Syncope | Clinical Medicine

foreign what's up Ninja nerds in this video today we're going to be talking a little bit about syncope this is a part of our clinical medicine section also just real quick if you guys like this video it helps you it supports you please support us and you can do that by hitting that like button commenting down the comment section and please subscribe I really urge you guys if you guys have a moment a quick second take and go down in the description box below there's a link to our website on there we have a lot of cool stuff that we can offer that's not here on our YouTube site so we have things like notes illustrations we're even developing some exam prep courses for those of you preparing for step one step two pants Etc so get ready and keep your eyes peeled open for that plus check out some merchandise get yourself some swagoo all right without continuing on about that let's talk a little bit about syncope so Chicopee is a patient who has a transient Global hypo perfusion to the brain where they have a transient loss of consciousness and they can quickly return back to their normal Baseline that's the concept of syncope is where a patient has Global hypoperfusion a transient loss of consciousness and then quickly back to their Baseline the question then becomes what causes the global hyperfusion that's really what syncope is all about so when a patient syncopizes they come to the hospital you have to kind of figure out what was the reason behind it oftentimes history and physical exam is the key but let's go through here there's three types reflex syncope orthostatic syncope and cardiogenic syncope sometimes you may hear this one listed as kind of a neurocardiogenic syncope and actually makes sense here in a y in just a second but reflex syncope is actually an umbrella term for three different types of syncope that kind of fits in the causes section it's a vasovagal a situational type of syncope and what's called carotid sinus hypersensitivity I'll explain all of this in a second the concept behind reflex and could be is really interesting there's some stimulus and what the stimulus is doing let's use this color here real quick here's going to be your vagus nerve right that dorsal nucleus of Vegas and it'll send down this information via the vagus nerve and what the vagus nerve will do is it'll act on your vasculature and it'll act on the heart and what it'll do is it'll release what's called acetylcholine right so here let's actually mark this down here this is actually going to be cranial nerve which is the vagus nerve the 10th nerve so cranial nerve 10. it'll go to release acetylcholine onto the heart and what it'll do is it'll exhibit two types of effects here one is what's called a cardio inhibitory effect so this is called a cardio inhibitory effect and what that means is acetylcholine will actually hit some of the muscular interceptors on the bundle the actual conduction system and slow down the heart rate so patients will actually develop a reduction in their heart rate when you drop a patient's heart rate what will you do to their cardiac output you drop the cardiac output a little bit right and if you drop their cardiac output what would you potentially do to their systolic blood pressure drop this systolic blood pressure a little bit so these patients can exhibit as a result here from dropping their heart rate from that vagus nerve input or outflow they can drop their heart rate drop their cardiac output and drop their systolic blood pressure all of these can happen as just one of the effects from that vagal outflow because this puppy is on hyperdrive so we're going to kind of say that it's really kind of it's actually inhibiting it but here we'll just say that this puppy is really really this dorsal nucleosphagus is really on hyperdrive that's one effect the second effect here is on some of the actual parts of your vascular system and it'll do something called a Vaso we'll actually put it like right here we'll put a Vaso depressor effect and what this may do is this may either shut off the sympathetic nervous system amplify the parasympathetic nervous system but basically what happens is your vessels will actually start to dilute and so now because of that when I actually get this vasodilating effect what does that do to my systemic vascular resistance well I increase the diameter so the resistance should go down when your systemic vascular resistance goes down what would that do to your blood pressure it'll drop it it generally will drop the diastolic blood pressure but that's what you're going to see is you're going to see a drop in the resistance and a drop in the diastolic blood pressure as a result you're going to see a drop in the blood pressure and complete concept here when you drop the patient's blood pressure what will you do to their actual perfusion it's going to reduce so as an effect of both of these look what starts happening here as an effect of both of these you're going to decrease your cerebral perfusion and now if you reduce your cerebral perfusion what did I say was the definition of syncope it's Global hypoperfusion that then leads to less blood flow going to the brain and what will the patient have a loss of consciousness and we're going to put a transient loss of consciousness that's the concept here so there's vagal nerve outflow cardio inhibitory effect dropping the heart rate cardiac output and blood pressure vasodepressor effect dropping the actual systemic vascular resistance in the blood pressure if you drop the blood pressure in general you drop the cerebral perfusion they'll have transient loss of consciousness the question that arises here which is very interesting here which is why in the heck is this vagal outflow so intense right and there's three reasons why the vagal outflow can be super intense one is called a vasovagal response so what do I mean here is that the patient is usually in some way shape or form having lots of pain there's some particular phobia or they have been standing for a very very long period of time when there's lots of pain a phobia or prolonged standing what this will do is this will activate your vagal outflow so remember that vagus nerve which is right here this puppy becomes super activated and goes down and does everything that we talked about before with the cardio inhibitory effect and the vasodepressor effect this is the concept that I want you guys to understand so if you hear within the history oh they had you know they stabbed their foot or something like that and then they passed out or that you showed them a spider and they have a phobia of spiders and they passed out or they've been standing for long periods of time at a concert and they passed out that's a perfect example of a vasovagal syncope and you don't really have to go much further because the history really suggests it situational is a little bit different it's very interesting I don't know what the heck this thing is right here let me fix that but situational is usually due to some type of straining event right so usually what happens is you see in the the particular scenario a patient has been like coughing and coughing and coughing and then they syncopize because they're straining and that can really activate the vagus nerve but even a bigger one is micturition so when a patient is trying to actually go to the bathroom and pee and pee and pee sometimes what that can do is that really can activate that vagal nerve outflow for some weird reason so ask the patient did they pass out after they were having a terrible coughing fit or while they were trying to really Force themselves to urinate the last one here is really interesting and this is usually due to a carotid sinus type of compression so you have to remember here one of the inputs to your actual central nervous system is you have here your carotid sinus right here at the Carotid signs this actually made this a lot better this is a really ugly carotid sinus let's fix that here here we're going to have the carotid sinus here we go and that will give your external and your internal kind of carotid arteries so common carotid internal external and then right here on that sinus area here there is these like little areas these little like receptors these pressure receptors and so sometimes whenever you activate these these can through some weird way kind of connect with the glossopharyngeal nerve and the vagus nerve and guess what these can go and do they can activate that vagal outflow so if you compress these so the whole concept is you have to compress these that'll activate it that can trigger this vagal outflow what are the things that will compress it one is when you do a carotid sinus massage they do this a lot in patients who have SVT so their heart rate's really fast and they really kind of mash on that that's going to compress this send vagal outflow and drop the heart rate hopefully so one of those would be a carotid sinus that was an ugly one sinus massage pretty cool I would say try to avoid this one in true reality for SVT but nonetheless the other one will be a tight collar believe it or not if you're going like straight like tight collars whenever you're wearing like a weird Polo that could be one or a button up so tight collars another time that I've seen these is um sometimes in patients who are shaving so when they're shaving that could also be another way that they're doing that because they're applying pressure over that area and then the other one is head turning so again you really want to try to ask the patient have they had any syncopal event from a carotid sinus massage wearing really really tight collars shaving while they were doing it or turning their head and that also caused it these are all things that are going to activate the vagal outflow depress the actual activate cause the cardio inhibitory system to become activated and the vasodepressor system to become activated all right let's go to the next one the next one here is going to be orthostatic Syncopy this is actually a really really interesting one super super common the concept behind this one is you have a patient who is usually in some way shape or form having a reduction in venous return that's honestly the biggest concept so you know blood is supposed to run here right so it'll run out from the arterial system and then come back via the venous system and then naturally it should come back into the heart and fill generate a good cardiac output but in some patients let's say that this pathway is affected and so because of this let's say that they have a very low venous return all right so they have a very low venous return when venous return is extremely low you don't fill the heart what is that called whenever you have less filling of the heart so if you have less filling of the heart you have a less preload or a edv right because of that if you drop your preload you drop your stroke volume you drop your cardiac output and you drop your blood pressure so all of these are kind of making sense right so if you drop your your Venus return you will subsequently drop your preload your stroke volume your cardiac output your blood pressure let's fix this one it's an ugly looking Arrow there preload and then if you drop your blood pressure what will happen to the actual cerebral perfusion it'll be reduced so as a result here 's cerebral perfusion will drop and if your cerebral perfusion drops then I'm not getting enough blood flow to the brain then right and as a result of me getting less of this blood flow to the brain what will then happen as a response the global hyperfusion and transient loss of consciousness so this would be the effect here and we'll actually kind of just Mash this up here unfortunately but this will be the transient loss of consciousness okay now question that arises in this scenario which Vegas outflow was increased we figured out the causes for that venous return is low we got to figure out the causes for that reasons why the venous return would be low is usually three particular reasons one is your volume within the vessel is significantly depleted relatively common right it's like this is really really common if a patient has diarrhea or vomiting they're not absorbing that fluid if they have peeing tons and tons and tons of fluid from their kidneys from diuretic abuse that could be another reason or if they have Burns or they're sweating like a banshee that would also cause them to lose a lot of fluid so if they're losing fluid from all of these sources or what's another way that you can lose fluid not as common but it would be terrifying bleeding so if it's from a fluid loss or blood loss what is that doing to your actual blood volume it's reducing it so these patients will have a reduced volume because all of their volume is being lost from these organs or from the blood vessel itself when you drop your blood volume we're going to abbreviate BV you drop your Venus return my friends and that will then subsequently lead to that orthostatic change which is you'll have a transient type of launch of Consciousness due to global hypoperfusion all right that's one concept another one is you're dilating the vessels so if you dilate the vessels you actually reduce the systemic vascular resistance and that reduces venous return so the whole concept behind this one is same thing you're reducing the systemic vascular resistance on the veins they're not squeezing normally veins are not high pressure system and they usually it's just going to be a slow flow but if you squeeze on the veins you can push the blood flow up to the heart well if you're not squeezing at all and they're really really relaxed or dilated that that venous return is going to be significantly reduced so a decrease in the svr will then reduce your preload or your venous return in this particular scenario now you have to then ask yourself the question what are the things that are causing this vessel to become super dilated it's dilating drugs one is going to be your calcium channel blockers they love to do this and then your Alpha One blockers so calcium channel blockers this is going to be drugs like um nifedipine amlodipine right Alpha One blockers will be things like tamsulosin prazasin doxazosin Etc these are going to cause the vessels to dilate they in other words their venous or their systemic vascular resistance is low they're not going to get a good venous return last one here is autonomic neuropathy this one's really interesting it's not the vagus nerve that's being affected let's use this color here we're going to have some sympathetic nerves that should be releasing things like norepinephrine and epinephrine Etc which should cause the vessel to Vino constrict if you constrict it the resistance goes up you squeeze blood up to the heart good venous return but what if I jack this thing up or I jack up the central part of it so now I have a neuropathy that's actually present and it's not sending these signals so there's a reduction of this as a result there is a reduction in the venal constriction if there's a reduction of venous constriction the svr goes down and the venous return consequently goes down so does the preload so does the stroke volume the cardiac output the blood pressure and then boom patients on the ground so these are decreased Vino constriction mechanisms just drugs versus neuropathy this one is your volume down okay we come to the last one here talking about the pathophys and causes here cardiogenic syncope in this particular scenario it's actually relatively straightforward it's not a message that's actually coming so you've kind of noticed here that in this one there was no real message from the brain to the actual cardiovascular system and this one it was the message from the brain to the cardiovascular system this one was a message from the cardiovascular system to the brain this is going to be the same thing a message from the cardiovascular system to the brain so what do I mean by that in this scenario it was a reduction in venous return in this one it's a generalized drop in cardiac output and that could be a bunch of different reasons which we'll talk about but in this problem the heart is not doing a very good job of getting blood out of the left ventricle and into your systemic circulation so there is going to be very very little blood flow circulating through the systemic circulation if I have very little blood floating through the systemic circulation that means very little blood getting to the actual central nervous system so the question is is okay we know out of this scenario here that there is a reduction in cardiac output we will talk about all the reasons why the cardiac output is reduced it's just it's different in this situation because it has nothing to do with venous return it's all other mechanisms in this scenario cardiac output drops if cardiac output drops then what do we know we know that that will drop your your blood pressure preferably the systolic blood pressure but in general we're going to say blood pressure that's going to cause cerebral perfusion to be reduced if you drop your cerebral perfusion you will have a transient loss of consciousness that'll actually occur right so this is the mechanism that we've constantly become acquainted with it's just in each one of these scenarios it was a little bit different as how we got to it Venus return vasodepressor cardio inhibitory response this one is there's a reduction of cardiac output let's talk about why this is the problem here when it comes down to a reduction in pure cardiac output from the heart the heart is the problem it's not the vessels it's not the venous return it's nothing to do with the Vegas outflow it's the heart is the problem there's two reasons why one is it's arithmogenic or it's a mechanical cause what do I mean well let's say that my heart rate is too high or my heart rate is too low may sound super simple here but whenever your heart rate is too high what you do is is you actually reduce your diastolic filling in other words you don't give the heart any time to fill with blood because you're trying to beat so fast you're beating fast you don't give it time to fill when you reduce diastolic filling you reduce what your preload and that reduces your stroke volume and that reduces cardiac output and that's how we got that concept there so what you'll notice here is that you reduce diastolic filling reduce stroke volume and reduce the patient's cardiac output but you have to really be going pretty fast generally greater than 150 beats per minute for the ventricles in order to really reduce diastolic filling so the time that you would see this is in a patient who has v-tac or v-fib that's why sometimes patients will syncopize in these particular events the other one is if the heart rate is super low because this is directly tied to cardiac output intensely so if a patient's heart rate is really low you directly we know cardiac output is equal to heart rate time stroke volume so if heart rate drops you will directly directly drop their cardiac output we don't even have to go through all of this mess it will directly drop their cardiac output this would usually be patients who have like complete or like very severe heart blocks so I'm talking generally like a second or third degree AV block and their cardiac output is so low that they're not able to perfuse the brain properly okay so that's generally going to be the concept here let me fix this I know Rob behind the camera is actually screaming right now so let me go ahead and fix this right here all right [Laughter] all right we're going on to the next concept here mechanical causes when we talk about these it has nothing to do with the heart rate it has something to do with the true ventricular function and usually this is it comes down to a couple causes one is the contractility stinks second they can't fill third they can't get blood out because of an afterload problem so three things one is a reduced contractility this one is usually due to reduced filling massively reduced filling and this one is high afterload so let's write those down so decrease contractility so there's something wrong with the pump the pump is not doing good here you can't fill like massively I'm not talking like a little bit you can't fill it all and third is the afterload which is the amount of like pressure and the work it takes to get blood out of the heart is massively increased things that would do this all of these things will drop your cardiac output I don't need to go through the whole mechanism this will drop your cardiac output this will drop your cardiac output this will drop your cardiac output but the question is why usually this is a massive myocardial infarction or it could be if a patient has a very severe heart failure usually with a reduced ejection fraction decreased filling is usually due to tension pneumothorax so this is because they have so much mediastinal shift that it compresses their right heart and their superior vena cava but they can't get blood into the Heart Another disease that acts like this is tamponade so these are other scenarios where this would be absolutely catastrophic you can see how these are much more scary than someone coughing or straining to pee the last one is increase afterload this would usually be this is classic please don't forget this one hypertrophic cardiomyopathy a young kind of athlete another disease similar to this one called aortic stenosis and the last one I've seen this before is a pulmonary embolism HTM and aortic stenosis it's hard to get blood out of the left ventricle into the aorta PE it's hard to get blood from the right ventricle into the pulmonary arteries and again you won't get any filling of the left side and you can't get blood out of the left side as well so these are catastrophic scenarios where your cardiac output drops to finish up we have now talked about the pathophysiology the causes but one thing I have to say here is that we have to briefly briefly briefly kind of come up with another way of defining the differences in the way that these present there's no true like complications that are like individualized to syncope but it is important when the patient presents you really listen to their story for reflex syncope usually the cause will be elucidated but the way that they say that they syncopized is really crucial for a reflex syncope you really want to hear this terminology of a prodrome that occurred before they lost Consciousness what the heck do I mean they saw a big orangutan running after them all of a sudden they got diaphoretic they got nauseous their Vision got blurry and they passed out that is a prodrome that preceded the loss of consciousness that's only critical to reflex syncope okay orthostatic syncope is positional this is super super important we know the causes patient could be hypovolemic they're taking medications or they have a neuropathic disease that improve that alters their venous return Venus return is super important when you're going from a seated or supine to a standing position if you do that you literally depend on those Vino constrictive mechanisms and volume to get blood to your heart so if you lose that the patient will then lose a lot of cardiac output and syncopize very quickly so it's usually a positional change the last one is cardiogenic this one is actually scary because these don't give you a prodrome they're not positional they're sudden so this could be two ways we could say here that's where I can actually put underneath it sudden or one other scenario exertional and what I mean by exertional is this is classic classic for your afterload problems your HCM so if a patient all of a sudden no prodrome no particular trigger boom they pass out you really want to think about arrhythmias if all of a sudden they're exerting themselves they're going to be making it harder especially for this afterload problem and then they pass out you really want to think more about the mechanical causes so exertional mechanical arrhythmia is usually sudden that covers this concept of syncope now it's going to how he diagnostically approach it with the diagnostic approach to syncope the first thing that I want you guys to think about is getting orthostatic vitals on a 12 lead ECG reason why is this is going to help you right away to tell you do I have an arithmogenic cause of syncope or do I have orthostatic syncope if I have them going from a seated to a standing position and during that time frame when I have the blood pressure checks between those two they're systolic drop more than 20. in that time frame going from seated to standing that would be diagnostic of orthostatic syncope another one would be if they're diastolic it was greater than 10 millimeter mercury drop that would also be suggestive this last one not as important but the heart rate should shoot up as a reflex to this drop in blood pressure but these are the findings that will be super suggestive of orthostatic syncope if a patient has an ECG that's abnormal and it shows hey they got a third degree AV block or a second degree move it's two or six sinus syndrome or v-tac or tors odds well then I've already concluded it's a cardiogenic syncope of a rhythmic origin but if the ECG is really normal and I just maybe miss them being in that occult arrhythmia then I can go ahead and do an EP study or a halter Monitor and see hey did I miss that particular arrhythmia if there is no arrhythmias but I think that their history is suggestive of a mechanical cause if it's super obvious like tamponade or tension pneumothorax or PE those are really kind of going to be super clinically obvious to you the ones that will probably miss is going to be the ones like aortic stenosis HCM maybe the heart failure or the cardiomyopathy so in those scenarios I would get an echocardiogram because that's really going to help me to see do they have a reduction in their ejection fraction do they have almost abnormality is there a synonym aortic valve is there septal hypertrophy these are great things to rule out the mechanical causes of cardiogenic syncope now if you've done this in the ECG is normal their orthostatic vitals are normal then I would kind of say it's probably some sort of reflex I just don't know if it's carotid sinus hypersensitivity if it's situational or if it's vasovagal so carotid sinus hybrid sensitivity is really interesting in the sense that if I rip you know kind of rep I'd say provide the same kind of event that put them into that type of arrhythmia or that type of event I could do what's called a carotid sinus massage and if I do that what it should do is it should kind of precipitate the body to think that the blood pressure is high and it should drop the systolic blood pressure and drop the heart rate so what I would see is I would see a systolic blood pressure drop of greater than 50 or asystole for at least more than three seconds and that's boom diagnostic if the patient has a prodrum it means that they get lightheaded they get nauseous they get kind of dizzy they feel like things are kind of they're getting dark and then they pass out that super suggestive of either vasovagal or situational so think about it was there a situational experience were they coughing or were they peeing and then they were really forcing that and then they passed out that's suggestive of situational whereas if the prodrome was present with them being in insane pain or they just saw like a spider or bear was chasing them or they were standing for a long period of time that's more suggestive of a vasovagal syncope and if you're still not sure you can sometimes do what's called a tilt table test and that can sometimes be helpful in that scenario but that's how we'd approach syncope one quick thing is sometimes there can be this differentiating factor that you really have to discern did the patient syncopize or did they develop a seizure because sometimes it can be difficult reason why a seizure is you can lose Consciousness syncope you can lose consciousness one of the differences here is that in seizures you'll see tonic clonic activity that usually occurs with this loss of consciousness whereas you will not see tonic clonic activity with syncope you may see some type of jerky movements but it should not be in this tonic clonic fashion the other thing is an aura so auras are definitely present in seizures whereas in syncope you want to look for that prodrome if they potentially have a reflex syncope and lastly tongue biting is more suggestive of seizures it should not be present in syncope and same thing incontinence losing control of bowel or bladder function is more common in seizures it should not be present in syncope lastly this post-dictal state after the patient seizes they have this period of confusion agitation they don't remember what kind of happened whereas the syncope they have a transient loss of consciousness and they should be able to have complete remembrance or return of their Consciousness with saying oh yeah I remembered what happened particularly and that's what really would help us to classify syncope from seizures when we have a patient who has syncope regardless of the cause whether it's reflex whether it's in this case orthostatic or cardiogenic syncope we really want to be able to treat these accordingly so reflex syncope is potentially treating the underlying cause in other words avoiding any of those triggers that causes the patient to pass out they may seem super obvious but it's the obvious answer in these scenarios orthostatic is probably where you may get a question or two and the concept behind this is remembering the causes volume loss or its decreased Vino constriction that's occurring here so fluids can sometimes be beneficial if the patient is hypovolemic avoiding vasodilator medications alpha blockers or any other kind of drugs such as a calcium channel blocker this will be super helpful because if it's a vasodilating cause you don't want to be having that medication on a patient who is chronically orthostatic for what maybe a chronic like autonomic nervous system neuropathy of some sort then in these scenarios you probably want to put them on something that'll give them a little bit of squeeze to their vessels and help them to maintain fluid volume so midodrine will squeeze their veins and fluger cortisone will help to remain a kind of maintain a good sodium and water balance in the body last one is cardiogenic Syncopy and it's pretty straightforward treat the underlying cause for example if they have an arrhythmia they need an aicd or a permanent pacemaker aicd for vtac or b-fib and then a permanent pacemaker for the bradycardia and if it's mechanical you have to treat that cause is it aortic stenosis HCM treat the cause accordingly all right my friends that cover Syncopy hope it made sense I hope that you guys enjoyed it as always until next time [Music] thank you [Music]