EKG Interpretation: Beyond the Basics

so over the next 30 minutes or so I thought I would just show you a few key examples that I think are important that you might encounter in your offices or obviously up in the hospital and certainly this is not meant to be a conclusive representation or comprehensive representation of electrocardiography but I thought maybe some take-home points here this is an example of hyperkalemia and Oh renal failure patient taken care of by one of our nephrologists and I think the underlying story here is it’s important as an office based practitioner or in the hospital to recognize electrolyte abnormalities because the electrocardiogram may be the first indicator of an electrolyte abnormality typically this pertains to calcium and potassium disorders potassium affecting initially the T wave is in this case with a peaked symmetric t way with a narrow base notice that the T wave amplitude may not be all that high but in fact it’s more the symmetry and the narrow based portion of the T wave that’s most important in addition and more pronounced cases of hyperkalemia you can have QRS complex duration prolongation you can have PR interval prolongation as well with hypokalemia you will see a prominent T wave and often a prolonged QT you segment because the UAV gains more prominence in calcium disorders it’ll typically affect the QT interval and spare the QRS complex per se and the PR interval this next particularly patient is an example of wolff-parkinson-white syndrome and ventricular pre excitation and the take-home message here is sure the PR interval is short you can see that the PR interval is short and all leads there’s a delayed upstroke to the QRS complex and that delayed upstroke reflects early activation of the ventricle down the accessory pathway what you want to be careful of here is interpreting an agent determinate myocardial infarction so some people might want to identify the inferior leads as having prominent fairly long duration Q waves supporting an agent determinate for your myocardial infarction but that’s where you can get into trouble in fact the accessory pathway conduction is opposite the inferior leads in this case so your getting an initial negative QRS complex deflection due to the fact that the accessory pathway vector is away from the inferior lead so in this case you’d want to steer away from an agent determinant myocardial infarction but instead stick with the accessory pathway this patient may in fact have coronary artery disease but that would you’d have to rely on another test to make that diagnosis this particular patient does have coronary artery disease well I can’t conclusively tell you that the patient has coronary artery disease based on the electrocardiogram there is a hint here first of all he’s being taken care of by an interventional cardiologist that that always helps but not all of you are from Cleveland Clinic so you may not know that this patient demonstrates normal sinus rhythm with complete right bundle branch block that’s a fairly routine finding on an electrocardiogram and is very nonspecific so what is somewhat more specific regarding coronary artery disease well look at the T waves and leads v1 and v2 they are actually positive or concordant with the QRS complex that is abnormal in the setting of complete right bundle branch block that is an example of a primary T wave change in the setting of complete right bundle branch block and suggests the possibility of posterior circulation abnormalities and and in fact this patient had a dominant left circumflex which had been occluded and the patient had a prior posterior myocardial infarction is it diagnostic from this electrocardiogram no is it suggested that there may be a problem yes based on the t wave and QRS complex concordance so when you see this it should raise your attention to the possibility of a posterior circulatory problem and I think you should do more investigation more investigation is subject to discussion it might include include a history and physical and if there’s any concern particularly in terms of their aggregate cardiac risk factors you might consider some sort of cardiac stress imaging this is a patient with sinus rhythm may be borderline first-degree atrial ventricular block and complete left bundle branch block and this patient had profound left ventricular systolic dysfunction on a non ischemic basis the patient had a heart cath which demonstrated normal coronary arteries there is some correlation between the duration of the QRS complex and the level of degree of LV dysfunction the wider the QRS complex suggests and somewhat correlates with more profound left ventricular systolic dysfunction provided the patient’s not on any anti rhythmic poisons such as amiodarone or something else which also can prolong the cures complex why am i showing this EKG because it’s basically complete left bundle branch block which you’ve all seen well there’s inferior q waves and leads three and a VF and we have to know that both the strengths and limitations of any test with regard to

electrocardiograph II it’s not really a good idea it’s not permissible to code an agent determinate myocardial infarction in the presence of complete left bundle branch block if you think about it the left ventricle is too polarized last it’s the right ventricle that’s depolarize first and then there’s right to left ventricular depolarization the polarization is slowed entry is first into the distal conduction system and therefore the Curos complex is displayed extremely apparently and there’s not a prompt initial reflection of left ventricular events given the lack of visualization or ability to interpret prompt left ventricular events the inferior q waves really are out of bounds there you really shouldn’t derive any conclusions from those you might notice that a patient has a somewhat a left or a taxes but even in lead to the Curos complex is positive so I would leave this alone and say sinus rhythm first degree AV block complete left bundle branch block and the inferior Q waves are not informative in this particular instance this next patient actually does demonstrate findings where you can diagnose an age and determine myocardial infarction this patient demonstrates sinus rhythm rate may be slightly greater than 60 per minute the PR interval is markedly prolonged greater than 200 milliseconds the cure s complex vector is positive and lead 1 and negative and leads to three and a VF so the patient has left anterior Hemi block there’s no evidence of an age of determinant inferior myocardial infarction because our waves are still present and leads to three and a VF so we’re gonna stick with left anterior fascicular block there is a QR pattern q RR prime pattern and leads v1 and lead v2 the QRS complex is delayed so that looks like a complete right bundle branch block because the cure s complex is at 120 milliseconds or longer so this patient actually has first your gravy block left anterior fascicular block and complete right bundle branch block if they had synch to be this would be a patient who you’d send a friend Fred Jagger or one of our electrophysiologists this patient also has coronary artery disease again cared for by dr. Whitlow one of my interventional colleagues notice the Q waves and leads v2 and v3 so we had complete left bundle branch block we couldn’t derive any conclusions about Q waves because the left ventricle is depolarized late incomplete right bundle branch block the left ventricle is actually depolarized early it’s a depolarize first so there’s no superimposed right ventricular events with left ventricular depolarization and you see what would I consider a more pure electrical reflection on the surface EKG of left ventricular events and this patient actually demonstrates an agent a term at a neuro septal or a a neuro septal myocardial infarction because it looks like v4 may be spared so this patient does have coronary artery disease and you can make that determination in the presence of complete right bundle branch block because the left ventricle is depolarized initially here’s a patient it’d be unlikely for them to walk in your office perhaps in the hospital or perhaps in the Muenster room this patient has a hemodynamically significant pericardial effusion this patient has diffused low-voltage qrs and the concept of electrical alternans i think you can all see that each every other QRS complex demonstrates a differing but regular amplitude so there’s very there’s regularization to this every other Kuras complex amplitude there’s diffused low-voltage qrs somewhat rightward axis and this patient had unfortunately a metastatic malignancy including a large pericardial effusion this should not be confused with what we see as the respiratory variation on an electrocardiogram where it might be more like this in terms of its variation it’s not an every other variation but you might see a slight variation of curves complex amplitude as the patient takes a deep breath and then exhales this is a and actually with a ventricular pacemaker ventricular pacemakers can be tricky to see on an electrocardiogram however there is a small discrete deflection before each QRS complex supporting the presence of a ventricular pacemaker notice that the QRS complex is negative and leads to three and a VF and also it’s a left bundle branch block morphology the the ventricular pacemaker lead is in the right ventricular apex so that by definition is going to give you a left bundle branch block morphology because the right ventricle is being depolarize first remember this is a nada biventricular pacemaker pacemaker we’re pacing the right ventricular apex so we get a left bundle branch block morphology since we’re pacing the apex it’s going to be able to base depolarization opposite what normal the polarization is so that means you’re actually activating the heart away from the inferior leads toward the upper aspects of the heart so maybe toward AVL and lead one so from Baystate from apex to base and that’s why you get the negative QRS complex and leads to three and a VF away from those leads now I wouldn’t have shown you this EKG just

solely for that this patient also has retrograde atrial activation so if in fact you see say let’s look at the lead v1 rhythm strip you can see retrograde P waves within the ST segment and that means that there’s retrograde ventricular atrial depolarization the atria are actually contracting against closed mitral and tricuspid valves and those in that circumstance patients can actually present with exertional intolerance shortness of breath fatigue and this can be equated with the at least the electrocardiogram presence of the pacemaker syndrome so this is a type of patient if you have a patient who’s not thriving doing poorly for one reason or another and has an electrocardiogram that looks like this they need to be referred to your pacemaker clinic because reprogramming of their pacemaker is indicated this is actually an interesting EKG it’s an interesting coronary artery disease pattern that you don’t see all that frequently so this patient has let’s say sinus rhythm a rate of around 60 65 per minute notice that there’s a prominent our wave in lead v1 the R wave is greater than the S wave in lead v1 that suggests the possibility of posterior territory pathology well is there something else on this electrocardiogram that supports that finding well there’s Q waves and leads one in AVL and that’s the high lateral leads so the high lateral leads appear to be infected the posterior leads may be affected and notice also in leads v5 and v6 you actually demonstrate our wave regression with the presence of Q waves so this is an example actually of a postural lateral and high lateral myocardial infarction almost certainly the left circumflex coronary artery distribution notice the prominent R waves and leads to three and a VF this does not support right coronary or involvement but instead a posterolateral and high lateral infarction that you may see with circumflex disease and not a terribly common electrocardiogram but one that you may run across a run across over time this is more of a Show and Tell this is an electrocardiograph example of a patient with a secundum atrial septal defect and again if you see a lot of primary care patients in your high-volume practice the patient may be asymptomatic particularly if they’re in a younger age group the left to right shun isn’t all that significant but this is an example of an atrial septal defect is it diagnostic no is it highly suggestive yes I’m not really into pattern recognition when trying to educate colleagues regarding electrocardiograms but this is one of those cases where you should recognize the pattern notice and lead v1 which I would consider the money lead here the somewhat unusual appearing delayed double positive inscription of the QRS complex this this reflects in this particular case initially left ventricular and then followed by delayed right ventricular depolarization so sort of a double QRS complex not classic for a complete or incomplete right bundle branch block but indicative of right ventricular conduction delay due to a left-to-right shunt right ventricular enlargement and dilatation and slowed right ventricular depolarization if you critically look at leads v4 v5 and v6 you can see that there’s somewhat of a terminal s wave delay there as well and that’s also indicative of right ventricular depolarization which is slowed if you think about it lead v6 is extreme left ventricle so if there’s delayed right ventricular depolarization it’s going to be very far away from lead v6 and it’s going to be delayed and that’s why it’s a negative delayed inscription on this electrocardiogram so keep in mind lead v1 and if you run across that pattern take a good history do a physical and consider a transthoracic echocardiogram if your suspicions are reasonably high and that transthoracic echo would be with intravenous saline contrast as well to look for the intercardiac shunt the reason I’m showing this EKG is to try to distinguish between premature atrial complexes and premature ventricular complexes and many folks would be led to believe that this represents non sustained ventricular tachycardia well in fact these are premature atrial complexes with right bundle branch block aberrancy so how do you make that distinction on this electrocardiogram well if we go back to the basics first of all we have sinus rhythm rate of around 60 and maybe a little bit of a leftward axis we’re positive in one slightly negative and lead to and negative in leads three and a VF so we’re going to say we have a leftward axis with sinus rhythm if you go across the EKG what I try to do is I land on anything that looks familiar and in that I can readily make the diagnosis of then I try to work backwards in this particular case is a premature or atrial complex it’s preceded by AP wave within the T wave of the preceding torus

complex and even before that complex there’s another premature so those are 2 premature or atrial complexes in succession one of which does not conduct with aberrancy the next one does conduct with the barren sea and those that occur three in a row actually conduct with maximal aberrancy so going backwards you can actually see a P wave within the T wave deforming the terminal aspect of the T wave which precedes this atrial triplet so this is a nice example of premature atrial complexes with a Barron see otherwise a normal electric cardiogram with the exception of perhaps a left axis of the QRS complex this is sort of what Fred Jagger just showed us with regard to what you don’t want to see this was a young woman who was unfortunately very ill with some sort of malignancy receiving chemotherapy and had a potassium level less than three so this is a 12-lead electrocardiogram example of torse odd in a patient with a markedly prolonged QT interval best exemplified in leads v4 v5 and v6 where at the initial left-hand portion of the EKG they actually demonstrate an R on T phenomena where the PVC occurs on top of the T wave during the probable vulnerable period which initiates a period or torus odd this particular case actually is a very important EKG if it’s a little bit blurry I apologize this demonstrates sinus rhythm with left anterior fascicular block positive QRS complex and lead one negative QRS complex vector and leads to three and a VF so that’s a relatively simple electrocardiogram and most people would code this is otherwise a normal electric cardiogram but this EKG actually shows something even more important than that and that’s called a negative u wave and I’m not sure how many of you have heard of a negative u wave before but let’s look and leaves v4 v5 and v6 just following the T wave you will see a negative deflection and that’s a negative u way for negative u ways are typically found in two circumstances one is ischemic heart disease and the other is left ventricular hypertrophy this patient doesn’t have marked cures complex voltage or repolarization changes to suggest left ventricular hypertrophy or LV mass and I distinctly remember this patient even though it says dr. Topol on the EKG I think it was during an American College of Cardiology meeting I was much younger I was of course asked to stay back for the meeting and to see one of dr. toklas patients and this patient had a history of an led angioplasty and a stent in the past and had been doing well but over the past week or so had recurrent angina so I saw him and this and clinically it was apparent he had angina but I saw this EKG I said myself okay this guy’s got negative view waves I looked at his prior EKG he didn’t have one negative view waves so these actually can be transient finding in the presence of active ischemic heart disease so he underwent a calf a repeat intervention and sure enough I saw him and follow up about a month later and his negative view waves have gone away and that was about ten years ago and he’s been my patient ever since and he’s continued to do clinically extremely well so this is where the negative view waves can come in handy and if you if you read a lot of EKGs or if you see a lot of patients preoperatively particularly in patients with say peripheral arterial disease those are the patients where you’ll see this so if there’s a high pretest probability for a negative UA where there’s cut where you suspect coronary artery disease take a look at leads v4 v5 and v6 there’s more of these floating out there than you realize so this is a nice example actually of paying attention to the underlying atrial rhythm in the setting of ventricular pacing toward the right-hand portion of the EKG hopefully everyone can see that there’s a paroxysm of ventricular pacing and then to the extreme right hand side of the EKG the ventricular pacing seems to go away and in fact the native QRS complex conduction resumes to the left-hand side of the EKG you see what appears to be native QRS complexes without any identifiable interactivity so this patient actually demonstrates atrial fibrillation with a variable but controlled ventricular response in addition there’s a Q wave at least in lead a VF raising the likelihood of an agent determinant inferior myocardial infarction and then for some reason the ventricular conduction slows and then the pacemaker kicks in and then toward the end actually the native QRS complex takes over in the pacemaker once again becomes quiet in fact the second to last QRS complex is both an intermediate paced and native QRS complex is what we call a pacemaker fusion complex so that complex is partially paced partial native conduction and it’s a hybrid between the fully paced and the non paced complex the important take-home message on this EKG is as follows it’s important to pay attention as best you can to the underlying atrial rhythm even if the patient’s ventricular lee paced because if this patient had

inappropriate chads2 score and a cardio embolic risk which was felt to be significant of course this patient would need to be anticoagulated so that’s the really the take-home message on this EKG this is a calcium disorder and one that I think I’ve overlooked many times but this one I got right this was a patient who had primary hyperparathyroidism in hypercalcemia and the finding on this EKG actually is basically no ST segment there’s a cure s complex and then it’s the T wave and the fact that there’s a lack of an ST segment suggests to me a calcium disorder and in this case it was profound hypercalcemia hypocalcemia you’ll see the opposite a more prolonged and straitened ST segment and the T wave is relatively spared unlike hyperkalemia or hypokalemia so many many people would call this a normal EKG including me but the key is the lack of the ST segment should raise your suspicions for hypercalcemia this is a patient who presented with an acute coronary syndrome and those of you who might see patients in the emergency room are acutely in the hospital or if you’re really unlucky in your office and someone presents like that you might say well this looks like a relatively normal EKG maybe a little bit of Jay point elevation in leads v1 v2 v3 but the ST segments don’t look too bad they’re still up concave upwards they don’t look terribly coved or anything like that but in fact this patient had a diagonal branch of the led that was acutely occluded and the only finding on this EKG that is fairly solid are the biphasic T waves particularly in leads 1 an AVL so if you look in lead AVL you can see that the j-point is elevated the ST segment is a bit straightened and elevated and the T wave demonstrates biphasic t-wave inversion terminal e and that actually indicates in this particular patient the diagonal branch occlusion reflecting the high lateral leads so the circumflex coronary artery is the most underrepresented coronary artery on the surface electrocardiogram and sometimes you have to be you have to double and triple-check to look for an abnormality it may not be present apparently but may involve evolve over time and when I use the circumflex and the diagonal interchangeably well I shouldn’t do that for this EKG because it was it’s oftentimes overlapping or similar territories depending on the actual coronary artery variability from one patient to the next this is an example of pericarditis and I think we’ve all seen an EKG like this but sometimes distinguishing between pericarditis and acute coronary syndrome can be very difficult in this particular patient diffuse ST segment elevation and j-point elevation is seen not contiguous to one coronary artery territory in addition the often sort of unforgotten or excuse me too often forgotten electrocardiogram lead as lead AVR if you look in lead AVR there’s a special segment called the PR segment it’s not the PR interval the PR segment is the terminal aspect of the p-wave just prior to the QRS complex and that small segment is actually elevated in this patient PR segment and that’s the positive electrocardiographic finding which the reciprocal being PR segment depression but if you see the PR segment elevated and lead AVR coupled with diffuse ST segment elevation not coinciding to one particular coronary artery distribution and the lack of reciprocal ST depression and other leads supports pericarditis and the most common cause of pericarditis and any major tertiary care hospital is open-heart surgery okay so I don’t typically like to ascribe the electrocardiographic diagnosis of myocardial ischemia on a 12-lead electrocardiogram but if you’re gonna do so this would be the one of the best EKGs you could do it so this is a positive stress test at rest unfortunately this patient didn’t make it had a general surgery major procedure was I think has some sort of perforated bowel so went into the procedure not with a very good prognosis emerged with an even worse prognosis and end of it and ended up passing away but at any rate this was a profound hypotension sepsis anemia whatever you know whatever the malignant combination was and this patient ended up ruling in for a myocardial infarction so this turned out to be a non-st segment elevation myocardial infarction but I wanted to show you at least a profound what appears to be global ischemic pattern on an electrocardiogram just a few more here so we can stay on time this is a patient who presented with an acute coronary syndrome clearly they have inferior ST elevation and q waves so there’s no doubt this patient suffering a firm innate acute inferior myocardial infarction this patient also demonstrates acute right ventricular myocardial injury so you might say well how am i able to make that assessment from a 12-lead EKG I thought you had to do right-sided chest leads to make that determination well not always look and lead v1 can you see the ST segment

elevation there in lead v1 also in lead v2 to a lesser extent in lead v3 remember the right ventricle is an anterior structure right below the sternum so that your best leads to look at the right ventricular leads v1 and v2 and sometimes you will pick up acute myocardial injury of the right ventricle in the setting of an inferior injury pattern but I put it just taking a closer look at leads v1 and v2 and that dramatically can change your management plan I think I’ll end on this EKG there might be a few more that you can look in your syllabus online if you’d like after the course this patient demonstrates sinus bradycardia with complete left bundle branch block and remember I said before you can may not make the diagnosis of an agent determinate myocardial infarction and complete left bundle branch block well I was kind of teasing a little bit there so let me show you the native QRS complexes and then there’s a by geminal pattern so this patient actually has a sinus rhythm complete left bundle branch block and ventricular bigeminy and you can see the PVCs in the lead v1 rhythm strip have a right bundle branch block morphology so these PVCs with a right bundle branch block morphology are coming from where they’re coming from the left ventricle that’s why they have a right bundle branch block morphology so if we look at the PVCs that are occurring from the left ventricle we may get some insight in terms of what’s going on with initial left ventricular depolarization if you believe that now there are a few skeptics out there I suspect with this but if you look say and lead AV F at the PVC there’s a very prominent Q wave there and you can also see it slightly within the PVC and lead three just to the left of it so this patient actually had ischemic left ventricular systolic dysfunction and a prior right coronary artery territory myocardial infarction and that is suggested but not confirmed by these left ventricular originating PVCs right bundle branch block morphology in the presence of complete left bundle branch block so please we can’t take this to the bank but we can at least it gives you some insight in terms of why this patient may be suffering from the complete left bundle