Making Sense of Syncope

Ajouté : 2026-05-28

[00:00:00]Good afternoon everybody.

[00:00:02]You all are welcome to the third session of lunchtime feeds organized by Sri Lanka College of Internal Medicine. My name is Dr. Rohit Amaritana specialist in internal medicine the moderator of the today's session.

[00:00:19]Lunchtime feeds is an 1h hour online session.

[00:00:24]The speaker is a specialist in medicine and address clinical medicine with current updates.

[00:00:32]Uh at the end of the lecture we have 10 minutes to discuss questions from the virtual participants. Please send your questions to Q&A box.

[00:00:44]uh from today session we share two true or false questions before the sessions as and at the end of the sessions so you can go to the Q&A box and get the the links please answer the questions before and after the session and submit to get your CPD points and CPD certificates Now I would like to invite Dr. Madwan Hetaraji the president of the Sri Lanka College of Internal Medicine to address the participants.

[00:01:23]Over to you Mad.

[00:01:24]>> Uh very good afternoon to all of you. Uh thank you very much Rohita. It's it's a great pleasure to see you all uh with yet another SLCM lunchtime feed session and we are indeed privileged to have uh today Dr. Kiti Bandul consultant cardio electrophysiologist at national hospital candi delivering today's lecture of making sense of sinko uh it's actually a topic with which is uh relevant uh to us clinically immensely and um it's it's of practical importance as well to our day-to-day practice. Uh the the session truly reflects uh uh the spirit of our theme actually a decade of inspiration a future of innovation and by revisiting core clinical problems like sync copy through a more structured and evidence-based uh practical lens we continue to strengthen our clinical reasoning while embracing the evolving knowledge which is an essential step towards meaningful innovation in patient care and I would like to thank Dr. Amarra for coordinating uh and moderating this session today whose guidance will undoubtedly enrich uh today's discussion as well as ensure a highly interactive session and I would like to express my gratitude to my uh executive committee Dr. Ysef Dr. Anga who are the joy joint secretaries and Dr. Dura honorary joint treasurer for their time uh behind the scene efforts as well as our office team Dr. Tishila, Dr. W and Dr. Nusaha along with Mrs. Chin Tani and my heartfelt gratitude to the Gates team as always for their excellent clinical technical coordination in making this session session possible. Finally, I thank all of you for the participants for it's very uh it's uh uh I'm actually happy to see the uh continuous engagement and uh your commitment to learning and your presence is actually very important for us to continue these webinars. And a gentle reminder again we from today onwards we'll be uh having a pre-est questionnaire and the same questionnaire will be uh asked at the end of the lecture as well. So this is the QR code for the pre-EST. Please scan this and answer the questions now and at the end of the lecture we'll take this out and after the lecture it will be a post test questionnaire. please answer it also and then make sure you will submit these to get the CPD certificate which would be mandatory from here onwards for all our webinars. So I'm actually uh uh uh expecting that you would adhere to this so that it will be a fruitful uh learning uh endure. Uh and thank you again very much for everyone of you for your for and uh I invite you to engage through the discussion and learn uh what is new in syncopy. Uh over to you Rohit for formal introduction of Dr. Kitri.

[00:04:37]Thank you.

[00:04:41]Thank you Dr. Madwanti. Uh let me to introduce uh today's speaker Dr. Kiti Dula consultant cardiac electrophysiologist National Hospital Candy.

[00:04:57]He is going to talk on making sense of syncop.

[00:05:02]Dr. Keith B. Dulver MBBS MD was graduated from faculty of medicine University of Colbo 2009.

[00:05:15]He completed his post-graduate training at PGIM Colbo and offered cardiac rhythm management fellowship from Royal Pepworth Hospital Cambridge Biomedical Campus, United Kingdom. He served at teaching hospital Kurunagala before taking up a specialist post at National Hospital Candi. His main areas of research interests are sudden cardiac death and syncopy.

[00:05:46]Over to you Dr. Kiti.

[00:05:50]>> Very good afternoon on to all. Uh I take this opportunity to extend my sincerest gratitude to Dr. Maduantiari the president of Sri Lanka College of Internal Medicine and her council for arranging this type of lunchtime talk in order to expand and uh innovate uh uh knowledge among colleagues at the same time would extend my warm invited me to deliver this lecture. Uh so this to uh as a practicing electrophysiologist for the last uh uh few years uh syncopy had been one of the major clinical problem that I have encountered in my practice and uh and then I realized uh even though the the problem is big sometimes this simple problem get neglected u um not only because uh lack of knowledge but as well as the the clinical burden of the rest of the work that we all have. But uh um I felt this is one of the important clinical signs or symptoms as a matter of fact uh which uh had which leads to farreaching uh consequences in terms of individual p personal level as well as uh as a whole to our national health system. So a lot of my the patients that were referred to me come in from uh internal medicine specialist uh other specialists like neurologist, cardiologist even our surgical colleagues. So as as one of the largest center in the country candy national hospital electrophysiologist of who are present with copy uh a given year. So I felt creating awareness about syncopy is actually one of the clinical need uh with utmost validity. Therefore I thought of sharing my experience and knowledge about contemporary management of uh syncopy among our colleagues.

[00:08:04]So the today's disposition I wanted to make this uh presentations uh sort of init that are important to clinical management and moving from that how do we assets or set about a patient who's presenting presenting with a similar symptoms and giving a strong weight on how do we restratify how with which patient Do you think having the highest risk of unnecessary consequence of having a syncopy as against a person who is tends to have a fairly benign cause then we'll discuss about some of the commonest causes and finally uh lead into the treatment options.

[00:09:02]Before talking about syncopy, I wanted to uh draw your attention to few other topics that are directly related to the the topic that we are talking.

[00:09:13]Um little bit of philosophy the this American physician George Lber has put put this in universal problem that we all is actually permanent sessation of all life function. uh whether we ex exist after death is just a it's a a matter of philosophy. Uh but there is no scientific indication whatsoever. Uh so he thinks that death is not the enemy. The human death is normal. We all agree. We all die. The real enemies are actually the premature death, the disability, the pain, human suffering and the prolong of prongation of death.

[00:10:01]So all the rest is mostly noise.

[00:10:05]So you might wonder why I talk about death to begin with because death is the end. But you will realize during this present course of slides that uh syncopy and death is almost simultaneously on the same course.

[00:10:25]So as we know that everyone would die but who after going through or analyzing heap of data not only individual, personal, medical and economical uh data as well.

[00:10:49]So WH thinks that anyone who premature death and apparently is a significant global health problem. So uh preventing premature deaths does not necessarily mean anyone who lives beyond 70 is unnecessary.

[00:11:09]uh you would understand the of it. uh but anyone who happens to die less than 70 years of age product life is actually they all interlink to one another and there's important uh new day I wanted to highlight uh 20 in 2024 uh European association or heart rhythm association has declared a new day to uh create or raise awareness about heart health which we call it pulse day which normally falls on first of March of each and every year.

[00:11:55]So in we mo most of the time we talk about diabetes, schemic, heart disease, uh heart attacks, kidney problem, high blood pressure but we never think about we give far less attention to the the very important structure the rhythm of our life the heartbeat or the pulse which drives and everything all of our life depends on on the heartbeat and yet we give very little uh weight to the service it delivers and to to understand the magnitude of the issue you could see that one in three individual is at a risk of significant heart rhythm problem in their lifetime. So this piece of information highlight as to why we should create awareness regarding heart rhythm issues and even more so important in time to come. So this day is actually uh to indicate that uh uh to create an among awareness among normal population to check their pulse and uh especially after age of 65 uh as a regular basis because that can uh lead to recognition of uh serious ious underlying cardiac rhythm issues before they another sudden cardiac death.

[00:13:35]So any death that occurs as a part due to cardiac cause which normally start by sudden loss of consciousness within an hour of acute symptoms. So it highlights the importance that the that is you can see that the the glimpse of sync copy fell into the diagnosis of sudden cardia.

[00:13:59]So anyone who presented with sync copy they are actually at a risk of dying suddenly. So sudden cardiac death is a major global issue. Did you know that three out of four cardiac arrests happen at home away from the hospital and it can strike anyone at any time and in order to understand the gravity of the doomed nature of the uh the problem is only one would one of us if there's 10 of us in here and we all suffer a cardiac arrest we are far more likely to to suffer it at home rather than at the hospital. and only one of us would be able to survive a cardiac arrest outside the hospital. So this raises the importance of uh immediate CPR which can double or even triple the chance of survival. You know that if a cardiac arrest happens to you, you could be counting on someone you love to save your life. It goes the other way. If a loved one of you suffers a cardiac arrest probably you are the one who stand between death and life of that love person. So this would I wanted to create the awareness give the necessity initiative to uh begin the the important talk. So let me bring up some of the cases that I have encounters in our practice to highlight the the importance of the topic of the day. So this is a 20 year old male with a history of 3 months onset daily brief disease spells and disturbed sleep with chest titis and nocturnal sweating. He didn't have a significant past medical history. Family history was completely negative. They had had multiple ECGs done all the time. The ECG was only showing sinus techy episode. A halter was off is a 24-hour ambulatory monitoring.

[00:16:09]And this was one of the halter tracing.

[00:16:13]If you carefully see it, you can see at the beginning the P waves and the QRS complex are there. All of a sudden QRS complexes disappeared only P waves. So this is called complete AV dissociation without an escape rhythm. This is called ventricular stand still. So this patient was developing this uh ECG phenomenon every now and then and when he develops this there's no cardiac outer uh fainting episode. you could see that uh he was even experienced these things especially during night when he was stressed. So the diagnosis was only certain when we did the uh hold. So this is one of the uh uh interesting case patient that I have come across. He ended up receing a pacemaker and his problem was solved. The second case was another I would say somewhat tragic. It's a 24 32 year old general of house officer who was working in a district general hospital developed a dropped during labor room duty. It was assumed to be simple faint but uh easy simp was taken that was all fine. However, he got admitted to the ICU and he was monitored hooked with the halter and this was the whole recording mind.

[00:17:45]Believe me, the the a rather unfortunate nature that even though he was in the ICU, he had this event recorded on his tur for nearly 3 minutes and unfortunately nobody picked this up.

[00:18:00]Nobody picked this up and he he was for fortunate enough that the arithmia resolved on its own. You could see this is called short couple PVC induced polymorphic PT. You can see the QRS complex and the PVC happening right on the T-wave initiating the polymorphic VT. He was degenerated into VF and for his luck he was spontaneously organized into sustained arythmia and resolved and final freedom. So he was in this arythmia for nearly 3 minutes. He was asleep. This has happened early in the morning. Nobody noticed it. this happened and he suffered minor brain injury. He was lucky to survive.

[00:18:45]Uh he eventually ended up needing an ICD. Here's another uh uh interesting case. 7 year old girl who was experiencing reclin blackouts beat unresponsive episodes with jerky movements of arm exclusive at classroom and ground both seated and standing position. spot ECG is echoal eg oa normal we subjected her to a tilt table test uh I'm not sure whether you can clearly see it uh so I will talk about table test in time in in coming slide so she was slightly bloody cardic at rest with a relatively low normal blood pressure she was put to the tilt and heart rate has gone up all of a sudden the blood pressure started to plummeted and she became acy stalled so this is the ECG strip we were taken You can see there there's uh this uh only artifact there's no pways there's no QRS complexes uh in fact there's one QRS complex in the middle so there's patient was in complete asytoic and as we uh gradually monitoring uh we gave atropine and you might see towards the end of the thing the the Q uh QRS complexes started to appear so this was a classic case of astoic uh um uh reflexing copy severe form of reflexing copy.

[00:20:09]The fourth case rather another uh interesting scenario is a 27 year old female who has a history of mital valve prolapse MVP one of the commonest clinical finding we normally see especially in female patients had mital valve regulation as well and she experienced episode of palpitations and prein couple episode just before one week uh before her wedding and she came with a halter and you could appreciate a 12 lead halter showing a nonsustain arhythmic episode. So she was actually diagnosis with malignant mital valve syndrome is one of the novel clinical condition which was which has been there for many decades but uh it has been only nearly two years since this was described it as a syndrome. It's called malignant mital valve syndrome. It normally that condition happens patients with MBP. There had been couple of uh sudden cardiac uh deaths associated with this condition. Actually one of our colleague who also suffered an incident like this and uh uh so this is something something recently recognized condition.

[00:21:30]So this laid the foundation to talk about uh trans loss of consciousness and syncopy.

[00:21:36]So uh consciousness is a complex phenomenon. We exactly don't know how the human brain uh evolve into the maintaining consciousness. So it it's a it's a conceptual thing. Uh we don't yet to fully understand it. It's a complete uh uh uh uh awareness about the surrounding that include perception, cognitions and ability to response. And we normally assess the uh uh consciousness by use of glasco scale.

[00:22:15]Uh so when we define transial loss of conscious or the t it's a state of real apparent loss of consciousness or loss of awareness which comes with four distinct features. The the person is normally amnesic for the period of unconsciousness. It could be followed up with retrograde or antigrade amnesia and the motorone is normally uh gone. So they will have uh loss of motorone or abnormal motorone. The person becomes unresponsive for the period and by the hallmark is it is short duration that is the distinct feature uh which divide it from cardiac arrest.

[00:22:59]Cardiac arrest un unless we intervene it doesn't resolve whereas TLO even if we do not intervene it should recover that is the distinction between the uh uh uh loss of uh TLO or a sync copy uh versus cardiac arrest. So T-lock has a very broad differential diagnosis. Classically uh uh dichromatize into non-traumatic T-locks and T- locks due to head trauma.

[00:23:32]Mind we if someone suffers a T-lock they might there's a possibility of them them suffering or sustaining a blow to the head impact to the head and other injuries. So even our surgical colleagues they need to be aware of sometimes the uh uh the underlying pathology is actually a sync copy that has led to uh the sustain injuries and ended up needing surgical care and and and all these chaos in the midst of all this chaos and primary syncopy might get lost middle. So that is something we need to keep aware. So sustaining injuries even dropping or ro suspiciousness being detected whether this could there could have been an element of syncopy related to this presentation. So what is syncopy?

[00:24:37]Syncopy is a due to pathophysiologically driven by cerebral hyper syncopy is a cerebral hyperusion. So it's rapid onset. So deep short degradation and by definition it should recover spontaneously without even without an intervention. So if we going back to basics of physics phys physiology we understood in our medical school days. So we know systolic blood pressure is a product of cardiac output against total peripheral resistance. So reduction in cardiac output or total peripheral resistance if it happens simultaneously or on its own rights giving rise to sync copy. So is only capable of maintaining its function run out within 4 seconds if the heart stops. So you you can be conscious for 4 seconds in upright position.

[00:25:45]uh once your heart is stopped.

[00:25:50]So cardiac output drops due to rhythm failure or pump failure. We'll discuss the and about these things in details and total peripheral resistant drops due to v was dilotation.

[00:26:04]So in many case the important point that we need to remember is that syncopy is herald by more than one mechanism.

[00:26:12]So breaking down syncopy conventionally we break into three different terms. We call it reflex sync copy, static syncopy and cardiac syncopy. But the novel understanding is such way that we have two separate arm we categorize everything cardiac as cardiac synopy and the rest all the rest is non-cardiac synopy. So based on the eology uh rather than the eology uh division includes giving more focus into the the mechanism leading to the uh uh t. So cardiac V means the primary cardiac uh pathology leading to ser whereas non cardiac means the autonomic nervous system is primarily responsible for causing either presentation or bradicardi presentation. Now the interesting feature is I wanted to highlight is when a sync copy presented with cardia that does it.

[00:27:44]So there due to the departure we call it.

[00:27:52]So uh cardiac synopy is far more common. The probability of a person coming to to have a non-cardiac synopy far far greater compared to a cardioyncopy and out of that even hypertensive phenotype is the commonest one.

[00:28:11]So uh the problem happens there's at least 34% of patients who are presented with sync copy may not be able to uh put it into one single box at the end of the initial ED evolution evaluation that is the problem that's the problem so that that is the percentage of people that would require uh further more elaborative exhaustive undertaking to the nature of their uh sync copy.

[00:28:49]So the how the depth and width of the problem of so at least one of see during their Sir, there is a technical error. We we try to get uh immediately connect corrected right.

[00:30:30]Yeah. Sorry for that. I think you you should be able to hear me.

[00:30:36]>> Yes, now we can hear you.

[00:30:37]>> Yeah. Yeah. Sorry for that. I think all of a sudden connection got lost. Yeah.

[00:30:41]So uh uh we were talking about the prevalence of saying cap you could appreciate the graph that there's bimodal peaks and uh and uh the the prevalence is least when we turn to 20s 30s and then gradually we can see the prevalence is going up and generally the syncopy is common among females would be as high as 50% % uh when we go beyond age of 80. So this will uh give you a glimpse of to the the depth and width of the problem we are facing.

[00:31:20]So why do we so uh need to talk about syncopy is a so we we establish that a syncopy can be indicative of serious underlying health issue because the body has a remarkable ability to compensate for uh one or two you know injuries that happens in the body but body's ability to cope up with compensating mechanism started to uh fall apart and person will start manifesting symptoms. So if anyone experiences syncopy that indicates if something is seriously wrong in that person and as we know we all are people with ego and pride to various text.

[00:32:06]Imagine one of you suffer in a sink of interest of a crowd uh how embarrassing you would find it about yourself. So and the kind of stigma in the society you remember we had a similar kind of stigma uh related to epilepsy but the there had been a huge campaign was done to uh eliminate that stigma around epilepsy.

[00:32:31]See and uh surprisingly I felt that the awareness about efficac is far greater than the awareness about syncopy. We our understanding about syncop is poor. The general knowledge about the community knowledge about the syncop is poor and that has that has been greatly reflected by the fact that most of the time a person who suffer a syncopy would ended up in a neurologic scare. You may have seen it and uh and and sometimes most of the synop there's a 30% probability of synop mis classified as a true synop. So there's a the significant u uh lack of knowledge among the society and I've seen some of the cases especially school children who suffered the blackouts in the in the classroom or or assembly they have been instructed to and forced to not to come to school and leading to significant uh disadvantage to the their education as well. So it's a serious medical problem not only the uh medical component that it comes with the associated psychosocial adverse outcome.

[00:33:38]So education empowers the society to uh understand this problem and take measures and improve the quality of life.

[00:33:55]So you can see some of the real world data indicates that at least 12% and motor accidents those uh has a history of synergy and driving is one of the important area. Unfortunately, still we don't have a uh proper guidance for this. We sometimes follow uh uh European or UK VI uh DA DVLA recommendations.

[00:34:40]Uh so uh syncopy has a significant impact uh implications with driving especially commercial driving is normally get banned uh uh with syncopy.

[00:34:52]So uh many patients uh in our line of work uh who develop syncopy actually depend on their driving skill for to make end meets and and as well as we have the responsibility of uh especially those who drives commercial vehicles. Uh so syncopy has you can understand how seriously the implications are and so we need a proper guideance for uh patients with uh syncopy uh in Sri Lankan setup.

[00:35:27]So we discussed this relationship between synop.

[00:35:36]So we establish this fact that the syncopic can proceed with school. Uh so in the western world one in five deaths uh among individuals between age 20 to 80 die suddenly that's significant. One in five by cardiac arrest due to ventricular arhythmia and the chances of survival is 1 in 10 or 10%. So syncopy as a risk factor for premature death and sudden cardiac death. These uh these studies have highlighted the importance of uh the gravity of sync copy as a predictor of dying suddenly. So those who suffer a cardiac uh syncopy the oneear mortality as high as 30% in some other studies.

[00:36:27]So this one other study that was conducted in ED setup those anyone who with a synopy has 1.13 31% uh increased risk of dying from any cause and 1.27% of risk suffering from uh strokes. Some of the patients who are presenting strokes you may have realized sometime they only complain of syncopy or presynopic. What happens is as we grow older uh uh it leads to the uh drop in blood pressure leading to uh relative underperfion of certain areas of the brain and presenting them as a stroke.

[00:37:10]Uh so the all these data is about you know 30% mortality rate. So if you take 100 people coming to the ED with a syncopy at least one person would be dead by end of 30 days. another four purple persons would ended up having some serious medical outcomes. So this indicates that the severity of the problem and those especially those who are with background history of structural heart disease or heart failure if they present with syncopy that is an serious indication that the compensatory mechanism the body is failing and that person is extremely higher risk of dying suddenly.

[00:37:54]So the syncopy increases the hazard ratio for and the relative risk uh significantly in patients with structural heart disease and uh heart failure cohort.

[00:38:04]Uh so you could see that uh uh normally cardiac syncopy uh reduce the longevity of sing uh of a given person uh compared to other uh types of syncopy.

[00:38:18]So we were talking about the individual impact how the economic burden. So this is uh some of the data from US. So 1.3 million annual ED visits and $2.4 4 billion dollar annual hospitalization cost and 5 nearly $5,000 for average cost per admission and those who coming with sync copy 30% for them of them get admitted and the the the interesting point is 33 billion dollars wasted annually on low yielding diagnostics. So this puts really into the perspective that some of the tests that we do we do not uh calculate the cost of this. So the syncopy is a very expensive you would realize how many investigation we do for a patient who's coming with syncopy and most of the time none of them give us a clue and and to make the matter worse only 9% of syncopy workup yield a positive finding. So, so this will tell the economic impact cover if it translate into uh financial matrix. It's a huge burden to our economy. This is only for the the diagnostic field and uh if you are to mind about the treatment option most of these cardiac uh treatment option that are available for cardiac syncopy is really expensive. So, syncopy is a expensive undertaking.

[00:39:55]So let me give some of the condition that can get easily confused with syncopy. There are several differential diagnosis. neurological conditions like epilepsy, vertebra and uh metabolic conditions like hypoglycemic other hypoxia uh those thing can get get confused with syncopy and and in the middle sometime psychoggenic syncopies pseudocyncopy pseudo seizures can also come up in the mix.

[00:40:26]So this uh 1020 rule high or help us to determine especially the the major clinical problem. I remember even as a uh part one MD selection exam one station was about a person who is giving history and we were supposed to determine which is which. So this rule apparently scientifically backed to differentiate between a syncopy and seizure and so remember this having myioonic jerks does not rule out uh probability of syncopy.

[00:41:02]Normally in a person who develops syncopy they tends to exhibit less uh jerks number of jerks compared to a person who develop actual feet. So more than 20 m injly to be seizure. Uh less than 10 microns likely to be syncopy. But the question is who is going to count this? Uh luckily if you have a witness or a or a CCT camera recording you able to do the counting. So uh sometimes this u uh the eyewitness account may not as reliable as one one want to it to be. uh so I'm not so sure whether this uh this can be very helpful in our setup. So we need to we need to forget the fact that jerk we need to remember the fact that myioonic jerks does not differentiate between syncopy or uh epilepsy.

[00:41:55]So some of the features that are in uh far more uh indicative of a seizure are lateral tongue bite and head turning during an event and prolonged post drowsing confusion and absence of prod.

[00:42:11]So the absence of prod you have to take a pinch of salt sometime aura can be confused as the prodrome.

[00:42:20]So from uh this now we'll take about the diagnostic evalu evaluation and reertification of synth topic. So this redeso is uh is uh virtually the the cornerstone of al uh uh ed acronym uh uh which was recently actually introduced um to use uh as uh uh assessing a patient who presented with syncopy to the emergency department. So our indicative of recognize we need to confirm the syncopy and and refute the other differential diagnosis and we have to make sure that there's no uh immediate life-threatening condition such as pulmonary emolism aotic dissection acute syndrome sh uh ruptured aotic canulism or any GI bleed and uh then we need to do the initial evaluation. So remember the initial evaluation include the detail history taking with physical examination 12 ECG and active standing blood pressure measurement. Then we have to determine uh by using uh restertification uh tool to decide the setting of care.

[00:43:35]Whether we can discharge a person safely, whether we need to obser observe the patient for another 24 hours to 48 hours, whether we need to admit the patient directly to a uh uh uh treating uh facility.

[00:43:51]Uh so based on the restification uh they have introduced syncopy units uh where we can 24 hours to 48 hours that and then we need to have a uh uh clear strategy and stratify uh whether whether this is a cardiac syncopy or a non-cardiac synopy.

[00:44:20]syncopy and plan the management.

[00:44:24]So the step one is differentiating mimics we discussed this about. So this slide would in sometimes we've seen patients especially young people coming with cudo p c p c p c p c p c p c p c p c p c p csychogenic pseudo syncopy which put a very dramatic presentation and alarms the parents and the guardian and it can be very difficult to convince that this is something but uh functional because of the dramatic nature. Some of these features can be helpful to differentiate between bit uh uh between a true syncopy or a cure or a cudogenic or cudos syncopy psychoggenic pseudo sync copy.

[00:45:03]Then uh so detail history taking and physical examination and uh and the cornerstone is actually doing a 12DCG and uh and they taking orthostatic vital by doing a active stand up uh 3 minutes rule uh taking blood pressure measurement and it advice advocate highly against doing a panel of broad number of investigation including routine tropin HCTS uh uh so we need to utilize these risk risk scores carefully in order to minimize doing unnecessary investigations to cut the cost and sometimes this investigation may not yield much of a uh important information.

[00:45:51]So identifying red flags if there is this patient having high risk features uh like syncopy during exertion syncopy during supine position lack of produ palpitation those who are above age of 65 patients structural and patients who are anemic and those who features allow us to sometimes uh discharge the patient directly from the EDU.

[00:46:33]So uh sometimes uh the diagnosis of synopy may not be as apparent as at the initial evaluation. then we need to uh apply risk classification score systems in order to objectively uh assess the risk and plan the management.

[00:46:52]So there are various different reertification scores, Canadian syncopy scores. All these scoring system has their strength and we can as uh the Canadian synctopus score is good at assessing third event uh and is detecting the probability of cardiacology.

[00:47:17]So uh all these uh scoring system has their own uh uh uh strength and weaknesses. So they in Canadian synopy score they it based on clinical fees features and probable diagnos based on we give scoring system categorize patient into very low medium and high risk and very high risk. uh and then that will allow us to uh decide whether that patient can go treatment.

[00:48:01]The same way the oal risk score which is good for uh predicting the uh 12 month old cause mortality after syncopy uh it contains uh basically clinical features as well as the abnormal ECD finding. It's a simple scoring system.

[00:48:22]This evaluation of guid guidelines in syncopy study score uh uh they utilize uh abnormal ECG criteria and uh symptoms such as palpitation, syncopy during effort, syncopy in supine position as positive uh plus uh plus values with the negative predictor such treating factors like uh some of the symptoms and uh like prolonged uh standing and uh the some of the situational triggers such as fear in uh pain indicative of a non-cardiac synopy. So based on the sing scoring um uh they can categorize them into three different groups groups and uh it is predictive of a cardiac cause as a uh as the reason for the this present present uh syncopal episode.

[00:49:26]So detailed history taking is cornerstone. Uh really need to take a detailed history regarding the present event. I normally start with what were you doing? Give an open question. Allow them to uh elaborate their history and sometimes I would ask what time did you wake up? I start taking the history from that point on onward and what did you feel exactly before and after whether there has intercon illness and circumstance of the event the eyewitness account previous attacks of of sync copy and history of even feats road traffic accident drowning drop attacks even fractures.

[00:50:08]So all these are crucial sometimes uh uh gathering all this information because uh this is like a detective scenario and uh sometime uh getting the right answer the past medical history obviously and the family history of syncopy cardiac ailments premature or sudden cardiac death and and also giving away to the occupational and recreational activity as well. So close from the history uh if a syncopy happens in supine position uh sometimes occasionally vaso veagal syncopy can happen happen with a clear trigger uh and pseudocyncopy can happen at any position even arrhythmia. So during seat normally either epilepsy or arrhythmia sitting it could be voagal orthostatic arhythmia all these are possible standing for some period a vaso veagal is orthotic hypertention form likely but that does not necessarily rule out having an arythmia as well couple of step after standing and straightening from bending or squatting position normally it is orthostatic hypertension a mixturation defication normally vagical but remember even a cardiac ariththmia can lead to severe veagal activation. So they might get the urge to make churito defecate that might confuse things. So cough normally voagal swallowing voagal during and after meal normally voagal but one of the exception is after meal is actually bugata bugata syndrome postprandial ariththmia can be seen in bugata patient. uh if a syncopy happens with neck movements, thyroidit sinus syndrome is a possibility or even sometimes uh like one of the other misleading differential diagnosis autotic crisis that is partly due to the brain uh balance malfunction of the brain mal uh balancing system. The fear pain instrumentation generally voagal but sometimes severe uh adrenal surge can even initiate arhythmias during physical physiological during physical exertion normally cardiac but untrained unneatized a person who start doing something extraordinary rarely voagal activation can occur during uh activities but Most it should be the cardiac syncopy suspected as the prime uh suspect recovery period after exertion normally voagel but some other arhythmias like bugard can manifest after a period of exercise.

[00:52:51]Uh the palpitation indicates arrhythmia.

[00:52:54]Uh but even pots and vasagal there is a element of palpitation because the heart rate goes up before the syncopy.

[00:53:02]Uh and strong emotion both can be there.

[00:53:06]Startling response long syndrome uh during fever voel same bugata syndrome patients they are likely to develop arithmia during fever. Sleep deprivation generally favors the wave vehicle. Uh heat uh change in climate, change in weather normally triggers uh non-cardiac syncopies. If you're lucky to have a eyewitness account, the fall kneeling over steep generally indicates epilepsy.

[00:53:36]Flaccid collapse could be syncopy but catatonic sometime uh real atonic epilepsy. movement before fall generally epilepsy.

[00:53:48]So remember the head turning with the uh with losing consciousness generally indicative of epilepsy. Movement after fall could be epilepsy or syncopy movement within the lock epilepsy indicative epilepsy and movement countless so more than 20 m indicative epilepsy movements are limited especially less than 10 sync copy.

[00:54:14]So uh I'm revisiting the same thing. So if a syncopy event a new one set of chest discomfort so headache palpitation abdominal pain uh these considered as high risk features uh during excertion or supine and sudden onset palpitation no warning symptoms and family history of schemic heart disease or background history of medical es schemic heart disease they all indicative of iris features and uh post medic past medical history if a person is having long history of recurrent syncopy from young age. It's far more likely to be benign rather than pathological. And patients already have a diagnosed history of structural or uh schemic cardis heart failure or arhythmia you have to suspect arhythmic uh cardiac synopy. However the mild symptoms are so the duration of syncopy uh not having injuries the dramatic nature none of them are uh strong enough to differenti between uh uh bas uh non-cardiac synopy against cardiac. So symptom severity does not indicate the underlying pathology.

[00:55:29]Sometimes I've seen this plain and simple syncopy presenting as so dramatic to a point that you think this is cardiac but that is not the case. So normally the the dramatic nature of the syncopy the dramatic nature the patient whether they have sustained injuries none of them are indicative of the ethiology. So other it's actually the other factors that help us to determine which is which because whatever it happens the brain loses blood blood supply. So the patient passed out after that whatever it happens uh it does not tell the eeology. So physical examination unexpressure evidence of GI bleeding persistent radic cardia new systolic mas they all cardia.

[00:56:18]Keep in mind that different types of syncopy are prone to happen or can be more severe in the presence of several other factors like active medication, the consumption of alcohol, dehydration, respiratory syn diseases with hypoxia and environmental condition and anemia. So all these things has to kept in keep to kept in mind when we evaluating a patient think of it.

[00:56:50]I'll skip all all the factors we were discussing uh during the presentation.

[00:56:55]So I wanted to bring uh this uh ECG clues that are pointing towards cardiac syncopy earlyization ST segment elevation with the bugata pattern uh T-wave abnormalities LVH so absence of P waves AV block requires meticulous methodical assessment of ECD to pick up the subtle changes.

[00:57:25]Uh so both repolarization abnormality, depolarization abnormalities and uh all these can indicative of uh uh clues to uh uh probable uh cardiac in nature in that indexing of a presentation. So let me bring up some of the ECGs so you would be able to spot. So this CCG shows uh so this patient shows uh you can see left axis vision with the right bundle branch block. So that means the P there's an indication of this patient is having infraodal conduction system disease and this ECG shows you can see various degree of AV blocks and this ECG shows uh no non-sustained ventricular tachihythmia. So you can see premature ventricular complexes uh more than three. So if you have one it's a single PVC two couplers three and beyond that we call it non-sustained ventricular tacharithmia. If an arythmia lasts less than 30 seconds we call it non-sustain arythmia. If it is lasting beyond 30% 30 seconds it is it is labeled as sustained ventricular arhythmia. So if you spot these things a person who's presenting with a sync copy you have to suspect cardiac sync copy.

[00:58:56]So this ECG demonstrate this patient is in sinus rhythm. You can see a PVC occurring very close to the T-wave. So this is called short couple PVC.

[00:59:08]Uh PVC occurring nearly on top of the QRS uh T-wave. Uh so T-wave represent the uh repolarization.

[00:59:17]So this PVC occurring at the vulnerable period and and this is an indicative of a uh some these type of scenarios will uh can cause polymorphic PT and presenting them as uh syncopy.

[00:59:35]So the first TCG shows myiosinus predicardia if remember if the heart rate less than 40 that has to be taken seriously and this TCG showing I don't know whether you can appreciate uh pre-exitation so short PR interval P and QRS are merge and QRS complex are wide so so uh I'm showing some of the subtle ECGs uh so that really needs uh a focusing and and methodical assessment of ECG to pick up what is not so apparent that could really be the game changer.

[01:00:12]This CCG uh is obvious demonstrating spontaneous type one. This co type of ST segment elevation with T inversion is right trio V_sub_1 and V_sub_2. So this is a classic spontaneous type one bugata pattern.

[01:00:27]This ECG shows that abnormal T waves with QT prolongation. You can see we can appreciate broad T waves inverted T waves. So this is lo and this is I have highlighted you can see you can appreciate that the SC segment is really short. This is called early repolization short QT syndrome.

[01:00:49]These are rare conditions. But sometimes if you you do not I mean if you fail to methodically assess each and every component of the ECG you might miss this. So that's the important that I'm highlighting that the need for the methodical assessment of ECG and can you appreciate the abnormality in here? You can see that subtle ST elevation uh saddle bed type of ST elevation in inferior leads. This is called early reporization or Jwave syndrome. these condition these subtle changes might indicative of an abnormal uh cardiac conduction system disease.

[01:01:36]So uh one of the other classical problem that we encounter those who do athletics athletes presenting with syncopy is a really challenging uh so this require significant expertise. So people have different between athlete the easy in detail uh for these ECG changes. So uh there are a few features that indicative of so the understanding of his condition compared to a uh false sinister condition card stratification the patient uh can patient can be discharged straight away from the ED or sorry we I'm like repeatedly getting Yeah.

[01:02:45]>> Yes. Okay. So uh so the importance of establishing syncopy units I suggest actually uh to as a project to you know uh and you can be uh to you know be the leader and uh guideing specialized units that will improve We can see now BC medical setup the uh divided divided attention.

[01:03:39]So there are four highlighting important copy units across the country that will definitely management.

[01:03:51]So we will moving from that uh further assessment investigation both equal.

[01:04:20]Can you hear me now better?

[01:04:22]>> Yes. Yes, we can hear now.

[01:04:23]>> Yeah. Okay. So, so the further synopy assessment of syncopy uh based on the uh so we have to think uh think both cardiac and non-cardiac courses given an equal opportunity and plan our investigations.

[01:04:47]So based on uh so there's a heap of investigations that are available to us to determine the the pathophysiological basis or eological causes for the uh sync copy. Then we have to plan our investigation according to the available resources and uh and giving equal weights to the probable causes. So if you're thinking of uh uh in line of assessing the rhythm uh and the blood pressure you could use ambulatory rhythm monitoring and ambulatory blood pressure monitoring and if you wanted to assess the cardiac structure go for the echo cardiogram combined with uh CTCA coronary angiogram and cardiac MRIs then tilt table test and carotric sinus massage and uh if you are going further down the line you could utilize electrophysiological assessment by bringing down the patient into the catlabs and as I mentioned earlier blood investigations should be determined by the clinical probability and sending the investigations without any specific reasons may not derive the uh uh desired results. So when it's come to rhythm assessment in syncopy the one of the important thing feature that we need to establish is that the frequency of symptoms and the in investigation what we order should be able to match the the patient's frequency of symptoms otherwise we will just be doing an investigation with the relatively your low yield. So that is why it is mentioned that establishing the symptoms ECG correlation will guide us to uh establish the probable diagnosis.

[01:06:39]Otherwise uh if an investigation is carried out h it does not give us it does not gives us uh uh patient symptoms. So that ECG that investigation might not uh yield a positive results. So we are spending lot of money on a investigation which doesn't give enough information. So we are still back to the square and we are not moving one step further than we should be.

[01:07:16]So u I wanted to highlight the importance of uh uh utilizing implantable loop recorders in terms of managing a patients who are presented with sync copy. So implanted loop recorder is a small diagnostic tool the USB stick like device which we put under the patient's skins and has the capability of monitoring patient symptoms for 2 three years. So especially those who are presenting sympto with infrequence frequencies uh uh evidence for ILR making a positive diagnosis is uh significant and you you these some of these invest studies have shown that it's far superiority in terms of picking up paroxismal AF in evaluation in the evaluation of patients who are presented with strokes.

[01:08:10]The cost the problem is actually the uh rather expensive nature of a implantable loop recorder. Currently in Sri Lankan context implantable loop recorder cost around 1.5 million rupees. So as compared to the rest of the investigation that are available to us uh implantable loop recorder is really expensive. However, uh by ordering so many test, if you can uh implant a loop loop recorder preparation, that will give a far more uh information in a rather uh speedly and avoiding other heap of unnecessary investigations. So collectively implanting a loop recorder might be economical compared to ordering uh several rounds of alters and all the other investigation and and and if we count the number of admission and the cost related to those admissions.

[01:09:07]Uh now in we are in the era of variable devices and smart watches. So can we use these smart watches and some of the other u uh variable features that are capable of even recording blood sugar even measuring blood pressure. So this is a recent study published actually very recently has uh shown the validity or usability of smart watches and this um variable other devices that are capable of monitoring uh heart rhythm issues as well as even taking blood pressure measurements. So this become a new normal for us and everyone is having a smartphone and a smart watches. So we can utilize and they become complimentary and the technology has advanced into a level that some of these measurement as at accurate as other laboratory investigations we we do we do as well as some of these smart watches can pick up even fall and some of the elderly people they might not recall even when they sustain a fall and might uh might fail to report that they have suffered a fall. uh if the but if they are wearing smart watches the smart watches itself can in uh detect the fall and alert the uh guardians or the hospital facilities. So uh these clinical symptoms otherwise might get lost can be acquired and assessed and treated accordingly. So we are be we are seeing uh so much of information now even AI algorithms are now being developed. So it becomes rather accurate that uh the the the uh the kind of information provide by these mach uh smart watches and other variable devices uh be going to be a very good clean uh um informative tools that we can utilize and this might even a time come that some of these expensive inward monitoring become uh in null and void once these technology ologist become a standard day-to-day practice.

[01:11:20]So when we suspect cardiac syncopy, rhythm assessment going beyond doing uh ambulatory monitoring include exercise testing sometime we bring them down to the catlap and do certain invasive measurement.

[01:11:34]the structural assessment uh by a course cardio uh coronary angiogram CT coronary angog and u cardiac MR cardiac MR has become an important tool of assessing uh uh arrhythmia probability of arythmia especially in patients who with structural heart disease.

[01:11:58]So uh when a patient uh is suspected to be having non-cardiac syncopy now the current novel approach is to uh evaluate in the line of what was the possible mechanism that has led to the uh sync copy. So this this means rather than going for probable eological causes we wanted to highlight what was the exact reason that has led to the uh blackout or the syncopy in these patients. So it could goes either by dropping the blood pressure or uh as a result of dropping the heart rate. So based on that uh short cardiac autonomic functional testings uh group of test that we do a patient when we suspect uh uh suffered suspect to suffer the non-cardiac synop.

[01:12:55]So those investigation include active standing the bedside test that we do remember 3 minute active standing and taking blood pressures and then we do the tilt table testing and valva maneuver caroted sinus massage as well as ambulatory blood pressure monitoring.

[01:13:10]So we don't need to do advanced autonomic testing sometimes in order to pick these patients.

[01:13:18]So orthostatic challenge uh unlike other animals we evolve into freeing our hands and stay on our feet and as a result the brain is always at the top and uh the this this gravity uh gravitational pull leads to Venus pooling and eventually drop in cardiac. So there are mechanisms that are in place directed by the brain through the autonomic system in order to make sure that the brain g become being the most important controller of the body to make sure that the brain gets enough blood supply during upright position.

[01:14:01]So we know but during our physiology days that uh as we stand up the heart blood pressure slightly dropped the heart rate goes up then was constriction occur squeeze the blood up and maintain the blood pressure. So this same physiology phenomena is used as an investigative tool in terms of assessing patients capability and assessing the this uh corrective reflex mechanism that are in place to make sure the the brain is get enough blood.

[01:14:34]So uh the the simple test is what we do is active standing test the bedside test that we do and if you have to do further uh elaborative test we do the head-up tilt table test. So this is the tilt table test. We put the patient flat and then we put put the patient up in a tilted position and measure the hemodynamic and as well as recording the ECG. So adapt test become an important tool assessing patients who develop syncopy especially in upright position in terms of deciding whether there was a hypertensive hypotensive uh uh uh syncopy or whether it was a bradic cardic syncopy whether it was a uh mix syncopy I'm not going to go to the details of describing these things but this is an important tool we use uh in our day-to-day practice we do have till table test available to our dis uh our use. So we'll be carrying out these investigations and test you remember that the first case that I described the case number three young female who presented with blackout and we we did did the tilt patient develop uh significant bradic card. So that was a non-cardiac uh bradic cardic uh syncopy uh and we were able to simulate symptoms as well as the ECG correlation during the tilt table test and reproduce the symptoms and thereby making the diagnosis.

[01:16:05]So this is the tilt response. So when we put a patient into the uh initially we put the supine procedure then we patient put up and we taking the time. So you can see uh in in the tilt table test the person person is standing the legs are not actively moving only maintain the posture. So you can see the blood pressure gradually drops as well as the heart rate tries to uh tries to go up and compensate. So it will come to a point that this compensatory mechanism started to fail. The brain start experiencing hyperfusion and as a result brain initiate reflex through the vagus nerve either cut down the blood pressure or bring down the heart rate and inducing the blackout. So this is this blackout in non-cardiac syncopy is induced by the brain as a result. So what happens is uh it's a maladaptive response. The brain cuts down and initiate the syncopy. So the person goes down and patient po person the intention is to goes down and assume the supine position. So the uh disequilibrium is settled and the brain at the heart becomes remain at the same level. So the brain start getting blood supply. So this is a maladaptive mechanism and that is the current understanding. So it can happen in both days. Sometimes the heart rate drops sometimes the blood pressures of uh uh so the tilt table test can still be helpful in diagnosing classical various form of orthostatic hypertension as well.

[01:17:47]So ports it's not a synop the tilt table test can also be helpful in diagnosing ports. So we this test is combined with caroted sinus massage in order to elicit uh this uh phenomena called caloted sinus syndrome. So stimulation over stimulation of the caroted sinus leading to severe veagal mediated bradic cardia and drop in blood pressure. This is a condition especially common in uh elderly population. One of the uh drastic condition that give rise to syncopy in elderly population. So you can appreciate that when we do the kerotic massage patient become radicardi. That's the same mechanism we are using to treat SVTs because when we stimulate the kotid sinus it leads to veagal activation or veagal surge and making bradicardic.

[01:18:39]So uh reflexing copy if you are going into a little bit of uh ethiology. So reflex is a neuro we call it neurocardio inhibitory reflex syncopy or simply reflex syncopy. It is where uh uh we we don't fully understand the condition. It happens from the uh brain hypothalamus and rest of the other deep brain structures are participating. It happens through the part uh navigate its effects through the autonomic nervous system. So we don't fully understand the behavior of the autonomic uh system nervous system. So in the presence of what we call triggers may it be orthostatic challenge and lot of other psych physical psychological triggers can uh initiate this mechanism reflex through the brain through the autonomic nervous system leading to either vaso depression or cardio inhibition and patient will experience a blackout.

[01:19:40]So there are various type of reflex syncopies. The commonest one is called vasovagal or orthostatic syncopy. The kind of syncopy happens in upright position especially if a person standing or seated for prolonged period. And there are other uncommon various v types of syncopies which I'm not going to discuss. we call them situational syncopies and carot sinus syncopy is one another other classic uh uh condition that fall into the same umbrella. So reflexopy it is common in young people most of these school children remember those these hot weather uh hot days dry days and especially during school sport meets or in in assemblies children come many childrens comes with synopel episode and mostly they are reflexing due to uh the common type what we call orthostatic or reflex voagal synop so uh the orthostatic Hypertension we mentioned now we no longer the use this term but for the completeness of sake the orthostatic hypertension occurs due to uh failing mechanism uh that are in place to make sure the brain gets enough blood. The condition get aggravated by various different things we do uh volume depletions and sometimes the kind of medication we give to treat uh high blood pressure, diuretics, other these tricyclic anti-depressent nitrates all these can condition leads to orthostatic hypertension and primarily some uh neuro neurological conditions uh leads to autonomic nerve dysfunction can also manifest as orthostatic hypertension.

[01:21:26]So cardiac syncopy we know basically it most of the time happen due to electrical instability really it can occur due to uh mechanical problems such as c seviotic stenosis mital stenosis hydrophic cardiammyopathy uh and pulmonary emulation even cardiac temponardic uh I wanted to highlight this condition remember the fourth case that I was discing the young female with the MVP who presented with the precinct couple episode and Walter was demonstrating non-sustained polymorph equities. This is a condition recently entertained. It has been there uh there are so many literatures even 30 40 years before those who uh seemingly uh normal. We tends to these ignore MVP and neglect this as a benign condition but MVP can sometime now have been understood can be pathological especially those who have bio bioentrical MVP and and there's another distinct echo feature called mitalular dysfunction. So those who are with MBP they should not be neglected completely.

[01:22:37]They need to be assessed and they should be warned against the probability of having arrhythmia and this is something recently recognized and enclosed as malignant mitro valve syndrome. Um so these patients relatively young female patients having MP they come with palpitation and ECG in sinus rhythm normally you would see T-wave inversion in inferior leads and they tends to develop uh premature ventricular complexes originating from the papillary muscle of the left ventricle.

[01:23:11]So this is uh uh something uh people uh we all have to remember one of the uh important uh condition this MVP is quite prevalent in Sri Lankan setup. I've seen if you see a 100 echos at least you would spot 10 people or so having MVP uh documenting in their echos. So it does not mean all of them but uh we have to keep keep in mind that some of them actually runs the risk of developing malignant arythmias.

[01:23:41]So we are moving to the final part of the presentation how to treat syncopy.

[01:23:46]So our goal of treatment is to reduce the recurrence and uh and reduce the relevant impact by involving the patient in decision making process by eliminating the morbidity and mortality associated with as well as improving the quality of life. So this point I wanted to highlight that thorough evaluation itself reduces the recurrence of syncopy by 50%. So giving or paying the due attention it requires can actually itself be therapeutic on its own.

[01:24:19]So treating cardiac synup is very easy.

[01:24:21]If you have this abnormative bradic cardia you would consider giving them a pacemaker. And remember even asymptomatic AV block patients uh second degree third degree AV block patient however asymptomatic they are they should always receive a pacemaker. The problems come when the the when patients present with bifasicular blocks, left axis stevision, right bundle branch block and and when they are coming with presyncopy sometimes it could mean that the patient is developing intermittent advanced AV block. So you may have to do implant them in ILR or even subject to a EP study or requires rather close followup in order to pick up and treat them with pacing therapy. Those who present with tacky obviously sweet cathelation is a cho treatment of choice and almost 90% of the time these STS can be completely cured by cathablation.

[01:25:19]Those who are presenting in VT they should require to have an ICD putin and they also can benefit from cathablation apart from being on antiarithmic medication.

[01:25:30]You can see that treatment treating with anti-arithmic medication now fall into class 2A as compared to cathablation and ICD implantation which is now which are now considered as class one. So most of these arrhythmias now can be treated and completely cured by modern cathedation treatment options.

[01:25:51]The other problem when we encounter is those who already have rhythm issue diagnosed like inherited arhythmia syndrome or structural heart disease coming with syncopy but when you do a ECG they are normal. So that is a clear distinct clinical scenario that we encounter day-to-day practice.

[01:26:10]So uh depending on the condition sometimes say syncopy should be taken very seriously those who already have a background cardiac issue. So syncopy is equivalent to presumed arithmic until proven otherwise and most of them actually considered as a high-risisk procure and they should be considered ICD implantation even we are unable to uh pick up an arythmia on monitoring same goes with the patients who already have a structural heart disease unexplain copy we have found it is indicative that they are at very high risk of having uh having fatal event in time to come. So it increases the both 30-day and one year motility. They should be considered treating with patients who are with hypertrophic cardia with ARVC they should also be considered having ICD put in even we are we were unable to identify arymas.

[01:27:16]So ICD is now freely available. So all these cardiac patients with cardiac uh syncopy suspected cardiac syncopy even we are unable to uh pinpoint uh or find the culprit arithmia already established cardiac uh structural heart disease or inherited arythmia syndrome patient they should be considered having an ICD.

[01:27:41]uh so uh moving from that uh the novel approach is for the treatment of non-cardiac synopy based on the mechanism.

[01:27:51]So if we uh find out by our investigation the patient is having hypertension but a patient is already on treatment for hypertension. So remember patients who are hypertensive can also presented with reflex hypertension. So uh the first option is to whether we can deal. So sometimes what happens we overtreat them and other mistake what happens is most of the time this office blood pressure can be erroneously high. We call it re reactive hypertension and we escalate the treatment and the patient next day patient become hypertensive because of the the medication that we have prescribed. And unfortunately in our setup we don't have the luxury of using these long acting medication. Still in our uh hospital setup we have only short active medication like you know presine uh so these patients are at high risk of developing drug induced hypotensive episodes. So dispersescription is an important step of managing these type patients. So especially those who are with hypertensive we should focus on deprescribing them and those who were present with bradicardia.

[01:29:01]So as part of non-cardiac synopy this is called reflex predicardia depending on the age we decide the treatment if they are young uh less than less than 60 years of weight we can treat with the sympathy like theophilene and there's another newer novel operation it's called cardo cardio neuronal ablation unfortunately we don't have it in Sri Lanka we can go and put catheter into the heart and ablate the veagal relays into the heart these ganglions can be updated. So patient uh will no longer develop vag mediated bloody arithmas and those who are above 60 years of weight if they develop bradic cardia normally the pace is indicated even they are reflex in nature. So in in in order to summarize uh conventionally the reflex copy we normally manage with education and giving uh uh and uh improving hydration and ask advising them to increase uh salt and avoidance the triggers and they and they also need to learn the physical counter pressure manual which I will demonstrate in a moment and depending on the phenotype whether either they are hypertensive you could kiss treating with them flutortisone and make sure you do the endocrine panel and rule out conditions like hypothyroidism and uh Addison's disease uh before starting fluocortisone and those who are severe refractory sometimes they need uh especially those who become predicard they need either pacemic implantation or cardio ablation.

[01:30:39]So these are these counterress maneuvers. So remember most of the commonant reflex copy uh phenotype is orthostatic happens in upright position.

[01:30:49]So they can do this arm tensing, leg crossing and butt clenching uh to improve the circulation and uh and thereby minimizing the activation of the reflex and thereby preventing having suffer suffering a uh uh sync coffee. So counter pressure manuals you can see it improves the blood pressure uh uh and thereby minimizing the symptoms.

[01:31:17]So the advice normally we should be giving is uh they should be able to recognize the the prod. So we should educate them to recognize the prod and take measures. What happens is some people when they feeling that something is not normal. Uh if you are standing and going and sitting down is not sufficient because still the brain is above the mechanism is still in place.

[01:31:42]What you really need to is to bring the head to the heart level. So that means you need to lie down and if someone is around what they can do is they can lift the legs up. So, so the other if you are in a situation where you can't lie flat down, what we normally advise you to bend down, bring the head as low as possible and clench your teeth and cross your legs and cross your fingers and tighten the grip. So thereby um uh disposition counter pressure manuals and improving the circulation and the same time drinking chilled water uh seems to improve symptoms quite rapidly.

[01:32:22]So this is the cardio neural ablation.

[01:32:25]We put catheters into the heart and find these ganglionic overlays uh and uh into the cardiac conduction system and we can upgrade those ganglas and thereby preventing uh reflex mediated bloody episodes. Sometimes even complete heart block can now be treated by doing this abdation. So some patient can get away without having to put a pacemaker in.

[01:32:51]So uh managing orthostatic hypertension.

[01:32:54]So we mentioned these prescribing is an important step and volume and lifestyle modification calf muscle strengthening.

[01:33:01]Then you can use a mechanical support wearing abdominal binders and lower volume compression garment to minimize venus pooling. So uh as much as we emphasize on strict blood pressure control it comes with the risk increased risk of hypertensions. So I really normally I made the habit of doing ambulatory blood pressure even if you find out blood pressures are high. Uh sometimes when you do ambulatory blood pressure you would find their blood pressure is actually very normal even though they are having very high blood pressure recorded during office visits.

[01:33:38]So thereby uh minimizing the over prescription of antihypotensives based on re uh office blood pressure.

[01:33:48]So syncopy in athletes it's a a topic on its own right. So the what the key message that I wanted to give is if a athletes who comes with syncopy uh make sure that they get them referred to a sport medicine units. Now we across the country we have sports medicine units and assessing ECG who uh in athletes can be quite challenging because as I mentioned earlier some of the ECG changes that we considered abnormal in otherwise normal people can all well be normal in syncopy uh in athletes. So therefore it required a special attention and especially when they come for this clearance for event participation it is always best to get involved of a uh sports medicine specialist.

[01:34:34]So uh uh finally uh uh in order to wind up the session I wanted to highlight these uh 10 uh key takeaways to uh uh if you can take these 10 takeaways from this presentation I think I have done a good job. So remember the cardiac synopic kills the mortality is 30%. One year motility and if you understand the mechanism uh it'll it help us to treat the patients more effectively. So most of the time you you are witnessing a patient who's coming with syncopy like it are far more likely them to have hypotensive episode than anything else.

[01:35:18]and taking detailed history is your most powerful tool. Even initial EV if you do a thorough initial EV evaluation at ED level you are at least 50% of the time will come up with the definite diagnosis and as I mentioned earlier they remember this 1020 rule to say misdiagnosis so sometime 30% of the time syncopy is misdiagnosis epilepsy so this jerks presence or absence of a jerk should not be a strong indicator to determine between syncopy or uh uh syncopy and between syncopy and epilepsy. So keep your mind open uh and uh and uh do the evaluation in both ways and uh do the reertification every patient. Try not to believe your gut feeling most of the time. uh uh use the uh the scoring system to uh do an objective evaluation of a patient and and uh man plan your treatment, plan your management and investigation based on the uh the scoring you get from the scoring system.

[01:36:29]Uh and syncopy I wanted to highlight the fact that we need to establish dedicated syncopy units. I think uh this is the message I wanted to high give to uh the Sri Lanka College of Internal Medicine.

[01:36:43]Uh so you could should be that you should be taking the lead. Uh establishing these syncop units this is one of the unmet needs uh in the country that's what I feel. So establishing syncop unit will transform the management of syncopy patients and remember the one single point exertional syncopy should always be considered as anti-cardiac. So taking this piece of information this tiny piece of information whether the patient experiencing copy during or after the activity will change will be the game changer.

[01:37:19]uh so we need to make sure that availability of ILR uh in in terms of assessing uh sync copy because we are wasting on so much of research doing unnecessary investigations uh and especially without giving due regard to the frequency symptoms just by doing a halter uh actually even less than 10% of the time we are not coming out with the reasonable answer by doing a 24-hour so rather than wasting on uh multiple rounds of investigation, multiple hospital administ uh admission without a clear diagnosis that can be cut shorted by uh offering ILR services more frequently and make sure every syncopy patient get evaluated thoroughly because the eval evaluation has a therapeutic value and it reduced the syncopy frequency by at least 50%.

[01:38:15]And uh so remember real syncopy has a real world consequences. It involves patients and not only their day-to-day life but as well as a whole uh it gives a huge economical burden uh to a national health services around the globe.

[01:38:36]So if you do cannot if at least if you can remember these three key things I want to highlight make sure that you check your pulse and know your CPR and take your and your patient in copy seriously. Uh thank you uh for listening and these are my further readings and if you're interested in uh and thank you very much have a pleasant day.

[01:39:29]Yeah. Uh thank you so much Dr. K for a very uh comprehensive and very interesting lecture uh very informative lecture on uh syncopy. So now we are coming to the end of the uh session today. Uh actually now you all can see this uh the QR code. Please scan the QR code and answer for the post test questions and uh submit your informations to get your CPD certificate. Uh yes >> and I I want to apologize for this technical glitches leading to this.

[01:40:11]>> Yes. So actually like you know it was taking almost more than hour beyond this due time.

[01:40:21]>> Yes. Sure. So yes. Okay. So basically we apologize for this uh technical uh error and uh incon inconvenience for you all and actually we are coming to the end now and uh let me thanks uh uh our speaker today Dr. Kit consultant electropysiologist in National Hospital of Candy for excellent presentation. Uh and also I would like to thanks uh respected virtual participants audiovisisual team Mr. Dishan and Mr. Nimanta and also sponsors Gwama and SLIM team for their valuable support. Thank you very much and next session will be held on 27th May 2026.

[01:41:17]Thank you.