr. Christopher Short, followed by a didactic by Dr. Anu Abler-Depi, who will review ways in which ultrasound can be used to optimize mechanical ventilation and diuresis in patients with acute respiratory failure. This will be followed by a controversy on whether you can use ultrasound in the evaluation of cerebral edema. Stick around for the Game On part, where these three intensivists stump you and each other in a pro-con debate over each of these applications and a case-based review of how ultrasound did or did not change management. Enjoy the session. Hello. My name is Christopher Short. I'm an associate professor of critical care and emergency medicine at the University of Pittsburgh and VA Pittsburgh Health Care System. In this session, I'll be discussing whether or not we should apply point-of-care ultrasound to all patients presenting in shock. I have no disclosures related to this presentation. Providers who routinely use point-of-care ultrasound can recall countless anecdotal stories of how it changed their care for a patient. I easily recall multiple instances of being surprised by what I saw when I put the probe onto a patient. I had patients that were presumed to be in septic shock that turned out to have cardiac tamponade or presented for acute liver failure that ended up being due to congestive hepatopathy from heart failure, not suspected until visualized on the bedside ultrasound. In this talk, I will provide the data on why point-of-care ultrasound should be used in all patients with shock, but with the caveat of having the appropriate training to recognize the limitations of its use. Point-of-care ultrasound was initially established in the 1980s and 90s with a focused assessment with sonography and trauma as a way to determine at the point of care whether or not a patient presenting with blunt abdominal trauma that was hemodynamically unstable had pathology that could be treated intraoperatively. It was subsequently used to reduce invasive procedures such as the diagnostic peritoneal lavage or DPL and has been shown to have decreased time to treatment in the OR and decreased mortality in this patient population. Point-of-care ultrasound has since evolved to becoming a focused or goal-directed tool to answer specific diagnostic questions or guide performance of an invasive procedure. It has subsequently become a core competency for emergency and critical care medicine and is expanded to other specialties such as internal medicine, anesthesia, surgery, and many others. Point-of-care ultrasound can be used in multiple ways for the treatment of a patient in shock. It has diagnostic applications helping to determine the etiology of shock during an initial patient evaluation. It can readily help identify cardiogenic, obstructive, and hypovolemic causes of shock. It can be subsequently used to guide resuscitation looking for evidence of fluid responsiveness and fluid tolerance as ongoing resuscitation occurs. It can also be used for procedural guidance, particularly for vascular access. Over the years there have been numerous publications of various protocols for point-of-care ultrasound to help determine the etiology of shock. Some of the early and most notable protocols include the FATE, FAST, RUSH, FEEL, and BLUE protocols among many others. In essence, they all look at the pump, tank, and pipes as described in the RUSH protocol as ways of determining what the cause of shock is through evaluating the heart's contractility, looking for evidence of obstruction or hypovolemia, and then putting together all of these findings through the various protocols. Let's use an example case. Here we have a patient with a relatively normal LV systolic function and what is starting to appear as an enlarged right ventricle in the parasternal long axis view. Turning to the parasternal short axis view, we can see again that there is preserved LV systolic function, but there is evidence of RV impairment and strain as the intraventricular septum is bowing into the LV. This finding, seen here, is referred to as the D sign. In the apical 4-chamber view from this patient, we see that the RV is so enlarged it is now larger than the left ventricle. There is reduced contractility and motion of the RV free wall, but with preserved contractility at the apex, a constellation of findings known as the McConnell sign. On evaluation of the lungs, we see there is lung sliding present bilaterally in all fields examined. On assessment of the patient's deep venous system, a non-compressible popliteal vein with echogenic material in the lumen is concerning for a DVT. Putting the findings together, we do not see evidence of a clinically significant pericardial fusion, normal or preserved LV systolic function, right ventricular strain with increased pressure producing the D sign, an enlarged RV with the McConnell constellation of findings, lung sliding present bilaterally, and a DVT in the right popliteal vein. The summation of these findings suggests that this patient may be in shock from a massive pulmonary embolism. This is an example of how point-of-care ultrasound can help provide information right at the bedside to determine if or which further testing may be needed, as well as beginning early resuscitation targeting the specific cause of shock for your patient. Transthoracic echocardiography can also be used in the setting of a cardiac arrest. This table is from a paper that looked at the use of POCUS in patients during a cardiac arrest and found that in the patients with pulseless electrical activity, or PEA, 38 of the 51 had what was referred to as pseudo-PEA, where the patient had evidence of cardiac activity but poor enough that there was no palpable pulse during the ACLS pulse rhythm checks. These were due to etiologies such as hypovolemia, severe LV hypokinesis, or obstructive shock from massive pulmonary embolism or tension pneumothorax. There have been subsequent meta-analyses looking at the use of POCUS during cardiac arrest. There is a trend toward showing that if cardiac activity is seen during pulse and rhythm checks, there is a highly likelihood for successful return of spontaneous circulation, as opposed to the absence of cardiac activity having an increased likelihood ratio of not obtaining ROSC. However, this is not an absolute and should not be used for definitive prognostication, but is another tool to help guide resuscitation as well as recognize when there may be futility. Recently, transesophageal echocardiography, or TEE, has been integrated into the care of patients in cardiac arrest. This has been supported by the American College of Emergency Physicians. These views can further demonstrate true versus pseudo-PEA and identify other reversible causes, sometimes with clearer views than the transthoracic approach. It can also be used to assess the adequacy of chest compressions, where literature has demonstrated that compressions over the central or upper sternum may not be appropriate in all patients. Inappropriate compression location may cause harm from left ventricular outflow tract obstruction rather than ventricular compressions to produce adequate perfusion. However, it is important to recognize the limitations for the use of TEE in cardiac arrest. It is essential that it cannot lead to delays in compressions. It is also important to note that not all the causes of an arrest that can be seen on TEE are easily treated or correctable. Before starting a TEE program, it is essential to have the appropriate training for providers as well as developing protocols for cleaning and disinfection of the devices and storage for easy access. As I noted before, point-of-care ultrasound can be used to guide resuscitation after initial diagnosis. In particular, point-of-care ultrasound can specifically answer questions about whether or not your patient can tolerate further IV fluid administration as well as if you will see benefit from further IV fluid administration. Here, I am demonstrating some of the specific information that can be obtained from point-of-care ultrasound. On the left side of the screen, I have listed ways in which point-of-care ultrasound can help determine whether or not your patient's right heart can tolerate further IV fluids. For example, measurement of the IBC collapsibility in spontaneously breathing patients can provide an estimate of their central venous or right atrial pressure. Looking at the tricuspid and ulnar plane systolic excursion, or TAPSI, provides information about your patient's right ventricular systolic function. We can even estimate the patient's pulmonary artery pressures. We can look at the patient's lung for evidence of pulmonary edema. I have also included ways of determining if the left ventricle can tolerate fluid administration at the bottom by using spectral pulse Doppler and tissue Doppler imaging to calculate their E to A mitral valve inflow and the E to E prime ratio as measures of acute diastolic dysfunction from increased afterload. On the right side of the screen are a couple of ways to predict if the patient's cardiac output would benefit from further IV fluid administration. One way is to obtain an apical 5-chamber view where you would use the pulse Doppler imaging through the left ventricular outflow track and measure the maximum and minimum velocities across a respiratory cycle to calculate stroke volume variation. You can also perform a passive leg raise maneuver in the same view looking for changes in the velocity time integral from when the patient is sitting upright to after they have had an autotransfusion from the passive leg raise. Let's look at a couple of examples. Imagine you have a 78-year-old patient admitted for septic shock secondary to pneumonia. In obtaining the parasternal long axis view, we don't see a pericardial effusion. We can see the LV systolic function is normal to hyperdynamic. Looking at the inferior vena cava, we can see that it is small in maximum diameter with almost complete collapse during inspiration. Assessment of the lungs bilaterally demonstrates lungs sliding throughout in an A profile. Assessment of the right heart in an apical 4-chamber view demonstrates a TAPSY measurement that is above the cutoff for normal and may even be hyperdynamic. Performing the passive leg raise in this patient demonstrates a change in the velocity time integral of 13.7%. Putting all of this data together, we have a hyperdynamic EF with no evidence of pericardial effusion, an IVC that is suggestive of a low CVP or right atrial pressure, dry lungs, a normal TAPSY measurement, and a passive leg raise VTI change greater than 12.5%. This data would suggest that the patient is both able to tolerate IV fluids as well as predict that you will likely see improved cardiac output with further IV fluid administration. Now let's look at the same patient, but with a different set of ultrasound findings. Here we see evidence of decreased LV systolic function in both the parasternal long axis and parasternal short axis views and no evidence of a pericardial effusion. Looking at the IVC here, it is plethoric, dilated with minimum change during respirations. These lungs demonstrate evidence of sliding with B-lines throughout, suggestive of an interstitial process, potentially pulmonary edema. This patient's TAPSY measurement is decreased at only 12.6 millimeters of change between systole and diastole. When we perform a passive leg raise maneuver, we only see a difference of 6.7%. Putting the data together for this patient, we observed a decreased EF with no evidence of a pericardial effusion, a plethoric IVC suggestive of elevated central venous pressure, lungs that appeared to be wet, decreased right heart systolic function, and decreased responsiveness to an autotransfusion with a passive leg raise maneuver. Therefore, this patient is not likely to tolerate further IV fluids and predict that we are not likely to see an increased in cardiac output with any further fluid administration. In this scenario, you may elect to focus therapies more on vasopressor and or inotropic support based on these ultrasound findings. There are several other important pearls and pitfalls to keep in mind. Point-of-care ultrasound is incredibly operator-dependent. It is simply another tool that may be used by the provider at bedside and is not an intervention in and of itself. It requires quality image acquisition before even being able to make an accurate interpretation. The provider needs to not only recognize their own limitations if unable to obtain quality views to make an interpretation, as well as recognize the limitations of the measurements themselves. Many of the ones that predict fluid responsiveness were done on patients that were breathing passively with mechanical ventilation on total volumes of 8 cc per kg ideal body weight and may not be applicable to patients breathing spontaneously. They were also done on patients in normal sinus rhythm. The data may be inaccurate or skewed if the patient has underlying conditions such as pulmonary hypertension, valvular pathology, or other complicating cardiopulmonary conditions. Point-of-care ultrasound can more easily rule in findings that are seen rather than ruling out a diagnosis that the operator may not see. It does not replace other data you may have, such as laboratory studies, arterial lines, or other monitoring devices. Therefore, it is always important to correlate your findings and data to the clinical context of the patient in front of you. In summary, point-of-care ultrasound can help demonstrate the etiology of shock as well as guide resuscitation. In cardiac arrest, it can help identify reversible causes as well as distinguish true from pseudo-PEA. However, point-of-care ultrasound requires appropriate training to achieve competency in both image acquisition and interpretation. Ultimately, it is a tool to provide additional data at the bedside. Similar to the Swan-Ganz catheter, point-of-care ultrasound is not an intervention. Its utility depends on the operator to correctly obtain and interpret the data. But with the appropriate training and competency, point-of-care ultrasound is a valuable tool in the contemporary care of patients in shock. Thank you. Hi. My name is Enya Ablardepi. I'm from Washington University, where I serve as the co-director of the Critical Care Ultrasound Training Program and the director of the Emergency Ultrasound Research. Today, I want to talk to you about using ultrasound to guide and optimize mechanical ventilation and guide diuresis in patients with acute respiratory failure. I have no disclosures. A lot of the images you'll see today are not my own. So the first question is, should ultrasound be used to guide and optimize mechanical ventilation and guide diuresis? But I think for the talk, I'll spend most of my time on, can ultrasound be used for these applications? I think now with the era of coronavirus and having a lot of pulmonary pathologies related to that virus, certainly this is a very useful and relative application, point-of-care ultrasound and restorative failure. I want to break it up into sort of three sections, thinking about how ultrasound can help us optimize pulmonary mechanics and guide diuresis. First thinking about lung pathologies that we can see with point-of-care ultrasound, then looking at infrastructure, specifically diaphragm, and then the supporting structures, which is going to be cardiac ultrasound. So first to the lung pathology portion, I think this is probably the easiest, probably the one that's probably most well-versed, and I think probably people have the most clinical familiarity. There are three primary applications that we'll talk about, which is evaluation for pneumothorax, pleural fusion, and consolidations or interstitial syndrome. I think this slide is very depictive and exemplary if you're not as familiar with how ultrasound works to see what we're talking about. So the air-fluid ratios that are seen in each of these three pathologies helps explain what we see sort of graphically down here. So first with pneumothorax, which is probably the primary application, certainly can help us with acute restorative failure on the ventilator, is evaluation of the pneumothorax. So we know that some of the physics of ultrasound, that because the echoes do not come back to the probe when they hit air, we can exclude if there is air between the parietal and visceral pleura. The literature for that is well-saturated, well-known, with good sensitivity and specificity for point-of-care ultrasound over our supine chest radiographs. How do we do it? The kind of pneumothoraces that we're typically catching on point-of-care ultrasound are going to be the anterior ones because that's where the probe is placed, and I think this is really important because those anterior ones are the ones that are missed on chest x-rays because you will continue to see pleural markings all the way down. Sensitivities there for the anterior pneumothoraces are somewhere now 80s and 90s, and more on the higher when there's good clinical training and competence. Essentially, here in this picture, you're starting with a high-frequency probe, soft tissue is seen. You must first identify the rib, which is seen here, and then the pleura will be this hyper-echoic bright line that's present, and you can clearly see this back-and-forth motion that's present. That's the parietal and visceral pleura opposing each other when somebody's spontaneously breathing. That tells us that there's no air between the parietal and visceral pleura. When a pneumothorax is seen, we look for the same structure, so high-frequency probe again, soft tissue, rib is seen here, and then the pleura hyper-echoic line here, and what we're looking for is that this hyper-echoic line is always the parietal pleura, but the movement of the visceral pleura as the person is breathing is not seen here because there's air between the parietal and visceral pleura. What about for pleural fusions? Pornicure Auction can help us look at that as well. Many of you have had chest x-rays like this on your ventilated patients, and you can see here there's a pacification of the right lung. The question here is that do we need to bronch this patient, do we need to give some diuresis, or do we need to increase the peak? Pornicure Auction can be very useful in helping us determine lung pathologies here, specifically pleural fusions. Typically, we'll use a lower-frequency probe. The patient is supine, so we'll put the probe in the mid-axillary point, and again, we'll find the most important structure, which is going to be the diaphragm or this bright hyper-echoic line, and we're looking towards the patient's head, which is over here for anechoic or black fluid that is present. Visually here, here's a large pleural fusion. First identify the diaphragm, which is this hyper-echoic line here, and then all this dark fluid here is the large pleural fusion with adipocytic lung that's present down here. Consolidations and pulmonary edema are also well-visualized on pornicure ultrasound, again, can help us not only come up with a diagnosis of why the patient is in restorative failure, but can help us follow while they're mechanically ventilated and maybe determine if there are ways to optimize them to expedite them being extubated. And again, certainly with our COVID-19 process and lots of pulmonary manifestations of that, we're having more experience with pulmonary edema and consolidations. Sonographically, what will we see? We'll see B-lines, and so B-lines are a resonance artifact that is very common to air and water interfaces. It's a bright vertical line that comes from the pleural all the way down the screen. It does not fade, and it faces A-lines. A-lines are those reflections of the pleural line. It is common to have one, maybe even two B-lines within a pleural space. Here is a rib on the side, and this bright line vertically down is one B-line. You can see it correlating here with a CT scan that looks relatively good. As the pathology for the lung seen on CT gets worse, you can see that the B-lines become more. On this picture here, you can see that there are several B-lines. I like to start at the bottom of the screen to identify a B-line so that we can be sure that that's definitely the artifact that's seen here as it should not fade. The more confluent those B-lines are, the more lung water that's present in the lungs. It's important here to note that the ultrasound is telling us that there's lung water. The etiology of that lung water is based on clinical explanation. So pulmonary contusions will have B-lines, as well as non-cardiogenic pulmonary edema, as well as pneumonia will have B-lines, and so you have to use the rest of the story to see them. On actual moving clips, here's what that looks like. Here's a low-frequency probe, ribs on the side. Here's our pleura, and we can see a few B-lines that are present. So that might be a chest CT that looks like this one or this one. The nice thing here about B-lines is that they also exclude pneumothoraces for us to be able to see. As the person's lung pathology gets worse, the B-lines become more confluent, and you can see this entire lung interface here is filled with B-lines present. So B-lines are identified, the patient has pulmonary infiltrates and such, and so how can lung ultrasound go beyond just identification of the B-lines and help us perhaps optimize on the ventilator? There are these scoring systems that are reported in the literature that don't look at just one spot of the lung, but look at the entire lung broken up into the superficial, inferior, anterior, lateral, and posterior segments of the lung. And typically, their score, some of the point-of-care systems have a picture like this embedded within the machine for you so that you can score each segment of the lung. And in general, you're scoring it from a zero to a three, a zero being normal lung, meaning that you see a pleural line and the reflections of those pleural lines, which are called A-lines, so that would be normal, and progressing from those to a score of one, which that there are a few B-lines present, as seen here in picture B, and then in picture C, where there are more confluent B-lines seen, and then finally to consolidation, taking you from a score of zero to 36, 36 being a maximal worst score. Visually seen, again, on some of your point-of-care systems, you may be able to show all processes of the lungs and depict a score here of 27. That correlates with this person who has a very poor PF ratio of 82, with lots of areas where there is evidence of lung water with diffuse B-lines present. So what can you do with these B-lines? Again, there's some literature suggesting that you can use the B-lines to help guide how much PEEP a patient needs to be on, for example. This is a study that looked at taking patients who had B-lines present, up titrating the PEEP on those patients to places where the B-lines resolved, to let us know that we had maximal inflation of the lungs and that increasing PEEP would not be beneficial for those patients. In this example here, you start to see that there's a confluence of B-lines, and these are patients who are on 5 of PEEP, and as the PEEP increases from 12 here to 16, you can see, hopefully in the picture, that the B-lines decrease and now more A-lines are present. Again, A-lines are normal pathologies, demonstrating that there's good distention of the alveoli, and you wouldn't want to increase beyond 18, 16 in this particular case, which clearly for ARDS and management, we typically don't go that high anyway, but depicting here that going high would not be beneficial, it would actually increase your risk of hyperinflation seen somnographically. So those are the lung pathologies that can be done with ultrasound. What about the infrastructure, or specifically diaphragm ultrasound? I think it's a little bit harder as the punchline, and probably the data is not as clear, but certainly can be used and is reported in the literature to help both not only predict who is going to tolerate extubation, but may help guide and optimize the patients who are mechanically ventilated. So diaphragm ultrasound typically can be done at a point of care. Most of your facilities may have options for you to order a diaphragm ultrasound, and they're usually being used to diagnose diaphragm dysfunction, whether paralysis or weakness, and certainly using neuromuscular blockade for these patients that are at high risk for having diaphragmatic weakness. So potentially this can help us predict who will be successful and not successful from weaning from mechanical ventilation. So the two types of diaphragm ultrasound that are pretty common, I think, for point of care are going to be evaluation of the movement or excursion of the diaphragm, and then the thickness or fractional thickening, and the data is by certain very heterogeneous, but probably the punchline here is that excursion of the diaphragm, that's about a centimeter or less than a centimeter, certainly associated with knee failures, with decent sensitivity and specificity. You can see it's about 75% here. And again, there's a lot of heterogeneity, which makes sense because these studies may be done when a patient is not quite ready to do a spontaneous breathing trial, maybe related to other clinical processes, their wakefulness, and the like. Some of the details of how point of care ultrasound for the diaphragm are depicted, especially when you order a comprehensive radiology ultrasound. Here are looking for motion of the diaphragm, specifically looking for evidence of weakness or paralysis, weakness by low amplitude, and we said one centimeter is your kind of mark, or paradoxical movement where it's moving in the opposite direction. The amplitude of that movement, the force of velocity, and the thickness or the fractional thickening, and even displacement of other organs has been well correlated to, again, the likelihood of patients being able to tolerate extubation if there's evidence of diaphragm pathology. And of course, we know that that's not the only thing that's important for if patients can tolerate extubation or not. I thought this was a nice slide and hopefully useful for you to see that there are many applications here of the respiratory muscle, which I call sort of the infrastructure of the lungs, right? The diaphragm and the pleural or the, excuse me, the intercostal ribs and muscle architecture in terms of the strength to be able to tolerate being extubated. Again, lung diaphragm or diaphragm ultrasound is being depicted here using a low-frequency probe. The diaphragm is seen here. The probe is typically placed near the, on the anterior abdomen on the right side. The mode is used to easily identify the excursion of that diaphragm and the measurement of that during passive and deep inspiration and expiration is measured. Here's some more examples of that. Again, in the literature, there's some varying numbers, again, depending on the age of the, or excuse me, the gender of the patient, whether there's passive breathing or quiet breathing, voluntary sniffing, or deep breathing. There's some expected normals and how those normals sort of correlate with the ability to stay off the ventilator is what is being studied. And again, probably the number I saw most frequently in the literature was somewhere around one centimeter or 10 millimeters. Looking at the fractional or thickening of the diaphragm has also been supported about 30% fractional thickening to be suggestive of patients who can tolerate extubation. And this is an example of paradoxical movement. So compared to this one here, there should be diaphragm moving up during our inspiration. And here the diaphragm is moving down, suggesting that there's diaphragm paralysis present. Okay, so what about then the support, right? So looking at cardiac ultrasound and how it influences pulmonary mechanics and a patient's ability to tolerate extubation or to optimize them while on the ventilator. We know that hypervolemia is bad, but we know that there are parts of it that are necessary, especially our patients being critically ill who may need resuscitation. This is a nice graph that helps explain probably why the supporting portion of the heart in terms of diuresis is so useful, that there's a resuscitative phase, an optimization phase, stabilization, and an evacuation stage. And I think for the evacuation stage, that's where diuresis is probably more commonly used, but there's some literature suggesting that perhaps in optimization or stabilization, early diuresis or at least decreasing the amount of volume patients are getting may be very useful. So we'll talk about how ultrasound can help us decide which patient would benefit from diuresis in these two areas. So diuresis for patients who are mechanically ventilated, when we know that they have heart failure or HFREF is very easy, we can either look at their comprehensive echo or we can do a bedside and see that the systolic function is very decreased. But I think that it's important to also consider that there are patients who have HFREF and if they don't have a diagnostic comprehensive echo that demonstrates that when you're using point of care, you can easily miss that this person also has heart failure, though it's not a systolic heart failure, but diastolic heart failure. There is this nice scoring system to help us think about patients who are at risk for heart failure with preserved systolic function, this HF score. And the higher your risk or the more points you have, the more likely that you likely have heart failure. And that means for these patients that decreasing how much fluid they're getting and or a diuresis while mechanically ventilated can help increase their chances of staying extubated. So how do we currently think about the supporting structure of the heart as it embeds around the lung here? Well, certainly we are familiar with IVC data. We know that IVC, when it is small and collapsible, suggests that the preload on the right heart is small and that's great and can be useful. We know that when the IVC is large and plethoric, that it suggests that there's high pressures on the right side or high volume on the right side. And I think in those cases that there's good information and probably good clinical familiarity with using perhaps plethoric IVCs to help guide diuresis. And, but that may not be all. I think there's also this segment of looking at the volume or the preload on the left side with point-of-care ultrasound to be able to, again, determine which patients in that group may need ongoing diuresis. So we get into a bit of diastology and while that is a very complex and certainly needs some additional training and competence, there's some easy applications that we can use at point-of-care. So again, diastolic dysfunction, according to the ASC, has certain criteria. And these three, these four criteria, excuse me, that are here, we'll talk about the first two. But the average EDE prime, if it's greater than 14, the septal and lateral E prime velocities, TR velocities, meaning that patients have high pulmonary artery pressures, and then large LAs are all suggestive of having a diastolic dysfunction. And those are patients who have the HEF or the heart failure with preserved systolic function. So we'll talk about EDE prime, which I think can be done very easily at the bedside to, again, determine if diuresis for your patient with acute respiratory failure is needed. The EDE prime is measured first using an apical four-chamber view with all of the criteria for adequate imaging. You're gonna put pulsative Doppler at the tips of the mitral valve as they open and close, and that peak first inflection, which is early diastolic filling, the peak of that will be measured, that is the E. Next, you're gonna measure the E prime, and that E prime is simply now talking about not blood velocity, but tissue velocity. So in diastole, what does the tissue on the mitral annulus do? And so using tissue Doppler, then septal and laterally, you're going to measure the peak of that as well using the tissue Doppler. Here's an example of how that actually looks. So here's mitral inflow called the E wave. Pulse wave Doppler is placed at the tips of the mitral valve. You're gonna get a reflection that looks like so. The first one is usually early diastolic filling, and you're gonna measure the peak of that. For this particular case, it's about 0.9 meters per second. It's measured twice for accuracy, 0.89. And then in this case, we're gonna go to tissue Doppler. This example is looking at just the lateral tissue Doppler. We're putting tissue Doppler now on the lateral annulus of the mitral valve. Subsequently, you'd also put it on the septal if you had the time or were able to. You put it on the lateral and the downward deflection, that first one after systole is early diastolic movement of the tissue, and you're gonna measure the peak of that as well. Here it is 0.10 meters per second. So the E to E prime here, based on these two measurements is nine. We'll talk about how useful that number is to help guide diuresis for your patients on the ventilator. That number, that E to E prime, can help us estimate the left atrial pressure. Left atrial pressure is sort of a good surrogate for your wedge pressure. And I think that this is where probably understanding that somebody may have high LD preload or high LD filling pressure can be useful. So you take the E to E prime, you add four, and that's about the left atrial pressure. And why is that important? Well, we just talked about lung ultrasound using B-lines, but B-lines don't tell you that this is a cardiogenic cause. It's important for us to remember that. So if somebody has B-lines that are present and their wedge pressure in this case, or their E to E prime is high, typically greater than 15, that means that their wedge would be 15 plus four. That's a high wedge pressure suggesting that there's certainly cardiac pathology or cardiac etiology to that pulmonary edema versus somebody who has pulmonary edema and B-lines on their lung ultrasound and you check their E to E prime and let's say it's six, then their wedge pressure will be six plus four, 10. That's a generally normal wedge pressure. Now, giving that patient diuresis does not mean that they will not make urine. They absolutely will. They're like any one of us. If you were to give us some diuresis, we would make some, but the benefit of that and how it would decrease your pulmonary infiltrates is where there's a question and probably would increase the risk of them developing an AKI since that patient with a low E to E prime is more likely euthylenic than not. So again, looking at this radiograph, I think it's very easy for all of us to want to give a diuresis to this patient who's mechanically ventilated. I think using markers like E to E prime, the most commonly, if it's less than eight, I think suggests really good wedge, normal wedge pressure. Probably diuresis is not necessary in this case. Certainly will not fix their lung pathology. There may be other reasons why they have extracellular water, such as low albumin or perhaps a clinical condition or infection that has a leaky capillaries, but E to E prime that's greater than 15 certainly suggests that probably this person has a high wedge pressure, would definitely need the strength of the heart, a low preload to be able to tolerate extubation. Diuresis here would be useful. And of course, like many things in medicine, there is this gray zone where other clinical factors are going to be important. Well cited in the literature regarding mechanically ventilated patients supports the same, that a high E to E prime, and in this case, greater than 7.5, was suggestive of wedge pressures that were 15 or higher. And then E to E primes that were low were suggestive of wedge pressures that were low. But in general, I think most people feel very comfortable in this range. Less than eight means diuresis is not going to be helpful or not necessary. And then greater than 15, meaning that it would be important. I will also take this point to mention that it's important to understand when you can and cannot use this E to E prime. In general, patients need to have heart rates that are about 100 or less, and they cannot have any mitral pathology. And also in general, these are for patients who have some moderate amount of LV function present. I found this slide here to be very useful. This is from an article that looked at a comprehensive approach to think about weeding from the ventilator while using ultrasound. Uses this ABCDE approach, E standing for aeration and pleural fusions. We talked about that with lung ultrasound. Even how you can use B-lines to help titrate your peep to improve your aeration score. Below the diaphragm, which talks about having ascites and other pathologies that may increase the pressure in the lung or increase the pressures in the pulmonary and thoracic cavity and affect lung compliance. Cardiac, both systolic and diastolic dysfunction, looking at E to E primes. Diaphragm excursion and thickening that helps support the lung when patients are mechanically ventilated and if they're able to wean from that. And then extra diaphragmatic processes such as the respiratory muscles themselves and the intercostals. So in summary, should ultrasound be used to optimize mechanical ventilation guide diuresis? I demonstrated to you here that there are certainly the possibility that ultrasound can. There's varying degrees of literature support and complexity to the pathology, but certainly with more training and more evidence, I think that this can be a part of what we do every day, both looking at lung pathologies, the infrastructure diaphragm, and then the support looking at cardiac ultrasound. Thank you so much for your time. Hello, I'm Aarti Sarwal. I'm a neurointensivist at Wake Forest School of Medicine in Winston-Salem. In the next few minutes, I'll share my perspectives on the controversial topic, should we use ultrasound for every patient with suspected cerebral edema? I have no relevant financial disclosures, although I do have a intellectual disclosure that most of the indications and practices discussed in this talk are exploratory and need further investigative research before we can incorporate that into standard clinical care algorithms. As a neurointensivist, when I think of suspected cerebral edema, I think of Mundell-Kelly hypothesis. There are only few things that can contribute to high ICPs in the brain. Three compartments, the brain tissue, CSF, and blood essentially drive the pathophysiology of cerebral edema in the brain because of a closed skull structure. When I think of cerebral pathology in the parenchyma itself, I also think of brain or skull as a house. There are structural issues which cause parenchymal damage or bone damage. There are chemical issues, too much neurotransmitter or not enough neurotransmitters. Electrical issues, too much electricity as in seizures or not enough electricity as in hypoactive delirium. And plumbing issues, too much blood or blood flow or not enough blood flow. And the plumbing part is the one that is amenable to assessment by diagnostic testing for cerebral hemodynamics. And transcranial Doppler makes one of the ultrasound-based modalities that gives us these assessments for the plumbing part of the brain. Not many people know this, but ultrasound was a gift to medicine essentially from the sonar technology that came from defense use. And echoencephalography, which was use of sonar to look for midline shift, was one of the first medical indications of ultrasound. CT MRI obviously replaced lots of these indications and cranial ultrasound fell in the background until transcranial Doppler indications came around for some valid indications. And now with emerging point-of-care use in emergency and critical care medicine, neuroultrasound applications are seeing a new reemergence in interest. Since neuroultrasound is not a very well-recognized speciality outside neurosciences, I will do a very brief overview of what modalities in ultrasound can be used in evaluation with suspected cerebral edema before I give you my perspectives. The skull impedes our ability to ultrasound the brain, except in a very small portion of the temporal bone where the echo probe or the phased array probe or also called the transcranial Doppler probe can be used to assess the ultrasound picture of the brain in the axial plane. And this axial plane looks like this with opposite skull with some lesions visible here, a midbrain, which you can see here as a butterfly, and the third ventricle. Cranial ultrasound in this B-mode imaging can detect intracranial hemorrhages with a decent accuracy. Again, in no way suggesting it can replace CT scans, but this is a lesion hyperechoic that is being produced by this intracranial hemorrhage in the patient's basal ganglia. So cranial ultrasound can be used for evaluation of the panchyma for incidental bleeds, subdural hemorrhages, epidural hemorrhages can also be detected. The caveat, very high supratentorial bleeds or infratentorial bleeds cannot be detected by this. The same way we measure midline shift on the CT scan, we can use the B-mode axial section of the brain to measure midline shift in ultrasound imaging. So here the third ventricle is being used as a midline structure and temporal insonation with distance from ipsilateral probe to the midline and midline to the opposite skull is being used to calculate midline shift. This is a B-mode description of third ventricular assessment for size to look for hydrocephalus. Again, no way reflecting that it can replace CT scan, but in a patient that is not amenable to CT imaging because of accessibility, high risk or radiation issues, patient's seal assessments can assess third ventricular size and in this case, the other hyperdensity is being produced by either an intracranial bleed or choral plexus calcifications, both of which can cause hyper-eco-eclisions. This is the ultrasound version of papilledema, which is optic disc bulging into the posterior chamber and caused by high ICPs transmitting to the optic nerve sheath. This is also called the crescent sign. In this case, the optic nerve sheath diameter is being used as a non-invasive surrogate for intracranial pressure. The challenges behind reproducing an exact transverse plane to get these exact transverse diameter has been the challenge in coming up with cutoffs for showing sensitivity for distinguishing high ICP versus low ICP state. But again, serial measurements, if a standardized protocol is consistently followed, can be used as a non-invasive surrogate of cerebral edema. For transcranial Doppler per se, we can use color Doppler to look for blood vessels. Here, you're looking at the midbrain in the axial section, opposite skull. This is the circle of Willis in the color Doppler and you can use pulse Doppler to identify a segment and in this case, this segment of distal MCA is being insulated to give you spectral waveforms that show the cerebral blood flow. Suboccipital windows behind the occiput can be insulated to give you the vertebral basilar system. In this case, you're insulating the basilar artery flow going away from the probe because the probe is sitting under your neck looking towards your glabella. In this case, arterial waveforms can be seen from the distal PCA and the basilar venofrazental venous waveforms are being insulated along with the arterial waveforms. How does color Doppler help in assessment of cerebral edema? Well, typical intracranial circulation is low resistance. What does that mean? Throughout the cardiac cycle, this part is systole, this part is diastole, blood flow is extremely positive and no part of the cardiac cycle is systolic or diastolic blood flow limited or close to the baseline. Compared to high resistance circulation where systolic part is pretty robust but the diastolic part is pretty diminished. And in this case, another extreme of high resistance circulation where some part of the cardiac cycle, the blood flow is actually reversed or zero. Typical intonation of the femoral artery will reveal these waveforms. Typical intonation of the middle cerebral artery will reveal these waveforms. So presence of these waveforms in the brain tell you that there is significantly high resistance in this case or this case. These focal increases in resistance can actually help you figure out hemodynamically significant intracranial stenosis. This is normal cerebral artery waveform that can progress to a resistive waveform when insulated just before the stenotic lesion. You can see the impaired diastole, but robust systole to where diastolic is completely obliterated. Post-stenotic phenomena, just like what we see in aortic stenosis, parvus et tardus, delayed upstroke and blunted peaks can be seen when patient's vessels are insulated distal to the stenosis. And this pattern of spectral waveforms can help localize a focal intracranial stenosis. These patterns can also be reproduced in recanalization. So if a patient was recanalized for a thrombosed vessel, the patient's blood vessels will start showing blunted waveforms followed by normal waveforms restoring blood flow. When this resistance is global, say as an increased ICP, you can see a global increase in patient's waveform characteristics with low resistance waveforms corresponding to normal intracranial circulation progressing to high resistance waveforms with impaired diastole compared to the systole, reversed diastole compared to the systole called an oscillating waveform pattern when the ICPs exceed your diastolic significantly to blunted waveforms and no cerebral blood flow. The oscillating waveforms are kind of the the challenging transition where if not reversed in real time can herald impending cerebral circulatory arrest. Now, why would you use ultrasound for critically ill patient when you have a CT scan or MRI? Well, if you've taken care of such a patient in your ICU, you know that there are higher situations like very high ventilator settings, systemic instability due to high need of vasopressors, ECMO patients, HFO patients, balloon pump patients and CRRT where even if you had a mobile CT scanner, the movement of the patients and the transfer of the patients may be very high risk. You can make it happen, but it's high risk. So what if you had a serial assessment tool that is non-invasive, can be done without moving the patient and can be useful in extreme cases even if it doesn't help you in every single case? That's where ultrasound has a role. Patients with cerebral venous sinus thrombosis, hepatic encephalopathy or thrombocytopoietic patients from chemotherapy, they may need serial assessments for intracranial hemorrhage for ICP monitoring because of a poor exam. Their lack of invasive monitoring strategies can help be replaced by ultrasound. Medical surge units as well as neuro units all have some indications where ultrasound can be helpful in evaluation of hydrocephalus, subuteral hemorrhage, intracranial hemorrhage. Again, by no means recommending that we replace CT scan with ultrasound, but in patients where CT scan is not amenable or transport is high risk, these indications can help us evaluate cerebral pathology when it doesn't exist before. Patients with liver failure, post-cardiac arrest syndrome, patients with cerebral edema on TTM, ECMO patients, as well as septic patients. Lots of indications are evolving where ultrasound can be helpful in understanding the pathology and pathophysiology of acute brain injury. Let me give an example. What if you had a VV ECMO patient, very high risk and otherwise paralyzed, sedated, doesn't have an exam, and the logistics of the case paradigm dictate that we are concerned about anticoagulation in this patient. There might be a bleed and the team is discussing goals of care, whether it's worthwhile getting a CT scan. If you scan this patient with ultrasound and you see these oscillating waveforms, that gives you a very strong indication that the patient has malignant ICP increases. And this can give you some evidence of undertaking a high risk mobile CT scanner or a transport to the CT scanner or can even guide goals of care discussion compared to say a VA ECMO patient where you're looking at non-pulsatile waveforms, but you can see robust CPPs on both sides, the left and the right MCA. And this can give you an indication that the patient's cerebral perfusion is pretty positive, almost close to normal mean values of MCA, and there is no gross asymmetry. This can give you some confidence that at least the patient is not having extremes of brain injury that will dictate goals of care. Now, traditionally we used to think these oscillating waveforms seen in cerebral edema are irreversible, but lately with using escalated osmotic therapy or surgical evacuation, in some patients we have found that if reversed in real time, these may not portend a bad prognosis like we used to think before. This is a published case report of a patient with subarachnoid hemorrhage that had global cerebral edema with normal waveforms progressing to high resistance waveforms and even oscillating waveforms. There were no significant changes in the radiology findings of the patient, but these were used to escalate osmotic therapy and reversed, and the patient actually did relatively well for what could have been. And the goals of care were not addressed here as they would have been if a benefit of doubt was not given. If you're familiar with the ICP monitoring paradigms and Lundberg waves, the plateau waves of Lundberg sometimes decrease in the compliance of the brain because of pathology, and these patterns of P1, P2, P3, P1, P2, P3 that are seen in ICP monitor can also be reproduced on TCD waveforms. When a brain becomes non-compliant because of new pathology or new edema, P2 becomes equal to P1 or higher than P1, and these patients may need lower ICP thresholds for impairing the cerebral perfusion pressure. So in these cases, the osmotic therapy goals need to be titrated because they may suffer a neurological decline at lower ICPs than before. When a typical patient suffers from an ICP crisis, the low resistance waveforms will convert to high resistance waveforms and sometimes even oscillating waveforms, and these can be a good target for driving osmotic therapy as well. People have used this phenomena called the Windkessel effect where P2 becomes higher than P1 in patients with evolving cerebral edema as a target to titrate hepatic encephalopathy therapy. So lots of benefit in exploring the spectral waveform patterns and their evolution where a routine ICP monitor may not be helpful. If you look at ICP target literature, the holy grail of ICP management or cerebral edema management has been refuted by at least six different schools of ICP management or cerebral edema management that have not proven to be beneficial compared to one another. Whether you target ICP goals, whether you target Rossner protocol with CPP goals, or you add brain tissue oxygenation as in the Edinburgh protocol or the LUNCH protocol, which just defies every other clinical practice by really decreasing catecholamines in these patients, cooling these patients and avoiding vasopressors and CPP directed goals at all costs versus auto-regulation targeted goals by Brain Trauma Foundation or the chestnut way of doing things which is look at exam and radiology and that's as good as trying to target an ICP number. What is missing in these trials that has really failed to deliver a good cerebral edema management strategy? Maybe it's cerebral hemodynamic assessment. Think of it. If your patient had an increased ICP at 55 with say a brain that has tightness and some uncle herniation, a waveform that looks like this basically means a malignant ICP crisis versus if I was to insulate this patient with ICP of 55 and a full brain with some false herniation, uncle herniation, but no pupillary dilatation and this is my waveform. That's a very different pathophysiology of how this patient is going to suffer acute brain injury. And I wonder if these two distinctions need to be made when selecting patients for escalating ICP management therapy. This food for thought also came from emerging studies from invasive monitoring where a published report showed that every time a patient had a seizure that was detected only by continuous EG monitoring and not clinical, patient had an ICP crisis, increased brain temperature and increased CPP and blood flow. You wonder how many of these periodic ICP crisis are truly caused by parenchymal issues that need mannitol and 3% or surgical evacuation. How many of these may actually be caused by increased blood flow that was driven by seizures that were occult on surface EG. That's where TCGA could have a role in distinguishing patient's positive cerebral perfusion pressure with a high ICP versus an impaired cerebral perfusion pressure. So I'll request you to investigate the possibility that if you have a patient with suspected cerebral edema where imaging is not significantly changed, the presence of high resistive waveforms, oscillating waveforms versus the presence of normal waveforms or even hyperionic waveforms should guide different kinds of therapies rather than an impaired cerebral edema management strategy. This can be a useful guide in screening patients that are otherwise not amenable to neuroimaging such as a VA ECMO patient and markers of compliance, transition of normal waveforms to non-compliant waveforms as seen in this picture should herald a changed cerebral edema management strategy rather than just single ICP calls. So let me end this by a few descriptive case studies. A poor grade subarachnoid with same exam, same CT scan gets TCD on one day that shows normal velocities that's less than 80 with normal PIs which is a marker of distal resistance and normal waveforms. The next morning, nothing has changed. CT scan is the same, exam is the same. I would not have done anything different from a management perspective except the patient's ICPs have gone up occultly from about nine to 15. I would not have targeted osmotic therapy based on 15 but patients transcranial Doppler shows now resistive waveforms with very high PIs globally. And this for me indicated increased ICP and became a target for therapy. Now again, further investigative research is needed to ensure that we have good evidence to use this as standard of care, but another exploratory idea. Another patient, high frequency oscillator patient, four year old was transitioned from VV ECMO to high frequency oscillator because of an intracranial hemorrhage that was not deemed to be adverse prognosticator but could not allow therapeutic anticoagulation for ECMO to continue. The ICP monitor that was placed could not give reliable waveforms because of the oscillations impairing waveform analysis. We used point of care assessment with transcranial Dopplers to look at both MCAs, ipsilateral basal vena frosenthal and deep venous system that showed robust venous flow, as well as midline shifts to continue giving information to the critical care team managing this patient, that patient has not progressed in cerebral edema in a manner that would made us back off the supportive care going on through high frequency oscillator. Seven days of non-invasive monitoring, on the eighth day patient was able to get a CT scan and we confirmed that the patient's ICPs cerebral edema had not progressed and otherwise had the same prognosis that would have been at the start of this therapy. So this is a good screening tool in that sense. I hope these few minutes helped you at least accept the possibility of use of ultrasound as a complimentary neuroimaging in assessing cerebral perfusion physiology, in assessing patient with compliance to assess which patients are high risk for decline. Maybe spectral waveforms can be a goal in the goal-directed therapy of cerebral edema management. And definitely as a useful tool in screening for the presence of malignant cerebral edema where current imaging is not amenable or high risk. Thank you for your time. Thank you, Chris and Inyo, for such an energizing presentation on applying ultrasound in patients with shock and using ultrasound to guide mechanical ventilation and diuresis clinical decisions by bedside. And I hope that the Cerebral Edema talk gave you some new perspectives on neuroultrasound. My question to you, Chris, is what are your thoughts on integrating POCUS that is done by trainees with their learning curve, knowing that there'll be false negatives, false positives? What are your thoughts, perspectives, and lessons that you have learned from your practice in integrating POCUS into training programs during clinical service? Yeah, that's an excellent question, because you have to balance education against patient safety, and there's certainly a potential for harm if you make the incorrect diagnosis or anchor incorrectly based on an incorrect finding or an artifact. So one of the key elements is to have archiving, whether that be a digital solution or some sort of way of being able to go back and review to do quality assurance so that you can both ensure patient safety. So I'd recommend there being a point expert champion or an ultrasound director who can do that. And again, if you can do it in real time to be able to balance the safety element as well as providing constructive feedback to help our trainees improve. That's a great point. Dr. Abduldabi, I'm going to ask you, I know you're joining us from Detroit Airport. If you're able to join us, can you give us your perspective? We learned so much from your talk. We learned about PEEP titration, diaphragm ultrasound, learned about diastology. How do you see all these modalities and lung ultrasound integrating into your clinical service rounds with so many trainees around and their learning curve? Yeah, I think that's a great question. So for me, especially in the training environment, I think it's best to think about in the multiple applications of ultrasound, which ones are binary, which ones are like, it's an easy yes or no. That's usually a good place to start, especially easy things like lung ultrasound. Is there a pneumothorax? Are there B-lines? Very binary questions. And then once you get a solid foundation on that, then I think you can improve on the nuances of the technique in terms of diastolic dysfunction or diaphragm measurement or etc. So it starts with a solid foundation of ultrasound knowledge, and then kind of a strong reinforcement of those principles with some daily applications. And then you tailor the type of ultrasound you're doing based on the clinical need at that time. Great points. And we have another question from the attendees. We love the idea of diaphragm ultrasound, especially in patients that are difficult to ream. What are your recommendations from the perspective of performing diaphragm ultrasound daily or every other day in chronic vent-dependent patients, or what are your thoughts about that? Yeah, I think that diaphragm ultrasound is a place that definitely has the room to further knowledge. The data is there. It's a bit sparse. It's, you know, hit or miss. There's a signal, but I think that for myself, I don't do it every other day. I think for the chronically ventilated patient, that's challenging. I think you just need to sort of think about the entire infrastructure of what's keeping them ventilated. And diaphragm ultrasound can certainly supplement and help add with that. I think the obvious binary hemiparalysis or obvious non-moving is good, but if you can get comprehensive studies, that's probably definitely going to be the more accurate way to apply the finding on that diaphragm ultrasound. Great points. Dr. Sarwal, I've got a question for you. What advice do you have for people who may not have access to TCD presets on their ultrasound machines? Well, great question, Chris. Thankfully, the new point-of-care machines are incorporating TCDs or neuroultrasound because of the increased recognition, but if you don't, you can use the abdominal preset in most of the older point-of-care machines. The only thing you have to make sure is that you keep the multi-beam on and the tissue harmonic imaging off for Doppler imaging. So the beam mode will be easy just with abdominal presets, but for the actual TCD Doppler part, multi-beam on and THI off can help you get these similar images to the ones that I showed. Sounds good. So seems like we're up on the hour and stick around. We have an exciting pro and con debate that we hope that we get to stump you. Chris is going to start this pro and con debate by giving very descriptive cases from his own personal practice on the focus in shock. This will be followed by Dr. Ablur-Duppie talking about use of focus in acute respiratory failure and guiding diuresis in, again, descriptive cases from her practice. And then I'll finish off by my perspectives on pro and con use of neuroultrasound in cerebellar edema. Please make sure to post your questions. And on to Dr. Chris Schott. All right, guys, well, good morning, good afternoon, depending on where you are in the country right now. So thank you guys very much. And as Dr. Sarwal said, we're going to go ahead and present some cases that both present the pro and the con sides of using ultrasound for these various applications. So the first case I want to present is from when I was covering a shift in the emergency department. I had a young patient in their 20s coming in. They had been diagnosed with pericarditis three weeks prior. And today we're presenting with generalized weakness, some additional chest pain, shortness of breath, nausea. And you can see their vital signs here where they were tachycardic, but otherwise hemodynamically OK. So on initial arrival, an EKG was obtained. So we can see what the EKG looks like here. And then moving on, the patient went over to radiology very quickly. And here is the chest X-ray. And we did get the readback quickly describing some marked global cardiomegaly with some congestion and bilateral effusions. It was brought to our attention that the patient upon arrival back from radiology was now hypotensive, was more tachycardic to the 130s, 140s. Blood pressure had now dropped to 80s to 90s systolic. And so I was requested to come in and see. So I'm going to open up to the panel and just start to see what is your differential diagnosis for this patient? Well, COVID-19 always could be, but I don't think that alone explains the new cardiomegaly that they reported. So you're thinking about things like heart failure, tamponade perhaps. And I would agree with that. I think with the scenario around, that would be the first thing, especially COVID being everywhere and the new strains coming around. But I almost wonder if there is some tamponade situation going on. OK. So that's what I was worried about too. And so I went ahead and I put the point-of-care ultrasound probe on. And so here I obtained a couple of images. On the left side of the screen is an attempted parasternal long axis view. And on the right side of the screen is a parasternal short axis view. So I'll let that play for a few seconds, then I'll go on to another clip. OK. And now I obtained, oops, let me see if I may have gone by too quickly there. Wow. So if we take a look, go ahead. This is the epical view. You wanna go back to the last views again? Yep, so these were the peristernal long and short axis views that we have here. And then I'll go on to the apical four chamber. So what are you guys seeing and observing on this view? I mean, there's so much. I mean, you definitely see a heart that's encased with a very, very large pericardial fusion. There's some obvious movement abnormally of the RV free wall and the heart's doing a lot of extra moving that should not normally be happening. Yeah, and the other things you're noticing, so you mentioned it moving, it almost looks like it's swaying back and forth, kind of that electrical alternance pattern. The other thing is I almost start to see, and I'm not sure if my arrow on my mouse is coming across, but you can almost see some fibrinous stranding occurring here as well. So I went ahead and I did a couple other images on this patient. Let's see if I can advance. So on the left side of the screen is the subxiphoid four chamber view, and on the right side is a view of the patient's inferior vena cava. So I'm going to go ahead and move on and let's focus on that inferior vena cava for a moment because we've talked about that in a few of the cases. So again, I want to open up to the panelists. What do you guys think? Just looking at this in a B-mode qualitative image, what do you think? Can you estimate this patient's radiatrial pressure, CVP? Is it 11 to 20 or what the heck are you talking about? I got to put in a central line or a swan to actually measure that. Well, Chris, I am just a neurologist, but I can tell you this is not a very collapsible IVC. And whenever in doubt, say the answer C, but I think knowing the story, how it's building up and seeing the previous views, I would argue for C. Yeah, I agree. And again, I don't have specific measurements. If I look at the markers on the right side of the screen, that does look to be a little bit larger than two centimeters. I'm not seeing at least not more than 50% collapse with inspiration in a spontaneously breathing patient. So this does seem like a higher radiatrial pressure. I had enough time that then I went ahead and actually did some pulse Doppler imaging across the patient's valve. So I put the pulse Doppler gate here right across the mitral valve in the left ventricle. And what I found was as the patient was breathing, the difference between the maximum and minimum velocities was 26.88%. And some of the literature supports that more than a 25% correlates with pulses paradoxes that you would normally see when measuring a blood pressure for respiratory variation. And then for academic purposes, I went ahead and I put the probe over the mitral valve. And here I saw a variation between respiration on a scale of about 66% where the literature suggests that more than 40% pulses paradoxes. So let's go ahead and see now based on these findings, does that help increase or decrease kind of your pre-test probability for any of these conditions? Yeah, for sure. I think that those variations definitely support there being tamponade physiology and still could be COVID though. I'm glad we're at a point where we can laugh about it now. But yeah, I would definitely have a very high concern for cardiac tamponade. So with that findings, with that constellation of findings, when I spoke to our cardiologists, the interventional cardiologists, they really, it was a very quick decision for them to take the patient then to the cardiac cath lab. And they said that ultimately 1.8 liters of fluid was removed from the pericardium. And that as soon as they put the drain in, the patient immediately had improvement in their hemodynamics. So I presented this case as kind of a nice, easy save by point of care ultrasound and how that was able to quickly expedite the patient getting the definitive care that they needed. So I'm gonna go ahead and move on to a second case. And this comes, I'm sorry. Yes. This is a question from the audience, which actually elaborates on the question we asked before. This was a very descriptive case, out in the very visual to kind of give you this is tamponade and literally change the diagnosis. What do you think are the strategies of decreasing the barriers to performing focus like this in literally every patient? I mean, I think there's several barriers. The first is the foundation of training that we have to have people who even know how to obtain these views than what they're looking for. This case was helped by the fact that when the images were archived and saved into the EMR, it was easy to share with my colleagues in cardiology. So I'm not just telling them over the phone, but they can see and agree as well. And we're quite surprised by those findings to help expedite the care. There will also be concerns at the hospital level when it comes to credentialing and privileging to ensure that people who are using it have the appropriate amount of training and are using it within their scope of practice. And the biggest barrier in all of the literature that comes up in the top three from every paper I've read always seems to be a lack of training for in-practice providers. So to continue to educate people already in practice on how we can use these skills. And that's a great point. And as a very avid focus user myself, I literally don't take care of any shock patient without focus anymore, but I was very intrigued by your use of the sonographic version of Pulse's Paradoxes. That takes extra time. How do you integrate that, you know, the time component in a heavy clinical service with the burdens of documentation? And I would be interested in seeing Emil's perspective on that as well. Sure. So for me, there was actually, I attended a lecture earlier in the year, or earlier in the Congress, where they talked about using ultrasound in cardiac arrest. And some of the evidence they presented there was that it should be the most senior person and the most experienced person who can do it efficiently. And I agree, the more you practice, the more experience you get, the less time consuming it is. I mean, once I had the apical forward chamber view, it was just a matter of hitting the button to activate pulse doppler, lining up and getting it. At this point, I think the patient had a very clear and straightforward case of cardiac tamponade. And just as I was waiting in the room in case he decompensated, I obtained those measurements for academic purposes to have for presenting cases like this. But it also helps when maybe there isn't as clear cut evidence of tamponade, maybe not as large of a fluid collection to be able to argue with, not argue, to be able to discuss with the cardiology service that there actually does need to be a more emergent treatment. But that again goes to the importance of having, the more you practice, the more you're prepared when the situation arises, you can jump in. And I'd be curious if you have anything else to add. No, I totally echo everything that you said. It has to do with training and confidence. I call it the three Cs, competence, confidence, and comfort to be able to use the ultrasound, interpret it, and then integrate it into what you're going to do to change care for the patient. And so, yeah, I totally agree with you. If time allows, or if I need to convince, then I will do more. But in the, for tamponade specifically, abnormal vital signs, a big pericardial effusion, that's enough to go ahead and pull the trigger and ensure while you're waiting, while you're resuscitating, those more diagnostic values, I think can help guide the management while you're waiting for a final intervention. Thank you. Well, let's hear your second case. All right, so this case comes from, this was done with a fellow of mine. So I actually, each year, have a critical care ultrasound mentee, and this is an individual in his second year of critical care who already passed the echo boards and completed their portfolio. So somebody who is really well-trained and well-qualified in the use of trans-thoracic echocardiography. This was a patient that was in the hospital post-op day three after a CABG-4 ischemic cardiomyopathy, when we had what's called a condition C at our institute or the equivalent of a rapid response called for decrease in blood pressure and hypotension. So the patient apparently had been saying that they felt unwell throughout the day. On examination, they were cool, pale to palpation. We transferred them back to the cardiothoracic ICU and arterial line was placed. The map was found to be between 55 and 65. And with the arterial line monitor, they had very large pulse pressure variation. So based off of that limited history, what are you guys thinking in terms of potential causes? All right, it could be all the above. You're missing E, all the above. Yeah. And I think I even maybe could have included a graft going down as well after a CABG, another option. Yeah, right, it could be all of these. So we applied ultrasound to see if that could help us narrow the differential diagnosis. And here is the parasternal long axis view that my fellow was able to get. So I'm gonna take this view and I wanna ask you guys, I mean, you guys are ultrasound experts, maybe a little bit more neuro than a cardiothoracic, but I labeled the structure on there with the asterisk. What do you guys think? What did I label there? What structure is that, parasternal long axis view? Come on, Chris. That's a left atrium in the parasternal long axis. What's there in the RV? Let's go back. Let's take a look at it real quick in a video. Yeah, I don't know. Maybe there is something up there in the right ventricle. There's something that looks a little cloudy up there. Okay. Anyo, anything else to add on? Yeah, I mean, I don't know if you saw me, but whenever I'm looking at ultrasound images, if I have to lean in, that means that the image quality is, you know, it's a little tough because I have to really sort of see what it is that I'm trying to look at. So I was trying to look clearly. I also saw the thing, the RV, I don't know what that was. I don't see a large pericardial fusion. I can't really tell about the LV function. But, you know, I probably need either more views or better pictures. All right. Ask and you shall receive. So here I've got on the left side, on the left side of the screen, we've got a peristernal short axis view. And on the right side of the screen is an apical four chamber view. So you asked Dr. Anyo, what do you have on here? What do you think based off of these findings? I'm still leaning in, which means that the image quality is still suboptimal. I'm feeling judged now. I'm seeing this short axis and I, you know, the heart is beating. And I'm seeing this five chamber. I see the aortic valve, maybe looks a little funny. The RV doesn't look as big for, if PE was in my differential, but I still can't see really well. Yeah, so go ahead. I like Anyo's lean in test, that if you really have to lean in to see the images and I'm really having to lean in, but it kind of looks normal to me from my perspective. Again, what do I know? I'm just a neurologist. So we, I completely agree that when we did these views, we recognize that. And so we already talked about the differential. I don't know if this necessarily helps rule in and rule out enough that I think we were struggling with these views. And so that was one of the things we recognize is that this is a patient who had just undergone a thoracotomy. So that alone makes it harder to get trans thoracic views. And on top of that, some of the machines we use at the bedside, they're not the same as when we order a consultative echo and they come in with the full ability of what they can see. So we did, we went ahead and we ordered a consultative trans thoracic echo to see if that can help clarify some of our views. And this is the consultative trans thoracic echo that we obtained on this patient. What do you guys think of this? Again, it's now the peristernal long axis view again. Yeah, what is that? Is that something at the LA area? I don't know if it's a dissection of the wall itself or it's like a clot in the pericardium that's compressing the LA. There's something funky going on there. Yeah, funky for sure. I mean, that's so, that's a great picture. I did not have to lean in. And I'm appreciating that there's like two high, you know, like anechoic or hypochoic areas where I thought the left atrium was. And so, yeah, I'm a little, that looks like a clot or something echogenic within the pericardium of some sort. Yeah, so I'm gonna go ahead. And so now that we have the same exact area, I've got that structure label. I'm pretty sure you guys said confidently that was the left atrium. So now what do you guys think? Sticking with left atrium? No, you see the mitral valve. No, that's not the left atrium. It's probably that small little squish thing above the asterisks. Yeah, the left atrium is probably right up around here. All right, so let's go ahead and compare then what we had. So now on the left side of the screen is the image that I obtained using point-of-care ultrasound. And on the right side of the screen is then the transesophageal, I'm sorry, the transthoracic using a consultative echo. Yeah, that's the challenge of focus versus a diagnostic image. Okay, and then they went ahead and they got the same views. I wanna show by comparison, they're peristral short and then they're apical four. The one thing I wanna highlight here too is I love on their apical four chamber view, you can see how much that this, what is essentially a more solid hematoma that is formed is completely compressing the left atrium. In fact, it looks obliterated and you can see that much more clearly here. So now that we've gotten these consultative images, does that change your differential? Oh yeah. Well, yeah, well, I did notice that I think on the previous pictures, the LD function did not look very good either. So regarding congestive heart failure, was that new or old for the person? Yeah, no, that's an excellent point. And that's one of the challenges too is recognizing if there's something new or chronic. The ejection fraction was considered to be moderately reduced, but was unchanged from what their perioperative, the postoperative TEE showed. So that was not an acute decrease. And Chris, I'm kind of unfamiliar with this population obviously, but I wasn't aware that you can have such a focal tamponade and ECHO is probably the only way of figuring that out. Yeah, no, that actually is a very common complication in post-cardiac surgery. And compared to patients that develop tamponade from other conditions, from malignancies, rheumatologic conditions, post-viral pericarditis as we saw, when it's not as fluid, it won't form as circumferential finding and so when it's due to blood clot, especially if the chest tube drains, the sternal drains aren't stripped appropriately, there can be just a resultant pocket that then solidifies and then that firm hematoma can actually cause that much more compression on the adjacent structures. And then as the patients tend to be a little bit more supine or at least recumbent in bed, it can be more dependent in posterior. So that is a limitation where the transthoracic approach is a lot harder to even get a view after having open heart surgery, your chest is open and where the location is. So a more ideal test would actually even be a transesophageal ECHO to locate those. Wow, I don't know about you, Neil, but I was stumped by the first case from the magnanimous city of the findings and the second case, I mean, I just wasn't aware that this happens. Yeah, so then with that finding, we reached back out to the CT surgeons who took them emergently to the operating room and was found to have 500 CCs of clotted blood that again, once the pericardium was open and was relieved, had immediate improvement in hemodynamics. So the reason I put these two cases together is to emphasize, I think again, we need to make sure we're aware of the limitations of the use of ultrasound, that again, it is an incredible tool, it is growing in terms of how much it changes our practice, but to be aware that depending on the capabilities of the devices themselves, your own skill as a user, the patient's body habitus and conditions, and in this case, being post-operative. Point-of-care ultrasound, I find, tends to be a lot better to rule in diagnoses. So in the first case, you saw the effusion, I mean, it made it a lot easier. In the second case, I couldn't see an effusion, so maybe I couldn't necessarily rule it out. And then the key thing is still the clinical correlation, not all the cases will have obvious findings. I know people, obviously we're huge enthusiasts of ultrasound, but it still is not the holy grail. It is just further data to supplement your care. And I like to teach people to use it as more of kind of Bayesian theorem reasoning. So you go in with a certain pretest, but it helps alter your ultimate diagnosis. So those are my cases for a shock, and now we will go ahead and hand it over to see some cases involving acute respiratory failure. And before Inyo starts, I have a question from the audience for you, Chris. Okay. What single view would you recommend in sick patients, either during a cold or worsening shock, if you literally had less than a minute of time with somebody who's very fairly familiar with point-of-care echo? Sure, so in the setting of a full-on cardiac arrest, the view I would use would be a sub-costal view. So I'm out of the way of compressions that are occurring. It's not gonna give me a lot more data other than just simply, is the heart beating at a pulse check and any gross abnormalities we can try to reverse. If time is limited, the two views that I really prefer are the parasternal long axis view and the apical four. Now the apical four is certainly one of the more challenging views to get, but it also gives me some of the most information. I would say probably 80% of echo reports, the information is derived from an apical four and apical five chamber view. So I would take a pickup between a parasternal long and an apical four. Awesome. And another person asked, were these images taken with a portable handheld ultrasound or what kind of machine was the POCUS images acquired from? I will try to remain brand neutral, but it was more of a CART-based device that actually is a very good high quality image. Both cases were from the exact same device type. So it wasn't a portable handheld, it was more of the traditional machines that would be on a stand, kind of like the computers on wheels that we roll around. Thank you. Let's see in your cases and see how you stump us. Okay. Are we ready for case three? Okay. So a 45-year-old male presents with acute shortness of breath after getting some Narcan because of an accidental fentanyl overdose. They're coming to your ER or they're coming to your ICU from outside hospital transfer, let's say, after and you hear reports that they've had two episodes of bloody emesis. Their vital signs are listed there. You can see that they're type of heartache, 140 is their heart rate, tachypneic in the 40s, blood pressure is 160 systolic, hypoxic 85% on 15 liters. You get some lab work there that suggests that leukocytosis, elevated lactate, some acidemia, and a chest radiograph that looks like that. So we're going to talk about how we can use Ultrasound to help us kind of comprehensively think about all the things that are going on with this person's respiratory failure and what we can do to optimize it. So we do the ABCDE, if again, time allots and if you're able to. So we'll just regard the images here and then we'll go over some of the questions to try to stump our panelists. So here are our images of the right. And then here are images of the left. Then here's our cardiacs and heart was the preferred if you only have one, here you go. As well as some calculations from our LD, filling pressure, disolic measurements, EDE prime listed there. And then diaphragm ultrasound, looking at some thickness. So as you guys sort of, panelists, as you sort of regard this and just look, we'll get on to the next questions using this as our frame of reference. So the person's vital signs that I mentioned are listed there, tachycardic, tachypneic, hypoxic. They're talking though, they're telling you that they're, you know, having a little trouble breathing, but not too bad. Here's again, their lung ultrasound using a lower frequency probe back on the left chest. What do you think and which options would you like to do? So I think, let me walk through this. You showed us some high frequency probe and low frequency probe pictures of lung ultrasound, showed beautiful sliding. So I don't think it's pneumothorax, so A is out. And then you showed us some good apical view pictures of what sounded like a normal heart on the four chamber view. And then I don't do diastology by bedside, but as you taught us in the lecture, the EE prime ratio seems to be less than eight. I think it was 4.1, it's something on the previous one. I wish COVID was a choice, but since that's not a choice, how about, he's talking, so I don't want to intubate him, BiPAP, you know, I don't know if he's aspirating. I don't know what his ability to protect airway is. Let's go with OptiFlow. What do you think, Chris? Yeah, I agree. I certainly would not think there's a need for a chest tube with the lung sliding that we're seeing in the B lines. If he's still on 15 liters and he's not responding, I think we need to step up. So I think you can easily make, and I wouldn't say we need to intubate him at this point. So I think you can make an argument for either BiPAP or OptiFlow. But I agree also with what you said. I don't think he's got high filling pressures that I really need Pete to drive that. So I would probably go with the high flow, OptiFlow at this point. Well, you know, that's what our team did exactly. We opted to try OptiFlow. And just to make the point here that, you know, the pointy-coated ultrasound absolutely is a supplement to what your pretest probability is. I mean, there are patients who have x-rays that are lung ultrasounds that look normal and they look terrible, like they should be intubated. So you're certainly not using it to tell you clinically what you should do. You're using it to supplement what you're seeing clinically. And in this patient, we have evidence that there's some lung, interstitial lung processes that are occurring consistent with the chest x-ray. All right. So you go ahead and use OptiFlow. Stats are improving. Tachypnea is a little bit better. Heart rate has come down to the one teens. And then here's that ultrasound that we talked about. Here's our, just our apical four chamber, and then some of our filling pressure measurements with the ED prime specifically that we discussed. So based on that, people want to know, should I give this patient fluids or diuresis them to try to help with their heart or help with their lungs based on that radiograph and that lung ultrasound that we saw? What do you guys think? Is it a choice to just observe him and kind of see how he does on OptiFlow? What do you think? Yeah, I agree. I mean, I agree. I think the EF looks good. I mean, I don't think he needs to be diuresed. You know, again, as we talked about with both the IVC and the ED prime, having a low number doesn't mean you need fluids, right? I mean, that's normal. So I suspect and I hope looking at each of us, our IVCs would be small and collapsible and we'd have a low ED prime. So it doesn't mean he needs fluid right now. And then in terms of diuresis, yeah, I think he doesn't look, he's not showing signs of fluid overload. I mean, using the ED prime as a surrogate for a wedge pressure, that looks good. So I would suggest that this is a non-cardiogenic cause of pulmonary edema. Yeah, that's exactly right. And I think for our purposes, whatever the clinical thing you want to do is, right? That pretest probability where the fluids or diuresis, then you're using the ultrasound to say, is this drug, both fluid as a drug and the diuresis as a drug, is this in the best interest based on the images I see here? So for fluids, I'm not using the low ED prime to tell me to give fluids. I'm using it to see if the patient can tolerate the fluids that I think might be clinically indicated. And then for diuresis, the same thing. If they have a low ED prime, the likelihood is that they don't have high. that it's important to remember that you should make sure that there's no regional wall motion abnormalities and that the heart rate is low and that, you know, sort of those sorts of things. So just be aware of exactly how to apply this tool. All right, so let's go to the next question. It's now day four. You've got the person on OptiFlow. You have made sure that their volume status is optimized by using some of your diastolic measurements to do that. And then on day four, they're getting a little bit better radiographically, but then they start reporting some more dyspnea. Oxidation status is unchanged and labs are pending. And you decide, let's go ahead and be comprehensive and go ahead and try this lung ultrasound that we talked about today. Based on their lung ultrasound, what do you guys think? So let's first just talk about what we see on the lung ultrasound. On the first clip, it's playing twice, but on the right versus the left. I think I'm going back and forth between the pulmonary edema images and the diaphragm images, but I'm going to try and troubleshoot these diaphragm images. The one on the right seems to have some effusion and you can see the liver and the diaphragm seems to be moving up and down pretty decently. I'm assuming this patient is still spontaneously breathing. I'm sorry, to clarify, you're saying the one labeled as right, which is the left side of the screen. Correct. Yep. I'm going by the label, the right, and then the one that is labeled as left looks like a splenic view. And you can see the spleen, a little bit of pleural effusion, but compared to the other side, I really don't see much movement of the diaphragm on the splenic side. Is that what you're saying, Professor Bell? Yeah, I agree. Is that a new finding? Did you look at the diaphragm before this? Yeah, that brings up a great point. So you get this new finding and like an EKG or like a white count, that one number, I don't know what it means because if you didn't look at it before, does that really help me now? We did, unfortunately, did not look at it before to be able to help guide that. But had you looked at it before and they were both normal and now they're abnormal, then what would you do based on that diaphragm ultrasound? Wait for your labs and give Lasix, initiate BiPAP, go ahead and intubate now, or go ahead after hearing an excellent neuro talk, order that, with your mind on neuro, order an electromyogram. Well, knowing that we're shooting for the diaphragm here, I can speak on behalf of my neuro ICU community. I really don't think it's a good idea to order electromyogram in a patient in active respiratory distress in the ICU. So I think let's take that out. I think it's a great elective test. I necessarily would intubate this patient, especially if they're still saturating well, ventilating well, you know, labs, ABG, Lasix, probably not. So I would initiate BiPAP for possible neuromuscular component and kind of troubleshoot the cause of diaphragm weakness and how much it's contributing to the patient's respiratory distress. Yeah, I'm gonna agree with the neurologist on this one, that I think that in the acute setting, I'm not sure how helpful that is. So I would just continue to support them until they can be a little bit more stable and then work it up. Yeah, but that's a great point to the sense that, you know, if you haven't, if you didn't do it before, it's hard to know what it looks like now. These are serial testing, and I think there's room for point-of-care ultrasound to be very useful in our application by serially checking. So what did it look like before and comparing it to what it looks like now? So we, for this particular case, then BiPAP was what the option was. All right, ready for the next case? Similar radiographic findings. Let's see if the ultrasound is the same. You got a 63-year-old female, shortness of breath, four days. Don't know anything about their cardiac history, just hypertension and GERD. They're intubated for respiratory failure. Let's say they do have COVID. If you wanna go ahead and bring that to the table here, their ventilator settings, they're on a PIPA 7.5 and 70% FiO2. There's some labs that are listed there. There's their chest radiograph, which, you know, and then they're a slice of a CT scan, let's say. So again, let's be comprehensive and think about, for that patient, as we're taking care of them and as we're optimizing them, are there things that point-of-care ultrasound can help us do to get them off the ventilator faster or optimize them while they're on the ventilator? So we, again, look at the lungs, we look at the heart, we look at the diaphragm. So let's start with the lungs, and again, just regard these images as they play. Okay, kind of thinking about some of the findings that we talked about there. A lot of B-lines. Yeah, yeah, there you go. Those B-lines, bad lines. Okay, and then here we're looking, exactly, B-line, bad lines. So here we're looking, again, at the lung and the mid-axillary phosphorphonic sort of area. And then we're looking at the heart. We've obtained some filling pressure diastolic measurements at ED prime here, it's 18.3. And then here we do have a pre, let's just assume that it's the same on both sides with diaphragmatic excursion in M-mode. Sorry, let me go back one. All right, so for that person, you've got them ventilated. I've told you the PIPA is 7.5. Sats are, or FIO2 is 70%, so their sats are 90. Now we're talking about how do we use point-of-care ultrasound to titrate the PEEP? So I'll play each of these clips here for you, and you guys get to decide which level of PEEP and plateau pressure in accordance with the point-of-care ultrasound that you think would be appropriate for this patient. Let me go back again. I think I'm- Go back one more and then go forward. Got it. Okay, ready? Oh, there they are. Lots of B lines in A. Okay, lots of bad lines in A. Bad lines in B. More or less in A? Not as much in D. So C and D seems to be a good thing that there's no B lines, but let's see, the PEEP is 10, plateau pressure is 28, PEEP is 12, and plateau pressure is 31. So I think I kind of like the idea of no B lines, but I don't like the idea of plateau pressure of 31. So how about going with C? Chris, what do you think? Yeah, no, I completely agree. I think that this is something, the literature is starting to support doing it. It certainly isn't prime time, ready to go from major studies, but I think it's really helpful, particularly in patients that have larger body habitus, where there may be a lot of basilar atelectasis. This is a great way to help recruit up because as the chest wall expands, or there's other limitations that can falsely elevate your measured pressures, this is a way of kind of helping visualize that you're getting appropriate filling. So I would go with C as well for those same reasons that Dr. Sarwal said. It's got a good enough PEEP that you've removed the B lines, but not too high to potentially cause ventilator lung trauma. That's exactly right. So you're using cortical ultrasound in this case, not as a binary of Chanel, but you're using it to sort of optimize and pick the perfect spot if possible to avoid over ventilation, to avoid atelectasis or under ventilation. And you're right, there's definitely room in the literature to make it more robust, but there's definitely, with the appropriate training to be able to do so. Okay, so the person's mechanically ventilated. You've adjusted their PEEP. They were at 7.5. You went ahead and used option C and took them to a PEEP of 10, and they have improvement of their B lines. Their radiograph over time starts to look better, but obviously they still have a lung pathology from their COVID, let's say. You have a creatinine on them initially, that's 1.27. You gave them some Lasix based on, some clinical assessment and perhaps their imaging before. They had good urine output, 1.5 liters. The next day your creatinine goes up to 1.5. Your EMR flags and says that there's an AKI, and you decide there's a question amongst your team about redosing the Lasix or diuresing them again. So you decide to take chronic care ultrasound back to the bedside to see if it can help guide you. So the first frame, we're looking at images of the lung using, again, a low frequency probe. What do you guys think you're seeing there? Oh, wow. So I think the EE prime ratio is still pretty high. The IVC still looks pretty plump. I don't see any variability. And then we obviously saw the B-lines. Well, I kind of want to give diuresis. Focus does support the need for further diuresis. So I'm going to go with C. C is always the right answer. I'm not a good test-making person, I see. But I'm going to go with C as well. I think the lungs still look wet. You've got those evidence of B-lines, which don't necessarily mean wet. I mean, you can see that even with any other interstitial process. The IVC itself, the fact that they're intubated now on that much PEEP, it's hard to really say what value it's showing, even though there isn't a lot of change. I'm going to focus back on the diastolic measurement you did, the ED prime of 18.3. I mean, that's still really, really high. And that's, again, the equivalent of a really high wedge pressure, suggesting that this is a cardiogenic pulmonary edema. So I'm going to advocate that this patient can benefit from further diuresis. Yeah, I really like how you guys really pieced that together. That's the beauty of point-of-care ultrasound, is that in addition to, again, doing binary assessments, perhaps as an early trainee, as you get more advanced, being able to put all of the pieces together in context, appreciating that B-lines mean that there's interstitial lung water or pathology of variable explanations, that the IVC may be dilated, that the context matters, the PEEP they're on, and if they're ventilated or not. And then the wedge pressure estimates or surrogate here, this EDE prime, putting that all together suggests that this person's body still has probably high volume rather than low volume, in which case we agreed with you that diuresis here would be beneficial in spite of the creatinine elevation and proceeded to still do that. What do you guys think of push-pull and ultrasound help us with that? Don't do it. My unit, that's what you get. Don't do it. All right, final question here. Yes. Question from the audience about this really interesting case. They're asking, one, how much do you, how long do you wait for PEEP titration to see changes on B-lines? Is it a matter of seconds? Is it a matter of minutes? And another person asked, what's your strategy on how many lung fields, how many zones bilateral versus unilateral? So what's your strategy on PEEP titration with the probe and fields? Yeah, my belief is that definitely the more information, the better. Part of being an intensivist and working in sort of these clinical environments is so that sometimes we don't have time, either time because of a patient, a clinical condition or other clinical priorities. But certainly the more, if you can get bilateral, all of the lung fields, then you have a better assessment of what's happening. I would say more practically though, people are typically getting bilateral, more anterior zone one, two, and three sort of broad strokes along the anterior and mid axillary line looking for gross pathology and sort of following the blue protocol if you've read about that in terms of if the B-lines exist or not. In terms of titration, how long you should wait, that's probably still not quite finalized. One would expect like anything else with recruitment, it may take a few minutes. I don't know that it's a second for that to happen, but it may be a situation where you put them on a PEEP, come back 15 minutes later, maybe 30 minutes later and check to see if there's resolution or improvement. I'm not sure there's good literature about kind of how the up titration, but I think for myself, practically something like, 30 minutes or so is probably what I would do. The other panelists, what do you guys think if you are doing those or? Yeah, I agree. So I probably on the scale of minutes to hours, like you said, 15 minutes, I'd say minimum, 30 minutes, pretty good, maybe even an hour to go and come back. And again, depending on the situation, depending on how many fill-in-your-blank city units a patient is, I also really look a lot at the lung bases for consolidation there too, because I know if I can be reaching those basilar segments, that that helps. Yeah. Okay, final question so we can get on to the rest of the cases here. It's day four, the person is not passing, but not grade their institutional spontaneous breathing trial. Go ahead and again, look to the diaphragm ultrasound to help understand why they keep not doing as great as maybe perhaps you desire. So we're just looking at the fractional thickness of the diaphragm, both in M mode and then also the actual clip of it here, let you guys regard that. And again, we'll just go to our neurology ultrasound guru here and see what she thinks of this diaphragm excursion and the thickness reported here and how it correlates potentially with being able to estimate the person. So I think if I'm looking at it correctly, in the before pictures, I'm seeing a thickness change of about 36% from inspiration to expiration. And on the after picture, I'm seeing about change from 1.6 to 1.2 millimeters. That's about four millimeter change, 25% change. So 25, 36% seems to be kind of in the normative category. I think the challenging part in your diaphragm ultrasound is as you said it very nicely in the literature review, when you talk about millimeters, there are two things you have to consider. One is the resolution allows reliability. It's very hard to say one to two millimeter changes. And the second is I don't think the literature is there yet to give you definite cutoffs to predict extubation failure. So I think this is the case where unless the diaphragm thickening fraction was in extremes, I don't think I would use this diaphragm ultrasound finding to decide my extubation decision and the clinical decision of extubation would be paramount. Now, if I had seen literally zero on one side, that's a different thing. Yeah, Chris, what do you think of the answers? Which one would you pick there? Yeah, I completely agree with what Dr. Sarwal said. I would really, I don't think this changes my clinical course and I would still be correlating clinically to how the patient is doing on their trial. Yeah, I think we do have to know the limitations of ultrasound when we can and cannot use it. All right, that's my case. Awesome. Well, I'm stumped. I just want to keep going on, but here, let me present my neural ultrasound case. 19 year old guy with urea cycle disorder, non-compliant, has the ammonia of about 377 and comes with altered mental status and these seizure-like episodes, gets a benzo load, gets an EEG. Everybody's worried about seizures, but we don't find seizures. And then the focus changes to hepatic encephalopathy and we are suspecting cerebral edema. So we start therapies as we kind of looking at diagnostic studies. We start hemodialysis, all the nitrogen scavenger, paradigms kind of kick in, and the exam stays poor. So we take this patient to CT scan. And you can see the CT scan on the right side. There is some edema and gray-white de-differentiation in most of the CT scan, although you can see the silica at the top. So, and you can see the ventricles pretty decently with basal cisterns. So with this CT scan, we also get an MRI on this patient. Oops. So this is the MRI on this patient. And on the left, you can see there is significant hyperammonemia changes of restricted diffusion. And on the right, you kind of confirming there is cerebral edema, there is some kind of early uncle herniation, and you can see gray-white changes at the top as well, but you're worried about cerebral edema. So this patient gets this concern for cerebral edema and ICP monitor is placed, attempts at EBD fail. So bolt is placed. And over the next three weeks, his ICPs are very refractory. As you can see, here we are showing the actual shots from the patient's EMR. And these are your left-sided markers. At the top, you have systemic hemodynamics, and at the bottom, you have ICPs. So in the first few weeks, every time we try to move this patient, his head of the bed is elevated, maximum osmotic therapy, maximum ICP lowering therapy. But anytime his ICP goes up, you're kind of seeing this pattern of his blood pressure going up. So he's auto-regulating very nicely. And this trend kind of continues, but it's been almost two weeks now and patient's ICPs are not getting better and we can't even put him flat for another imaging. And as the weeks go by, you kind of start seeing a different trend now. And instead of the auto-regulation happening, now the blood pressure and the ICP changes have kind of disjointed from each other and are not changing in relation to each other. So it gives you kind of an understanding the patient is just auto-regulated now. And obviously, you know, I come on. So I'm going to stop there and ask you guys, you've seen this guy for two and a half weeks now, what's your next big step in management? Would you continue current osmotic therapy, which is maximized? Would you call a neurosurgeon for a bilateral bucket handle hemicraniectomy? Or would you perform a neural ultrasound, especially if you listen to my talk? Or engage ethics and palliative care? Definitely C or three in your case, lung ultrasound, I mean, neural ultrasound. Yeah, I mean, I think there does sound like there may be a lot for engaging in ethics. I don't know how much a bilateral bucket handle cranioctomy would help, but yeah, I think based on your talk, I'd be curious to see what the actual flows are. Awesome. So the mother refused any talks about palliative care period and obviously bucket handle for a medical cause would be a little blasphemous here. So obviously I come on service and that morning, I look at this transition from intact to impaired auto-regulation and the patient ICPs have now gone up to 90s. And we've already gone through two bolts and one EVD. And when I do the ultrasound on this patient, this is what it shows. So if you pay attention in the talk, this is my B-mode image with the midbrain in the center. And then you can see the color Doppler. And then here we are imaging the PCA, ipsilateral MCA and contralateral MCA. And these are the waveforms. And if you remember my talk, these are low resistance waveforms. You have beautiful flow throughout the cardiac cycle. Diastolic flow is a third to half of the systole. And the flow looks pretty intact. So what do you think, Chris? Yeah, so I have to admit, I am not somebody who does a lot of transcranial Doppler. I am not a neurologist. But so based on what you said and looking at these, this looks very much, I'm used to doing this more with resistive indices looking at transplants through the hepatic vein and looking at renal arteries. So that to me looks like there's good flow. That doesn't look like the restrictive pattern that would suggest a high pressure edema because the diastology, there's really, yeah, it looks good. The resistive index looks appropriate. And to give you the RIs, we actually did quantitative measures as well. So here you can see on the left upper part of the screen, the mean flow velocity is 58, which is pretty normal. You can calculate RI for the brain as well. It's 0.52, so very low resistance. We typically follow PIs, which is 0.6 to 1.2 normal. And so from my perspective, both the right MCA and the left MCA in these two pictures represent pretty normal cerebral perfusion. So in this case, if you remember our talks on how the waveforms change, typically you would have high resistance waveforms with very impaired diastolic or even reversed diastolic. And then typical TCP waveforms are low resistance waveforms with a very robust diastolic. And as your ICP goes up, you expect this transition from low resistance waveforms to high resistance waveforms. And in this case, obviously, we're not seeing any patterns of high resistance. Both right and left MCA show pretty normal cerebral perfusion pressure. So how do you reconcile that? Now, so there are two scenarios. We all know the Mondro-Kelly hypothesis, and the green represents the brain, red represents the blood, and blue represents the CSF. So there are two ways pressure can increase in the brain. Either the brain got swollen and started compromising the CSF and the blood, in which case you typically will see this high resistance waveform because blood is not getting through the brain because of high pressures. And high pressure is coming from having too much brain edema, in which case you will see these high resistance waveforms, diastolics are even reversed. But the other two compartments can play a role in ICP too. So if you look at the right of the screen, you have the same patient with increased ICPs, which was my patient. Here, the increased pressure in the skull is not coming from the brain, but from too much blood flow going into the brain. And in this case, because of disorder regulation, even at normal blood pressures, the patient's blood flow in the brain, in the cranium is so high that that's contributing to the ICPs. So in the left side, when I have the resistive waveforms, I would probably give osmotic therapy and I would contract or constrict the brain, shrink the brain. But on the right side, I'll actually drop the blood pressures. I'm really curious about that. So the concern, again, the normal paradigm is that in order to maintain appropriate cerebral perfusion with a high ICP, you have to increase the MAP. So you're actually decreasing the MAP to bring down the ICP. Does the cerebral perfusion pressure follow that linearly? And did you do serial exams to ensure that? Because like an LVOT, outflow tract obstruction, we have to paradoxically give a beta block or people are gonna look at you kind of funny. Is that the approach? Is that what you did? How do you do that? You are right on point, Chris, there. So on the ICP of 55, when you have resistive waveforms, you actually want to increase their MAPs to maintain their CPPs because blood is being compromised, which can cause more ischemia. But on the right-hand side, it's the hyperemia because of impaired auto-regulation that is driving the ICPs. So you will actually normalize this patient's blood pressure, normalize their MAPs. And for people who are familiar with the ICP schools of management, this is the LUNS protocol or LUNS school of management. Cool, yeah, that's pretty critical. That's cool. Thanks. Yeah, I think it also just highlights really nicely what point of care really, how it brings value that previously others were doing what they thought was right based on how we are being taught to take care of the patient and the point of care should totally change how one should act. And I think I showed this case in my lecture. Great point. So I showed this case in my lecture. You can have non-convulsive seizures that are driving high blood flow. And this was a case published from invasive neuromonitoring, but you can diagnose that with point of care ultrasound. And we've seen similar trends in post-cardiac arrest patients that are undergoing TTM during rewarming, where you can distinguish their hyperemic waveforms, reperfusion versus high resistance waveforms using point of care ultrasound. And obviously, we did formal diagnostics in this patient and over the next two weeks, I discontinued all osmotic therapy with a gradual VEEN, discontinued sedation, paralysis, used CETL-TCD monitorings to make sure that the patient's waveforms have not transitioned to high resistance waveforms. And the patient's actually doing well right now in rehab, extubated, awake, interactive, and participating in ADLs. Any questions or thoughts there? Okay. So that was a positive case, but I think, I hope I convinced you guys to try to do ultrasound in every suspected cerebral edema. And here's another case. So 47-year-old woman, pretty protracted, impaired history of social misbehavior with alcohol abuse, alcohol rehab, and getting out of it. And in the alcohol rehab, she's found altered within cephalopathy, but non-focal findings. And there is a concern that she might be ingesting hand sanitizers with ample availability these days for obvious reasons. And she comes to the community ER where they find high osmolar gap confirming that. And while they resuscitate her, they find a CT scan finding of bilateral ICH. And they transfer her to Wake Forest Baptist ICU. She's intubated, sedated, and paralyzed during transport to prevent any ICP increases. Even as of the last documented exam, she's confused and disoriented, but she's moving all four extremities before she was sedated and paralyzed. So this is her CT scan. Bilateral ICHs, but no significant herniation. And obviously we are a very neuro ultrasound savvy unit. And we say, let's do optic nerve sheath diameters in her. So at the top picture, you can see one side of the optic nerve sheath diameter, which is a 0.3 behind the retina. And it gives you a measurement of about four. And on the opposite side, it's labeled left, but we actually did two different sides. You're getting a measurement of 6.4 millimeters. And if you look at the measurements, they were exactly done as the protocol says. So what do you guys think? Based on these findings, would you initiate high dose osmotic therapy? Would you transport the patient to a head CT? Would you perform a neuro ultrasound? Or would you engage ethics in palliative care to withdraw care? I mean, I kind of feel like there, I'm leaning towards needing a head CT. I don't know how much I really trust some of those images. Like when you go back, the one you can really clearly see the optic nerve sheath. The other one, yeah, the one on the right of the screen, I can really see that. And also the one that's labeled bottom left. That top one, I don't know how well that's measuring the optic sheath versus the optic nerve. Yeah, so I don't know if I would really trust, and especially like, yeah, I would go with the CT. You knew anything? I would go neuro ultrasound. You go neuro ultrasound, yeah. Neuro ultrasound. And I do also just want to highlight again about the images, just again, subtle differences, millimeter differences, but that's the difference between the competence and sort of just running wild with like too little knowledge and making wrong decisions. We have to, you know, that's a great point that I don't really see the sheath. That's not gonna be an accurate measurement. That's a great point. So the parents of the family that were DPOA basically refused any further diagnostic testing and wanted withdrawal of care. She was rapidly deteriorating with hypotension and hypothermia evolving. We decided not to transport the patient to a head CT, but as the discussions for goals of care were going on, I really wanted to kind of reconcile what we saw. And before I do that, these are very quickly, you know, this is the papilledema version of ultrasound that we just talked about. And this picture kind of Chris said very nicely, this is a very classical picture of what optic nerve sheaths should look like, but it's very difficult to get these pictures in point of care on a day-to-day basis. And there's so much variability of optic nerve sheath. You have different ways, different angles, you look at it. And this is the MRI until you really align the angle of insonation to go and get the longitudinal axis and really cut it off in a longitudinal axis. It's very hard to get a true transverse axis. And even then the variability of the anatomy itself, you can see an MRI and a ultrasound correlate, even a millimeter difference of what you can measure can make a huge difference in these cutoffs. And this is probably, you know, why the cutoffs have not really correlated well as great tools for non-invasive ICP surrogate. You can see here on the right side, a very tortuous optic nerve. You know, how do you measure this? And where do you reconcile this? Versus people have tried to have this target eye approach. So lots of challenges in not just the acquisition of the image, but also creating these cutoffs. And this is where we tried to do, you know, three millimeters each side, but as you can see the challenges of really identifying the optic nerve sheath, and even that one millimeter difference, how big a problem it can create. So this is why we haven't quite seen optic nerve sheath translate. And in this case, I obviously didn't need an ultrasound to basically close the loop on the irreversibility of the disease. And this is cranial ultrasound showing ICH on each side, and the waveforms from ACS confirming very nicely that the patient is oscillating waveforms and irreversible brain injury with very high ICPs. So I hope that these three cases and the lectures gave you a perspective on how POCUS is really growing in scope and has really expanded head to toe in ICU patient. You have to balance evidence against standard of care and kind of understand what the evidence says. And just because you can, doesn't mean you should. I mean, we showed you some really descriptive cases of great stumping movements that wow, ultrasound change management here. But then we also showed you some cases where we should pause and say, do I really have enough information based on what I'm looking at that translates into a different clinical decision? I can't ignore the big picture. And that's where you have to remember that POCUS is one extra tool to help you supplement, not replace your clinical judgment. And we have multiple times during these last two hours, education and training is the foundation where we need to be spending significant amount of time. There are lots of learning opportunities that you can learn ultrasound head to toe. And you can also follow us on Twitter, hashtag ultrasound and hashtag POCUS are some of the most trending hashtags. And there, I will open the floor to questions and any comments from Chris or Enyo about these cases. And I look out for audience questions. Yeah, thanks guys. So there is an audience question that came in that says, awesome presentation. In the case of the hyperemia causing increased ICPs, if we are not proficient in neuro ultrasound, what other modes of diagnostic would you recommend to confirm? So if you have invasive monitoring, obviously you can always use blood flow parameters. Like I told you, optic nerve sheath quite, hasn't quite seen the day where we can suggest cutoffs. Cranial ultrasound is not very hard to learn. And we mentioned earlier in the course that you can use abdominal presets to perform basic MCA. So you don't have to be proficient in transcranial Doppler. You can have basic training in just getting MCA insulations. And say, if you have a facility available for formal TCDs, you can use formal TCDs as full diagnostic TCDs performed by the diagnostic lab to give you that information. So I think having that POCUS tool obviously is helpful. You know, all ICP crisis happen at three in the morning or seven at night, but you can use formal diagnostic TCDs. And then another question came up. What are some resources for learning neuro POCUS? Well, the biggest resources, the advanced ultrasound course coming up in the summer. SCCM has added neuro ultrasound as of last year, which I'm really grateful for. And the neuro ultrasound chapter was also added as the introductory chapter for the second edition of the Critical Care Ultrasound book. And if you look up, there are also other transcranial Doppler and neuro ultrasound CME opportunities available. And then I just want to go back and comment on, sorry, just real quick. I think that, you know, for like myself, who doesn't do a lot of neuro ultrasound, I was really fascinated by your cases and the diagnostics that I learned. And it reminded me that, well, why don't I learn how to do it or at least start getting more proficient about what that means? And so I just wanted to make the point that if at your facility you don't have, or you don't feel that you are able to do all these applications of ultrasound, but you have diagnostic or comprehensive testing or radiologic testing available, while you get those, compare that to the point of care studies that you're getting and compare your images, assuming they're at the same time and, you know, intervention scope, that kind of thing. I think that helps build confidence, helps you see the standard that is expected, even in point of care. Like in your case, Arne, you talked about how you did the TCD, you saw the low resistance, and then on the comprehensive, that's what they saw as well. I mean, that's great confidence that you've got the right diagnosis and that you're making the right. And I do that with lung and cardiac, all my point of care cardiac, if I get a comprehensive, I look at them as well. So I would just advocate for not only doing the training with SCCM, getting the resources, but go ahead and do the point of care and compare it to diagnostic testing. If that capability is available, I think you'll get good benefit out of that. That's a great point. Chris, your thoughts? Yeah, no, actually that's one of the requirements for my trainees is the second they order an X-ray, I say, go and do the ultrasound, or the second they order an echo or a lower extremity Doppler, I ask them to go do it. The other thing I wanna go back to is for any, one of the things you did on your cases that I really like is talking about the use of diastology. And I know a couple of years ago when we introduced our advanced workshop locally, I struggled a little bit with trying to explain why it was so important. And a lot of our trainees who may have been coming from outpatient, thinking about diastology in the sense of LVH and longstanding hypertension, how does that apply to me in the ICU? And I just wanted to say, I think your cases did a really good job of showing how you can use the diastology to look for evidence of increased afterload resistance and as a surrogate for wedge pressures for cardiogenic or non-cardiogenic pulmonary edema. So I thought that was a really good example in your cases. Yeah, and I just wanna make a comment. I feel like when I first started learning echo, it was all about the LV and LV is important, yes. And then we kind of started talking about the forgotten ventricle, right? Which was talking about the right ventricle and all of the applications and utilities. And now we realize that systolic function is not everything. We have got to understand how the heart relaxes and how the pressures that it takes to really, again, comprehensively understand it. I use it very frequently now because I now respect fluids as a drug. And in order to be able to use that drug effectively, I need to understand maybe better than some of the later markers what's happening. So I encourage people to get in with that knowledge. I think there's growing evidence that it can be very useful for us, not just outpatient, but in the ICU active patients. Yeah, and especially because echo is really one of the few ways to even assess diastology. So that's a really great marker. And I think identify your local resources, identify local people who are doing these diagnostically and make friends with them. I think once you start raising the awareness of clinical applications, it's only a matter of time you'll find it useful to do it yourself. So we ran a little bit over time. Any parting comments, Chris? No, I think we answered all the questions that were written in and these were great cases, guys. Thank you very much. It was a pleasure to share this time with you. Thank you. You know, any parting thoughts? Same, I mean, I have my hashtag now or one thing I say is just focus it. You know, instead of just do it, just focus it. Meaning that it's a tool, it's there, it's in our space and our patients deserve for us to be really good at it so that we can apply it and use it for them when appropriate. So you got to get the training. And I, again, thank you guys so much for the cases and the re-education on the point. Well, as a parting thought, thank you, Chris. And thank you, Inyo, for making the time and putting together such a great lineup of not just educating us about use of focus and shock, diuresis and titrating mechanical ventilation and letting me have the opportunity of showcasing my perspectives on your ultrasound. And I hope that we guys gave you at least enough food for thought to try it out and integrate focus in your day-to-day care. I really appreciate everybody's time attending this Congress and please stay safe. Please stay well and keep ultrasounding. Thank you guys. Goodbye. Thanks guys. Take care. Bye.

point-of-care ultrasound

POCUS

clinical applications

evaluating shock

resuscitation

procedural guidance

mechanical ventilation

diuresis

acute respiratory failure

lung pathologies

diaphragm function

left ventricular filling pressure

cerebral edema

limitations

case presentation