I want you to look at this EKG and tell me what the diagnosis is what do you use to car ride bundle what duration do you need for incomplete and complete based on the ACC criteria in order to Define complete bundle branch block you need to be over 120 milliseconds and incomplete bundle branch block it is between 110 and9 milliseconds less than 110 millisecond is not a bundle branch block same to Define non-specific intraventricular conduction delay you need a QRS over 110 millisecs without a specific feature for right or left bundle branch block so here actually I don't think we have delayed conduction it's two maybe barely two and a half boxes so it's less than 110 milliseconds so there is no bundle branch block so what you have on this EKG you have right Axis deviation Qs negative in one and upright in avf and you have an upright R in V1 that is larger than S actually there is monophasic R here so the diagnosis is straightforward this is right ventricular hypertrophy and this patient's QRS is less than one 10 milliseconds so you don't have that dilemma of trying to diagnose rvh the setting of right bundle branch block which I'm going to explain shortly so this patient has rvh and this is how rvh is defined is right Axis deviation more than plus 90° or sometimes a little less but close to plus 90° you know maybe plus 80° and so you need right Axis deviation unlike LVH you don't need left axis deviation and actually with LVH you tend to get a leftward axis you don't usually get fullblown left axis less than minus 30 de actually with LVH if you have a fullblown left axis it's usually something else associated with it it's either left bundle branch block or more commonly left anterior facular block when it's a fullblown less than minus 30° axis okay in rvh on the other hand it's mandatory to have right Axis deviation to define rvh or close to right Axis and on top of that you need Big R wve in the right lead V1 most importantly R bigger than S or if not bigger than S more than 7 mm another Criterion and here are some morphologies you can have R bigger than S or more than 7 millimeter in lead V1 or you can have the whole QRS is a small with a tiny s less than 2 mm another feature is big S bigger than R wve in lead V6 this feature is less specific and I don't like it too much because this may be seen in anything that turns the heart axis posteriorly you may see it with LVH with left anterior facular Block in which case is however the axis is not right you may see it with long disease that pushes the heart posteriorly and in Long disease you may have right Axis deviation and S bigger than R in lead V6 that nonetheless does not imply rvh so for those reasons s bigger than R in V6 is not specific for [Music] rvh so those are the most important criteria in r rvh and the reason we get those criteria in rvh is that in rvh the heart is extending down in the frontal plane and it's extending anteriorly the depolarization axis is extending anteriorly in the horizontal plane therefore those anterior forces are pronounced in V1 V2 the anterior forces cause big positivity in the right leads V1 V2 and they cause big negativity in the left leads V5 V6 and one AVL and the big positivity could be Big R but sometimes it's just a tinier s than usual like I mentioned less than 2 Millet and sometimes you get an rsr Prime pattern which I will explain this is another EKG what's the diagnosis here this is right Axis deviation with an rsr Prime pattern in lead V1 less than 110 milliseconds with an R Prime bigger than S that is indicative of rvh the same way R bigger than S indicates rvh when you have a standard QRS pattern RP Prime bigger than S when you have rsr Prime pattern is in indicative of rvh particularly when the QRS is less than 110 sometimes when it's 110 to 120 or more than 120 as well so this is rvh no ride bundle branch block and no incomplete R bundle branch block now I want to explain that more it's easy to diagnose rvh one QRS is less than 110 milliseconds it's more difficult and less specific and less sensitive positive to diagnose rvh when your QRS is wider and when you have right bundle branch block so I want to elaborate on this somewhat complex issue the overlap between rvh and right bundle branch block so rsr Prime in V1 is normal if the QRS is less than 110 millisecond and the axis is normal and S bigger than R and RP Prime it's a common normal variant I try not to even comment on it when I read the EKG rsr Prime in V1 is Right bound branch block whether incomplete or complete if it is more than 110 millisecond in which case RP Prime it's not only wide it's also RP Prime is definitely taller than R and frequently taller than S so that indicates pathology width and a change in the height parameter S rsr Prime is rvh if QRS is less than 110 milliseconds but you have R Prime bigger than S with right Axis deviation so this is a pure rvh if c s less than 110 with this RP Prime more than S and right Axis as in this patient now rsr Prime could be combined rvh with right bound bran block if QRS is over 110 milliseconds and R Prime bigger than S with the right Axis an important idea here you need to recognize right bundle brancher block does not cause by itself right Axis deviation so when you have right Axis deviation in conjunction with the right bundle branch block it's something else on top of it and that's usually your hint to rvh right BND the branch block with RP Prime bigger than S and right Axis is very possibly rvh now I didn't say it's definitely rvh associated with it why because what's the other option it's left posterior facular block so a right mod brancher block with right Axis could be left posterior facular block or more commonly rvh because left posterior facular block is an uncommon conduction disease it's the least common conduction disease further suggest of rvh will be R Prime bigger than S or R Prime as I will explain more than 10 to 15 mm and the reason right Bond bran block doesn't cause right Axis is that always we Define a frontal axis by looking at the first two boxes of the QRS we don't integrate the vector of the whole QRS QRS could be 150 milliseconds but we're not integrating all the forces by definition a frontal axis is defined by looking at the forces of the first 80 milliseconds so in right bundle you may have area under the curve of this s bigger than the area under the curve of this narrow R so that will make the axis potentially rightward if you integrate all of the forces under under the curve but by convention the frontal axis is defined by using the first 80 milliseconds so we're going to truncate that swave and you'll end up with a normal axis in right bonded branch block and how to diagnose rvh when there is right bonded branch block know the following idea most incomplete and complete right bundle bran block are benign and not related to rvh and in a lot of Nordic studies they are not associated with impaired longterm cardiac prognosis on the flip side most rvh from volume overload has some degree of rsr prime or incomplete or even complete right bundle branch block all this being due to the sluggish spread of depolarization across a dilated dri ventricle so incomplete right bundle branch block may be worrisome for rvh if it has these features R Prime more than S and more than 10 plus right Axis in complete right B branch block rvh diagnosis is less specific compared to again the left side I explained yesterday when you have left Bounder branch block you inherently assume there is LVH in most of the cases most often left bound branch block is not pure conduction disease it is conduction disease with some myocardial disease most commonly LVH could be more dilated carom myopathy and systolic dysfunction a right bondle branch block is is different and that's why it's hard to make the rvh diagnosis with right Bond branch block simply because right Bond branch block is most often a pure conduction disease so unlike left bundler branch block which is often related to Intrinsic LV disease and LVH often hypertensive disease most right BND branch block are not rvh they are just pure conduction disease and it's important to try to diagnose whether rvh is present or not so look at look at this EKG and tell me here what's the diagnosis this is wide this is very wide it's it is 120 and more than 120 when we measure the QRS width always pick the lead where it's wi this you can see in V5 V6 it's quite wide that QRS so it is so it is complete right bundle branch block the question is there rvh what other findings you have here this patient has sinus cardia he has right bundle branch block with a QRS over 120 milliseconds and he has right Axis deviation so you have right bundle branch block with right Axis deviation it's either right bundle branch block plus left posterior fular block or plus rvh supportive feature of rvh on top of the right Axis will be RP Prime more than 10 or better yet more than 15 mm but even that is not specific so you can have ride bundle with a big RP Prime and no rvh purely due to conduction disease conversely you can have rvh with right bundle and RP Prime less than 10 or 15 so again you lose sensitivity and specificity in right bound branch block most often when I see right Axis I assume it is rvh in conjunction with the right bundle branch block but I take always the clinical picture in context this particular patient with he sinus tachicardia this is not just conduction disease he was coming with dmia and he was diagnosed with PE he did have actually rvh on his Echo that this Criterion would have missed to diagnose right atrial enlargement you need to have the height of the p wve in lead to more than 2 and a half mm and it is here around that number that could suggest right atal enlargement or alternatively to call it right atan enlargement the positivity of p wve in lead V1 would be over 1.5 mm as you may see here the positivity in V1 becomes over 1.5 mm or the height of pwa in Le 2 would be over 2.5 mm meters either one of those he doesn't have the V1 Criterion here the catch when you have sinus sardia the p-wave height increases so much so that the criteria for right atal enlargment become less specific so having a p wve taller than 2 and a half millim or barely 2 and a half millimet in somebody with with s sardia is less specific for right large than the regular sinus rhythm this is another EKG what's the diagnosis always start by analyzing the QRS width before you jump to the height it's two small boxes looking any lead it's not more than two and a half small boxes so we have right Axis deviation we have a QRS that's about 100 to 110 milliseconds there is no bundle branch block here and importantly you have that what I call the QR pattern you see QR pattern in lead V1 this is definite rvh there is no other option here this is not left posterior facular block left posterior facular block gives you right Axis deviation but doesn't give you any abnormality in the precordial leads you have no reason to have rsr prime or QR or Big R unless you have Associated right Bond branch block but this being narrow this is a QR pattern of rvh with right Axis deviation and the reason I'm showing this is that you need to recognize that specific QR pattern of rvh which I will explain another Finding on this EKG is you do have definitely right atra enlargement the p wve in lead2 it's tall over 2 and a half millim in height uh it doesn't quite make the cut off in lead V1 where the positivity should be more than one and a half millimeters you do have a feature of left atal enlargement it's deeper than 1 mm and wide 1 mm so you have byal enlargement you also have something else suggestive of left eral enlargement that prolonged somewhat Notch p in lead usually you would see it in lead two but you see here in lead one but the more important diagnosis for me is rvh with a QR pattern and here is why I want you to know that rvh I mentioned you may have rsrp Prime pattern and and I mentioned the rsr prime pattern is suggestive of volume overload you lose some specificity The Wider the rsr prime is but regardless it does suggest a volume overload type of rvh if it is rvh on the other hand when you you have a QR pattern as in here or if you have monophasic r as in this one it's a monophasic r notched but monophasic there is no s it's a notched R so when you have a QR or monophasic r instead of RS or rsrp prime pattern this is suggestive of severely increased right ventricular pressure severe pressure overload type of rvh and usually suggests that the RV systolic pressure is equal or higher than the systemic pressure so you frequently see that in pulmonic stenosis or in severe pulmonary hypertension so be familiar with that QR pattern or monophasic R without widen QRS which is suggestive of pressure overload the widen QRS rsr Prime is suggestive of volume overall simply because the RV is dilated in volume overload and therefore the electrical depolarization takes longer to spread throughout that R ventricle and you get that QRS prolongation and rsr Prime rvh like LVH may lead to secondary St abnormalities so and those secondary St abnormalities will look in opposite direction to the QRS so it leads V1 through V3 you will have S depression opposite to the QRS you tend to get more T inversion than S depression with rvh just because usually the RV mass is smaller than the LV Mass so we get more strain pattern more s depression with LVH then you do get with rvh but you definitely can get straight pattern with rvh depending on the severity of the rvh and it will be a CD de pression with t inversion again more commonly T inversion than a CD de pression and more pronounced Inver SD depression but regardless you can get both and this is what you're having here this you're having here rvh with a strain pattern this is a patient with very severe pulmonary hypertension and RV pressure overload and you're getting those secondary St abnormality so left bundle branch block inherently causes opposite change stct elevation and depressions LVH may cause the same discordant St changes as well rvh and right bound ban block may lead to ST depression and T inversion but they do not lead to Elevation and that's a major difference between the right sided issues versus the Left sided issues one difference is that the ST depression you get to the right sided issues is usually not as pronounced as the one you get with the left-sided issues although it can be pronounced it's less commonly pronounced and number two you do not get St elevation with the right sided issues so St elevation with rvh or right B bran block even if looks discordant it's always abnormal and suggestive of a primary process such as an MI I showed this EKG earlier and I just want to explain this idea lung disease pattern is different from right ventricular hypertrophy you can have long disease pattern without right ventricular hypertrophy and what it means you have a lot of chest air and increased size chest cavity which will press the heart and make make it more vertical in a frontal plane and push it posteriorly in a horizontal plane so this is what lung disease leads to it will lead to a vertical heart axis in the frontal plane and it will cause posterior heart shift meaning deep s wave throughout all of the precordial leaves and poor precordial R wve progression so we'll have small R big S throughout all the precordial leaves because the heart is pushed posteriorly to the right Axis the S bigger than RM V6 can mimic rvh so by EKG it can mimic rvh but it is different than rvh and there are specific criteria to diagnose rvh in context so this chronic lung disease pattern may simulate rvh through rvh in conjunction with lung disease requires additional features and I'll explain that so whenever you have an EKG like this you have right Axis but you also have that small R big S throughout most of the precordial leads with an overall QRS that is not large and may even fill the features of low voltage you're thinking lung disease so right Axis small R big S throughout the pical leads with a total QRS height that is not large this is very suggestive of lung disease to diagnose rvh on top of that you need additional features and the additional features are those you want large r or small s in V1 so it's not just that you have deep s throughout well maybe in V1 the r is bigger than s or that s that is bigger than R is still very small like the whole complex is small and S is less than 2 Millers or you will have the strain pattern that will suggest rvh T inversion in V1 V2 so that will suggest rvh in conjunction with lung disease or you will have an rsr Prime pattern that will suggest rvh on top of lung disease including rsr Prime less than 11 milliseconds also p monali is less helpful because with lung disease as the heart becomes more vertical the Atria plane of diarization becomes more vertical so you can get a high p wve in lead to so P monali may be seen with lung disease even without rvh or right atal enlargement so people Wali becomes less specific for rvh or R Atri enlargement so you understand that pattern I want you to know that when I was a fellow used to get confused is lung disease pattern rvh there is overlap that's why I tried to explain to you also rvh and right Bond branch block overlap there's a lot of overlap between those pathologies so I mentioned that the lung disease pattern may simulate rvh I mentioned the criteria for that also as I mentioned previously The Chronic lung disease pattern may simulate an old interior enteral Mi where an R is diminished all across the precordial leads and in the lateral leads one an AVL and you get that right Axis so I showed that EKG and I showed it's hard to tell this EKG may be long disease pattern but may very well be an old inter lateral Mi with poor precordial R progression and Tiny R in the lateral limes and in the lateral lead V5 okay another idea I mentioned yesterday in conjunction with the explanation about LVH I mentioned the differential diagnosis of poor r-wave progression and how to sort out whether there is an MI or not and you need to know the causes of poor rwa progression left anterior phical block LVH left bundle COPD and lead misplacement or proper lead placement but the heart is too low compared to the lead or the heart is too posterior compared to the lead there is the flip side of that which is Big R wve it's the opposite it's the early transition you have Big R wve in lead V1 bigger than S or those same ideas apply to Big R waving lead V2 bigger than S the so-called early transition R wve and you need to know the differential diagnosis whenever you see a big rwa W I mentioned that when you analyze the QRS you look at four things you look at the Q waves first you look at QRS width QRS height and r-wave transition in the precordial leads including poor transition poor precordial rwa progression or early transition so it's an important whenever you analyze QRS just follow systematically those four steps qwave QRS width sare height and the transition and when you see Big R wve in V1 this is a differential diagnosis could be rvh in which case you'll have that Associated right Axis deviation it could be right bundle branch block QRS would be wide it could be posterior wall infarction in which case you'll get a Big R in V1 or V2 but it's also not just big it tends to be wide like a qwave an abnormal Q is not just deep but it's wide so you tend to have a wide R wve more than one box in V1 V2 and sometimes if it is rsr prime pattern with a posterior infar it will be wide initial R wve more than one box not just wide RP Prime so it will be a special rsr Prime with a wide initial R and frequently unlike rvh and R bundle when you have have posterior wall infarction the t-wave is upright in leads V1 V2 it's not inverted and frequently you will have and you should think of doing posterior leads and see if you have a Q waves in those posterior leads the reason T is upright because posteriorly T will inverted as an infar another differential diagnosis is wpw with left accessory pathway you need to know those very well those four a less the fifth one is less common it's hypertrophic caromi opathy believe it or not it's hypertrophic colopathy of the left ventricle so you typically get Big R wve in the Le V5 V6 and big s in V1 V2 but on occasionally that localized very localized sepal basil hypertrophic carom opathy you may have Big R in V1 and big Q in V5 56 when it's very localized without much hypertrophy on the lateral end posterior or even entol lateral wall okay another entity is duchan muscle hypertrophy because it causes posterior wall fibrosis like a posterior am I you need to know those you cannot be a cardiologist and not know those Basics honestly however the most common cause of early transition Big R in V1 or V2 is just a normal variance it is more common in young individuals where the heart is swung more anteriorly than older individuals older individuals may have poor r-wave progression as a normal variant younger individual may have that early transition as a normal variant because their heart is swung more anteriorly also that normal variant early r-wave could be just Lal position of the electrodes V1 V2 unlike poor rwa progression the electrodes V1 V2 are too high compared to the heart early rwa progression maybe1 V2 are too close to the level of the heart those leads will see better the anterior theorization and you'll get that pronounce R wave in V1 V2 you need to print that and that but especially this one because most fellows don't know it also when it is a normal variant early transition the key is that you don't have other Associated feature no R bundle branch block no abnormality of strain pattern of St and T no widening of the QRS it's an isolated early transition that's how you know it's a normal variant okay I'll move on to this EKG can anybody tell me what's the diagnosis on this EKG we have LVH by voltage criteria you have have the sof and lions criteria you have S in V1 plus r in V5 or V6 way over 35 mm mainly met because of V5 and V6 you have the Cornell criteria sv3 plus RN AVL it's way over 28 mm or 5 and a half boxes you also have the Criterion of RN V5 or RN V6 more than 26 mm or five boxes there is also a widen QRS with a right bundle branch block pattern in lead V1 but this is an unusual right bundle branch block this is rsr prime s pre okay RS RP Prime S Prime not the usual rsrp Prime so what we call that fractured right bondle branch block is very suggestive of some myocardial disease it's not your typical right bondle branch block fracture the more notching and fracture in the QRS the more you think of myocar disese what else in the QRS what's the QRS axis here QRS is negative in lead avf and is negative in lead one but close to equ phasic so you're negative in avf you're in this Zone and you're close to equ phasic to one so you're about here you're close to Min - 90° but you're a little negative in one so so you're in reality in this Northwest axis area does he have rvh here's something unusual you don't often see on EKG okay you told me he has LVH think about it LVH gives you big s in the right preoral leads and Big R in the left preoral leads well look at this patient he has a huge R in the electrical but he also has has a huge s look at the s in lead V6 and V5 they are abutting each other and going all the way down it's hard to tell where they finish he doesn't have just Big R he has a huge s in the left preoral lead and interestingly the s in the right preoral lead is not that pronounced you meet the soal flying criteria based on the size of the r in the left leads not so much because of the s in the right leads so what does this tell you and you have a Northwest axis which I said LVH doesn't cause major axis shift by itself here you have a Northwest axis so what's the diagnosis is it B ventricular hypertrophy yes yes it's B ventricular hypertrophy it's massive biventricular hypertrophy there are so many criterias for that and there is one Criterion I want you to know in the the mid to lateral precordial leads when you have a huge basic QRS huge R and huge s with the summation of RNs the whole QRS more than 50 mm this is what we call it has a name cats wakel it's a highly specific sign of biventricular hypertrophy plus he has biatrial enlargement you have a huge peyp wve in lead two way more than 2 and a half mm and you have a peaky first positivity of p wve in V1 more than 1 and a half millimet you also have deep negativity more than 1 MIM so you has by aan enlargement based on V1 and he definitely has right Aton enlargement based on lead two so this is the final diagnosis you have sinus rhythm byon enlargement right bundle branch block with a fractured rsr Prime S Prime pattern suggestive of myoc caral disease severe LVH voltage but also rvh based on the unusual axis accompanying that LVH whether you have right Axis or Northwest axis that will be suggestive of rvh in conjunction with LVH also the cat swel sign that tall basic QRS in V4 V5 V6 and another hint despite LVH you're having small negative forces in V1 that's also suggestive of rvh in conjunction of LBH that rvh is diminishing those negative forces in V1 another thing is the strain pattern so we have LVH strain here but you also have a c depression in those leads V2 V3 that is concordant with the QRS that is not due to LVH that LVH gives you s depression opposite to the QRS QRS is up S depression will be down but here you have a depression those leads where there is dominant QRS negativity this in conjunction with everything else is suggestive of RV straight pattern so that also supports B ventricular hypertrophy so on this EKG in the setting of LVH rvh and therefore biventricular hypertrophy is suggested by the axis whether right or in this case Northwest axis the paradoxically small SNS Prime lead V1 discrepant with LVH the estd depression on the right precordial lead a form of right ventricular strain marked by atrial enlargement the fragmented right BND branch block pattern which indicates right heart pathology and the cats wakel phenomenon those tall basic preoral QRS complexes in V4 V6 this patient had moderately large vsd with biventricular failure clinically and B ventricular enlargement on Echo and this is how we diagnose B ventricular enlargement as from my book you have any of those one voltage criteria for both LVH and rvh this usually means you have tall R wve in V5 V6 of LVH with a small swave in V1 paradoxically small swaave in V1 or R bigger than S in V1 R is not going to be large in V1 when you have B ventricular hypertrophy because you have both ventricle pulling that r and s in different direction but R is bigger than S even though it's not that big but it's still bigger than S a second feature is LVH with right Axis deviation and that to me is the most common one you have LVH that you have right Axis or Northwest that's B ventricular enlargement third is LVH with right atal or bial enlargement fourth is LVH with t inversion in V1 V2 meaning a right heart strain pattern which suggests B ventricular hypertrophy although T inversion V1 and V2 or and ST depression V1 V2 could be RV strain but could also be anterior ischemia so we have to analyze it in context that concordant ST depression could be right heart strain or could be eske in this EKG context is clearly right heart strain but in another context it might be anterior esia and the fifth feature is that tall R and Tall s and mid or lateral precordial leads the cat's wakel sign this is another EKG what's the diagnosis on that EKG so there is atra flutter agree 3:1 atra flutter unusual atra flutter what else incomplete what right bundle how come why right bundle in order to call it right bundle it's not enough to have rsr Prime in you want R Prime should be pronounced should be closed in size to the swave and the slurred s in V5 V6 should be by definition wider than the initial R wave so when the S is narrower or equal width to the r this is not right bound bran block so analyze systematically go Q waves QRS width QRS height and the transition zone those are the four steps one there is no Q wave abnormal qave two how wide it's about 110 millisecond it's not boxes in any lead okay wide we'll have to Define what type of bundle or non-specific intraventricular conduction delay I don't think it's right bundle like I explained to you it's clearly also not left bundle you don't have a slurring of the r wve on those lateral leads so it could be unspecific conduction delay another thing I want to tell you that in terms of a QRS width when the QRS is between 110 and 12 20 and you don't have right or left bundle branch block criteria it could be non-specific intraventricular conduction delay but it may also be QRS widening from ventricular hypertrophy so both rvh and LVH can give you QRS 1 I mentioned rvh can give you rsr prime pattern with a QRS 110 to 120 milliseconds LVH can also give you QRS widening with Progressive incomplete then complete left bundle branch block but sometimes you have a mild QRS widening with LVH that is 110 to 120 M seconds without loss of qwave in leads V one and AVL so I would not call it LVH plus incomplete left bundle branch block I would call it LVH with QRS widening anyway do we have LVH voltage here what is the Cornell here SN V3 plus r in AVL is 20 mm which fits the Cornell criteria for LVH in a woman or in a man if he has big ight t-wave in lead V1 it's hard to tell the t-wave status in lead V1 here I don't think it is more than 2 mm in a man the criteria are lower you you move to 1222 women 12 man 22 mm if you have big upright t-wave in lead V1 she doesn't actually but she's a woman so she fulfill the Cornell criteria what else so she has LVH what else you have LVH with right Axis it's simple so to summarize it this is this patient has atal flutter mostly 3:1 AV block she has Cornel criteria for [Music] LVH based on S 3 plus r and AVL about 20 mm her QRS is about 110 milliseconds and it's likely QRS widening related to left ventricular hypertrophy she also has right Axis deviation so LVH with right Axis deviation inherently it's biventricular hypertrophy there is also close to the gold Burger criteria I described earlier pronounce voltage in preoral Le reduce voltage the Lim Le so it could be also suggestive of dilated copath and this is what this patient had eventually B ventricular dilatation this is a 75y old man with heart failure what are the findings on this EKG so you have inferior and anterior infar yes so what's the diagnosis in this patient anterior and inferior am I if you have an infar from an LED especially mid LED you an apy those are the patients where you get acutely diffused St elevation and chronically you get diffused Q waves you get them in the anterior and in the inferior lead it's an LED that traps around the Apex so you get injury in All Leads because the Apex looks at All Leads so it could be that when you see that EKG one diagnosis should pop in your head yes it could be am I but there is something else I'll tell you okay you think it's Mi well his Echo shows normal F and no segmental wall motion abnormality now what's the diagnosis amiloidosis yes so let me summarize it here so this patient has sinus rhythm with a long PR interval he has low voltage in the limb leads less than 5 millimeter QRS voltage in the limb leads not quite low in the precordial leads they are to call them low in the precordial leads they need to be less than 10 mm in all the leads not quite fulfilling that but still relatively low voltage in the preoral leads you have extensive Q waves in the inferior leads and in leads V1 through V4 so the possibilities are that he has esic carom myopathy and a prior anterior and inferior infar usually the LV will dilate in those cases you will get Ecentric hypertrophy you will get more pronounced voltage except in end state copath with a lot of Scar you will lose voltage however whenever you see that infar pattern with low voltage think amiloidosis because this is what AM amiloidosis lead to low voltage especially the limb leads you may not fulfill it the low voltage Criterion in the preoral leads or low voltage that's progressively reduced over time so it may not look low in absolute but if you compare to older EKGs you'll see Progressive decline in the QRS and very important you get pseudo Q waves in amiloidosis so you get you can get extensive Q waves just because that Amo tissue is replacing active myocardial cells you're having inert electrically inert tissue in The myocardium and that will cause qwave it's a tissue that doesn't have electrical activity a truly low voltage in both pror and Lim lead is insensitive and is only seen in 30% of transitin amiloidosis to 50% of Al amiloidosis however the near Universal finding in Amo dois is QRS voltage that is not high you cannot have LVH voltage and QRS voltages gradually decrease over time or is low in the limb leads it fulfills the criteria of low voltage in the limb leads or disproportionately low relatively to the LV thickness so you you see an LV thickness of 15 16 mm yet the QRS height is normal or somewhat reduced or bluntly low in the limb leads so that's a hint for you it's very important because for example this patient I showed here I suspected when the echo came back showing normally f i suspected Amis so I did PP scan and the serum and urine imun fixation those were negative but we insisted on the diagnosis and eventually we did endomyocardial biopsy and that was the only way we established diagnosis in this patient he had a l Lambda type amiloidosis interestingly even his septum wasn't thick initially normally to suggest am dois on Echo you want some thickening of the septum typically for or above his septum wasn't even even thick initially so that EKG was really the only hint to amid dois in this patient his IV septum progressively thickened over time this is another kind of similar case 72y old man heart failure normally F that we admitted recently to the hospital again low voltage this time he's fulfilling low voltage in both the limb and the precordial leads there are Q waves in the inferior leads you see them in two and avf and there are extensive Q waves throughout all of the precordial leads with this normally F this is very suggestive amiloidosis they show you that on board you should think amiloidosis so I did on this patient pyp scan and the imuno fixation type of work all those came negative so we ordered karak MRI and we're waiting for the result if kak MRI shows diffuse subendocardial LGE we might end up doing a biopsy especially if he continues to have a progressive heart failure to prove the diagnosis