Transcribed by Mallika Prakash

CVS3 - ECGs and Heart Sounds cont.- by Dr. Kinnally

3.10.14

(19) [Fig.11.3G Correspondence of AP and ECG] Ok so first of all there is no Q here. It is a different lead. There are 12 or 16 leads in an EKG. What that means is they put the electrodes in different places and so the wave looks differently. (Points to image) So the QRS- this is what happens to the QRS. And the T when you have an action potential going through the heart so you have the rapid depolarization that often results in an R wave, then the whole heart is depolarized at this point and you are back at baseline. I know it is not perfectly flat but this is what was in the book. And then when you repolarize thats when you get the T wave. So there is a coordination of QRST with the action potential duration within the heart Now Im going to back up one slide- and talk about the ST segment. This tells you if you have had a heart attack. The ST segment is normally at baseline when the heart is completely depolarized and it doesnt repolarize until you get to T. but if this segment is displaced to this section here (higher up), we call it an elevated T segment. And it means you have had a heart attack (20) [Fig 12.2J The ECG] Remember I had said this previously when we had talked about what the action potentials look like. The action potential in the SA node looks very different than it does in the ventricle. For one thing there is a pacemaker potential, you dont have the rapid depolarization that you do in the ventricles. And the timing is also different. This is in the SA node (top most graph) and look at the P wave- so this is where you have atrial depolarization and that gives you a p wave. Then you go back to baseline and then you have a QRS when the action potential hits the ventricles. Repolarization of the action potential gives rise to the T wave. But in this section here the heart is completely depolarized (points to image) and yet you are at baseline. its only when you get QRS when part of it is depolarized and part of it is not depolarized. So this is a recording from your arms and legs and various places. (21) [Fig 9-5G] So here we are going put it on your favorite slide the cardiac cycle. So P wave is depolarization of the atrium initiates atrial systole. Now why dont we see atrial repolarization? it essentially happens during the QRS which is a much larger wave so it just gets obliterated by it. So then you have your QRS, which happens right at the beginning of ventricular contraction. and then you contract and when you start to relax

thats when you end up with the T wave. So here the ventricles is completely depolarized but here its at its normal resting spot. So where you are in your normal EKG is going to determine whether or not you are hyperpolarized, depolarized or polarized. So being at baseline, being at 0, doesnt necessarily mean that youre depolarized or not depolarized. (22) [Fig 12.3 J A diagram of six-lead placements used for an ECG] This is a 6 lead placement for taking an EKG. So very often what theyll do is that theyll put 4 leads on. 1,2,3,4. I guess you could put them on the hands and feet. In olden times perhaps they did do that. In the first image you can see the PQRST, but in the 5th image its upside down. So depending on where the lead is, you see how its different. You would flip how it looks. So you can actually get a very detailed analysis of how the electrical impulse is travelling through the heart by moving those leads/electrodes around. And actually after they do the 6 lead they move the electrode laterally across the heart this way to get an even more precise indicator of where the electrical impulse is or how they are moving. This generates a vector. And normally it just goes down and to the left. Thats how propagation occurs. More than you need to know. Except you should know that when you have a heart attack or a myocardial infarction you change that vector ever so slightly, and that helps the cardiologist tell where the infarct occurred. Whether it is on the right or left side or what implications will be (23) [Normal ECG] This is just a summary of all the things I have said. Again the ST segment the voltage is expected to be flat. But if you have a myocardial infarction (MI) then you have a current of injury (24) [ECG is a Diagnostic Tool] So you can measure your own heart rate and what you will find is.. you can measure it in various places. One of the things that is very impressive is that its very regular. Everybodys heart has skipped a beat, it happens now and then. Especially if youre on drugs, for allergies. But your heart skips a beat it will feel funny. If you rub here what are you doing? you can do vagal stimulation. Isnt your vagus nerve somewhere around here? But anyways, if we vagally stimulate it. Wouldnt we change something? What would we change? We would decrease the heart rate and decrease propagation

through the AV node. So what happens to the EKG if you vagally stimulate it? The PR interval could get extended. (25) [Fig.12.8J: Elevated ST segment indicates injury; lead is diagnostic through vector analysis.] So this is an elevated ST segment. And this would be picked up in probably any of the leads. But this should be down at the bottom like this one is. So the elevated ST segment occurs because injured myocardium seems to be more negative is how they state it. (26) [Fig. 1.2 Kumars Gen Path] This is what it looks like (points to top most image) these are normal myocytes. This is the left ventricle. When you have sustained stress on the heart- Just like when you go to the gym to workout and you want big biceps. you hypertrophy them by lifting weight all the time. But if constantly have a strain on your heart as if you had what? High blood pressure! Then you can get hypertrophy (image on left). What happens to the size of the ventricle? it gets bigger? You think better would be better. But when the heart hypertrophies you fill it up with muscle. So what happens to your stroke volume? Gets lower and lower and lower. So that is not a good thing. Athletes have huge stroke volumes and that way they can have really low heart rates. So normally your heart rate doesnt really go below 60 except if youre in good shape and athletic. So sometimes when athletes go to sleep their heart rate can be like 45- thats low! I would wake them up! Thats a bradycardia ! but if theyre in really good shape, then its not a bad thing. (Image on right) this is when you have a myocardial infarction. This is dead cardiac tissue (yellow in color). Does dead cardiac tissue contract? not really, and it doesnt really replicate (if you survive), it gets replaced by fibrous material which is not very contractile either. Thats why it is hard to recover function after a major heart attack. (27) [Heart Rates] So this is a tachycardia, which is a 100 beats or more per min. And this is a bradycardia 60 or less beats per min. So normally sitting here, youre so excited to be in class I can tell. Youre heart rate is about 70beats/min. So usually what you do is you count how many beats there are in 15 seconds and multiply by 4. If you happen to have a watch except most of you dont! Does the exercise! Ready set go, and ill tell you when the 15 seconds is up. So hopefully no one counted to 25 or more that quickly because that

would be a tachycardia. And I guess 15 would be the other one. So everyone got between 15-25 and that would be normal. (28) [Causes of Cardiac Arrhythmias] Arrhythmias can be caused by several things. Ischemia which is reduced oxygen level, scar tissue calcification, inflammation. Abnormal rhythmicity of a pacemaker- if your heart is not beating normally it is very rhythmic, at a constant pace. But if you SA node gets knocked out then you may go to an area of..the shift of a pacemaker may be away from the SA node to another place which is maybe not as rhythmic. You can have blocks at different points of the transmission of the cardiac impulse. In particular if you have an infarct that would knock out the left bundle branch or the right bundle branch or some section of the purkinjee fibers. this would give rise to abnormal pathways of transmission in the heart. If you have left bundle branch block some of the electrical impulse will go around muscle cell to muscle cell to the rest of the ventricle. But it will not be a coordinated nice contraction. You also may have spontaneous generation of abnormal impulses that would usually be picked up as a premature beat. So if the heart is normally going bump! bump! bump. Then you will have bump bump!bump!bump! so the second bump would be a premature beat. And you get a lot of those from drugs or from an infarct (29) [Relationship of P to QRS waves] So were going to look at some of these. This is that wenckebach video is. The first thing they look at is the relationship of the P with the QRS. That is, is the atrium appropriately talking to the ventricle? And there are different degrees of block. So normally it takes about 0.16ms for the impulse to go from the atria to the ventricle. Most of that time is spent in the AV node where you have slow progression, because you want to separate atrial and ventricular contraction. So in the first-degree block- when the PR interval is longer than 0.21s. And second-degree block some of the Ps dont give rise to the QRS complex. In third degree block the Ps are gone along and QRSs are coming at a different rate. Short PR interval is sometimes called wolf Parkinson white syndrome. And thats when the interval is very short. The PR interval is very short. (30) [AV Block- Fig12-9G] This is what you call normal sinus rhythm- every p is followed by QRS, it is a very regular occurrence and the PR interval is between 0.16 and 0.21 seconds. In firstdegree block PR interval is longer than it should be. So there is a delay in conduction.

In second-degree block some of the P waves dont have a QRS. And in third degree block the Ps has no relation to the QRS, but importantly look at the QRS, does it look the same? No it probably a QRS arising outside the SA node, maybe even outside the QRS. Its wider than a normal QRS indicating that the conduction velocity is delayed so its probably not using the normal conduction pathways

3-Correct answer for question above

4- correct answer for question above Recording paused- skip all the way to the lidocaine slide (33) [Lidocaine] So you guys use novacines to numb the gums/gingiva. People in coronary care units use it to numb those aberrant foci that are throwing off PVCs (:/) what does lidocaine or novacaine do? it blocks sodium channels and so they have found that lidocaine is actually very effective in suppressing those foci that give you aberrant signals after a myocardial infarction and thats when they are most common. So it is used to decrease arrhythmia. Answers someones question- okay so muscle cells are at about -80 to -90 and normally they dont have a pacemaker potential in the ventricles, usually its flat. but when you injury it usually due to ischemia it becomes slightly depolarized, and it hits threshold and it gives rise to an action potential which is then propagated in the wrong direction so its a focci of injury that gives rise to electrical impulse that can take over the heart beat, like in ventricular tachycardia. When you have multiple ones you have multiple muscle cells that are depolarized and active and this is not good. One irritated spot is better than having many irritated spots in your heart (34) [Current of injury]

Damaged cardiac cells can be partially or completely depolarized. And they seem to leak current throughout the heartbeat. It can be heart infection, or ischemia. Ischemia is probably the most common or it can be mechanical trauma. But ischemia would be the most common. Mechanical trauma would be if you had a car accident or an infection (due to rheumatic fever for ex.). So the normal sinus rhythm ends up having an elevated ST segment and its pretty diagnostic of a myocardial infarct (35) [Figure 94 G] Because you have sodium channels your heart becomes refractive and thats why each action potential that initiates in the SA node is eliminated before the next heart beat and it is important that that happens. So the refractory period is important. if you have a premature contraction, usually that contraction is not as strong, that would be here, as it is when its separated in time. (36) [Circus Pathway to Fibrillation] But theres something called the circus pathway to fibrillation. Fibrillation is when you heart goes from this to this.. and this doesnt generate cardiac output. So it quivers. So it doesnt have a coordinated contraction. And this coordination is actually very important to having a good cardiac output. So one way that you can have that is due to dilation of the heart. Dilation of the ventricles is not a good thing because the overlap of the myosin and actin myofibrils tends to decline and if you go too far it doesnt recover. So dilation is bad for muscle contraction. But it is equally bad because of the possibility of fibrillation. When the heart becomes dilated the action potential takes a long time to get through the whole heart. So long, in fact that you may have another action potential before the heart is not completely refractory. So you can end up having this quivering (37) [Fibrillation image] Normally you have an action potential that travels through the entire heart and as it travels it leaves muscle cells behind that are refractory and at the end of a heart beat the entire heart is absolutely refractory. And then the sodium channels come out of their inactive mode and then they are ready or prepared to have another action potential. But when that pathway becomes long or is delayed then you have the action potential that takes such a long time to get back to the beginning that you leave part of the heart in relative refractory, and so of it is ready to get another action potential. And if it is the then this (points to the white and pink region) before this (orange part) is ready and the whole thing is going to end up being a quiver. Normally the action potential is

completely annihilated but sometimes it isnt if the heart is dilated or you dont have the normal conduction pathway functioning. As you would have in left bundle branch block for ex. So if this happens you dont have a pulse. Do you know how to use the machines outside? did you guys learn to use them yet? Good! (38) [Fibrillation] This is what it looks like electrically. The top one is atrial fibrillation- dont actually see any P waves. What you see is the quivering of the atrium. And what about this trace, can you tell me something else about this trace? its not regular! it doesnt have a consistent interval. One of the easiest ways to diagnose atrial fibrillation is to feel the pulse. And the pulse will be irregular because the SA node is not functioning. But its got a pretty decent rate, and you will have decent cardiac output even though you can be in atrial fibrillation. A lot of people can be in atrial fibrillation without any problem. No one is walking around with ventricular fibrillation- you will pass out in 4-5 seconds. But in ventricular fibrillation you dont get any cardiac output, which means that the heart is not getting any blood either which is bad. And this often reduces to something called asystole- where you just have a flat line. Ventricular fibrillation goes into asystole in time if it is not stopped. Because the heart is not getting any oxygen either. (39)[Fibrillation] So when you defibrillate, which is what that machine out there does, you pass a large current across the heart. What does that do? it resets and clears out the electrical activity which was kind of going around like that. IT activates all the sodium channels and they all become refractory and this was normal sinus rhythm can happen again. (40) [Asystole] And thats what asystole looks like (41) [Key points of ECGs] Okay and you can look at this on your own (42) [Whats mechanism of sympathetic NS regulation of HR?] I had written this out and I left it in the PowerPoint just because some people are unclear and it just brings it together on how sympathetic regulation occurs

Why does AC current electrocute you? and DC current will still electrocute you, you can die from DC current, but you need a lot more current. So you need a lot less AC current Lecture 7 CVS4 Hemodynamics by Dr. Kinnally (3) [Hemodynamics:] Hemodynamics is the movement of blood in the cardiovascular system (CVS). So the CVS is supposed to be a closed system. So unless you are hemorrhaging everything that flows out of the heart usually returns to the heart at some point. But what effects how the fluid flows is what we are going to talk about. So pressure differences and resistance. The blood flows because the heart generates a pressure gradient which goes through the entire circulatory system. (4) [Pressure Gradients] So fluid flows from high-pressure to low pressure. So where is the pressure the highest? In the left ventricle or the aorta. Where is it the lowest? The vena cava. The pressure is actually not the lowest in the capillaries because if it was then it wouldnt return to the heart. so the pressure in the capillaries must be greater than it is in the veins, otherwise the blood would not flow from the capillaries back to the heart. So Im an electrophysiologist so for me Ohms law is V=IR (Voltage= Current x Resistance) but in the cardiovascular world Flow= Pressure gradient/ Resistance. So flow is what we follow, the heart generates the pressure and something else controls the resistance. (5) [Resistance] But the resistance you need to know is affected by 3 major things. One is viscosity, one is the length of the tube, and the radius. It is directly proportional to the length and viscosity and inversely proportional to the radius4) so radius has a huge impact on flow and resistance. (6) [Blood is thicker than water] Back to viscosity. The viscosity of the blood is a function of the hematocrit. Normal hematocrit is between 40 and 50 and what is a hematocrit? If I were to take a known volume of blood. I dont know how they do it these days!Actually I do because I donate blood all the time. It used to be that you measure the hematocrit by putting blood into a tall capillary tube and then you centrifuge it. And lets say it was this big, if it filled up half way, if you spin the cells down and the cells took up half of the space the plasma would

be above it and the RBCs and stuff below it. The hematocrit would be 50%. So normally the blood cells make up half of the volume of the blood, so normal hematocrits are 4050%. So if you live at high altitude, what happens when you are at high altitude? Mexico city is high isnt it? your body responds to high altitude by generating more RBCs. So typically your hematocrit increases. Thats why athletes used to go to high altitude places two months before the Olympics, so that their ability to carry oxygen in the blood is increased. But also the viscosity of the blood increases (7) [Normal laminar flow of blood] So this describes the normal flow of the blood in a vessel. It is called normal laminar flow of blood, where the particles in the middle are not near the walls so they flow more quickly. So the velocity is higher in the middle than it is near the walls 8) [Turbulent Blood flow] But if you have turbulent blood flow, it is not normal laminar flow, you have increased resistance to blood flow. So if somebody has a shunt. Why would you have a shunt? A shunt is when they connect the vein and artery directly and skip the capillaries to give an area of high blood flow. If somebody is on renal dialysis they have a shunt here or here or someplace where they connect and artery and a vein. This high blood flow also gives rise to some turbulence. Another possibility is that you can a deformity in a blood vessel, which can also give rise to turbulence. But you can hear the turbulence in with a stethoscope. Its like a whirling kind of a sound. Oh thats what I meant to show you, one of those auscultation things actually lets you hear what the respiratory system sounds like with rails, rhonchi and normal!breath sounds if youre interested. Maybe Ill call it up when we talk about congestive heart failure or something. Because thats when you get rails and rhonchi in the respiratory system. (9) [Blood vessel diameter regulates resistance] Blood vessel diameter regulates the resistance in time. Normally in time the length of your blood vessels doesnt change. Normally in time the viscosity of your blood doesnt change. But everyday you have tremendous changes in your blood flow depending on your metabolic needs, whether youre running a marathon or working out at the gym vs. having a big meal vs. sleeping, the output changes. So vessel walls can dilate and constrict, larger diameter has lower resistance and the resistance is proportional to the reciprocal of radius to the fourth. But resistance can be in parallel or resistance can be

in series. And Im going to explain what that means because it makes a big difference in how you calculate it. (10) [Resistance in Series] I always think about one of those collapsible cups, with different radii. But if you had things that were in series like these things are then the total resistance is always greater than the largest resistance. So you add all the resistances together, so the resistance of the flow through this series of different diameters is equal to a resistance greater than any of them individually. (11) [Resistance in parallel] But if its in parallel it is a very different situation. So here the total resistance will always be less than the resistance of any individual tube. And you can see how it is calculated here. So its 0.2+0.04+0.01= reciprocal of 0.25= 4 which is smaller than any of these. So if you have things that are in parallel then the resistance is much smaller. Thin about capillaries. Are capillaries typically in parallel with each other? Youre making a choice whether youre going to light up this capillary bed or this capillary bed- theyre all in parallel. (12) [Resistance in CVS] But arteries arterioles and capillaries are arranged in series. So the different types of vessels are in series with each other. But within each type they are in parallel with each other. But the overall resistance to flow is actually.. ill get to it. (13) [Fig 120-4J] Again we have a changing diameter. So did you ever connect a hose to a faucet, and usually its a skinny hose, and man does that come out fast. And spins all over the space. And if we had a fat hose it wouldnt be as turbulent or as quick. In fact the velocity changes with diameter or the radius of that tube. So its very rapid when its small and much less when it is large. Given the same pressure reservoir which is what the heart wants to do, it always has this pressure reservoir field (14) [Cross Sectional Area in CVS] So if you think about the cardiovascular system and you look at the cross sectional areas in the cardiovascular system the aorta has very high diameter, but if you look at all of the capillaries together they have a huge cross sectional area. That means that the blood flows because its in parallel, the blood flows very slowly in the capillaries. And

is that important? Thats appropriate and important because thats where you have gaseous exchange, thats where nutrients come to the cells and wastes are removed. So it is very important that the capillaries have a high cross sectional area which means that the velocity of blood flow through those areas is very low. (15) [Velocity and cross sectional area in CVS] So its the cross sectional area in parallel blood vessels that determines the velocity. The velocity is high in the aorta because it is not in parallel with anything. And all the blood has to flow through that tube, but the cross sectional area of the capillaries is very large so the velocity is very low. (16) [Velocity decreases as cross-sectional area increases] This is a visualization of that velocity. it is very high in the aorta. As you go into the capillaries it becomes the slowest and as it comes back to the vena cava, it increases again. (17) [Resistance in the CVS] So because it has a very large radius, the resistance is relatively low in the aorta but in the arterioles the radius is much smaller and so the resistance is much higher and in fact the arterioles generate the biggest resistance to flow in the cardiovascular system. (18) [Pressure] This lets you see the pressure in the different types of vessels and remember these are all in series with one another. The biggest drop in the pressure occurs across the arterioles, and that is an indicator that is the region of the highest resistance. So the arterioles generate the highest resistance. (19) [TPR and Ohms Law] Now the total peripheral resistance (TPR) is regulated by the arteriole tone. So what controls the constriction in the arterioles? The sympathetic nervous system! So in your cardiac center, it is always looking at the blood pressure and controlling the constriction of the arterioles. So if the blood pressure drops it will constrict to increase the pressure. So the mean arterial pressure (MAP) is actually = Cardiac output x TPR. I told you how to calculate it before 1/3(pulse pressure) + diastolic = thats an approximation. How do you measure TPR? Its not that easy to measure in a person. So this approximation just makes it much easier

(20) [Mean Arterial Pressure = CO x TPR] So MAP can be increased by constricting the arterioles, which increases the TPR. This is probably one of the number one things. If you constrict the vessels you will increase venous return and that will increase cardiac output. Thanks to Frank-Starlings Law of the Heart. You can directly increase the cardiac output by increasing the heart rate and increasing the contractility of the heart. So those are 3 major ways of increasing MAP. (21) [Mean Arterial Pressure] The blood pressure is pulsatile. I already told you about the pulse pressure = systolic pressure diastolic pressure. And the way that you can approximate the MAP = 1/3(pulse pressure)+ diastolic pressure. One thing you should think about is that the pulse pressure actually depends on both the stroke volume and the capacitance. And what does capacitance mean? Its more or less the distensibility of the vessels. (22) [Graph] This is just illustrating what the pulse pressure is. I got ahead of myself. Sorry! (23) [Measurement of Arterial pressure] And this is how you would measure the arterial pressure using a cup like the one in the front. (24) [Measuring Systolic and Diastolic Pressures] You would hear the heart sounds. You would not get a heart sound when the pressure of the cuff is higher than your systolic pressure and as the pressure in the cuff is reduced, blood starts to flow. Sort of turbulent because its trying to get through a pressure. And then youll stop hearing it at the diastolic pressure. (25) [Blood Pressure Classification] This is something you should know, that normal may be less than 120/80mmHg but prehypertension is 120-140/something in the 80s mmHg. So in prehypertension typically what you do is if you are denoted as pre-hypertensive then you could try to reduce the stress in your life, lose weight, try and live a healthier.. whatever.. but the important thing is that you should monitor your blood pressure more frequently. I have white coat syndrome, my doctors always like your blood pressure is too high, but its only high when Im in his office. When I take it at home its 90/60 but when Im in his office its like

140/90. its like really crazy.. So that happens and everybodys blood pressure varies a little bit, but if you find that you routinely have elevated high blood pressure, especially in this pre-hypertensive range you really should take care of it, either by life style changes or you may have to go on drugs. I dont know. But well talk about those. Hypertension - stage 1 and stage 2. Hypertension not only gives you heart strain it can cause kidney disease and a myriad of other things that are not good to have. (26) [Capacitance] This is capacitance. Capacitance is the compliance of the vessel. Normally if you put a volume in to a vessel then the pressure will increase. So its sort of like having a heavy duty balloon vs. a light weight balloon. Its distensibility, how much pressure or volume you can put in a balloon and you can see it stretch. So as people age you can have a very large increase in volume with not too great of an increase in pressure, at your age. Now at my age, as you add volume you tend to increase the pressure because the stretch is gone. The elasticity of the vessels is reduced. So capacitance decreases with age. Now the capacitance of the veins is much greater than the capacitance of the arteries. IF you look at the structure of the veins vs. the arteries you see much less muscle and things like that on veins than on arteries. So its probably not surprising. But thats why the veins are a reservoir for the blood, and you can regulate that reservoir by tone and how much constriction you have on those veins. (27) [Veins are much more distensible than arteries] So this is just an illustration of the huge difference in capacitance in veins and arteries. (28) [Gravity] I used to teach comparative animal physiology so there were special examples in the world. When I think about hydrostatic pressure I think about giraffes. you know how they shift their necks and swing their heads up into the trees and then they swing! you realize how tall that hydrostatic pressure is on the neck of a giraffe. Imagine getting blood up to the brain of a giraffe. Pretty hard! So a large pressure gradient is generated by the hydrostatic column of blood when you stand up. You ever get up too fast and you go Woahhh!! Thats because the blood didnt get up to your brain. Normally arterioles constrict to buffer the high pressure caused by the hydrostatic column and also in veins they have a lot of capacitance, so blood could actually pool in the veins. So veins actually have one way valves that prevent the reverse flow when you from laying down to standing up. And there something called muscle contraction or venous or muscle

pump that when you walk you pump the blood back to the heart by contraction of muscle. This moves the blood back up to the heart. (29) [Try This] so this is to show you what a valve looks like. As I push, its right here in my hand, I can see how the blood .. its right there (pointing to an animation). So if you look at your hand, a lot of the times people walk out of here and they have these huge red marks. Really gently try to see if you can find something. You know these guys with the big veins in their muscle and stuff, it doesnt work on those.. I dont know why.. so dont try and get one of those giant ones to visualize! Anyways! (30) [Gravity] Another thing is that gravity can give rise to the mechanism underlying crucifixion. So when you have crucifixion, what happens is..okay so when a guy is crucified he is not moving his legs. Usually you contract the muscles in the legs to facilitate returning blood to the heart. And when you cant to do that, when youve been standing their for days, nailed to a cross, then fluid pressure starts to build up in the capillaries. Fluid flows out of the capillaries and into the tissues, and you have a reduction in blood volume and the person passes out and eventually they die. I thought you might find that interesting

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