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The Beat Webinar Series - Episode 1 - Management o ...
Episode 1: Management of Electrical Storm
Episode 1: Management of Electrical Storm
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Hello, I'm Michael Lloyd, professor of medicine at Emory University, and today we are going to talk about the management of electrical storm. I'd like to focus more on a review of the basic practical tips with an update on some exciting emerging therapies. When I say electrical storm, it's important to first define what exactly I am talking about. Just like a storm in meteorology, definitions are difficult and variable from person to person. There have been definitions such as three or more sustained ventricular tachyarrhythmy events within a 24-hour period, immediate recurrence of ventricular arrhythmy events after a treated episode, so much ventricular ectopy and non-sustained VT that it exceeds sinus rhythm, but I think the most useful and widely accepted definition is a recurrent greater than three clinically actionable ventricular arrhythmia cluster within a 24-hour time frame. So this encompasses ICD shocks, pace termination, salvos of symptomatic sustained VT, or even high-density non-sustained VT. Dr. Passman, in a nice website-based review, outlined the arrhythmia makeup of an electrical storm, and we can see that the majority are monomorphic VT. Some are VF, some are a combination, and some are polymorphous VT. Guerra and coworkers constructed a very nice meta-analysis on what exactly an electrical storm predicts or portends, and while some groups may disagree, this nice analysis showed fairly definitively that electrical storm, here right to the line of unity, is in fact associated with increased mortality, and most believe that this is associated with a roughly three-fold increase in mortality compared to the non-electrical storm counterparts. Okay, so let's get into some practical tips. First, I'd like to review some baseline assumptions of the talk, and the first is that the white complex tachycardia is already confirmed to be VF or VT. Second, that if the patient is coding, we're following basic ECLS guidelines. And third is that you're being consulted as the clinical cardiac electrophysiologist, and some initial measures have already been attempted. So this, I would like to focus more on the truly difficult, incessant VT-VF that doesn't respond instantly to, say, in the utero. With that in mind, let's begin. Because electrical storm is an urgent, emergent clinical event, it's important to take clinical action before all the information may be gathered. I've summarized these important common denominator actions as correct, support, and sedate. In this slide, because in the event of cardiogenic shock or low output state, we may not have time, and it may be urgently needed to do these before you know exactly what's going on. In the correct column, what I mean by that is electrolytes, potassium, and magnesium should be kept at higher levels. Do we have a thyroid stimulating hormone? Sometimes missed, but shouldn't be. Do we have a urine drug screen? And bear in mind that maxillitine, if the patient already has had a history of ventricular events, maxillitine will cause a false positive for amphetamines. But that aside, urine drug screen is important in your initial evaluation. And finally, is the patient actively ischemic? Now, I will tell you, most of our ischemic cardiomyopathies that have electrical storm, when we send them to cath, it usually results in nothing. However, and most of the time, if there is an electrical storm in the setting of ischemia, it is obvious, there's ST elevation. However, a coronary angiogram is recommended in those who it is suspected. By support, I mean hemodynamic support. Inotropes, of course, may worsen electrical storm because of their inherent arrhythmogenicity. So mostly we're focusing on mechanical. And I mean interaortic balloon counterpulsation, impella may be not favored because of ventricular ectopy causing events, and ECMO. The patient will be anxious. And sedation is an important initial step before you know the entire story because it interrupts the positive feedback loop of increased sympathetic tone after the pain and anxiety of defibrillator shows. Here's some data to support this initial correct support sedate step. This is a nice meta-analysis by Ling and coworkers from China showing a very favorable effect of Presidex or dexmedetomidine compared to propofol or morphine on ventricular arrhythmia events favoring dexmedetomidine consistently. Martens and coworkers from the French group also showed that in 116 patients with refractory electrical storm, rapid sequence induction followed by sedation, either with propofol or midazolam or sed, and an opioid resulted in a 47% acute response within 15 minutes, which is better than most of anything else we have. So sedation is critical, and interruption of that sympathetic positive feedback loop is critical. There are other ways to do it, and we'll discuss those later. A brief word on ECMO, as many hospitals are growing these programs and using them with frequency for a variety of disorders. Here's another series from Dr. Martens' group showing 26 patients with refractory ventricular fibrillation, and this is a bit confusing, but what it shows in panel B here is that mortality is about 50%, and those that had intermittent VF or VT did much better than those with truly refractory VF. And panel A here shows non-survivors and survivors, and anything that is non-white, which is predominantly everything after time zero after ECMO has been initiated, indicates the arrhythmia storm ends and then subsequent hospitalization begins. So this is a feasible approach, and most people were able to come off ECMO in a relatively timely fashion. Once those initial stabilization steps are in place, it's now time to triage and think about underlying causes. Dr. Green and his colleagues from Canada reviewed what they believed were the underlying causes in their series of ES electrical storm in 40 patients. About a third were unknown, a third were due to psychological or medication changes, and only 15% were from new or worsened CHF. This makeup may not be applicable to all institutions, and certainly at our center, worsened or decompensated congestive heart failure accounts for a large majority of our storm patients. So this is a highly institution-dependent demographic. So let's go to step two. After we've corrected, supported, sedated, now we're at the point of our initial take a step back and evaluate. And many schema have been developed for this approach. This is one of many that we tend to use. And our first branch point is the presence of structural heart disease, because the prognosis and therapies vary the most in electrical storm patients among those with poor hearts and those with, compared to those with structurally normal hearts. If a structural heart disease history is present, which is the vast majority, we then make a careful determination on if they are having active low output symptoms. Are they in shock or showing signs of end of organ hypoperfusion? And I'm not referring to deterioration during the ventricular arrhythmia episodes themselves, but is this underlying low output? And there's always an argument and a debate in these instances as to whether or not the storm caused the low output or the low output caused the storm. But I would submit that it doesn't matter. And aggressive hemodynamic support, predominantly in the form of mechanical support, should ensue at this point regardless. After that has been addressed, then we can go to basic medical antiarrhythmic options and device troubleshooting, which I'll mention. Because what you don't want to do is treat the arrhythmia first and hemodynamics later if there's an underlying low output as the cause. Because you will be burned in that order of steps. So we favor hemodynamic support followed by medication and device troubleshooting. Changing gears now, electrical storm in the structurally normal heart is entirely different animal altogether and is critical determined early rather than pouring amiodarone in everybody. Because some treatments are not only different for these specific subgroups, but are diametrically opposed to what you would do in someone with structural heart disease. And they get specific medication and possible device treatments. And then after this, we have the unfortunate people who continue to storm, which necessitates the escalation of therapy. And this is most often when we're called, and we're going to go into this in a minute. Let's first talk about basic antiarrhythmic medication and device troubleshooting. The two tiers of our initial storm therapy. For any arrhythmic therapy, the magic trio of beta-blockade, amiodarone, and lidocaine are the therapeutic mainstays. I indicated earlier that there's limited data available for most of our therapies in this discussion. The exception lies for both propranolol and amiodarone, as both clearly have fairly good data showing superiority over their rivals during the control of ventricular arrhythmia during electrical storm. Lidocaine is a third player and admittedly it is a weak antiarrhythmic, but I include it in our armamentarium because it has a demonstrated safety in its concomitant use with amiodarone, and everyone knows amiodarone plus lidocaine. And it is actually fairly good at binding to ischemic tissue, and we tend to favor this drug in ischemic substrates. And these of course are all temporary. As you all know, they will have side effects, especially lidocaine because it is not a question of if but when they will become lidocaine toxic. So these are short-term medications. On the right side of our slide here, we show a nice picture from the randomized trial by Dr. Chatzidou and co-workers from Athens showing a comparison of propranolol, 40 mg Q6 in blue, to metoprolol, 50 mg Q6, not a small dose, showing how well propranolol did over metoprolol in controlling ventricular arrhythmic events since ICU admission compared to propranolol. And this is probably because of its non-selective nature. People forget about this drug, but it is useful. And of course, Dr. Cowie, Dr. Scheinman, and many others have excellent data in demonstrating amiodarone's clear superiority for suppression of ventricular arrhythmias. Let's talk about tier two, which is device programming. I want to be clear. This does not mean implanting the device, which is clearly wrong in the midst of storm, but rather reprogramming or troubleshooting those with devices in the modern era. The far majority of patients being evaluated for electrical storm have a device implanted and allows them to survive to hospitalization. So there's a significant survival bias, and that's why most people with electrical storm that we see will have devices. I'd like to show two tracings from this very month on the arrhythmia service presenting to our hospital with electrical storm. This 12 lead is from a patient with a HeartMate 3, and you can see the LVAD artifact here who presented with repeated pause-dependent polymorphic ventricular tachycardia due to new onset AV block. Lots of Ps, no QRSs. His defibrillator, which was a dual chamber system, was programmed vi40, which is an appropriate pacing program. But when he hit block, then we had trouble with pause-dependent long QT polymorphous VT. So simply interrogating his device, increasing the base rate on his device, spared him days in the ICU and on excess amioroan, et cetera. And here I show some extraneous data just to show the April 3, 2022 hot off the presses case. Later that week is a Boston Scientific single chamber system, again, showing pause-dependent arrhythmia storm. Here's vPACE, vPACE, vPACE, vSENSE, vPACE, long, short, off to the races, resulting in ATP attempts, and finally, shock. This vSENSE episode was from over-sensing of myo-potentials, and simple reprogramming of sensitivity and increasing base rate averted this. Finally, a strip from Dr. Sweeney's very important article on the role of pacing algorithms that minimize ventricular pacing and allow for long, short sequences shows, again, more precipitation of arrhythmia. So avoidance of long, short, avoidance of bradycardia is an easy step in your device troubleshooting for those with electrical stroke. This is an older EKG from a patient with electrical storm several days after CRTD implantation. And this represents a specific subtype of electrical storm issue that's encountered frequently enough to be recognized in the literature. And this is CRT-induced electrical storm. And you can see the 12-lead showing a biventricular-paced QRS, not the narrowest I've seen, with some artifact, an ectopy here that appears epicardial and certainly could be the placement or near the placement of the LV-Lead. By simply disabling his biventricular system, we were able to first unmask a much narrower QRS than was afforded to him by the biV. And many times can be an antiarrhythmic shock-sparing measure when you have someone, especially recently, who is storming for no reason after a CRT implant. It's always a tool to consider disabling CRT in those with storm when other measures have been unsuccessful. And indeed, Bradfield and Dr. Shivkumar in this nice discussion analyzed this and suggested that the mechanism may be that the LV-Lead is amidst epicardial scar or near epicardial scar. And this is placed in zones of slow conduction, as evidenced in the long stimulus to QRS. And they found that exit sites during their VT studies and sites of successful ablation were in fact close to these LV pacing stimuli, suggesting there is a rhythmic tissue near this, which may account for the cause of this seemingly paradoxic phenomenon that we observed. So in summary for the general strategies around device reprogramming during electrical storm, first we ensure that pacing is at a fixed rate to avoid long short sequences. We then disable ATP if it's failing to terminate, or in many cases, accelerating the arrhythmia to a more unstable rhythm leading to shocks. We extended detection times and clinically tolerated arrhythmias. And we take that to the extreme sometimes, especially in LVAD patients or in people with very incessant, slow, hemodynamically tolerated VT to avoid repeated shocks and escalation of that sympathetic positive feedback loop. Well, what about those without preexisting structural disease or devices, these specific subgroup folks? This group of electrical storm disorders is rare in our center, but requires very tailored therapy that, as I mentioned, was often the opposite of what we would do in a heart failure patient. Diagnosis of and troubleshooting of this group relies heavily on the resting EKG. So let's talk about a few of these. The first is brugada, and to a lesser extent, early repolarization syndromes. This is not going to be a brugada talk, and we all know the characteristic brugada pattern on electrocardiogram. These patients can have electrical storm, and the medical treatment of choice is isoproteranol because it does prevent that unchecked ITO current. Temperature correction, as we know, hyperthermia can cause arrhythmia in brugada, so temperature correction is important. Quinidine, because of its blockade on the transient outward current, is very important in this disorder. And finally, targeting outflow-tracked late potentials, as shown in this slide here, taken from the Journal of Arrhythmia, is an important strategy once the storm has been somewhat quieted. The next specific subgroup I'd like to talk about are the sarcoid or inflammatory subgroup. Any inflammation of the myocardium, be it from sarcoid or myocarditis, can be suspected with the use of elevated biomarkers in the absence of overt coronary disease or epicardial coronary obstructive symptoms. This nice series by Kefiel and colleagues out of London described the use of really not heroic doses of methylprednisolone, 40 milligrams IV, for a few days. And this obviated the need for ablation in sarcoid, which we know has a very high recurrence rate and is a very difficult procedure. So steroid is in your armamentarium when you are suspicious of an inflammatory myopathy. Now, sarcoid and inflammatory electrical storm many times will not have structurally abnormal parts, and I grant that. It is a specific subgroup. Many times in people with new-onset severe cardiomyopathy, especially with elevated biomarkers, we will empirically try immunosuppressive agents if nothing else works. Long QT is of course another talk in itself. The mainstays of long QT syndrome medical treatment are beta blockers and when the rates are too slow, beta blockers plus pacing. The genotype, if known, should guide therapy as we know long QT3 responds well to flecainide therapy. Most frequently on our center's electrical storm is a first presentation of long QT and the long QT syndrome is a result of a combined underlying channelopathy in addition to one or more offending agents. Toxin evaluation is critical and removing long QT offending agents is important. Sympatholysis by means of beta blockade or by neuromodulation, which I'll discuss in a minute, is very useful in these patients as well. I'd like to mention idiopathic ventricular fibrillation from short coupled variants of ARVI or hisprokingy triggers. This is an interesting cause of storm and can cause the most severe storms I've encountered. And here on the electrocardiogram shows an early onset PVC well before the T wave triggering out of the Schutz VF. These are very responsive to quinity and are often unresponsive to standard measures. They respond well to sympatholysis as well and when the triggers are present, the triggering PVC ablation, either hisprokingy or early coupled RV outflow tract or inflow tract sources can be triggered and are useful. This 12 lead shows bidirectional VT and the bidirectional VT should call the mind three things for the electrophysiologist. CPVT, first and foremost, catecholaminergic polymorphous VT, digitalis intoxication and long QT7 or Anderson-Towell syndrome, that's rare. Exclude digitalis toxicity, beta blockade for CPVT is the most important therapy. Flecainide is a critical adjunct to beta blockers in CPVT storm and of course sedation. Anything that suppresses sympathetic tone is important in people who are storming from this disorder and frequently simple sedation enough is enough to settle the sympathetic surge and to quiet the storm so that you can go on for more definitive treatment. The final specific subgroup I wanna mention is that of our LVADs. This is a challenging and increasingly common electrical storms subgroup. These patients have late stage substrate and they're challenging. They have difficulties obviously with epicardial approaches to ablation and are, as I said, quite late stage. The minute we have an electrical storm with LVAD patients, we are on the phone with our LVAD techs and our heart failure specialist troubleshooting disorders. These two images here show a decompressed left ventricle, overly decompressed with an LVAD cannula banging against the wall or sucking, slamming these walls against each other. Suction events can cause a cardiac arrest cause ventricular arrhythmia storm. And by simply lowering flow rates, we can sometimes alleviate the arrhythmia. We have to exclude pump thrombus and low outflow states, which will be present and apparent on the monitor because this will acutely elevate ADP and be a cause of low output electrical storm. And as I said, ablation is difficult. We have attempted endocardial ablations in these patients. Epicardials are challenging. And the final thing I should mention is that in contrast to ECMO and other hemodynamic support bridges, LVAD is usually not the answer for a cure or an alleviation to electrical storm. Those who storm before LVAD tend to storm after LVAD in our patient cohort. So let's now assume all of that's been done. And this is where most of us get involved. What if the storm continues? And so I wanna finally discuss therapy escalation measures, which represents maybe the least well-studied, but most often requested set of therapies from our colleagues. I again need to mention that the data behind these are limited to cohort studies, observational studies, case series studies, and there is very little in the form of randomized or controlled studies in this. And this needs to be kept in mind when we mention these somewhat compassionate use or very new, or unfounded therapies. I intentionally avoided most novel medications because there's a laundry list, including rinolazine, which may be useful, and a host of others. Dilantin, you'll hear your more senior attendings mention. I will mention, however, the use of class one agents as a whole in electrical storm has been shown in a contemporary cohort to be associated with a higher mortality. And I would caution against these mixes and matches of procainamide, quinidine, amiodarone, as I think these are anecdotes and not useful as a general rule. I will mention this small study from Dr. Sindra Ferrer-Gonzalez, which used ventricular, in our case series of ventricular fibrillation refractory to standard measures in those with ischemic unrevascularized territories. I butylized on a scheduled fashion, and they showed a substantial number of shots pre-ibutilized with a marked reduction post-ibutilized after several doses of one milligram every several hours. And this is something that we have used with success as an adjunct to our usual amiodarone plus lidocaine. Of course, this is not the drug to pick in long QT storms, but those in unrevascularized refractory V. Next, probably the biggest realm of treatments that are non-medical and non-ablation for electrical storm are that of neuromodulation. Many series have been published with reasonable reduction in ICD shots with this technique. And during electrical storm, the easiest method to determine whether sympatholysis will be successful is the installation of bupivacaine and steroid into this middle cervical ganglion right above the vertebral process of C6 under ultrasound or fluoro. And this can be done very safely by your pain and anesthesia colleagues or by yourself if properly trained. And if there is response to your arrhythmias, and many others have shown a substantial response in arrhythmias, of all comers, defibrillations with no change in ejection fraction to this. If there is a response, you can then go on to ask your thoracic surgical colleagues to either remove the left sympathetic cervical chain, which innervates the ventricles predominantly, or you can have your interventional colleagues cryoablate this chain. I recommend a temporary blockade first to see if it works during storm, which can be done at the bedside. Dr. Markman and coworkers have employed a novel magnetic stimulation device to non-invasively do the exact same thing. And they've shown that over the 48 hours after this transcutaneous magnetic stimulation, they had substantial reduction, nine versus five ventricular arrhythmia episodes, and much less ventricular tachycardia. 41 external shocks were performed prior to treatment and none, importantly, were required after this treatment. So we'll wait and see if this pans out in future larger scale studies. You can also instill bupivacaine via an epidural catheter and take this focal or targeted area of the stellate ganglion out of the picture and simply administer spinal anesthesia between columns T1, T2, or T2, T3. And indeed, Doctors Ho and Shivkumar have published their series showing this method, which resulted in a substantial reduction in these or each patient's pre-thoracic epidural anesthesia to post in both ventricular tachycardia episodes and the number of shocks. And so this is something that can also be done by at the bedside and perhaps as they indicate in their trials, their series, save prolonged intubation sedation and get you to a more definitive step or let the storm settle after treatment. And it's not just the sympathetic chain in this neuromodulation. Gargan coworkers did a beautiful meta-analysis summarizing the effects of renal denervation, renal arterial denervation as seen in the antihypertensive trials. And they showed a short-term ventricular arrhythmia recurrence rate reduction of 63% and a low all-cause mortality. And you can see these panels here, substantial significant reduction in VT, reduction in ICD shocks and reduction in anti-tachycardia piece. But the most common request by our consulting colleagues is can we ablate this? And our reflex answer is yes. And in this large series as part of the larger VT ablation cohort, we see a, and this is the Della Bella group we see that those with a history of electrical storm in 676 patients, these are, this is a large series in those with prior electrical storm. Those that do well with ablation are those that were rendered non-inducible for non-clinical VTs or any inducible VTs. Those that had non-ischemic cardiomyopathy did less favorably. And so we can use these as a risk markers for who we may take to the lab. I wanna be clear that these ablations were not carried out in the throes of electrical storm, but those with a prior history. So it may not be applicable in the acute treatment, but after the storm has passed, after the storm has passed, after the dust has settled, we might use these data to guide our decision-making for who we take to the ablation, the EP lab. I am not going to mention ablation because that's in other lecture series in this format. Probably a more realistic group is published by this Cleveland Clinic group. And these people were predominantly taken on intraaerobic balloon pump. They were actively in decompensated hemodynamic states. They comprised 21 patients. Most were ischemic, average age 67. And of these 21, 17 were able to be liberated from mechanical support, although two died. Many were successfully ablated and 15 were discharged alive. These are not fantastic, overwhelming numbers, but should give you some perspective on how a very, very good group, the Cleveland Clinical Group, how they fare on ablation of acute decompensated VTs. So what's all this mean? Well, clinical features that may favor ablation in the setting of electrical storm, I believe, and the data would support, would be monomorphic ventricular tachycardia, an underlying ischemic substrate, PVC-induced arrhythmia that are from unifocal PVCs, and maybe letting the initial arrhythmia storm settle, but people that have had a high risk of recurrence should be taken to the lab. There's been a lot of talk about stereotactic body radiation therapy. This is the great new hope of VT treatment because it's non-invasive. They're taken down to the lab. They get one shot of 25 rays of radiation to a target that you can outline. And it's been employed very nicely in the seminal work by Drs. Kukulich and Thompson-Robinson, excuse me, at the Washington University with astounding numbers, 100% dramatic results. During refractory electrical storm, the results have not been so good. This is a beautiful cartoon by the Harvard Group showing the size of the circle representing sample size, the X-axis representing target volume, how much was radiated, and those with decompensated or refractory arrhythmias here down in these lower three spheres are much less effective, and the results are much less modest than those initially described. So the answer or the truth as a whole may lie somewhere in between, but it is an option for those who are undergoing repeated therapies from ventricular arrhythmias. I would like this, I'd like to bring this all home now with maybe a busy, but hopefully informative cartoon. On the X-axis, I have chance of success of electrical storm, of getting out of the storm favorably, and on the Y-axis, I have the relative frequency of occurrence at our center, so that the patients that we see most often at our facility are not ischemics, probably with low output or shock. They've had many procedures, and are now in VF storm or polymorphous storm. These are the most frequent, but also we have the worst outcomes. The next most frequent are those with ischemic myopathies, no revascularizable options, and monomorphic PT. These are very favorable outcomes and relatively high frequency. Those with ischemic cardiomyopathy, no revascularizable options, or those have been exhausted, and refractory VF are also fairly common, but have much less favorable outcomes. And finally, those with LVADs and storm with numerous ventricular tachycardia morphologies are thankfully not as common, although their frequency are increasing, and have low chance of a long-term resolution. The blue, yellow, and green spheres represent ablation, stereotactic body radiation, neuromodulation, as our therapy escalation groups. I've denoted for each of these groups by relative size of the spheres what we tend to lean towards most, so that in these patients, we are heavily leaning towards neuromodulation, the things I've discussed, and towards stereotactic body radiation more so than ablation, although ablation does have a role. In the ischemics, we're leaning heavily more towards the ablation and stereotactic body radiation, and less towards neuromodulation. The LVAD patients, neuromodulation can be helpful, and targeting substrate, since epicardial is important, with stereotactic radiation has been useful. And finally, those with VF in ischemics, we use a relatively high proportion of stereotactic radiation. And neuromodulation. And some ablation, more so than non-ischemics, but certainly it's not our go-to measure in the acute stage. This hopefully gives you an idea of what we're looking at, what the frequencies are, what our outcomes are at Emory, and what we favor in terms of the three therapy escalation groups. Finally, I need to mention the importance fact that all of the heroic efforts that we do may be useful, and they may help, but it's vital to remember that just like in weather, storms pass, so that non-controlled descriptions of these therapies may be obfuscated simply because of the passage of time. So controlled studies are needed. The second important aspect that we often forget with the passage of time is that psychological sequelae of these patients can be severe, and medical treatment in addition to psychotherapy or counseling is often warranted. This nice paper that I've referenced here shows risk markers for psychosocial distress. These are younger patients, they tend to be female, and may have pre-existing psychiatric diagnosis, but I think that almost all of our patients have PTSD, and that should be addressed in your follow-up once the storm passes, either from our therapies or simply from the passage of time. In summary, I hope I've imparted upon you that electrical storm is a heterogeneous event, and it's associated with approximately a threefold increase in mortality. Proper triage of the therapies that we use depends on the correct initial characterization of hemodynamic and structural state of the heart, and I hope my schema is useful in addition to other very nicely done schemas in the published literature. Most available therapies that I've mentioned in this talk have little randomized control data for their use. The mainstays include medication and device reprogramming. So before we go to these fancy stereotactic radiation considerations, or before we take them straight to the lab, remember that medications and some minor device adjustments are critical and should be your first priority. So let's go to the first step. Ablation, neuromodulation, and noninvasive radio ablation represent important potential therapeutic options, and hopefully randomized data will support their continued use and develop them and enhance them. I am happy to provide my email and my contact information here at the Emory University Hospital and our section, and I'd like to greatly thank the Heart Rhythm Society for allowing us to talk about this important topic and welcome questions by email. And thank you very much.
Video Summary
In this video, Professor Michael Lloyd from Emory University discusses the management of electrical storms, which are recurrent and severe episodes of ventricular arrhythmias. He begins by defining electrical storm as a recurrence of greater than three clinically actionable ventricular arrhythmia events within a 24-hour period. He highlights that electrical storm is associated with increased mortality, which is believed to be around three times higher compared to non-electrical storm patients. Professor Lloyd goes on to discuss practical tips for managing electrical storm, which include correcting electrolyte imbalances, supporting hemodynamics, and sedating the patient to interrupt the positive feedback loop of sympathetic tone. He emphasizes the importance of taking action before all information is gathered due to the urgent nature of electrical storm. Professor Lloyd also discusses various treatment options, including medication, device troubleshooting, and neuromodulation techniques such as sympathetic ganglion blockade and stereotactic radiation therapy. He concludes by mentioning that while these therapies may be helpful, controlled studies are needed, and psychological counseling should be considered as many patients experience severe psychological distress following electrical storm. Overall, Professor Lloyd provides an overview of the current understanding and management strategies for electrical storm.
Keywords
electrical storm
ventricular arrhythmias
management
mortality
sedating
treatment options
neuromodulation techniques
psychological distress
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