# The Complete Cardiology Masterclass: Exam-Ready in One Video

https://www.youtube.com/watch?v=VQWOLQ0iBNQ

[00:00] Hello, I'm Joseph Alpert, professor of medicine at the University of Arizona in the United States and also the editor-in-chief of the American Journal of Medicine.
[00:09] I'm going to be presenting a series of 14 lectures which are an introduction to cardiology.
[00:14] I hope none of you believe that you will be expert cardiologists at the end of listening to these 14.
[00:20] But I do believe that you will have a much greater understanding of cardiology.
[00:25] You will understand the various factors that lead to heart disease.
[00:31] You will understand how we make the diagnosis of heart disease and you will understand the various therapies that we have at our uh hands in our hands that we can use uh in order to help the patient with heart disease.
[00:45] So let's start with something very basic.
[00:48] Let's start with the anatomy of the heart and the blood vessels.
[00:52] Now, many of you, of course, receive hearts uh when you receive letters from friends or
[01:01] or close uh uh intimate uh relations.
[01:05] at Valentine's Day, we see the heart, of course, the the heart shape.
[01:09] Actually, the heart doesn't look anything like that.
[01:13] That's just a symbol for the heart.
[01:15] In fact, what you see here in this little diagram is a little bit more what the heart looks like.
[01:20] The heart is conicle in shape with a rounded point, not a sharp point.
[01:25] Um, and of course, uh, it is a pump.
[01:28] It's a muscle pump that keeps the circulation continuously going in a circle.
[01:33] So, uh, what happens, of course, I think everybody knows, is the heart pumps the blood out full of oxygen and nutrients to the cells throughout the body, and then waste products are given to the blood.
[01:44] The blood returns to the to the lungs a deep blue and is then reoxygenated, gets oxygen again and pumped out to the body.
[01:52] There's a continuous circle going on uh of the circulation.
[01:54] Here is a diagram that shows you how the heart lies in the chest.
[01:59] Notice that it's not directly in
[02:02] the center of the chest.
[02:04] In fact, it's slightly to the left.
[02:06] In this view, of course, it looks like it's to the right,
[02:08] but if you were standing behind this person,
[02:09] um where the heart bulges out would be the left.
[02:12] And you can see four points are marked on this skeleton uh with the with the heart drawn behind it
[02:18] behind the ribs of course and the breast bone which we call the sternum.
[02:23] You can see that there are four heart valves and the points that are that are marked here
[02:27] are the places where we listen with our stethoscope when we want to hear that particular valve.
[02:34] So, and we're going to go over the names of the valves and where they're located, but you just for introduction, you can see that they're the aortic valve, the pulmonic valve,
[02:43] the tricuspid valve, and the mitro valve.
[02:45] Now, here's a little diagram of the circulation.
[02:48] You can see it's made in two colors.
[02:51] Blue for the blood that's returning to uh the right side of the heart.
[02:53] It's exhausted of its oxygen.
[02:56] It's carrying waste products, particularly carbon dioxide.
[02:59] Carbon
[03:03] dioxide will be given off in the lungs.
[03:05] Oxygen will be introduced to the red blood cells and then they will get to the left side of the heart where they'll be pumped out to the body.
[03:10] So let's follow the circulation through the heart.
[03:15] You can see that there are two large veins here that drain into the right atrium.
[03:20] The superior vennea drains the blood from the upper body.
[03:26] The inferior vennea drains the blood from the lower body.
[03:28] They both empty into the right atrium and through then pass through the triricuspid valve into the right ventricle.
[03:37] They are pumped out through the pulmonic valve into the lungs.
[03:43] Um and then they return through pulmonary veins to the left atrium and then across the mitro valve into the left ventricle and the left ventricle pumps it out through the aortic valve to the aorta and to the whole body.
[03:54] What you see here is a small catheter working its way through the heart.
[03:59] We're going to talk more about that catheter.
[04:01] That's how we
[04:03] measure pressures and the flow the the amount of blood that the heart is pumping uh during a diagnostic caization.
[04:09] Um but again uh of course the blood is not exactly this color blue on the on the right side of the circulation.
[04:16] It's a little bit darker and it's quite bright red on the arterial side.
[04:24] Now, here is a more anatomically correct diagram.
[04:27] And there are a couple of points I want you to note about that.
[04:30] You'll still notice the superior vennea, the inferior vennea coming into the right atrium, draining the the uh if you will, deoxxygenated or tired blood into the right atrium.
[04:40] You can see the triricuspid valve the as the blood passes into the right ventricle.
[04:45] And then you can see it being pumped out into the pulmonary artery.
[04:48] Still all in blue.
[04:50] What's of interest here is that the left ventricle is a lot thicker than the right ventricle and in fact their shapes are slightly different.
[04:57] Why is that?
[05:00] It's because they have very different functions.
[05:02] The pressure in the
[05:04] lung is quite low.
[05:06] So that the right ventricle functions like a bellows like the blacksmith uses to create air for his fire uh that he's going to be uh melting the uh and working on horseshoes for example.
[05:21] So it produces large volumes of blood movement at low pressure.
[05:26] The left ventricle of course has to pump blood throughout the body.
[05:30] So it has to pump that blood at a much higher pressure.
[05:34] And consequently the walls of the left ventricle are much thicker than the walls of the right ventricle.
[05:38] It's functioning not like a bellows but rather like the piston in a car.
[05:44] a high pressure chamber that does a lot of pressure work as opposed to the right ventricle which does a lot of volume work at much lower pressure.
[05:53] Now here we see the heart diagrammed in comparison to the chest X-ray.
[05:59] You can see on the right hand side this is a so-called frontal X-ray like this.
[06:04] then on the left hand side there is a lateral X-ray taken like that from the side.
[06:09] And what you can see are several things.
[06:11] First of all again notice that the heart is not in the center of the chest but in fact is a little bit more in the left chest than the than the right chest.
[06:20] And the bulge that you see down in the in the left chest is actually the left ventricular outline.
[06:25] If you want to see the right ventricle, you have to look at the lateral view and you see it um in front of the left ventricle.
[06:35] Now people say, "Wait a minute, the heart actually has the right ventricle in front of the left ventricle."
[06:41] And in fact, that is exactly the case.
[06:43] We'll see that on some further uh x-rays um and uh uh uh and magnetic resonance image which will show you that in fact the right ventricle does lie in front closer to the breast bone than the left ventricle which lies a little bit behind.
[06:59] Uh and you can get a hint of that from the the two diagrams here that
[07:06] are reflecting um what you see in the chest x-rays below.
[07:08] Now, here is an MRI of the chest.
[07:14] What's at the top there is the front, the breast bone, and what's at the bottom of the picture is the spine.
[07:20] You can see a little area of the spinal uh uh vertebrae there.
[07:26] And you can see the heart right in the middle uh there uh of the diagram labeled RV is the right ventricle and LV is the left ventricle.
[07:34] And you can see that the right ventricle is lying in fact in front at is closer to the chest front wall compared to the left ventricle.
[07:46] And uh again here is again the diagram showing you where the heart is located and also where the different points are that you can best hear with your stethoscope the sounds made by the four heart valves.
[07:59] We're going to talk about those in in just a moment.
[08:01] Um but you see there are areas on the little bit
[08:06] upper right chest, a little bit upper left chest, lower right chest, and lower left chest.
[08:12] Um let's talk a little bit about the parts of the heart.
[08:15] The heart of course is a muscle pump.
[08:17] So that's the most important part, but that's not the only part.
[08:20] Of course, you have to have valves to keep the blood flowing in the right direction.
[08:24] If in fact you didn't have valves, all the blood would just slush back and forth within the heart.
[08:28] You have to have the valves to keep the blood flowing in the right direction.
[08:34] You also have electrical wiring.
[08:37] We're going to talk a lot more about this, but in fact, what triggers the contraction of the heart is an electrical signal that starts high in the right atrium of the heart with a little automatic pacemaker and passes right down through the heart muscle and results in contraction of the heart muscle.
[08:57] when the electrical signal gets there.
[08:59] Of course, you also have to have arteries to supply the heart with oxygen and nutrients so it can work.
[09:01] In other words, the fuel line for the heart to
[09:08] Put the fuel into the heart cells so they can contract.
[09:13] The veins uh are also important because they carry the tired blood, the blood that's lost its oxygen and some of its nutrients and is carrying waste products.
[09:21] Uh it returns to the right atrium along with the superior and inferior vennea uh to be circulated again from the right ventricle into the lungs to gain oxygenation and to give up its carbon dioxide.
[09:33] And then of course the entire heart is contained in a membrane a very tough membrane called the paricardium that protects the heart particularly for example from infections in the lung should they occur.
[09:44] Um and it also uh keeps the heart uh uh in a nice shape uh so that it doesn't uh expand or uh too much when it's working.
[09:53] Um the important lesson here in anatomy is that the heart is a muscle pump that it's going to continue um to pump blood in a continuous circle through the body and that it is meticulously and beautifully adapted uh to do this.
[10:05] Uh we will be
[10:09] talking about more detail of the various ways um that the heart uh does this.
[10:16] So here's the diagram again that you saw before.
[10:18] Once more to reiterate venus blood comes back to the right atrium through the tricuspid valve to the right ventricle out the pulmonary artery back oxygenated blood comes back to the left atrium through the pulmonary veins through the mitro valve and then pumped out the aortic valve to the body.
[10:37] Well, let's look in a little more detail inside these various chambers.
[10:40] Here you see a diagram inside uh the right ventricle.
[10:46] Uh and you can see of course it shows you the blood is blue.
[10:49] That's the deoxxygenated blood.
[10:51] Um you can see the right atrium above uh the right ventricle.
[10:56] Uh and you can see the pulmonary artery and uh the pulmonary valve uh below it.
[11:01] Um there are a variety of abnormalities that the heart can be uh uh found in in infants.
[11:10] example, the pulmonary valve can be stenotic or or closed uh has to be fixed at the early in life.
[11:17] Um there can be holes in the heart.
[11:20] For example, a connection between the right and left ventricle where there should be none.
[11:23] All of these are the area of the pediatric cardiologist who can make those diagnoses very early in life.
[11:29] And often these days infants are operated on and have these uh abnormalities corrected.
[11:33] But the normal right ventricle remember will be separated from the left ventricle with a muscle septum that will uh prevent blood from the right side from getting onto the left side.
[11:43] When blood from the right side gets onto the left side, the patient actually uh look has a faintly bluish tinge to themselves.
[11:53] And you we'll talk about that when we talk about physiology and diagnosis.
[11:55] Here we see a diagram of the right ventricle contracting.
[12:00] And as I said before, the right ventricle is working like a bellows.
[12:04] You'll see in the diagram on the left, that's the contracted right ventricle.
[12:08] And then on the right, you
[12:11] can see the filling right ventricle.
[12:13] It looks like a bellows, right?
[12:15] Just like the blacksmith's bellows that's used to to heat up the fire uh beneath uh the the horseshoes that the blacksmith is working on.
[12:23] Um the right ventricle again is thinwalled, much thinner walled than the left ventricle because it pumps at a much lower pressure than the uh left ventricle.
[12:34] Here we see a diagram of blood uh that uh is passing through the heart and the different pressures in the different chambers.
[12:41] We're going to be talking a lot more about this when we come to the physiology component, but it's important to see right here on the left hand side of the diagram low pressure in the right atrium.
[12:53] Then periodic high pressure followed by low pressure in the right ventricle.
[12:57] Then we see in the pulmonary artery high pressure followed by not such low blood pressure.
[13:03] And then the pulmonary capillaries which are a reflection of left atrial pressure also a low pressure uh about the same as the
[13:13] minimal pressure in the pulmonary artery.
[13:15] Um we see that the blood passes through the heart starting at a very low pressure in the right atrium.
[13:22] The tricuspid valve opens, blood flows into the right ventricle and it squeezes and then you see the pressure going up for the right ventricle.
[13:31] And then when the the pulmonary valve closes, the pressure falls again down to the baseline where the right the tricuspid valve opens again and blood flows into the right ventricle.
[13:42] Out in the pulmonary artery when the pulmonary valve closes, the pressure no longer falls anymore.
[13:47] Uh and you see uh a a sort of baseline pulmonary artery pressure that's transmitted across to the pulmonary capillaries and eventually to the pulmonary veins and the left atrium.
[13:59] Here are the four heart valves.
[14:01] Um, the ones in blue are the right sided ones, of course, and the ones in red are the left-sided one.
[14:09] Let's take the one at the top of the uh diagram because that's
[14:15] The front of the heart.
[14:17] And that's the triricuspid valve.
[14:20] Triricuspid means three cusps, three components.
[14:22] And you can see that, right?
[14:24] You can see that there are three parts to the tricuspid valve.
[14:26] So the blood is now passing through the tricuspid valve into the right ventricle and then there's going to be vent right ventricular contraction squeeze and the blood is going out the pulmonary artery.
[14:40] Look at the blue valve to the left.
[14:43] That's the pulmonary artery valve and you'll notice it's open because the right ventricle is squeezing blood through it.
[14:49] That blood goes to the lungs as we talked about, gets oxygenated, get picks up oxygen, comes back through the pulmonary veins to the left atrium and then passes through the valve, the red circled valve on the right hand side of the diagram.
[15:03] Notice that valve only has two cusps.
[15:07] So it is the only valve with two cusps.
[15:09] The other three valves have three cusps.
[15:12] The tricuspid valve, the pulmon pulmonic or
[15:15] pulmonary valve, the aortic valve all have three cusps.
[15:21] But the mitro valve which is between the left atrium and the left ventricle has only two cusps.
[15:26] In fact, it resembles it's named for the bishop's miter which is the crown that the bishop wears in the Catholic church which basically has just two sides to it.
[15:36] Uh resembling a little bit the mitral valve.
[15:38] Once the blood is in the left ventricle, the left ventricle contracts and the blood goes out the aortic valve.
[15:43] That's the one you see right in the center.
[15:45] And you'll notice it's also open.
[15:47] So what we're seeing here is right and left ventricular cy that is squeezed cy is squeezed.
[15:53] Uh and you see that the pulmonary valve pulmonic valve and the aortic valve are open and blood is flowing respectively into the pulmonary artery through the pulmonic valve and into the aorta through the aortic valve.
[16:07] Now I mentioned before that the heart has an electrical system.
[16:10] Uh indeed uh it's the electrical system which is the trigger for mechanical contraction.
[16:15] Without the
[16:17] electrical system the heart muscle will not contract.
[16:23] It's each heart cell responds to the electrical activity by contracting.
[16:27] So where does this electrical activity start?
[16:31] It starts at the top of the atrium.
[16:33] There's a pacemaker, an automatic pacemaker which can be influenced by adrenaline circulating or by nerves from the brain.
[16:40] It can accelerate or it can decelerate depending upon a variety of conditions which we'll be talking about later.
[16:47] Uh but in any case the impulse starts spontaneously passes through a number of little fibers in the atrium into what you see that little bulb there that's the AV node.
[16:56] It pauses there for a little bit.
[16:59] Why does it pause?
[17:01] Of course, you can't have the atria and the ventricle contracting at the same time.
[17:05] And if the impulse traveled rapidly through, you would have them contracting at the same time and the blood wouldn't be going anywhere.
[17:10] So, there's a certain pause while the atria finish their mechanical contraction.
[17:17] And then the electrical activity passes down from
[17:19] that AV node, also called the bundle of H, down into the branches that are in the ventricle.
[17:27] And at that point, the ventricular muscle contracts.
[17:29] You can see below it a a diagram of the electrocardiogram.
[17:34] The first wave is called the Pwave.
[17:36] That's atrial contraction.
[17:39] And the big deflection is called the QRS.
[17:41] That's the ventricular contraction.
[17:43] And you can even see the heart sounds in there with uh atrial contraction uh and ventricular contraction.
[17:48] You can see the first and second heart sounds.
[17:51] In fact, we record the electrical impulse passing through the heart with something called the electrocardiogram.
[17:58] I think most of you are well aware of this.
[18:00] I'm going to talk a lot more about this when we come to the diagnostic lecture.
[18:04] But in any case, here's a diagram that shows you six electrocardiographic leads.
[18:10] They're taken in the frontal plane.
[18:11] That is this plane right here.
[18:13] But they're taken from different angles.
[18:15] They're a little electrical biopsy from different angles around the heart.
[18:18] And we put all
[18:20] of this information together as we'll talk about later.
[18:22] It helps us to diagnose specific forms of heart disease.
[18:26] It also tells us a lot about how well the wave of deolarization is passing through the heart.
[18:31] Are there abnormalities in the electrical conduction system or are there abnormalities in uh some of the minerals in the blood for example potassium.
[18:39] So again uh let's talk a little bit about one of the other structures in the heart that's important the coronary arteries.
[18:47] The coronary arteries are like the fuel line in your car.
[18:52] If you don't have a good open fuel line and gasoline doesn't get in or diesel fuel doesn't get in your motor, you know what happens?
[18:58] The motor doesn't function.
[19:00] The same is true about the heart.
[19:02] It needs oxygenated blood to nourish it and to enable it to continue to do its mechanical activity.
[19:10] And the heart is a remarkable organ.
[19:12] Remember, it beats constantly.
[19:14] Has to continue beating, of course, if you want to stay alive.
[19:17] Sometimes for many, many years, 80, 90
[19:21] years, sometimes even a hundred years.
[19:23] It's a remarkable strong muscle uh that that is very resistant to injury uh except when certain diseases occur but in fact often tries to uh do its best job even when injured.
[19:34] So there are of course two main coronary arteries.
[19:37] There's the left coronary artery and the right coronary artery.
[19:40] You say to me, "Wait, wait, wait a minute.
[19:42] My uncle had a triple coronary bypass.
[19:43] Where's the third coronary artery?"
[19:47] The third coronary artery occurs because the left coronary artery branches early on after its origin.
[19:50] It branches into the left anterior descending coronary artery and the left circumflex coronary artery.
[19:52] So what are we talking about here?
[19:56] We're talking then about two main arteries that start but one very quickly divides into two main branches.
[19:58] So that's how we have the three coronary arteries that are talked about.
[20:00] We're going to come back and talk more about the coronary arteries and I'm going to show you some pictures from a CAT scan.
[20:03] But let's take
[20:21] a look inside the heart for a moment. Uh
[20:24] I wanted to just reiterate the return of
[20:27] Venus blood to the heart. What you're
[20:30] seeing here is a little diagram of the
[20:33] inside of the right atrium. And you'll
[20:35] notice that there are three circles. And
[20:37] these three circles represent the Venus
[20:40] drainage coming into uh the heart. The
[20:43] highest one, the one that's up top is
[20:45] the entrance of the blood from the
[20:47] superior vennea. That blood enters the
[20:50] right atrium uh and drains the the venus
[20:54] blood from the upper part of the body.
[20:56] Now, if you look at the second one just
[20:58] below that, that's the one from the
[21:00] inferior vennea that's draining blood
[21:03] from the bottom of the body. So, what's
[21:05] the opening there on the right hand
[21:07] side? That's the coronary sinus. That's
[21:09] the heart's venus system coming back in
[21:12] because of course the heart's getting
[21:14] oxygenated blood. It has to have venus
[21:16] return to the heart so it returns also
[21:19] to the right atrium. So the upper part
[21:21] of the body, the lower part of the body
[21:23] and the heart all drain into the right
[21:26] atrium. Uh and then of course they pass
[21:28] through the tricuspid valve into the
[21:30] right ventricle. They're pumped to the
[21:31] lung where the blue blood becomes red as
[21:34] it takes on oxygen and gives off carbon
[21:37] dioxide. So here we are uh back to the
[21:40] coronary arteries and uh this is
[21:43] actually a cat scan uh that shows you
[21:46] it's colorized by the way. These are
[21:48] artificial colors put in to make it look
[21:50] realistic. Uh but in fact you can see
[21:52] very clearly the coronary arteries here.
[21:55] Um you can see the right coronary
[21:56] artery, the left anterior descending and
[21:59] the left circumflex. The right coronary
[22:01] artery supplies the right ventricle,
[22:03] part of the septum, the the wall between
[22:06] the left and right ventricles and part
[22:08] of the back of the heart. The left
[22:10] anterior descending coronary artery
[22:12] supplies the front of the heart and part
[22:14] of the septum. And the left circumflex
[22:16] coronary artery supplies the lateral
[22:18] wall of the heart and also part of the
[22:20] back of the heart. And of course,
[22:22] blockage in any one of these can cause a
[22:24] myioardial inffection or a heart attack.
[22:27] Here you see the CT in its natural
[22:30] state, not colorized artificially. Uh
[22:33] but you can see very clearly the
[22:35] coronary arteries coming off the left,
[22:37] the right, the anter descending and the
[22:40] circumflex.
[22:42] So we've reviewed the heart anatomy. The
[22:45] one thing we haven't talked about is the
[22:47] paricardium. The paricardium of course
[22:50] is the constraint. It's the the plastic
[22:52] bag, if you will, that keeps the heart
[22:54] nicely shaped uh within the chest,
[22:57] doesn't allow it to overexpand uh and
[22:59] protects the heart as well. It's filled
[23:01] with a little bit of fluid so that the
[23:03] heart is able to move smoothly uh within
[23:05] the paricardium. When disease happens to
[23:08] the paricardium and it becomes thickened
[23:10] uh and or weeps fluid into that space,
[23:14] then of course we can have restriction
[23:15] of heart function. Uh and we're going to
[23:17] talk about paricardial diseases as we go
[23:19] along.
[23:21] Well, that was a quick run through
[23:23] cardiac anatomy. You see a few
[23:25] references here that can help you to
[23:27] read a little more about it. Um, I'd
[23:29] like to reiterate what I've done here is
[23:31] given you a very quick view, if you
[23:33] will, like in an airplane from 35,000
[23:35] ft. If you want to have a little more
[23:37] detailed look at the ground, you need to
[23:39] do some more reading uh to more fully
[23:42] understand the cardiac anatomy. We're
[23:44] looking forward now to the next lecture
[23:46] where we're going to talk about the
[23:48] function of the heart. that is its
[23:50] physiology.
[23:51] With that uh let's talk about the
[23:53] cardiovascular exam. So when you know
[23:57] the cardiac exam many things are
[24:00] possible. Now what do I mean by that?
[24:02] Many things are possible is actually not
[24:04] just a statement of fact. It's also an
[24:07] acronym. It's a useful way to remember
[24:10] um the heart valves. Many things are
[24:12] possible is mt.
[24:15] Let me just draw that here.
[24:18] M
[24:21] T
[24:23] A
[24:25] P. Those letters represent the sequence
[24:29] of closing of the four heart valves um
[24:32] in the heart. The mitral, the tricuspid,
[24:35] the aortic and the pulmonic. And using
[24:38] that acronym, many things are possible.
[24:40] You'll remember which sequence those
[24:42] valves are closing. You'll also remember
[24:44] where they're located. This is a circle
[24:46] mtap mtap which helps us to keep track
[24:50] of where we are when we're listening for
[24:52] particular murmurss and trying to find
[24:54] the ideology of a particular murmur that
[24:57] we hear based on the location on the
[24:59] anterior chest wall.
[25:01] The next thing to talk about is once we
[25:03] lay our stethoscopes on his chest uh
[25:05] we're going to be listening in
[25:07] particular to three phases of the of the
[25:10] cardiac cycle. You're going to listen
[25:12] first to heart sounds. That is your S1
[25:14] and S2, also known as your lovedub,
[25:17] loved dub, lovedub. We're going to
[25:19] listen to the S3 and S4 parts of the
[25:21] heart sounds. Those are your gallops,
[25:23] which can accompany your loved dub and
[25:25] loved. The second part is cy. So, we're
[25:28] going to focus very deliberately on
[25:29] listening to the space between S1 and
[25:32] S2. And then we're going to listen to
[25:34] diastily, the space between S2 and S1.
[25:38] And I found it really important when
[25:39] you're oscultating the chest to make
[25:42] sure you really very deliberately listen
[25:43] to one thing at a time. First the heart
[25:46] sounds then cy then diastily. That helps
[25:51] you to avoid the common mistake of
[25:52] getting so sucked into a very loud
[25:55] systolic murmur that you neglect to hear
[25:57] that more subtle diastolic murmur that's
[26:00] happening afterwards. All right. So with
[26:03] that opening outline heart sounds cy
[26:05] dastily. Let's start off by talking
[26:07] about the heart sounds. So S1 and S2
[26:11] loved dub. Loved dub. As we said before,
[26:14] many things are possible. So m and t are
[26:17] the first heart sounds. So that must
[26:19] represent s1. And then a p represent the
[26:23] second heart sound, s2. These are paired
[26:26] together because they're so closely
[26:27] occurring in space. We all we hear is a
[26:29] lub. Not two different sounds, just the
[26:31] lub. And then the dub is the a and the
[26:34] p.
[26:36] Now normally when you are simply
[26:38] breathing just comfortable tidal volume
[26:41] breathing the mitro and tricuspid valves
[26:44] are closing almost perfectly
[26:46] synchronously. However the aortic and
[26:48] the pulmonic valve will actually
[26:51] separate or split during the respiratory
[26:55] cycle ex specifically during
[26:57] inspiration. So what happens is if this
[27:00] is
[27:02] S1 here mitral and tricuspid and this is
[27:06] your S2 aortic and pulmonic when the
[27:10] person takes a deep breath the aortic
[27:12] and the pulmonic will actually separate
[27:14] like so
[27:17] [sighs and gasps]
[27:20] [snorts]
[27:23] [sighs]
[27:24] and that's normal physiology and that's
[27:26] driven by the fact that when you take a
[27:27] deep breath you're creating a negative
[27:29] space in his chest that's actually
[27:31] drawing more blood to the right side of
[27:33] the heart. If there's more blood in the
[27:35] right side of the heart, it's going to
[27:36] take longer for that pulmonic valve to
[27:38] close until the pulmonic valve moves
[27:41] farther away in time while the aortic
[27:44] valve stays largely in the same place.
[27:47] That's called physiologic splitting. We
[27:49] expect to hear that when you're
[27:50] listening to the chest in this area, you
[27:52] should listen to make sure that when
[27:54] he's inspiring, when he's inhaling those
[27:57] uh that second heart sound does split
[27:59] like that.
[28:01] In contrast, there are some instances
[28:03] where for example the aortic valve may
[28:06] actually uh be displaced in time,
[28:09] particularly with a left bundle branch
[28:10] block. Now, if you have a left bundle
[28:12] branch block, the left ventricle is
[28:14] going to uh contract later than it's
[28:17] supposed to. So rather than having your
[28:20] S1 here and your S2 here with aortic and
[28:24] pulmonic valve, these two are actually
[28:26] flipped like so. The aortic valve is now
[28:29] over here and the pulmonic valve is
[28:31] here. So when this person takes a deep
[28:33] breath, the pulmonic valve moves over.
[28:42] [sighs]
[28:43] So what you're hearing is paradoxic.
[28:46] You're hearing during inspiration the
[28:48] two heart sounds moving closer together.
[28:50] And that's because the pulmonic valve is
[28:52] moving the way it's supposed to, but the
[28:54] aortic valve is so delayed by the bundle
[28:56] branch block that you hear the pulmonic
[28:59] valve catching up with it during
[29:00] inhalation. So that's called paradoxic
[29:03] splitting that you'll see with left
[29:05] bundle branch block and a few other
[29:06] conditions. We're not going to go into
[29:08] all the details of the different things
[29:09] that can cause abnormal splitting. Um,
[29:12] but I just wanted to highlight that
[29:13] that's an important thing you can pick
[29:15] up on by just listening very closely to
[29:17] those heart sounds.
[29:19] Importantly, the S1 and S2 heart sounds
[29:22] are higher [snorts] in pitch than some
[29:24] other sounds that you might hear. And
[29:26] this leads me to a very important quick
[29:28] brief on your stethoscope. Your
[29:31] stethoscope has two heads on it. You've
[29:33] got a bell, you've got a diaphragm. And
[29:35] these are uh useful in different
[29:37] circumstances. In particular, the bell
[29:40] of your stethoscope is most useful for
[29:42] low pitch sounds. It actually by putting
[29:44] the bell on the chest and creating a
[29:46] seal, you are filtering out a lot of the
[29:48] higher pitched sounds. In contrast, the
[29:51] diaphragm is useful for hearing all of
[29:53] the different pitches within the heart,
[29:55] though with potentially a little bit of
[29:57] a focus on some of the higher pitch
[29:59] sounds. So, when you're lo using the
[30:00] diaphragm, you're thinking higher pitch.
[30:02] The bell, you're thinking lower pitch.
[30:04] So, I just said that the S1 and S2 heart
[30:06] sounds um we know that they're we're
[30:09] going to best hear S2 up here. We're
[30:12] going to best hear S1 down here. And
[30:15] typically you're listening with the
[30:16] diaphragm because they're both higher
[30:17] pitch sounds like so
[30:47] Now, in some patients, you may find that
[30:50] rather than just hearing this simple
[30:52] loved dub, loved dub, loved dub, maybe
[30:55] you hear an extra sound, something like
[30:57] a belubdub, belubdub, beloved dub. That
[31:01] is an extra heart sound. In this case, a
[31:03] b occurring before the lub. And that's
[31:06] called an s4. It immediately proceeds cy
[31:11] and it's called a fourth heart sound.
[31:13] It's part of the atrial kick. What's
[31:15] happening when you hear an S4
[31:18] is that the left ventricle has fully uh
[31:22] fully filled during diastily you had
[31:24] diastolic filling and at the end of
[31:26] diastily the left atrium is contracting
[31:29] and spitting out that last volume of
[31:30] blood from the atrium but it's hitting
[31:33] against a stiff left ventricular wall.
[31:35] And this is something that you'll hear
[31:37] in patients with left ventricular
[31:38] hypertrophy, potentially hypertrophic
[31:40] obstructive cardiomyopathy. Um, and it's
[31:44] a very characteristic feature that you
[31:45] you you'll find in a lot of folks and it
[31:47] does portend or suggest that a patient
[31:50] does have one of those conditions.
[31:52] Importantly, that belubdub, the B is a
[31:56] lower pitched sound. And as I said
[31:58] before, that means you're going to best
[32:00] catch it with the bell of your
[32:02] stethoscope. Before we find it though,
[32:04] let's just quickly talk about the other
[32:06] kind of abnormal gallop that you might
[32:08] hear. Rather than lubdub, lubdub lubdub,
[32:12] you might hear a loved bub.
[32:18] Uh, essentially that is a sound
[32:20] happening right after S2.
[32:23] So rather than lob, it's lobbub.
[32:26] Lovedub. And you can tell that that bub
[32:28] is coming right after the duh, which
[32:31] would have been a dub. And uh and that
[32:34] is an indication of an S3, a third heart
[32:37] sound. Now, a third heart sound is also
[32:39] emanating from the left ventricle down
[32:41] here at the apex of the heart. And
[32:43] rather than being associated with left
[32:45] ventricular hypertrophy, it's typically
[32:47] found in acute systolic heart failure
[32:49] with left ventricular dilation,
[32:52] potentially increased filling pressures
[32:54] and uh almost always some evidence of
[32:56] systolic heart failure whether it's in
[32:59] the setting of es schemic
[33:00] cardiammyopathy or potentially if
[33:02] somebody has aortic regurgitation with a
[33:05] surplus of blood backfilling into the
[33:07] heart um then has to be ejected. So that
[33:09] sound is also heard at the apex which is
[33:12] where of course the left ventricle is
[33:13] going to be best heard and it's also a
[33:15] low pitch sound just like the S4.
[33:19] So the ideal way to bring about that
[33:22] sound it's going to be with the bell and
[33:24] since we really want to try and
[33:26] accentuate that sound because it can be
[33:27] very subtle to hear. We're actually
[33:29] going to reposition our patient and lie
[33:31] him in the left lateral decubitous
[33:33] position to really bring out that heart
[33:35] sound.
[33:36] With that, let's take a listen to the uh
[33:39] apex of the heart. All right. So, now
[33:41] that we have Shawn in the left lateral
[33:44] decubitous position, this is the ideal
[33:46] place for us us to try to pick up a
[33:49] third or fourth heart sound.
[33:53] I've got the bell of my stethoscope
[33:55] lightly applied to his chest uh simply
[33:57] to provide a seal. If I push too hard,
[33:59] I'm actually just creating a diaphragm
[34:02] out of the skin. So, you just want to
[34:04] have light pressure at the apex.
[34:13] And that's it. Now, there's a couple
[34:16] different positions that you may see
[34:18] over the course of this next few
[34:19] minutes. Uh, depending upon what you're
[34:22] looking for, you may have him lying in
[34:23] the left lateral decubitous position.
[34:25] You may have him sitting upright. You
[34:27] may have him lying flat. uh in general
[34:30] you don't want to have to repeat the
[34:31] entire cardiac exam in all three
[34:33] positions. So as we go through each
[34:35] murmur each type of valvular disease
[34:37] I'll talk about which positions may be
[34:39] most appropriate. First of all it turns
[34:41] out that the human brain is particularly
[34:44] good at recognizing patterns. Um, and
[34:47] this is a genetic characteristic that
[34:48] was probably evolved millions and
[34:51] millions of years ago uh when you needed
[34:54] to recognize what was out there in front
[34:56] of you was something that might be able
[34:59] to be eaten or something that was
[35:00] looking to eat you. So that h what
[35:04] exactly what happens with the electroc
[35:05] cardiogram after a while when you become
[35:07] very expert your brain allows you to
[35:10] recognize the pattern immediately when
[35:12] you see it. Now, of course, you there's
[35:14] going to be some steps where you're
[35:16] going to have to make some measurements,
[35:17] but in fact, you will immediately know,
[35:19] oh, I recognize that that's a a a heart
[35:22] attack and so forth. So, and you I think
[35:24] after the end of this 10 uh lecture
[35:26] series, you'll be able to do that and
[35:29] with practice, you'll get very good at
[35:30] it. So, I'm sure you recognize
[35:34] immediately these two paintings, right?
[35:36] On the left is Van Go's starry sky. On
[35:39] the right is Leonardo da Vinci's Mona
[35:41] Lisa. How did you recognize them
[35:43] immediately because you know the pattern
[35:45] you've seen them so many times. In the
[35:47] end, I think you'll get to be able to
[35:49] read the electroc cardiogram in a very
[35:52] similar way. You'll immediately
[35:54] recognize something and then you'll go
[35:55] back and do a little more detailed work
[35:57] on it. So when did the electroc
[35:59] cardiogram start? It started in the
[36:02] early 20th century. A Dutch physician
[36:05] named Einhovven uh was the first to be
[36:08] able to record the electrical activity
[36:10] of the heart with any accuracy. Many had
[36:13] tried before but he was the first that
[36:15] was successful. Now you can see from
[36:17] this very primitive early electroc
[36:19] cardiogram. One had to have an arm in
[36:22] saltwater and a leg in saltwater and a
[36:24] huge apparatus in order to record the
[36:27] electroc cardiogram. Well, today of
[36:29] course with solid state uh instruments
[36:31] uh they're much more sophisticated. The
[36:34] amplification makes the uh images much
[36:36] clearer. Um and uh we now use a very
[36:40] standardized protocol all over the
[36:42] world. Uh the standards were arrived at
[36:45] a long time ago back in the 1930s uh by
[36:48] uh experts who came together to decide
[36:50] what would be the universal um rules for
[36:53] an electroc cardiogram. Um so um reading
[36:58] uh the electroc cardiogram as I said
[36:59] it's like examining a fine artwork.
[37:02] First of all you get an overall
[37:03] impression something leaps out at you
[37:05] particularly if it's acute heart attack
[37:08] uh acute myioardial inffection as we'll
[37:10] talk about but then secondly there has
[37:13] to be the more careful detailed analysis
[37:15] things like heart rate and the duration
[37:18] of the various intervals and we're going
[37:20] to go over that now. Um, so in the
[37:23] beginning, don't hurry. Take your time.
[37:26] Systematically check the heart rate, the
[37:28] timing of the intervals, and the
[37:30] presence or absence of Pwaves. And we're
[37:32] going to talk about what that means in a
[37:34] moment.
[37:35] Remember, many times you're going to be
[37:38] seeing a an electroc cardiogram that's
[37:40] been recorded by a computer, and the
[37:42] computer will have read uh a diagnosis.
[37:46] It'll give you some information. The
[37:48] computer's usually right about heart
[37:49] rate and intervals, but it's often not
[37:52] right uh about the underlying rhythm,
[37:55] and sometimes it even makes more serious
[37:57] mistakes. So, every computerized
[37:59] electroc cardiogram has to be overread
[38:01] by an experienced electroc
[38:03] cardiographer.
[38:04] So, the first thing you're going to look
[38:06] at is going to be the heart rate. That's
[38:08] the number of beats per minute. I'm
[38:10] going to give you a rule how you can
[38:12] calculate the heart rate from the EKG.
[38:14] Of course, it will already have been
[38:16] calculated for you if it's a computer
[38:18] read ECG. Then we're going to do the
[38:20] various intervals. Um that's the various
[38:23] points on the the electroc cardiographic
[38:26] complex that you see um on the right
[38:29] hand side. Um and we're going to go over
[38:32] how those intervals are derived and how
[38:34] long they are when it's normal. So let's
[38:37] start. The first wave in the electroc
[38:40] cardiogram is the Pwave. And this is the
[38:43] electrical signal made when the atria
[38:46] that's the upper chambers deolarize. Now
[38:48] you're going to ask why P QRS and T? Why
[38:52] not A, B, C, D, and E? Well, in fact, in
[38:55] the early years of where there were
[38:57] attempts in the early 20th century to
[38:59] try and and record the electroc
[39:00] cardiogram, there were many artifacts
[39:03] that were called A, B, and C and D and
[39:05] so forth all the way through the
[39:06] alphabet. And finally, Einhovven got to
[39:09] the letters PQ or RS and T which were
[39:11] the accurate ones. So all the earlier
[39:13] ones were artifacts. So that's why we
[39:15] use these terms. Um so here is a normal
[39:18] complex. You'll notice the Pwave, that's
[39:21] the electrical deolarization, the wave
[39:23] of electricity running down through the
[39:25] atria and then it arrives at the
[39:27] ventricle. That's the QRS. That big
[39:30] complex is the ventricle. Ventricle has
[39:32] much more heart muscle. So therefore
[39:34] it's a much bigger u complex. And then
[39:37] you have something called the ST segment
[39:39] which is a a little pause before the
[39:41] ventricle resets itself. And the
[39:43] resetting is the T-wave. And some
[39:46] patients will have a Uwave uh uh
[39:48] following the T-wave. This can be
[39:50] normal. It's absent in most electroc
[39:51] cardiograms and it is a little more
[39:54] commonly seen when patients have low
[39:56] blood potassium so-called hypocalemia.
[40:00] Um so here again are the various
[40:02] segments. You'll notice uh that the um
[40:05] that the so-called PR segment is the
[40:08] segment that runs all the way from the
[40:11] beginning of the Pwave to the QRS. It's
[40:13] divided into two segments. The duration
[40:15] of the Pwave and then the PR segment
[40:18] that is from the end of the Pwave uh to
[40:20] the beginning of the QRS. But for most
[40:22] daily reading of the electroc
[40:24] cardiogram, we just call the PR segment
[40:27] the entire period from the beginning of
[40:30] the Pwave to the beginning of the QRS.
[40:33] You then see in gray the QRS complex. Um
[40:37] that's the deolarization of the
[40:39] ventricle of both ventricles by the way
[40:41] right and left although the left has a
[40:43] lot more muscle. So the QRS is dominated
[40:46] by left ventricular muscle
[40:48] deolarization.
[40:50] There's then an ST segment um where a
[40:53] little pause while the ventricle
[40:55] finishes the deolarization and gets
[40:58] ready to repolarize. That is to get
[41:00] ready for the next beat. And that's
[41:02] during the T-wave. The T-wave is the
[41:04] repolarization wave. And then as I
[41:06] mentioned, the Uwave is often not
[41:08] present um but may be present as a very
[41:10] small wave following the T-wave.
[41:13] Um the electroc cardiogram is usually
[41:16] the first test done after the history
[41:18] and physical exam. It's often done in
[41:20] offices. It's very simple and many uh
[41:22] physicians offices have their own
[41:24] system. Usually it's done by a
[41:26] technician. Um in the office it may be
[41:28] done by the office nurse. In the
[41:30] hospital there's a whole series of
[41:32] technicians um who are on 24 hours a day
[41:35] to record accurate electroc cardiograms.
[41:38] It is again the simplest, cheapest and
[41:40] most easily obtained cardiovascular
[41:42] test. It has reasonable accuracy for a
[41:45] variety of heart conditions, for
[41:47] example, arrhythmias or myioardial
[41:49] inffection, a heart attack. Um, however,
[41:52] uh, it's not as accurate to determining
[41:54] the volume of heart muscle compared to
[41:56] an MRI, an echo or or a CT scan. Uh, but
[42:02] um, all of those are much more
[42:03] expensive. They require huge amounts of
[42:05] equipment and machinery. Um the electroc
[42:07] cardiogram is really inexpensive and
[42:10] very simple and is almost always the
[42:12] first test done. Um [snorts]
[42:14] one of the things one of the reasons it
[42:16] takes a long time to learn to read
[42:18] electroc cardiogram is there are many
[42:19] non-specific or non-diagnostic patterns
[42:22] and there are some differences between
[42:24] men and women and between different
[42:26] groups. For example, in the United
[42:28] States African-Americans have slightly
[42:30] different normal values from from
[42:32] European white males and so forth. So uh
[42:35] all of this of course is in the computer
[42:37] and the computer uh is told u before the
[42:39] EKG is taken what the patient's ethnic
[42:42] background is and so forth. So that
[42:44] helps in terms of the normals. Um and
[42:47] also you'll get to recognize these
[42:48] things as you practice reading many
[42:50] electroc cardiogram. So let's start with
[42:53] the most basic way of interpreting the
[42:55] ECG. Um the first thing you do is you
[42:59] have to check the voltage calibration.
[43:01] What's this about? This is about the
[43:02] amplification of the image that the ECG
[43:05] machine is going. Sometimes with
[43:07] arrhythmias we want to enlarge the
[43:09] complexes. So we will double the the
[43:12] amplification of the image. But usually
[43:15] for almost all routine ECGs, the
[43:18] calibration is so-called 10 um
[43:20] millimeters. That's 10 little boxes. And
[43:23] we'll show you examples of that. And
[43:24] it's always good to check that to begin
[43:26] with because if they had been using the
[43:28] machine at a higher amplification, the
[43:30] complexes are going to look bizarre.
[43:32] They're going to be big and so forth and
[43:33] you might make a mistake in reading. So,
[43:36] first make sure that that the
[43:38] calibration is correct. Usually the
[43:39] technician takes care of that that uh
[43:41] but it's there's a little box that shows
[43:43] you that the calibration is okay and
[43:45] I'll point that out later. The next
[43:47] thing is to determine the rhythm. And
[43:49] how do you do that? You're looking for
[43:51] Pwaves followed by QRS's. In other
[43:53] words, the normal progression, remember,
[43:55] starting up with the sinus node, atrial
[43:58] deolarization, Pwave, QRS, ventricular
[44:01] deolarization, T-wave resetting. Once
[44:05] you know what the rhythm is, in other
[44:06] words, is this a normal sinus rhythm, or
[44:08] is it not normal sinus rhythm, but a but
[44:11] an arrhythmia, and we're going to have
[44:12] whole lectures about the kinds of
[44:14] abnormal electrical events that can
[44:16] occur when it's not sinus rhythm. Um,
[44:20] you then calculate the heart rate, which
[44:22] is a there's a normals there, and I'm
[44:24] going to be going over the normals as we
[44:25] go along. Um, you then do the timing
[44:28] intervals. What's the PR interval from
[44:30] the beginning of the Pwave to the
[44:32] beginning of the QRS? What's the QRS
[44:34] duration? That's the period of
[44:36] ventricular deolarization. And then how
[44:38] long does it take for the whole uh
[44:40] contraction and resetting of the
[44:42] ventricle from the Qwave to the end of
[44:44] the T-wave? We would then determine the
[44:47] electrical axis. In other words, uh what
[44:51] is the main vector force of the
[44:54] electrical deolarization wave? What
[44:56] direction is it going in? Um and there's
[44:58] a certain normal area for that. Um and
[45:01] for example, if you have abnormalities
[45:04] of of the ventricular mass, uh you can
[45:06] get abnormal uh vectors uh abnormal uh
[45:10] electrical vectors. Um we want to look
[45:12] at the Pwave morphology to see if it's
[45:14] normal. We look at its voltage and its
[45:16] shape uh because certain abnormalities
[45:19] of Pwave morphology can occur with
[45:22] certain diseases. We want to do the same
[45:24] for the QRS morphology. Again, certain
[45:26] diseases um and for example, heart
[45:29] blocks, things that can lead to
[45:30] pacemakers will change the morphology of
[45:33] the QRS. We'll then look at the ST
[45:36] segment and the T-wave morphology.
[45:38] eskeemia, lack of blood flow in the
[45:40] heart that can lead to angula or heart
[45:42] attacks changes the ST segment and
[45:45] T-wave morphology. And if we're lucky
[45:47] enough to have an earlier baseline EKG,
[45:50] we compare it to see, hey, have there
[45:52] been changes? Is something going on
[45:54] here? That's something acute.
[45:56] So, let's start here is a normal ECG.
[46:00] Notice in the upper left corner there is
[46:04] a little green box. That's the standard.
[46:06] And that standard is if you count the
[46:08] little tiny boxes, 10 little boxes. Each
[46:12] one of the big boxes has five smaller
[46:14] boxes. So there'll be two of the big
[46:17] boxes um which constitute 10 small
[46:20] boxes. Each one of those boxes is one
[46:23] millimeter and corresponds to one
[46:25] millolt of electrical activity. Um so
[46:30] again uh this is the standard on all ECG
[46:33] machines. Uh and if you had set the
[46:36] standard to half then of course it would
[46:39] be each uh uh one of those little boxes
[46:42] uh would be uh less uh uh voltage. If
[46:45] you doubled it they would be uh more
[46:47] voltage but usually again almost all
[46:50] EKGs use this green box of the 10
[46:53] standard. You'll notice how the leads
[46:56] are placed here. On the left hand side
[46:59] there's lead 1, two, and three. Remember
[47:01] 0 degree plus 60 plus 120. The next
[47:05] three leads AVR, L and F, ARVR plus 210,
[47:10] AVL minus30, AVF + 90. And then come the
[47:14] precordial leads, the ones that are
[47:16] sticking through the heart like like
[47:17] needles in a sagittal plane. V1, V2, V3,
[47:22] four, five, and six. And this is a
[47:24] normal ECG. Notice there's a Pwave in
[47:27] front of each QRS. The QRS's are nice
[47:30] and narrow. There's a nice T-wave
[47:33] upright and and not way prolonged after
[47:36] each QRS. Um, this is sinus rhythm.
[47:39] Normal sinus rhythm that that's set off
[47:42] by the sinus node. Passes normally
[47:45] through the heart. There's no evidence
[47:46] here of eskeeia or heart attack or or
[47:49] hypertrophy of the heart muscle. As I
[47:52] said, you'll notice that there's sinus
[47:53] rhythm. In the green box, you'll see
[47:55] that each QRS is preceded by a Pwave.
[47:58] The atria, the atrium deolarizes before
[48:01] the ventricle. All the Pwaves are
[48:03] followed by a QRS. There's no blockage
[48:06] of the beat as it goes down through the
[48:08] heart. Each QRS is preceded by a P. And
[48:12] the Ps are all identical. They're
[48:14] upright in leads two and AVF. Um, and
[48:17] they're nice and narrow. They're not
[48:19] prolonged.
[48:20] Um, if any of the comments just made the
[48:24] answer was no, then you're talking about
[48:26] an arrhythmia. And as I said, we're
[48:27] going to have whole lectures on the
[48:28] arrhythmias later. So, right now, we're
[48:31] just worrying about the normal.
[48:33] Also, uh, you notice how nicely the
[48:37] QRS's progress. Uh, in fact, that whole
[48:40] strip along the bottom, even though
[48:42] they're different leads, it's
[48:44] continuous. So, you're actually seeing
[48:46] one set of Pwaves after another.
[48:50] In order to um obtain the heart rate,
[48:54] you count the number of big boxes
[48:56] between two QRS's and you divide by 300.
[49:00] So if there were two big boxes between
[49:02] the two QRS's, that would be two into
[49:05] 300 or 150. If there were three big
[49:08] boxes in between a QRS, that would be a
[49:10] rate of 100. 3 into 300. If there were
[49:13] four boxes in between the two QRS's,
[49:16] that would be 75. 4 into 300 is 75. You
[49:20] can also do it by counting the number of
[49:22] QRS's in 3 seconds. Remember the ECG is
[49:25] moving at a certain rate. You can
[49:27] calculate a number of seconds and then
[49:30] multiply by 20. But usually what we do
[49:32] is we use the rule of 300 mentioned
[49:34] before. It's important to note uh that
[49:38] the normal heartbeat is 60 to 100 beats
[49:42] per minute.
[49:44] So now we have the heart rate. By the
[49:46] way, the computer's almost always right
[49:48] on the heart rate. Um, again, let's talk
[49:51] about the intervals. So, a normal PR
[49:54] interval is 0.12 seconds to 20 seconds.
[49:58] That's three little boxes to five little
[50:01] boxes, right? You remember there's five
[50:03] little boxes within the big bigger box.
[50:06] So, the normal PR interval from the
[50:07] beginning of the Pwave to the beginning
[50:09] of the QRS is somewhere between three
[50:11] and five little boxes.12
[50:14] to.20 20 seconds. The normal QRS
[50:18] interval is less than 0.1. That's 2 and
[50:21] a half little boxes. And the normal QT,
[50:25] which is corrected for heart rate in a
[50:27] formula, is somewhere between 33 and 46
[50:31] seconds. Remember the QT from the
[50:33] beginning of the Qwave to the end of the
[50:36] T-wave.
[50:38] Um remember each small box is 0.04
[50:42] seconds. So a large box is 5 times 0.04
[50:45] seconds or.20 seconds. And there are
[50:48] five small boxes in each large box as
[50:51] I've said before. Again, what about the
[50:55] axis? Well, there's a general rule that
[50:57] most med students use, and that is if
[51:00] the QRS is upright in leads one and two,
[51:03] it's a normal axis. You can actually
[51:06] calculate the axis because the axis is
[51:09] perpendicular to any lead where the R
[51:12] and the S or the upstroke and the
[51:14] downstroke are equal. In this example,
[51:16] lead three. You see that pretty much the
[51:19] amount above the line and below the line
[51:21] is about the same. So the axis is going
[51:23] to be 90 degrees from lead three. So 90
[51:27] degrees plus 120. Lead three is 120.
[51:30] Remember that's 210. And that would be
[51:33] in other words um a the axis would be
[51:35] towards AVR or minus 90 from 120 would
[51:39] be 30 that would be somewhere need near
[51:41] lead 2 which is plus 60. Well you can
[51:44] see how do we tell where is the maximum
[51:47] Rwave? Well the maximum Rwave is around
[51:49] lead 2. It's there's no upright Rwave in
[51:52] AVR. So therefore the axis is actually
[51:56] uh something like a plus 30. Um, so
[52:00] again the the rule of thumb is you look
[52:02] to see where the the amount of voltage
[52:04] up and down is equal. It's 90 the axis
[52:07] is 90 degrees from that. Then you look
[52:09] for the lead with the maximum Rwave.
[52:11] That's the direction because you could
[52:13] go this way on the 90 degrees or you
[52:16] could go that way. What tells you which
[52:17] way you go is where's the maximum Rwave.
[52:20] In this one it's lead two. And uh again
[52:24] normal axis is between minus30 and plus
[52:27] 90. And if the axis is not between plus
[52:31] minus30 and plus 90 then it's an axis
[52:34] deviation. If it goes more minus that's
[52:37] so-called left axis deviation. If it
[52:39] goes more plus than 90 it's called right
[52:42] axis deviation. And we'll talk about how
[52:44] that's used in reading various electroc
[52:47] cardiographic diagnosis. So again, just
[52:50] to reiterate, the axis for the mean
[52:52] frontal plane electrical vector of the
[52:54] heart is near the limb lead with the
[52:56] tallest Rwave and perpendicular to the
[52:59] lead where the size of the upward
[53:01] deflection and the downward deflection
[53:04] are equal. Remember the upward
[53:06] deflection is called an Rwave. The
[53:08] downward deflection is called an S-wave.
[53:11] So let's take a look at the Pwave
[53:14] itself. The normal Pwave is going to be
[53:17] three little boxes or less in duration.
[53:20] Remember that the PR interval, that's
[53:22] the duration from the beginning of the
[53:24] Pwave to the beginning of the QRS, is
[53:26] going to be less than five little boxes.
[53:28] But the length of the Pwave itself,
[53:31] should be only three little boxes. And
[53:34] it should be upright in lead one and two
[53:38] and a negative deflection of less than
[53:41] one box wide or one box deep in V1. If
[53:45] the Pwave in lead V1
[53:48] is more negative than one box and wider
[53:52] than one box that suggests that the
[53:54] atrium is the left atrium is enlarged
[53:57] so-called left atrial enlargement.
[54:00] If the box is pointed and higher than
[54:04] two millimeters
[54:07] then uh and usually wider than two then
[54:10] that defines right atrial enlargement.
[54:14] Now these numbers are not anatomically
[54:16] perfect. The echo and the MRI and so
[54:19] forth would be more perfect but they
[54:20] carry prognostic information. They're
[54:23] very important because when they appear
[54:25] it really means that there's quite
[54:26] significant either left atrial
[54:28] dilitation or right atrial dilitation.
[54:32] Let's look at the Rwave. Now the normal
[54:34] Rwave should transit in the precordial
[54:37] lead. Starting with lead V1, there
[54:40] should be a very small Rwave and then it
[54:42] gets a little bigger in V2. And
[54:44] somewhere between V3 and V4, you have a
[54:47] dominant Rwave with not much S Swave.
[54:50] And then it progresses out to V6. Uh
[54:53] with usually the maximum Rwave somewhere
[54:56] in V4, five and six with the transition
[54:59] from more negative to positive somewhere
[55:03] around V3 or V4. small cues that is
[55:06] initial downward deflections of less
[55:09] than one little box um can occur um but
[55:13] uh that they are never longer than one
[55:15] box. If they're wider than one box it
[55:18] suggests that there's been damage uh to
[55:20] the myioardium
[55:22] and uh the voltage should be within a
[55:24] normal range.
[55:26] Also the ST segment should be isoctric
[55:29] that is it should be flat. um you can
[55:32] have a little bit of depression um but
[55:34] if it's substantially depressed more
[55:37] than a tiny amount it suggests a number
[55:39] of things let's look at what it suggests
[55:41] if there's a sort of curved sagging of
[55:44] the ST segment as in this example that
[55:46] means the patient is usually taking
[55:48] digitalis digitalis has that effect if
[55:51] there's eskeeia or lack of blood flow
[55:53] you see a squared off flattening of the
[55:56] ST segment we see that with positive
[55:58] exercise tests and we see that when
[56:00] patients come in and have uh so-called
[56:03] non-estee elevation mioardial infarct
[56:06] and we'll talk more about those
[56:07] definitions later. Um, and then in
[56:10] hypocalemia where the potassium is low,
[56:13] you may see a mildly downs sloping ST
[56:15] segment, the T-wave is often flattened.
[56:18] And as I mentioned before, you may see a
[56:20] little additional wave after the T-wave,
[56:22] the Uwave. Again, here's the normal EKG.
[56:26] Look at the ST segments here. They're
[56:29] all fine. They're not depressed. They're
[56:32] not elevated. They're in exactly the
[56:34] right sequence. This is going to give
[56:37] you a big overview of cardiac pathology.
[56:41] It's actually possible to bin to kind of
[56:44] compartmentalize the different cardiac
[56:46] pathologies into about six different
[56:47] categories. And if you understand kind
[56:50] of the big picture, the little picture
[56:52] just ends up being some details that are
[56:54] kind of cool but uh not as important as
[56:57] the big picture. With that introduction,
[56:59] we're going to see a lot of cool videos
[57:01] that were prepared with the assistance
[57:03] of Dr. Jose Mata who I am eternally
[57:06] grateful for for all of his help. Okay,
[57:10] so this is the normal heart. What it is
[57:13] normally doing is squeezing blood out in
[57:17] a controlled regulated fashion, in a
[57:20] rhythmic fashion to provide profusion to
[57:23] the lungs so that blood can get
[57:25] oxygenated, but also to the aorta and
[57:28] out to the rest of the body to provide
[57:30] oxygenated blood and metabolic nutrients
[57:34] to the rest of the body and eventually
[57:36] bring back Venus blood that will allow
[57:38] us to get rid of various waste products
[57:41] and also carbon diox. oxide. So the
[57:44] heart in its beauty is just squeezing in
[57:48] a regular fashion and it's got to be
[57:50] coordinated. There's a lot going on
[57:51] here. What's not shown yet are there are
[57:55] valves that are giving us unidirectional
[57:57] flow. There are coronary arteries that
[58:00] are providing adequate profusion to the
[58:02] heart and then there are all the big
[58:04] vessels that are responsible for
[58:07] carrying blood to various places. Okay,
[58:09] that's what it should look like. We're
[58:12] going to have some big picture things
[58:15] related to cardiac pathology. Number one
[58:19] on the hit parade is pump failure. And
[58:23] basically this can be due to a variety
[58:24] of causes but more commonly most
[58:26] commonly this is going to be due to es
[58:28] schemic heart disease. A big thrombosis
[58:32] of a coronary artery which causes loss
[58:36] of profusion to a part of the heart and
[58:38] that heart is not pumping anymore. So
[58:40] there's pump failure. In this particular
[58:43] image, the right ventricle is fine. It
[58:45] continues to pump, but the left
[58:46] ventricle is pretty much at a
[58:47] standstill. That's clearly not going to
[58:50] provide adequate perfusion blood supply
[58:52] to the rest of the body. So that's one
[58:55] major mode of cardiac pathology, pump
[58:58] failure. What's shown here is actually a
[59:01] heart attack. But you can also have this
[59:03] same failure mode if you have
[59:06] myocarditis. you have inflammation and
[59:09] other injury of the heart. You can have
[59:11] pump failure if you fill up the heart
[59:13] with an extracellular component called
[59:16] amaloid. So there are variety of ways
[59:18] that you can have pump failure. Okay,
[59:20] that's one. Next one is because the
[59:23] valves that are supposed to maintain
[59:25] unidirectional blood flow don't work
[59:28] appropriately. So we're looking down
[59:30] onto the top of the heart and right
[59:33] there in the middle looking proud is the
[59:35] aortic valve. That valve should open all
[59:37] the way up to provide to allow blood to
[59:41] flow out when the ventricle squeezes. In
[59:44] this case, we have a stenotic valve. We
[59:46] have flow obstruction. That will have a
[59:49] number of consequences including
[59:51] diminished profusion of all the distal
[59:54] tissues, but also the heart's going to
[59:56] have to work much harder to try to pump
[59:58] against that tight valve. So, flow
[01:00:00] obstruction is another major cardiac
[01:00:03] pathology. Well, if you have stenosis,
[01:00:06] you can also have regurgitation. So, the
[01:00:08] next one is regurgitant flow. This is
[01:00:11] looking at an aortic valve. Blood should
[01:00:13] only be going out through the aorta. It
[01:00:16] should not be going backwards into the
[01:00:18] left ventricle. That backwards
[01:00:21] regurgitant flow is going to cause
[01:00:23] volume and pressure overload in the left
[01:00:25] ventricle which eventually will
[01:00:27] translate back into the left atrium into
[01:00:29] the lungs and we will have heart
[01:00:31] failure. So regurgitant flow is also a
[01:00:35] major source of cardiac pathology.
[01:00:39] You can have shunted flow. So again
[01:00:41] blood is supposed to go from the
[01:00:43] inferior inferior and superior vennea
[01:00:46] into the right atrium into the right
[01:00:49] ventricle and out the pulmonary artery
[01:00:52] return through the pulmonary veins to
[01:00:54] the left atrium to the left ventricle
[01:00:56] and out through the aorta. But in a
[01:00:59] number of congenal heart diseases and
[01:01:01] sometimes acquired diseases, you can
[01:01:03] have abnormal flow from the left side to
[01:01:06] the right side. In general, that will
[01:01:09] be, as we'll talk about, the most common
[01:01:12] defect because the leftsided pressures
[01:01:15] are much higher than the right- sided
[01:01:16] pressures. If we make holes between the
[01:01:18] ventricles or between the atria, flow
[01:01:20] will tend to go left to right. There are
[01:01:24] exceptions to this, very important
[01:01:26] exceptions. when pulmonary pressure
[01:01:27] becomes very high. But shunted flow is
[01:01:31] also going to cause significant
[01:01:32] pathology. And in this particular case,
[01:01:34] that extra volume and pressure coming
[01:01:37] from the left ventricle through a
[01:01:39] ventricular septile defect into the
[01:01:41] right ventricle is going to cause
[01:01:43] pressure volume overload in the right
[01:01:45] ventricle causing one right heart
[01:01:47] failure but increase pressure and volume
[01:01:50] in the pulmonary circulation which can
[01:01:52] eventually cause pulmonary hypertension.
[01:01:54] So shunted flow is your fourth big
[01:01:57] picture cause of cardiac pathology.
[01:02:00] There can be abnormal cardiac
[01:02:04] conduction. So if the atria do not
[01:02:08] transmit the signal appropriately from
[01:02:10] the sinoatrial node to the a atrial
[01:02:13] ventricular node then you will have
[01:02:15] atrial fibrillation and then you will
[01:02:17] not have a coordinated squeezing of the
[01:02:19] atrium into the ventricles. Similarly,
[01:02:22] if the ventricle is quivering in
[01:02:24] ventricular fibrillation, that's another
[01:02:27] cause of cardiac pathology. So, the
[01:02:30] conduction system has to work
[01:02:32] appropriately. And we will talk in one
[01:02:34] of our our sessions together, you and I,
[01:02:37] about cardiac conduction abnormality
[01:02:40] specifically.
[01:02:42] And finally, we can have rupture of the
[01:02:44] heart or a major vessel. And basically,
[01:02:47] when that happens, you get excuation.
[01:02:49] that seems like a rather trivial cause
[01:02:51] of cardiac pathology, but can have major
[01:02:54] outcomes. Basically, it's a cause of
[01:02:55] death. And what we're looking at on this
[01:02:57] image is a a reconstruction of a patient
[01:03:01] with a dissecting aneurysm uh that was
[01:03:05] ultimately lethal because the blood got
[01:03:07] into the abnormal false lumen and then
[01:03:10] ruptured out into the paricardial sack
[01:03:13] causing tamponod.
[01:03:15] All right, with that we have covered the
[01:03:17] six major modes of cardiac pathology.
[01:03:20] And now in the subsequent talks that
[01:03:22] we're going to have together, it's just
[01:03:23] going to be interesting details. We're
[01:03:26] going to talk about a rather large but
[01:03:28] very important topic of basic heart
[01:03:30] muscle disease or cardiomyopathy.
[01:03:34] We're going to do an overview and then
[01:03:36] we will talk pretty much in three little
[01:03:39] bins or three larger bins about the
[01:03:42] various forms of cardiammyopathy. While
[01:03:44] we are understanding more and more of
[01:03:46] the genetic basis underlying many of
[01:03:48] these intrinsic heart muscle diseases,
[01:03:51] it's still best to think about them in
[01:03:53] terms of their pathophysiology.
[01:03:56] So we will talk about a dilated or
[01:03:58] globoid or kind of floppy heart. We'll
[01:04:01] talk about a very hyperdamic heart.
[01:04:03] That's hypertrophic cardiammyopathy. And
[01:04:05] then we will talk about restrictive
[01:04:06] cardiopathy which is a stiff heart.
[01:04:10] So let's start with a cardiammyopathy
[01:04:12] overview.
[01:04:14] As I've already stated,
[01:04:16] cardiammyopathies are basically a group
[01:04:18] of diseases that affect the heart muscle
[01:04:20] and decrease its ability to pump blood.
[01:04:23] And that may be because it doesn't fill
[01:04:26] very well or because it doesn't pump
[01:04:29] very well. And either one of those will
[01:04:31] lead to the overall effect that there is
[01:04:34] diminished ability to pump blood
[01:04:36] systemically to all the organs of the
[01:04:38] body.
[01:04:39] There can be primary causes of
[01:04:41] cardiammyopathy intrinsic to the cardiac
[01:04:43] muscle. There may be secondary forms due
[01:04:45] to diseases of other kinds that affect
[01:04:48] the cardiac muscle.
[01:04:53] We're going to use this kind of uh
[01:04:55] schematic to help understand the various
[01:04:58] forms of cardiammyopathy or the types.
[01:05:01] Looking at the normal heart, you can see
[01:05:03] then we've emphasized mainly the left
[01:05:05] ventricle and the left atrium and the
[01:05:07] aorta. But you can also in some of the
[01:05:10] images that we're going to show affect
[01:05:12] the right ventricle as well. But the
[01:05:14] normal heart has normal closure of
[01:05:17] valves, normal size left atrial, normal
[01:05:19] size left ventricle cavity, normal
[01:05:22] thickness of the mioardium in the left
[01:05:24] ventricle.
[01:05:26] In a dilated cardiammyopathy, we're
[01:05:28] going to see kind of a globoid dilation
[01:05:31] of the heart. This is actually the most
[01:05:33] common cause of cardiammyopathy. Roughly
[01:05:35] 85 to 90% of cases are going to be
[01:05:38] dilated cardiammyopathy. And along with
[01:05:41] this dilation of the chamber, you can
[01:05:44] see that we're pulling those papillary
[01:05:45] muscles a little bit apart which are
[01:05:47] tugging on the cordi tendin which are
[01:05:49] opening the mitral valve. And so there's
[01:05:51] marketked left atrial dilation. Those
[01:05:54] are all part and parcel of a dilated
[01:05:56] cardiammyopathy.
[01:05:58] [gasps]
[01:05:59] This also includes aray-ythmogenic
[01:06:02] cardiammyopathy previously called
[01:06:03] arythmogenic right ventricular
[01:06:05] cardiammyopathy because it predominantly
[01:06:08] affects the right ventricle. The
[01:06:10] important point about this is that it is
[01:06:12] a form of dilated cardiopathy. We'll
[01:06:14] cover it more later. So just keep that
[01:06:16] in mind. The flip side of the coin is
[01:06:19] hypertrophic cardiammyopathy.
[01:06:22] Hypertrophic cardiammyopathy is a
[01:06:24] thickened ventricle with a hyperdamic
[01:06:27] heart. So there's more cardiac muscle
[01:06:30] mass.
[01:06:32] The outcome though however because of
[01:06:34] obstruction to the left ventricular
[01:06:36] outflow due to the thickness of the
[01:06:37] interventricular septum myioardium can
[01:06:40] also lead to left atrial enlargement. So
[01:06:43] you can have some of the same general
[01:06:45] geographic effects. And then there's
[01:06:48] restrictive cardiopathy where the
[01:06:50] chambers of the heart look pretty
[01:06:51] normal. The thickness of the wall looks
[01:06:53] pretty normal but because we have
[01:06:55] infiltrated the myasytes or the the
[01:06:57] myioardium with various things like
[01:07:00] fibrous connective tissue or amaloid the
[01:07:03] walls are stiff. So they don't relax
[01:07:06] very well. Okay. We're going to cover
[01:07:09] each of these in turn these kind of
[01:07:11] basic pathophysiologic forms dilated
[01:07:14] hypertrophic restrictive and talk about
[01:07:16] the ideologies and the consequences.
[01:07:20] Let's start first with dilated
[01:07:22] cardiammyopathy
[01:07:23] in general split about 50/50
[01:07:26] and the numbers change because we're
[01:07:28] finding more genetic causes but roughly
[01:07:30] 50/50 genetic causes and non-getic
[01:07:33] causes.
[01:07:35] These dilated cardiammyopathies cause
[01:07:38] systolic dysfunction. So they don't
[01:07:41] squeeze very well. They actually fill
[01:07:44] pretty well. They're pretty floppy. So
[01:07:45] they they feel okay. They just don't
[01:07:48] squeeze the blood out. So ejection
[01:07:50] fractions will be marketkedly
[01:07:52] diminished.
[01:07:53] In hypertrophic cardiammyopathy, we know
[01:07:56] it's about 100% of cases have a genetic
[01:07:58] cause and we understand the vast
[01:08:00] majority of those. In this case, it's
[01:08:03] not systolic dysfunction. They squeeze
[01:08:06] great. In fact, they squeeze too well,
[01:08:08] but they don't relax very well. So,
[01:08:11] they're like hard driving medical
[01:08:12] students around the world. They work
[01:08:15] really hard and they don't relax very
[01:08:17] well. So, it's diastolic dysfunction.
[01:08:19] And then in restrictive cardiammyopathy,
[01:08:22] as I've already stated, it's associated
[01:08:24] with some systemic disorders or it may
[01:08:26] be idiopathic. And the fundamental
[01:08:28] problem is that it's diastolic
[01:08:29] dysfunction. It's a stiff heart. there's
[01:08:32] not a lot of muscle there or not
[01:08:34] excessive increases in muscle but it's
[01:08:37] stiff and therefore you have diastolic
[01:08:39] dysfunction. It doesn't relax to fill
[01:08:41] very well. In all the cases whether it's
[01:08:45] dilated, hypertrophic or restrictive the
[01:08:48] clinical presentations are pretty much
[01:08:50] the same. It's heart failure. We have
[01:08:52] inadequate pump function to peruse the
[01:08:56] rest of the body. And as the heart
[01:08:59] either dilates and the valves fail or as
[01:09:03] we have increased
[01:09:06] squeezing with poor relaxation,
[01:09:09] we don't we tend to get regurgitant flow
[01:09:12] into the atrium. We get left atrial
[01:09:15] enlargement that leads to atrial
[01:09:17] fibrillation.
[01:09:19] A combination of atrial fibrillation, a
[01:09:21] kind of quivering left atrium and
[01:09:25] diminished flow through that left atrium
[01:09:27] with a dilated left atrium is going to
[01:09:29] make that portion of the heart prone to
[01:09:31] forming thrombi. So patients can also
[01:09:35] present with stroke and with sudden
[01:09:38] cardiac death due to either embleization
[01:09:41] or to sudden arrhythmic events. So the
[01:09:45] final consequences of all these are
[01:09:47] pretty much the same. how we get there
[01:09:49] in each of them is a little bit
[01:09:51] different.
[01:09:53] All right, that's the overview. And if
[01:09:54] you've got that, then you've really
[01:09:56] understood about 80% of what we're going
[01:09:58] to be talking about. The next 20% are
[01:10:01] going to be details that are important
[01:10:02] for you to take care of patients and
[01:10:04] also to ace those board examinations.
[01:10:08] Let's start with dilated
[01:10:09] cardiammyopathy.
[01:10:10] We are looking at the the the schematic
[01:10:14] that we've used many many times to show
[01:10:16] the various chambers of the heart. We
[01:10:18] have the right-sided heart all in blue.
[01:10:21] The inferior and superior vennea to the
[01:10:23] right atrium to the tricuspid valve to
[01:10:26] the right ventricle pulmonic valve going
[01:10:28] out to the lungs and then returning in
[01:10:30] pink to the left atrium through the
[01:10:33] pulmonary veins across the mital valve
[01:10:36] into the left ventricle and out the
[01:10:38] aorta. Okay.
[01:10:42] In dilated cardiammyopathy, we get a
[01:10:44] progressive cardiac dilation for a
[01:10:46] variety of causes that we'll talk about.
[01:10:50] It's associated not only with that
[01:10:52] dilation, but because we are stretching
[01:10:54] the cardiac myasytes, we are actually
[01:10:57] causing a rearrangement of the gap
[01:11:01] junctions that connect between the
[01:11:02] myasytes. So, there's electrical and
[01:11:04] mechanical dysfunction
[01:11:07] and overall there's impaired systolic
[01:11:09] function. It just doesn't squeeze very
[01:11:11] well. It is the most common
[01:11:13] cardiammyopathy causing about 90% of
[01:11:15] cases of cardiammyopathy not otherwise
[01:11:18] specified. Most commonly diagnosed in 20
[01:11:22] to 50s somewhere in that ballpark but in
[01:11:24] fact you can have it much younger as
[01:11:26] we'll talk about. You can have it much
[01:11:28] later as we'll talk about.
[01:11:30] It is a lethal disease. One half of
[01:11:33] patients, 50% will be dead within a
[01:11:36] couple years if not successfully treated
[01:11:40] and only 25% a quarter will survive
[01:11:42] longer than 5 years. So this is as bad
[01:11:45] as or worse than many malignancies in
[01:11:49] terms of mortality.
[01:11:52] Again, it's 50/50 roughly for the the
[01:11:55] causes of dilated cardiammyopathy. We'll
[01:11:58] c we'll cover first the non-getic
[01:12:00] causes. So it turns out that infections
[01:12:03] in particular myocarditis
[01:12:06] will cause damage to the cardiac
[01:12:08] myioytes and then over a period of time
[01:12:10] you may develop a dilated
[01:12:12] cardiammyopathy. You may not even have
[01:12:16] recognized the original infection of the
[01:12:18] heart muscle but the consequences that
[01:12:20] we can see downstream will nevertheless
[01:12:23] chronically progress.
[01:12:26] toxic exposures and this can be a
[01:12:29] variety of chemotherapy agents. This can
[01:12:31] be heavy metals. This can be alcohol in
[01:12:35] alcohol use disorders. So all of those
[01:12:38] can cause it.
[01:12:40] A relatively unfortunately rare cause
[01:12:43] non-getic cause of dilated
[01:12:45] cardiammyopathy is pregnancy. So
[01:12:46] postpartum or parartum cardiammyopathy
[01:12:50] and we'll talk a little bit about those
[01:12:51] mechanisms. Essia. So es schemic heart
[01:12:54] disease is probably one of the greater
[01:12:57] non-getic causes and low levels of
[01:13:01] eskeeia not necessarily even frank
[01:13:03] infarction but low levels of eskemia can
[01:13:06] lead over time to progressive
[01:13:07] dysfunction with a dilated heart.
[01:13:10] You can have something called takotubo
[01:13:12] cardiammyopathy. This is uh the
[01:13:14] so-called broken heart syndrome due to
[01:13:18] stress. And what do we mean by stress?
[01:13:20] We mean actually elevated catacles which
[01:13:22] cause microvascular spasm. Microvascular
[01:13:25] spasm that lasts for greater than 20 to
[01:13:27] 30 minutes will cause microvascular
[01:13:30] inffort and then you get an eskeemic
[01:13:32] cardiammyopathy. So you can have stress
[01:13:34] cardiammyopathy or tacosubo
[01:13:37] tacocardia. So just having a very rapid
[01:13:40] heart rate for prolonged periods of time
[01:13:44] can also cause dilated cardiammyopathy.
[01:13:48] And the reason for that is it's it's
[01:13:51] part of high output failure. Uh it is
[01:13:54] actually a mechanism by which we can
[01:13:56] induce heart failure in experimental
[01:13:58] animals just pace them very quickly. And
[01:14:01] it is because over a period of time
[01:14:03] we've talked previously the normal
[01:14:06] cardiac cycle roughly a a third of a
[01:14:11] second is going to be for cy and 2/3 of
[01:14:13] a second for diastily.
[01:14:16] And if you have 60 beats per minute,
[01:14:18] that's kind of the the sequence. But now
[01:14:21] if I increase heart rate significantly,
[01:14:23] 120 180 beats per minute, the cy stays
[01:14:27] the same, but the diastily shortens. And
[01:14:29] remember, we only peruse the heart
[01:14:30] during diastily. So chronic tacocardia,
[01:14:34] chronic high output will actually drive
[01:14:38] a dilated cardiopathy due to an
[01:14:39] eskeemia. Iron overload diseases like
[01:14:42] hemocchromattosis
[01:14:44] um either whether it's primary or
[01:14:45] secondary will also cause a dilated
[01:14:48] cardiammyopathy. We'll talk about
[01:14:49] mechanisms shortly. Let's look at the
[01:14:52] genetic causes.
[01:14:54] Most of these are defects in a variety
[01:14:57] of proteins involved in the contractile
[01:15:00] apparatus of the sarcimeir. And I will
[01:15:02] say as we're getting more and more
[01:15:04] sophisticated, smarter and smarter and
[01:15:06] looking at more genes, we are finding
[01:15:09] increasing genetic causes of dilated
[01:15:12] cardiammyopathy. Things that had
[01:15:13] previously been called idiopathic.
[01:15:16] As I say, majority of these seem to be
[01:15:19] defects in force generation. So the way
[01:15:22] that the actin and meosin fibers
[01:15:24] interact with each other or regulated by
[01:15:26] troponin and tropomyiain, we don't get
[01:15:29] effective sarimeic contraction.
[01:15:31] But some of the genetic causes involve
[01:15:34] signal defects that we're not getting
[01:15:37] the appropriate movement say of ions
[01:15:40] within the myasytes or it may even be
[01:15:44] defective ATP generation.
[01:15:47] Regardless of the cause genetic or
[01:15:48] non-genetic in dilated cardiammyopathy
[01:15:51] again we over have we overall have
[01:15:53] decreased myioardial contractility and
[01:15:56] the phenotype for all of these
[01:15:59] regardless includes dilation of the
[01:16:02] cardiac chambers that's how we get the
[01:16:04] name dilated cardiammyopathy
[01:16:06] there is myasite hypertrophy. So in as
[01:16:09] we are getting less and less contractile
[01:16:12] the response the adaptation of the heart
[01:16:14] is to say well we we need to have
[01:16:17] stronger myasytes. So even as we're
[01:16:20] getting less contractile force the
[01:16:22] myasytes are undergoing hypertrophy so
[01:16:24] they will be enlarged.
[01:16:26] The abnormal
[01:16:28] volume and pressure will lead to the
[01:16:31] myofiberblast the fibiberblast within
[01:16:33] the heart to lay down increased
[01:16:36] fibrosis. That's going to also
[01:16:38] materially affect the contractility of
[01:16:41] the heart. And because we have these
[01:16:43] dilated chambers with diminished
[01:16:45] movement of blood through them, they're
[01:16:47] going to be prone to developing thrombi,
[01:16:50] which can eventually imolize.
[01:16:51] We are going to consider one of the most
[01:16:53] serious problems that faces a
[01:16:56] cardiologist, the patient with heart
[01:16:58] failure. Heart failure is very common
[01:17:01] and increasingly common these days. It's
[01:17:04] because it is a common complication of
[01:17:06] older individuals and of course the
[01:17:09] older population is increasing
[01:17:11] throughout North America and Western
[01:17:13] Europe as well as Asia. Heart failure is
[01:17:17] defined differently in different
[01:17:20] circumstances by different cardiologists
[01:17:22] but basically it's an inability of the
[01:17:25] heart to pump enough blood to meet the
[01:17:27] demands of the body. In other words, if
[01:17:31] one exercises, one requires an increase
[01:17:34] in blood flow to the body. And if you
[01:17:36] can't do that, you may develop the
[01:17:38] symptoms of heart failure. As we're
[01:17:40] going to see, there are a number of
[01:17:41] compensatory mechanisms that get set off
[01:17:44] in heart failure. And some of them
[01:17:46] actually work to increase symptoms in
[01:17:49] these patients.
[01:17:52] The major issue here is that the heart
[01:17:55] has an inadequate or decreased cardiac
[01:17:58] output. Remember cardiac output that's
[01:18:01] stroke volume times heart rate. That is
[01:18:03] the amount of blood the heart puts out
[01:18:04] each beat times the heart rate. And in
[01:18:08] this setting what you see is that the
[01:18:11] patient has an increase in blood volume
[01:18:15] because of compensatory mechanisms that
[01:18:18] work to correct the heart failure state.
[01:18:22] Unfortunately, this leads to fluid
[01:18:25] accumulation in the body and even edema
[01:18:27] that is swelling in the body.
[01:18:31] This can also be associated with
[01:18:33] circulatory congestion for example in
[01:18:36] the lungs. So you have increased fluid
[01:18:39] in the lungs. So the patients are short
[01:18:40] of breath. And [snorts] in addition uh
[01:18:43] you may see uh patients being
[01:18:45] marketkedly fatigued because they're not
[01:18:47] getting adequate heart pumping. As I
[01:18:50] said before, it's a very common problem.
[01:18:52] There are more than three million
[01:18:54] patients in the United States with heart
[01:18:55] failure. There's a number of new
[01:18:58] patients presenting every year. And
[01:19:00] unfortunately, heart failure has a very
[01:19:03] poor prognosis. Often a prognosis just
[01:19:06] as bad as many forms of cancer.
[01:19:09] Heart failure is um more common in
[01:19:12] African-Americans. Um and uh uh it's
[01:19:16] interesting that these patients seem to
[01:19:18] do better briefly in when they're
[01:19:20] admitted to the hospital, but their
[01:19:22] long-term outlook is worse. Some of this
[01:19:25] may be because of uh lower socioeconomic
[01:19:28] conditions in many African-Americans.
[01:19:32] The heart failure frequency in the US
[01:19:34] has been increasing with an increasing
[01:19:37] population. A statistic I like to quote
[01:19:40] is that in the United States in every
[01:19:42] 24-hour period more people will become
[01:19:45] age 85 than will be born. So you can
[01:19:48] imagine if heart failure is a very
[01:19:50] common problem in the elderly just as
[01:19:52] atrial fibrillation is a common problem
[01:19:54] in the elderly. Both of these are what I
[01:19:56] call quote growth industries.
[01:20:00] Um and again uh women uh tend to be a
[01:20:03] little less frequently affected by heart
[01:20:05] failure. men is a little more common
[01:20:07] early on, but once we get into the
[01:20:09] geriatric population above 65 to 70, the
[01:20:12] amount is about the same.
[01:20:15] There are a number of factors that are
[01:20:18] referred to when we talk about heart
[01:20:20] failure and you'll remember some of
[01:20:21] these factors from the basic lectures on
[01:20:25] heart function. Remember preload.
[01:20:27] Preload is filling of the heart. So that
[01:20:30] uh it's a manifestation of the size of
[01:20:35] the ventricle when it fills up. When you
[01:20:38] have increased blood volume, you
[01:20:40] increase the preload. That is the amount
[01:20:43] of volume that the heart has to squeeze
[01:20:45] out. This happens with some of the
[01:20:48] compensatory mechanisms that increase
[01:20:50] the blood volume and consequently
[01:20:52] preload may be increased in the heart
[01:20:54] and what increased preload leads to is
[01:20:56] increased filling pressures in the
[01:20:58] ventricle during diastily during the
[01:21:00] rest period. This leads to increased
[01:21:02] pressures in the ventricle during
[01:21:05] diastilly and those increased pressures
[01:21:07] are transmitted back to the lungs and
[01:21:09] even back to the rest of the body
[01:21:11] leading to fluid accumulation in the
[01:21:14] tissues of the lung and the rest of the
[01:21:16] body.
[01:21:18] Afterload is the work of the heart. It's
[01:21:20] the resistance the ventricle feels when
[01:21:23] it is pumping out. This is usually due
[01:21:25] to resistance in the vascular system.
[01:21:27] You'll remember that from the the basic
[01:21:30] lecture in cardiology. Increased
[01:21:32] peripheral vascular resistance leads to
[01:21:34] increased afterload, increased work of
[01:21:37] the heart. You can imagine that's not
[01:21:39] good in heart failure. And in fact,
[01:21:41] here's a clue when we talk about therapy
[01:21:44] of heart failure. One of the things is
[01:21:46] to decrease afterload to decrease the
[01:21:48] work of the ventricle and hope that it
[01:21:50] will recover uh from uh its depressed
[01:21:52] state.
[01:21:54] Um there are two forms of heart failure
[01:21:57] systolic and diastolic. In other words,
[01:22:00] sometimes uh let's take diastolic first.
[01:22:04] The ventricle squeezes all right but it
[01:22:07] fails to relax normally. It relaxes
[01:22:10] slowly or in a stiffened manner leading
[01:22:13] to increased pressure in there that gets
[01:22:16] transmitted throughout the circulation
[01:22:17] and leads to collection of fluid as we
[01:22:20] talked about before. edema. Systolic
[01:22:22] heart failure is when the ventricle
[01:22:24] fails to squeeze well. Um that can
[01:22:26] happen of course with a patient who's
[01:22:28] had heart attacks, happens to patients
[01:22:30] with cardiomyopathy, heart muscle
[01:22:32] disease and often systolic heart failure
[01:22:35] is associated also with diastolic. So
[01:22:38] most patients with heart failure have
[01:22:39] both systolic and diastolic. But there
[01:22:41] is a whole group of patients, a minority
[01:22:44] as you can see from the circle diagram
[01:22:46] here, who have pure diastolic heart
[01:22:48] failure. Interestingly, the long-term
[01:22:51] prognosis for diastolic heart failure is
[01:22:54] just as bad as for systolic heart
[01:22:56] failure. Diastolic heart failure tends
[01:22:58] to occur in older individuals, often
[01:23:00] with thickened heart muscle. Now, um
[01:23:03] there are a number of compensatory
[01:23:05] mechanisms that the body sets off when
[01:23:08] it sees heart failure. Remember, I
[01:23:11] mentioned them just a few moments ago.
[01:23:13] What are the compensatory mechanisms?
[01:23:15] Well, let's think. Why would the body
[01:23:17] compensate for decreased cardiac output
[01:23:20] for decreased pumping of the blood? The
[01:23:23] reason the body compensates is because
[01:23:26] it interprets heart failure as if there
[01:23:29] had been a hemorrhage, a blood loss or
[01:23:32] dehydration. In other words, the reduced
[01:23:35] pumping ability the body interprets as,
[01:23:38] oh, there's a lack of blood from a
[01:23:40] hemorrhage or there's a lack of fluid in
[01:23:42] the circulation because of dehydration.
[01:23:45] and it sets off a whole bunch of
[01:23:47] compensatory mechanisms aimed at holding
[01:23:50] on to fluid, water, and salt.
[01:23:55] Unfortunately,
[01:23:56] this is exactly the opposite of what we
[01:23:59] would want because in holding on to
[01:24:02] fluid, you actually create the setting
[01:24:04] where patients put some of that fluid
[01:24:06] into the tissues both in the legs as
[01:24:09] edema or in the lung as pulmonary edema.
[01:24:12] So the activation of these of the
[01:24:15] neuroumeral system that is central
[01:24:17] nervous system uh initiated activity to
[01:24:21] correct the heart failure
[01:24:24] situation actually makes the situation
[01:24:26] worse. These systems work great if
[01:24:29] there's dehydration. You're caught in
[01:24:30] the desert without water. They work
[01:24:32] great if there's a hemorrhage. You've
[01:24:33] been cut somewhere or you're bleeding
[01:24:35] from an ulcer in your stomach. But
[01:24:37] [snorts] they work unfortunately in a
[01:24:39] negative manner in the patient with
[01:24:41] heart failure.
[01:24:43] Let's just talk for a moment about why
[01:24:45] these compensatory mechanisms work. They
[01:24:48] work because of something I mentioned
[01:24:49] before, Starling's law, the so-called
[01:24:52] rubber band law of the heart. The more
[01:24:54] you fill it, the more it contracts. So
[01:24:57] what the compensatory mechanisms are
[01:24:59] trying to do is to increase the filling
[01:25:01] of the heart so it will squeeze more. As
[01:25:03] I've said, unfortunately that leads to
[01:25:05] elevated pressures that back up in the
[01:25:07] system and result in edema. But uh the
[01:25:10] rubber band law of the heart says that
[01:25:12] the force of contraction is related to
[01:25:15] how much you stretch the heart muscle
[01:25:17] cells and this increases contractility.
[01:25:20] So you see why the body is trying to
[01:25:23] increase the pumping ability of the
[01:25:25] heart. And this works fine if it's a
[01:25:27] hemorrhage or dehydration, but it
[01:25:30] doesn't work well when the patient has
[01:25:32] heart failure. So remember, stroke
[01:25:35] volume is the number of cubic
[01:25:38] centimeters that the heart puts out with
[01:25:40] each time it squeezes times heart rate.
[01:25:43] That's cardiac output. So when we have a
[01:25:46] reduction in stroke volume because the
[01:25:48] heart has been injured, sometimes you'll
[01:25:50] even see the heart rate go up because
[01:25:53] the central nervous system says, "Oh,
[01:25:55] cardiac output is falling. We have to
[01:25:58] increase the heart rate. We have to
[01:25:59] increase our ability to hold on to salt
[01:26:01] and water and increase the blood volume
[01:26:03] and use the stling law to increase the
[01:26:06] contractility of the heart." Again,
[01:26:09] unfortunately, it's not the right
[01:26:11] setting for that. And this leads to
[01:26:13] overfilling of the circulation,
[01:26:16] increased pressures in the circulation
[01:26:18] and increased fluid getting out into the
[01:26:21] lungs and into the tissues.
[01:26:24] So uh the central factor in heart
[01:26:27] failure of course is depression of uh of
[01:26:30] the heart muscle at least for systolic
[01:26:33] heart failure but also in diastolic
[01:26:35] heart failure the heart is supposed to
[01:26:37] actively relax and there's also
[01:26:39] depression of that but the commonest
[01:26:41] form of heart failure as you've seen in
[01:26:43] the previous slide was systolic and it
[01:26:46] is usually because there's been some
[01:26:48] injury to the heart muscle most commonly
[01:26:51] from eskeemic or coronary artery
[01:26:53] disease. with heart attacks. Um, and
[01:26:56] again, we've talked about the
[01:26:57] compensatory mechanisms. Here are the
[01:27:00] compensatory mechanisms listed. First of
[01:27:03] all, they're initiated by the central
[01:27:04] nervous system. One of them is a signal
[01:27:07] that's sent to the kidneys and that the
[01:27:10] kidney actually does on its own. The
[01:27:12] kidney is the regulator of the blood
[01:27:14] pressure in the body. it sees a drop in
[01:27:17] blood pressure, a drop in cardiac output
[01:27:19] and it releases compounds uh in
[01:27:22] something called the renan andotensson
[01:27:24] system which holds on to salt and water.
[01:27:28] It's hormones that that actively tell
[01:27:30] the kidney, hey, don't don't pee out uh
[01:27:33] uh sodium and water. Hold on to it
[01:27:36] because the circulatory system needs
[01:27:38] some volume. There are also hormones
[01:27:40] that are released from the pituitary
[01:27:44] so-called antidiuretic hormone which
[01:27:46] tells the kidney, "Hey, hold on to
[01:27:48] water. Don't let the water go out in the
[01:27:50] urine." In addition, uh you also will
[01:27:54] have activation of the sympathetic
[01:27:56] nervous system, which is part of the
[01:27:58] flight or fight system. This sends
[01:28:00] adrenaline to the heart muscle to try
[01:28:02] and get it to contract more vigorously.
[01:28:04] And it [snorts] also clamps down a
[01:28:07] little bit on the periphery in an
[01:28:09] attempt to shrink the volume that the
[01:28:11] heart has to pump into. All of these
[01:28:13] compensatory mechanisms, you can see
[01:28:16] they work great if we're talking about
[01:28:17] dehydration or hemorrhage, but they work
[01:28:21] in the wrong direction when the patient
[01:28:24] already has a depressed left ventricle.
[01:28:27] The other thing that happens is that the
[01:28:29] heart muscle remodels. It reconstructs
[01:28:32] itself if you will. You can see in this
[01:28:34] diagram on the left uh the there's one
[01:28:37] form of remodeling left ventricular
[01:28:39] hypertrophy where the ventricle
[01:28:41] marketkedly thickens for example with
[01:28:43] aortic stenosis as we talked about with
[01:28:45] the patient in the last lecture. On the
[01:28:47] other side is the sort of thing you see
[01:28:49] in a cardiomyopathy. The heart dilates
[01:28:51] thickens a little bit but predominantly
[01:28:54] what it does is it dilates. And you've
[01:28:56] all heard someone say, "Oh, so and so's
[01:28:58] in trouble. They have a quote big
[01:29:00] heart." That's because the heart's
[01:29:01] dilated. That's often the final stage of
[01:29:04] heart failure. When the heart has
[01:29:06] exhausted all of its other compensatory
[01:29:09] mechanisms uh to get the cardiac output
[01:29:11] up, then you start to see this
[01:29:13] dilitation of the left ventricle. Now
[01:29:16] again we talked about the different
[01:29:17] kinds of heart failure systolic and
[01:29:19] diastolic but sometimes there are
[01:29:23] definitions based upon which ventricle
[01:29:25] is in the most trouble. You most common
[01:29:28] is leftsided heart failure. That's
[01:29:30] because the left ventricle has been
[01:29:32] injured. But in some conditions such as
[01:29:35] um severe lung disease with high
[01:29:37] pressures in the lung you may just see
[01:29:40] isolated right-sided heart failure. So
[01:29:42] let's think about this for a moment.
[01:29:44] With leftsided heart failure, the backup
[01:29:46] is going to be uh into the lungs.
[01:29:48] Patients get fluid in the lungs and
[01:29:50] they're short of breath. So the edema is
[01:29:52] in the lungs with leftsided heart
[01:29:54] failure. With right-sided heart failure,
[01:29:57] the backup is into the veins. So you
[01:29:59] often see patients with fluid in the
[01:30:02] abdomen, fluid in the in the legs,
[01:30:05] so-called peripheral edema.
[01:30:08] uh and the left ventricle may be working
[01:30:10] just fine, but it's not getting any
[01:30:12] blood from the right ventricle because
[01:30:14] the right ventricle is failing. And of
[01:30:16] course, it's obvious what the left
[01:30:18] ventricle puts out depends on what the
[01:30:20] right ventricle puts out. It they have
[01:30:22] to balance out. If they don't balance
[01:30:24] out, all the blood is going to end up on
[01:30:25] one side of the circulation or the
[01:30:27] other. And then we've talked about
[01:30:29] before systolic heart failure, failure
[01:30:31] of contraction, diastolic heart failure,
[01:30:34] failure of relaxation.
[01:30:36] Patients with chronic heart failure can
[01:30:38] be divided into two broad categories
[01:30:40] based on whether their ejection fraction
[01:30:42] is normal or reduced. These two
[01:30:45] categories are heart failure with
[01:30:47] preserved ejection fraction called heft
[01:30:50] and heart failure with reduced ejection
[01:30:52] fraction called hepheref. Sometimes
[01:30:54] [snorts] a third category is is implied
[01:30:57] and used and that's heart failure with
[01:31:00] mildly reduced ejection fraction of 41
[01:31:03] to 49% because normal of course is above
[01:31:06] 50%. For the most part it's important to
[01:31:09] know the differences between the two
[01:31:10] distinct types of heart failure. About
[01:31:12] half of the patients with heart failure
[01:31:14] have hep and about half have heff. This
[01:31:18] distinction has prognostic value and it
[01:31:20] also helps guide therapy for the
[01:31:22] patients with heart failure since
[01:31:24] therapy is different for heft and heff
[01:31:28] is defined as a left ventricular
[01:31:30] ejection fraction of 50% or more in a
[01:31:33] patient with signs and symptoms of
[01:31:35] clinical heart failure. Although most
[01:31:37] patients with HEPF have diastolic
[01:31:39] dysfunction with elevated filling
[01:31:41] pressures, asymptomatic diastolic
[01:31:43] dysfunction can be seen with normal
[01:31:46] aging in individuals who do not have
[01:31:48] clinical symptoms. So although people
[01:31:51] with diastolic dysfunction have a risk
[01:31:53] factor for HEPF, these two terms are not
[01:31:56] synonymous. Heft must be distinguished
[01:31:59] from other causes of heart failure in
[01:32:01] patients with an ejection fraction
[01:32:03] greater than 50% and these include
[01:32:06] patients with valvular heart disease,
[01:32:08] paricardial disease, cardiac amaloidosis
[01:32:11] and high output heart failure such as
[01:32:13] that seen with severe anemia or
[01:32:16] hyperthyroidism.
[01:32:18] Heart failure with reduced ejection
[01:32:20] fraction or heffref is defined as a left
[01:32:23] ventricular ejection fraction less than
[01:32:25] 50%. Although an ejection fraction in
[01:32:27] the 40s is sometimes called mildly
[01:32:30] reduced ejection fraction. Patients with
[01:32:32] heff have difficulty with the pumping
[01:32:35] function of the left ventricle uh the
[01:32:38] heart um and by definition a reduced
[01:32:41] ejection fraction in the left ventricle
[01:32:43] known as impaired systolic function.
[01:32:46] Decreased ejection fraction leads to
[01:32:48] inadequate tissue profusion and of
[01:32:51] course influences the prognosis of the
[01:32:53] patient. As you might expect, the lower
[01:32:55] the ejection fraction, often the worse
[01:32:58] the patient does and the more symptoms
[01:33:00] they have. Cardiac remodeling is a
[01:33:02] response to hemodynamic load as well as
[01:33:05] neuro hormonal activation. Pathological
[01:33:08] remodeling can be seen with pressure
[01:33:10] overload due to hypertension or aortic
[01:33:13] stenosis. can also be seen with volume
[01:33:16] overload with valvular regurgitation or
[01:33:19] with cardiac injury for example
[01:33:21] myioardial inffection. The management of
[01:33:23] heft is quite different from the
[01:33:26] management of hep and it's important to
[01:33:29] know the differences.
[01:33:31] Here's just a little diagram to remind
[01:33:33] you how the whole body is a coordinated
[01:33:36] system. You see the brain is connected
[01:33:39] to the heart, the brain is connected to
[01:33:41] the kidneys. They're all connected to
[01:33:43] the peripheral blood vessels. Uh, and as
[01:33:45] we've talked about, when there's heart
[01:33:47] failure or when there's dehydration or
[01:33:50] when there's hemorrhage, all of these
[01:33:52] factors become activated in an attempt
[01:33:54] to a restore the blood volume and b
[01:33:57] restore the pumping ability of the
[01:33:59] heart. And here they are all listed
[01:34:02] again uh just as as we've talked about
[01:34:05] before. The central nervous system is
[01:34:07] critical. The sympathetic nervous system
[01:34:09] is activated. the kidney through the
[01:34:12] renal angotensin system is activated.
[01:34:14] Um, and the ventricle is gets increased
[01:34:17] volume and therefore uses the starling
[01:34:20] mechanism. All of these things work
[01:34:22] together. They work great if the
[01:34:24] patient's blood volume is down because
[01:34:25] of dehydration and hemorrhage. They work
[01:34:28] against you when the problem is that the
[01:34:30] heart is not pumping enough. Um, and
[01:34:33] again, here you see a diagram that just
[01:34:35] shows you how all of these interact. uh
[01:34:39] how the decreased cardiac output uh can
[01:34:42] lead to lung congestion um and uh how a
[01:34:46] par increased peripheral pressure uh can
[01:34:49] lead to peripheral edema. the neurosu uh
[01:34:52] hormonal activations through the kidney
[01:34:54] that go on. All of these things are
[01:34:56] working in a complete circus uh motion
[01:34:59] like the horse riding around uh uh the
[01:35:02] uh the track in a circus around and
[01:35:05] around that they keep reinforcing each
[01:35:07] other and unfortunately in heart failure
[01:35:10] lead to marked retention of water and
[01:35:12] salt that leads to the various um
[01:35:15] symptoms that the heart failure patient
[01:35:17] has. in the American Heart Association
[01:35:19] guidelines talk about various levels of
[01:35:22] heart failure. Um level A is somebody
[01:35:25] who's really predisposed to heart
[01:35:26] failure but has not developed it yet. So
[01:35:28] that's somebody with high blood
[01:35:30] pressure, diabetes, hyper
[01:35:32] cholesterolmia, hyper lipidmia, as we've
[01:35:34] talked about that leads to
[01:35:35] atheroscerosis. Heart failure hasn't
[01:35:37] developed yet, but the substrate, if you
[01:35:40] will, is ready to go on and cause a
[01:35:42] heart condition that will lead to heart
[01:35:44] failure. Grade [snorts] B is when you're
[01:35:46] starting to have some very early signs
[01:35:50] of heart failure by some of our fancy
[01:35:52] tests such as um from the echo
[01:35:54] cardiogram, but the patient is still
[01:35:57] asymptomatic. Stage C is when the
[01:35:59] patient is already having symptoms.
[01:36:01] They're tired, they're short of breath,
[01:36:03] they have peripheral edema, and stage D
[01:36:06] is when they're really incapacitated
[01:36:08] with heart failure, marked severe
[01:36:11] symptoms of heart failure. Now um it's
[01:36:15] important um to remember that heart
[01:36:18] failure relates to atherosclerosis
[01:36:21] in the majority of cases who present to
[01:36:24] the cardiologist with heart failure. No
[01:36:26] surprise. Remember we talked about the
[01:36:28] last time uh I spoke to you about the
[01:36:31] typical patient. That's the commonest
[01:36:33] patient that comes to the cardiologist.
[01:36:35] The patient with atherosclerotic heart
[01:36:37] disease. When that disease is advanced,
[01:36:40] particularly if the patient has had
[01:36:41] previous myioardial infarts or heart
[01:36:43] attacks, the ventricular function is
[01:36:46] compromised and the patient shows up
[01:36:48] with heart failure. So what are the risk
[01:36:50] factors for heart failure? They're the
[01:36:52] risk factors for athoscerotic heart
[01:36:54] disease. their hyper cholesterolimeia,
[01:36:56] hypertension, cigarette smoking,
[01:36:57] diabetes, all the things we talked about
[01:37:00] before that can lead to atherosclerosis.
[01:37:03] Um, and you can see that the commonest
[01:37:06] ones uh you know are uh problems leading
[01:37:09] to heart failure is eskeemic heart
[01:37:10] disease. But there's a number of other
[01:37:12] factors uh uh that are involved as well.
[01:37:15] But es schemic heart disease the number
[01:37:18] one cause of death in the world, number
[01:37:19] one cause of heart failure.
[01:37:22] Um there are uh a number of rarer causes
[01:37:26] of heart failure. I'm not going to go
[01:37:28] into this in any detail. Um but for
[01:37:30] example in the United States, one of the
[01:37:32] the commonest causes of cardiammyopathy
[01:37:35] is excessive alcohol intake. Alcohol is
[01:37:37] a poison for the myioardium taken in
[01:37:39] small amounts. It's good. Increases the
[01:37:42] HDL level. Can be very pleasant in a
[01:37:44] social setting. But excessive alcohol
[01:37:46] can lead to cardiammyopathy and of
[01:37:48] course a lot of other problems. Liver
[01:37:50] failure from cerosis. etc., etc. Um,
[01:37:53] there are in uh other things that can
[01:37:55] cause heart failure. We've talked about
[01:37:56] this before. Cardiammyopathy from a
[01:37:58] chronic viral infection. Certain drugs
[01:38:00] can do it. Um, one of the favorite drugs
[01:38:03] for chemotherapy for breast cancer also
[01:38:06] uh damages the heart. Um, and some drug
[01:38:08] other drugs can do the same thing. And
[01:38:11] of course, arrhythmias with longstanding
[01:38:14] fast heart rate that's uncontrolled can
[01:38:16] also lead to cardiac fatigue. These
[01:38:18] things are much rarer. Remember es
[01:38:20] schemic heart disease is number one
[01:38:22] public enemy.
[01:38:24] Um and uh here you just see all of the
[01:38:28] uh symptoms that patients will have um
[01:38:30] with heart failure. Um they will be
[01:38:33] disnic that is they'll be short of
[01:38:35] breath. Um you will find maybe their
[01:38:38] lips are blue because they're not
[01:38:39] pumping enough oxygenated blood around.
[01:38:42] There may be heart murmurss as we had in
[01:38:44] the patient in the last lecture with
[01:38:45] aortic stenosis. Sometimes on physical
[01:38:48] exam you will hear a loud extra heart
[01:38:51] sound that says the ventricle is really
[01:38:53] hurting, the patient's breathing fast.
[01:38:55] You may hear actually sounds from fluid
[01:38:57] in the lungs and so forth. There's a
[01:38:59] whole variety of physical findings that
[01:39:02] uh the doctor finds that confirms the
[01:39:05] diagnosis of heart failure. Remember
[01:39:07] from the last lecture, the most
[01:39:09] important thing are the symptoms. They
[01:39:11] give you the clue. 90% of the answer of
[01:39:14] the diagnosis is in the history. You
[01:39:16] then move to the physical exam. Oh yes,
[01:39:18] I'm hearing things. I'm seeing things
[01:39:20] that suggest that the reason the patient
[01:39:22] is tired, the reason the patient is
[01:39:24] short of breath, the reason the patient
[01:39:26] has swelling in their legs is because of
[01:39:29] heart failure.
[01:39:31] Right ventricular heart failure alone uh
[01:39:34] can cause a different uh set of symptoms
[01:39:36] and signs. Of course, the edema, the
[01:39:38] extra fluid is in the legs. Um, and you
[01:39:42] re will remember that you may have
[01:39:45] problems in the abdomen because the
[01:39:47] increased venus pressure backing up is
[01:39:50] not only in the legs, but it's also in
[01:39:52] the abdomen. The liver swells. There's
[01:39:54] also swelling um in the in uh fluid in
[01:39:58] the abdomen. Patients may find their
[01:40:01] their waist size gaining. They become
[01:40:03] very very tired. Um and uh uh often you
[01:40:07] can even feel on physical exam this
[01:40:10] bulging abdomen that's full of fluid. Um
[01:40:13] remember again right heart failure much
[01:40:15] less common than left heart failure.
[01:40:17] Commonest cause of left heart failure
[01:40:18] eskeemic heart disease that is previous
[01:40:20] heart attacks. So here's a few diagrams
[01:40:23] that just show you what the cardiologist
[01:40:26] sees when they see a patient usually
[01:40:27] with very clear and significant heart
[01:40:30] failure. And [snorts] you can see um the
[01:40:33] their [clears throat] pupils may be
[01:40:34] dilated from the from the adrenaline
[01:40:36] that's circulating. Um the skin may be
[01:40:39] gray or pale or or even blue cyanotic.
[01:40:43] Um and a whole bunch of things. They may
[01:40:45] be short of breath, breathing fast. Um
[01:40:47] they they may be uncomfortable lying
[01:40:50] back and feel more comfortable
[01:40:52] breathing, sitting up. There may
[01:40:54] actually be sounds in the lungs from
[01:40:56] fluid in the lungs, crackles or
[01:40:57] so-called rls. They may [clears throat]
[01:41:00] have a cough from the excess fluid
[01:41:02] that's in their system.
[01:41:04] There is um often uh increased uh
[01:41:09] pressure in the veins and you can
[01:41:10] actually see that in the neck. I'm going
[01:41:12] to show you a picture of that. And the
[01:41:13] blood pressure may be decreased because
[01:41:15] the cardiac output is down. Um and also
[01:41:19] the patient may even um have some uh
[01:41:23] discomfort in the abdomen, swelling and
[01:41:25] nausea and so forth. uh and of course
[01:41:28] you may see bulging of the abdomen as I
[01:41:30] mentioned and uh edema uh uh that is
[01:41:33] swelling in the legs. Uh all of these
[01:41:36] are not seen necessarily in one patient
[01:41:39] but in individuals you may see a number
[01:41:42] of these findings
[01:41:44] and of course uh patients uh anxiety
[01:41:48] level is increased of course because
[01:41:50] they're short of breath. One of the
[01:41:52] worst things that can happen to you is
[01:41:53] to be suffocated. it activates anxiety
[01:41:55] in a huge way. Um, and again uh you may
[01:41:59] see uh the uh fact that the patient has
[01:42:03] decreased oxygen saturation. Often we
[01:42:05] can test that with a little finger thing
[01:42:06] or an ear thing to see that the oxygen
[01:42:09] level in the blood is going down. Um the
[01:42:11] patients in advanced heart failure may
[01:42:13] be confused particularly in elderly
[01:42:15] patients. Um there may be uh as I'm
[01:42:17] going to show you a picture in a moment,
[01:42:19] the jugular vein is distended because of
[01:42:21] high filling pressures in the right
[01:42:23] atrium transmitted back to the jugular
[01:42:25] vein. Um [snorts] there can uh if the
[01:42:28] patient's had a heart attack, there may
[01:42:29] be chest discomfort in association um uh
[01:42:32] with this. Of course, the patient is
[01:42:34] marketkedly fatigued. Um and uh you may
[01:42:37] hear the heart sounds that I mentioned
[01:42:39] before this extra heart sound. the heart
[01:42:41] may be increased in rate. Uh and again
[01:42:43] you may feel swelling of the liver or
[01:42:46] the spleen from uh the v the venus
[01:42:48] congestion that goes back there and of
[01:42:50] course um there's decreased cardiac
[01:42:52] output um if you measure that uh often
[01:42:56] with an echo and the pulse may be
[01:42:58] therefore weak. The patient is often
[01:43:00] cool the skin may be sweaty. So here's a
[01:43:04] picture this is a lovely picture of a
[01:43:07] distended jugular vein. You can see it
[01:43:09] rising up from just above the uh the
[01:43:12] clavicle uh the the bone that's right
[01:43:14] here on the front of the chest and you
[01:43:16] can see rising up almost to the level of
[01:43:18] the jaw. So this is a patient with quite
[01:43:21] advanced heart failure. In this case
[01:43:24] it's a finding of right ventricular
[01:43:26] failure but the commonest cause of right
[01:43:28] ventricular failure is often left
[01:43:30] ventricular failure that increases
[01:43:31] pressure in the lungs increases the work
[01:43:34] of the right ventricle which eventually
[01:43:35] fails. So this could be a patient with
[01:43:38] left ventricular and right ventricular
[01:43:39] failure or it could be somebody with
[01:43:41] isolated right ventricular failure. And
[01:43:44] here we see an example of peripheral
[01:43:46] edema. You can see you push into the
[01:43:48] soft tissue of the leg. And you'll
[01:43:50] notice that the impression stays when
[01:43:53] you take your finger away. So this is a
[01:43:55] patient with advanced peripheral edema.
[01:43:57] It also looks to me like the skin
[01:43:59] doesn't have its normal tone, its normal
[01:44:02] color. It looks gray and modeled. Uh,
[01:44:04] and often this is because of decreased
[01:44:06] cardiac output. So, of course, we're
[01:44:08] going to do some tests to confirm our
[01:44:11] clinical impression. We've had the
[01:44:12] history. Oh, this suggests heart
[01:44:14] failure. The patient's short of breath.
[01:44:15] They have peripheral edema. Oh, we
[01:44:17] listen to the heart and we hear an extra
[01:44:19] sound, the S3 gallop. Okay, we now
[01:44:23] pretty sure the patient has heart
[01:44:24] failure. Then we do a chest X-ray. You
[01:44:26] can see the two examples here. The one
[01:44:28] on the one side is normal and the one on
[01:44:30] the other side shows an enlarged heart.
[01:44:33] Sometimes we will even see evidence of
[01:44:35] fluid in the lungs. Pretty obvious on
[01:44:37] this chest X-ray. This is called
[01:44:39] pulmonary edema. The left ventricle has
[01:44:42] failed significantly. And what we see is
[01:44:44] fluid throughout the lungs. Um and of
[01:44:47] course this patient is very short of
[01:44:50] breath. They might be breathing at 30 or
[01:44:52] 40 times a minute. Normal is about 12,
[01:44:55] 13, 14 times a minute. And they may you
[01:44:58] may actually hear gurgling from this
[01:45:01] fluid that's collecting in the small
[01:45:03] alvear sacks in the lung and being
[01:45:05] transmitted into the uh into the bigger
[01:45:08] uh bronchial tubes. Um this can uh drop
[01:45:11] the oxygen saturation in the blood can
[01:45:13] lead to fatal arrhythmias and people can
[01:45:15] die from this. Um and and this this is a
[01:45:18] medical emergency that requires urgent
[01:45:20] therapy. Um, and here is a chest X-ray
[01:45:24] showing a variety of findings of a
[01:45:26] little less serious heart failure. One
[01:45:28] can see edema uh in the lymphatics,
[01:45:30] so-called curly lines. One can see fluid
[01:45:33] collecting um in the plura. Uh you can
[01:45:36] see in the little angle there where the
[01:45:38] heart meets the chest that there's a
[01:45:39] little sort of rounded uh uh area that's
[01:45:42] actually fluid in the plural space, the
[01:45:45] space uh that surrounds the uh the
[01:45:47] lungs. Um there's a variety of other
[01:45:50] findings that the radiologist will
[01:45:52] [clears throat] often call you up and
[01:45:53] say your patient has heart failure. We
[01:45:56] often do an echo cardiogram to see how
[01:45:58] bad of the heart failure is. For
[01:46:00] example, is it left ventricular? Is it
[01:46:02] right ventricular? Um is it very
[01:46:04] advanced? Is the ejection fraction that
[01:46:06] is the percentage of blood squeezed out
[01:46:08] by the heart very low or is it only
[01:46:11] modestly reduced? This is an echo
[01:46:13] cardiogram from a patient with very
[01:46:15] advanced heart failure. The left
[01:46:17] ventricle is marketkedly dilated. Uh we
[01:46:19] don't see the the the film with it, but
[01:46:22] I'm sure if we saw the film, instead of
[01:46:24] the ventricle squeezing normally like
[01:46:25] this, it's doing this, hardly squeezing
[01:46:29] at all. And you can see also in this uh
[01:46:32] echo, the left ventricle is enlarged. So
[01:46:34] this is a patient with longstanding
[01:46:37] heart failure. Um so let's talk a little
[01:46:40] bit about a treatment. Clearly treatment
[01:46:44] goals are to reduce the edema, to reduce
[01:46:47] the excess fluid volume and to make the
[01:46:50] patient much more comfortable and able
[01:46:52] to have full activity. You'd also like
[01:46:54] to increase the pumping ability of the
[01:46:56] heart. Uh sometimes [clears throat] if
[01:46:59] it's for example in the patient we
[01:47:01] talked about in the last lecture,
[01:47:03] somebody with aortic stenosis, taking
[01:47:05] away the stenotic valve and putting in a
[01:47:08] good valve allows the ventricle to
[01:47:10] recover. Um in other settings if it's
[01:47:12] due to severe eskeeia lack of blood flow
[01:47:15] in the heart coronary bypass or
[01:47:16] angoplasty may improve the blood flow in
[01:47:19] the heart and may not always but may
[01:47:22] improve the function of the ventricle
[01:47:24] and again lead to resolution of
[01:47:26] symptoms. And there's a variety of drugs
[01:47:28] that help increase the removal of fluid
[01:47:32] from the body. For example, diuretics
[01:47:35] that increase renal excretion of water
[01:47:38] and salt will reduce the excess volume
[01:47:41] of salt and water in the body and often
[01:47:43] lead to marked improvement in the
[01:47:45] symptoms. Patients with heart failure,
[01:47:47] particularly new heart failure, require
[01:47:49] hospitalization. They require a number
[01:47:51] of tests to determine why they're in
[01:47:53] heart failure. And they also require a
[01:47:56] number of drugs um that are used to
[01:47:59] improve if possible the function of the
[01:48:02] heart and to decrease the work of the
[01:48:04] heart and to increase fluid and salt
[01:48:07] excretion.
[01:48:09] And what you do this uh uh step diagram
[01:48:12] is a complicated one. I'm not
[01:48:15] anticipating that anybody needs to learn
[01:48:17] this uh uh right away but it shows you
[01:48:20] as the heart failure increases the
[01:48:22] aggressiveness of our therapy increases.
[01:48:25] So in the beginning we use uh ACE
[01:48:28] inhibitors uh that is they vasoddilate
[01:48:31] the arterials they decrease the blood
[01:48:33] pressure a bit and they decrease the
[01:48:34] work of the heart. In a sense what we're
[01:48:36] trying to do is rest the heart make the
[01:48:38] heart's job the left ventricle's job a
[01:48:41] little easier. But as you go along
[01:48:43] there's a variety of other interventions
[01:48:45] that are used um both improving blood
[01:48:49] flow for example with angoplasty um we
[01:48:53] also use drugs um that rest the heart a
[01:48:56] little bit by decreasing the heart rate
[01:48:57] beta blockers um and then eventually you
[01:49:00] may even progress to devices that
[01:49:03] increase the pumping ability of the
[01:49:05] heart while you're getting ready to do
[01:49:06] something u more aggressive for example
[01:49:09] change a heart valve or even in the most
[01:49:12] severe stages, do a heart transplant,
[01:49:15] give the patient a new heart.
[01:49:18] It's important that patients have
[01:49:20] lifestyle changes, particularly with the
[01:49:22] milder forms of heart failure, because
[01:49:24] what we're trying to do is prevent heart
[01:49:26] failure from progressing. So, what are
[01:49:29] those lifestyle changes? Clearly,
[01:49:31] somebody who's obese, you've got a lot
[01:49:33] of extra weight around. If you have a
[01:49:35] big belly that has 40 or 50 pounds of
[01:49:38] extra weight, it's like you're carrying
[01:49:40] a 40 or 50 pound knapsack on your back
[01:49:42] and you're asking the heart to do that
[01:49:44] extra work. You can imagine that's a bad
[01:49:47] idea. So, dieting and reduction of
[01:49:50] obesity is important. Number two,
[01:49:52] cutting back on salt because the more
[01:49:55] salt you take in, the compensatory
[01:49:57] mechanisms of the body hold on to that
[01:49:59] salt and of course increase blood
[01:50:01] volume. So restriction of salt. It turns
[01:50:05] out that regular particularly in the
[01:50:07] beginning supervised
[01:50:09] exercise or physical activity actually
[01:50:12] improve the whole cardiovascular system
[01:50:14] and enable patients to do more work with
[01:50:17] the same cardiac output that they had
[01:50:19] before. Uh so uh and of course stopping
[01:50:22] things like cigarette smoking which are
[01:50:24] damaging to the blood vessels and which
[01:50:27] [clears throat] can cause acceleration
[01:50:28] of aththeroscerosis just as in we talked
[01:50:30] about in patients with a heart attack or
[01:50:32] coronary artery disease. There's a whole
[01:50:34] variety of lifestyle changes and often
[01:50:37] these are integrated between the
[01:50:38] cardiologist and a good cardiac
[01:50:40] rehabilitation program. Medication
[01:50:44] management is tailored to the type of
[01:50:46] heart failure that a patient has.
[01:50:48] whether they have heart failure with
[01:50:50] preserved ejection fraction as we
[01:50:52] already heard called heft or whether the
[01:50:55] heart failure patient has a reduced
[01:50:57] ejection fraction so-called heffref and
[01:51:01] of course medication management is
[01:51:03] tailored to the patient's symptoms and
[01:51:05] signs. If a patient has volume overload
[01:51:08] with dysmia or peripheral edema of
[01:51:11] course they need diaresis usually with a
[01:51:14] loop diuretic to remove excess fluid.
[01:51:17] For patients with a compelling
[01:51:18] indication for a specific type of
[01:51:20] anti-hypertensive medication, for
[01:51:22] example, if a patient has diabetes or
[01:51:25] chronic kidney disease, then an ACE
[01:51:27] inhibitor or an angotensin receptor
[01:51:29] blocker should be used before starting
[01:51:32] HEPF specific therapies such as
[01:51:36] mineralicorticoid blockers or SGL2
[01:51:38] inhibitors. Of course, you have to look
[01:51:41] carefully at the patient's renal
[01:51:43] function. If it is quite impaired then
[01:51:46] ACE inhibitors or ARBs are are
[01:51:48] contraindicated because they might make
[01:51:50] the renal failure worse. For patients
[01:51:53] without diabetes then heart failure
[01:51:56] specific medications are indicated. The
[01:51:59] next step is to add a sodium glucose
[01:52:02] corransporter to inhibitor SGLT2
[01:52:05] inhibitor. I like to call them because
[01:52:08] that's part of their um generic name. um
[01:52:11] or of course uh and or a
[01:52:14] mineralocorticoid receptor antagonist.
[01:52:17] SGL2 inhibitors are medications like
[01:52:20] empaglyphloin or dapaglyphloin.
[01:52:23] You notice the term flozzen in the
[01:52:25] middle of those terms. A
[01:52:26] mineralocorticoid receptor antagonist or
[01:52:29] a mineral or MRA as it's often known
[01:52:32] such as spironylactone or pleadinone can
[01:52:34] be added. If the patient has a systolic
[01:52:36] blood pressure below 100 or symptoms of
[01:52:39] hypotension such as dizziness or other
[01:52:42] orthostatic symptoms then other
[01:52:44] anti-hypertensive drugs should be
[01:52:46] decreased or discontinued otherwise
[01:52:48] you're liable to have severe symptomatic
[01:52:50] hypotension.
[01:52:52] The primary therapies for heart failure
[01:52:53] with reduced ejection fraction are ACE
[01:52:56] inhibitors. Angotensin receptor blockers
[01:52:59] called ARBs or the combination
[01:53:01] medication of an angotensin receptor
[01:53:03] blocker and a neprolysin inhibitor put
[01:53:07] together are called anri and the
[01:53:11] neprolysin inhibitor is known as
[01:53:13] sacubitril and it's a blocker of the
[01:53:17] breakdown enzymes um for atrial
[01:53:20] peptides. Thus the ANRI drug is a double
[01:53:24] vasod diilator and again you have to be
[01:53:26] careful about the blood pressure. Beta
[01:53:29] blockers should be added if there are no
[01:53:31] contra indications and the specific
[01:53:33] three that have been demonstrated to
[01:53:35] benefit patients with heart failure are
[01:53:37] carvdalol basopriol and extended release
[01:53:41] mtopriol suenate. If patients have
[01:53:43] contraindications to any of the renan
[01:53:46] andotensin systems antagonist, an
[01:53:48] alternative is hydraazine pressong
[01:53:51] acting nitrate. A typical
[01:53:52] contraindication to the renan andotensin
[01:53:55] system antagonist is advanced renal
[01:53:58] failure because these drugs could
[01:54:00] increase the level of renal
[01:54:02] insufficiency. In patients who still
[01:54:05] have symptomatic heart failure,
[01:54:07] secondary therapies may be added in
[01:54:10] addition to the initial medications. And
[01:54:12] there's considerable current debate
[01:54:14] about the order that we give these drugs
[01:54:16] uh which one should be first which one
[01:54:18] second and that is the subject of
[01:54:21] current ongoing heart failure research.
[01:54:24] These uh include the additional drugs
[01:54:27] that could be used for example
[01:54:29] mineralicorticoid receptor blockers as
[01:54:31] we've already said spiron lactone and a
[01:54:33] plerone or the SGL2 inhibitors um again
[01:54:37] that were just mentioned in certain
[01:54:39] symptomatic patients we may need to
[01:54:41] consider cardiac recynchronization
[01:54:43] therapy done with a a special form of
[01:54:46] pacemaker that also stimulates the left
[01:54:49] ventricle as well as the right ventricle
[01:54:52] or trans catheter Mitro valve repairer
[01:54:55] repair for example clipping uh a loose
[01:54:58] mitro leaflet that's allowing for severe
[01:55:00] mitro regurgitation you clip that to
[01:55:03] another leaflet and thereby you decrease
[01:55:06] the amount of mitro regurgge further
[01:55:09] secondary therapies uh newer medications
[01:55:12] include veraquat or aabradine so
[01:55:16] vericyquat is indicated for patients
[01:55:18] with New York heart association class 2
[01:55:20] to four heart failure with an ejection
[01:55:22] fraction less less than 45% who were
[01:55:25] either hospitalized in the last 6 months
[01:55:28] or require outpatient IV diuretics.
[01:55:31] Evabine is a very interesting new class
[01:55:34] of medication called hyperpolarization
[01:55:36] activated cyclic nucleotide gated
[01:55:39] channel blockers. What they do is they
[01:55:41] actually decrease the rate at [snorts]
[01:55:43] which the sodium channel leaks in sinus
[01:55:46] node cells and that results in a slowing
[01:55:49] of the heart rate. It's indicated for
[01:55:51] patients with an ejection fraction of
[01:55:53] 35% or less who are in sinus rhythm with
[01:55:56] a resting heart rate. That's at
[01:55:58] if beta blockers are either
[01:55:59] contraindicated or have caused problems
[01:56:02] then you can substitute a slowing drug
[01:56:04] using ivorine.
[01:56:06] Deoxxin can be added to patients with
[01:56:08] endstage heart failure who are not doing
[01:56:10] well despite optimal other pharmacologic
[01:56:13] therapies as well as cardiac
[01:56:15] recynchronization therapy. Lastly,
[01:56:18] mechanical circulatory support devices
[01:56:21] such as left ventricular bypass pumps
[01:56:24] and and intriotic balloons and and even
[01:56:27] cardiac transplantation
[01:56:29] um may be considered in se highly
[01:56:31] selected patients with refractory heart
[01:56:34] failure.
[01:56:35] And again um there are there's patient
[01:56:38] counseling. We already talked about the
[01:56:40] lifestyle. Alcohol is a depressant on
[01:56:43] the heart. So, we want patients drinking
[01:56:45] as little as possible. Smoking has to
[01:56:48] stop. We want weight control. Um, we
[01:56:51] want regular exercise. All of the
[01:56:53] lifestyle things again repeated to work
[01:56:56] with the medicines that we're giving or
[01:56:58] to work [snorts] with the interventions.
[01:57:00] For example, opening up a coronary
[01:57:02] artery or replacing a heart valve. And
[01:57:05] further patient counseling of course
[01:57:07] involves the medications. Are the
[01:57:09] patients taking the medications and are
[01:57:11] they taking them regularly? and as a as
[01:57:13] appropriately prescribed. This is a huge
[01:57:16] problem in the United States. Many
[01:57:18] patients fail to take their medications.
[01:57:20] If there are surgical or catheter
[01:57:22] interventions, what these contain uh and
[01:57:25] what they can do and what the potential
[01:57:26] complications are. One wants to reduce
[01:57:29] stress in the patient's life. One wants
[01:57:31] the patient to keep track of symptoms.
[01:57:33] Are they getting better? Are they
[01:57:34] getting worse? Is their weight gaining
[01:57:36] all of a sudden because of a marked
[01:57:38] increase in fluid retention? And of
[01:57:41] course uh we would like patients uh to
[01:57:44] not overindulge in fluid intake and
[01:57:47] certainly come for follow-up visits with
[01:57:49] the doctor or the nurse clinician in
[01:57:51] order for us to monitor how things are
[01:57:53] going with therapy and if we have to
[01:57:55] make further adjustments in therapy. So
[01:57:59] um in conclusion heart failure is a
[01:58:01] growth industry particularly in older
[01:58:03] individuals. It's caused by many
[01:58:05] diseases but in particular by
[01:58:07] atherosclerotic heart disease that
[01:58:09] causes damage to the left ventricle.
[01:58:12] Again left ventricular systolic heart
[01:58:14] failure is the commonest. The left
[01:58:16] ventricle doesn't squeeze as well and
[01:58:18] the commonest cause of that eskeemic
[01:58:20] heart disease. Prevention of course is
[01:58:22] better than cure. I don't have to tell
[01:58:24] you that. And how do we prevent that? By
[01:58:26] controlling atheroscerotic risk factors
[01:58:29] before they put the patient in the heart
[01:58:31] failure uh situation. Um, of course, um,
[01:58:35] there's a whole variety of diagnostic
[01:58:37] tests that we use when the patient
[01:58:39] presents with heart failure, but
[01:58:41] remember the clue is in the patient's
[01:58:43] symptoms with confirmation by the exam
[01:58:47] and then we do some sophisticated tests
[01:58:49] to see what's the cause of the heart
[01:58:51] failure and how severe is the
[01:58:52] ventricular damage. Uh, and then we
[01:58:55] introduce a whole variety of therapies
[01:58:57] both drugs and even uh, some of the
[01:59:00] newer device therapies. For example, we
[01:59:03] can open up blood vessels and even in
[01:59:05] extreme cases, we can take over with
[01:59:07] little pumps for the heart while we're
[01:59:09] trying to get it to respond and and come
[01:59:11] back to normal. And of course, uh then
[01:59:14] we're going to have to uh uh do a
[01:59:17] lifestyle changes. There's a new pacing
[01:59:19] protocol with a special pacemaker that
[01:59:21] can in some selected patients can
[01:59:24] improve the pumping of the heart. All of
[01:59:26] these are fairly extreme uh things done
[01:59:29] uh right at the end. And again uh we
[01:59:32] talked about uh the fact that there's a
[01:59:34] lot of technology here but the best deal
[01:59:36] is to stop the heart failure before it
[01:59:39] starts with reduction in risk factors or
[01:59:43] identifying it early and getting all of
[01:59:45] those things including the lifestyle
[01:59:47] changes implemented before the patient
[01:59:49] progresses to a point that they need
[01:59:51] things like bentricular pacing and heart
[01:59:54] lung machines and so forth. Thank you
[01:59:56] for listening to this lecture. I look
[01:59:58] forward to seeing you with the next one.
[02:00:00] So, let's start talking then about the
[02:00:02] drugs. The first class of drugs that I'm
[02:00:05] going to talk about are so-called beta
[02:00:07] blockers. What do I mean by a blocker?
[02:00:11] What's a blocker? Well, it turns out
[02:00:13] that on the surface of heart uh cells as
[02:00:17] well as other cells in the body, there
[02:00:19] are little let's call them keyholes in
[02:00:23] which certain keys are fit which then
[02:00:25] result in changes going on within the
[02:00:28] cell. So, let me tell you one example.
[02:00:31] One example example would be adrenaline.
[02:00:34] Adrenaline is released from nerve
[02:00:36] endings and it's released from the
[02:00:38] adrenal glands. We're going to talk
[02:00:40] about that system in just a moment,
[02:00:43] [snorts] but it's important to realize
[02:00:45] that when adrenaline plugs into the
[02:00:47] keyhole into the receptor on the cell
[02:00:51] membrane, it results in a number of
[02:00:53] biochemical changes within that cell.
[02:00:56] And [snorts] those biochemical changes
[02:00:59] are not just restricted to heart cells,
[02:01:01] but throughout the body and of course
[02:01:03] that can lead to the side effects or the
[02:01:05] complications that we just talked about.
[02:01:07] So, why are beta blockers useful? Beta
[02:01:10] blockers are useful because they
[02:01:12] decrease heart rate, they decrease blood
[02:01:15] pressure, and they decrease heart
[02:01:17] contractility.
[02:01:19] And you're going to see what they do is
[02:01:21] they block some of the actions of the
[02:01:23] autonomic nervous system. Beta blockers
[02:01:27] were discovered by this man, Dr. James
[02:01:29] Black, who was a chemist with Imperial
[02:01:32] Chemistry uh company in England in the
[02:01:35] 1960s. And by the way, for discovering
[02:01:38] beta blockers, he won the Nobel Prize in
[02:01:40] 1988.
[02:01:42] So what was the reason for developing
[02:01:44] beta blockers? Well, I think most of you
[02:01:47] are aware is that our entire circulatory
[02:01:51] system, our digestive system, many of
[02:01:54] the organs in the body are controlled by
[02:01:56] the brain. And one of the ways that the
[02:01:59] brain controls things is through
[02:02:01] something called the autonomic nervous
[02:02:03] system. I like to call it the automatic
[02:02:06] nervous system. It has two parts, a sort
[02:02:09] of an accelerator system and a brake
[02:02:12] system. The accelerator system, also
[02:02:15] called the flight oright system, is the
[02:02:17] sympathetic nervous system. That's the
[02:02:19] one that squeezes out adrenaline when
[02:02:22] you're in a near car accident or when
[02:02:25] you're threatened by somebody. It revs
[02:02:27] up your blood pressure. It revs up your
[02:02:29] energy. You're ready to flight or fight.
[02:02:33] Now the opposite effect occurs from the
[02:02:37] parasympathetic nervous system. That's
[02:02:39] when you eat a meal and you feel a
[02:02:41] little sleepy and you lie back and you
[02:02:43] relax. That nervous system increases the
[02:02:46] digestive activities which of course are
[02:02:49] the exact opposite of what you'd want if
[02:02:51] you were flying or fighting. You'd want
[02:02:54] to be revved up, not lying back relaxing
[02:02:57] and digesting. And these two nervous
[02:03:01] systems interact constantly depending
[02:03:04] upon what you're doing. If you're
[02:03:06] vigorously exercising, you're going to
[02:03:08] be turning on the sympathetic nervous
[02:03:10] system. If you're relaxing after eating
[02:03:12] a large meal, you're going to be turning
[02:03:14] off the sympathetic nervous system and
[02:03:16] turning on the parasympathetic nervous
[02:03:18] system. The parasympathetic nervous
[02:03:20] system is also run through a very large
[02:03:23] nerve that runs throughout the body
[02:03:25] called the vagus nerve. And [snorts]
[02:03:28] sometimes it will actually activate at a
[02:03:31] time where it drops blood pressure and
[02:03:32] even can cause people to feel lightaded
[02:03:34] or faint. That's a little excessive
[02:03:36] activity by the parasympathetic nervous
[02:03:39] system. Now the excess activity on the
[02:03:41] part of the vagus system or the
[02:03:43] parasympathetic system can slow the
[02:03:47] heart. It can decrease the blood
[02:03:50] pressure uh and it basically sets you up
[02:03:53] for what we call a vegetative state.
[02:03:55] That is for a digestive resting state.
[02:03:58] The sympathetic nervous system of course
[02:04:00] does the opposite. It revs you up ready
[02:04:02] to fight or to flee depending upon the
[02:04:06] circumstances. Raises your blood
[02:04:07] pressure, increases your heart rate,
[02:04:09] increases the pumping activity of the
[02:04:11] heart and starts putting a lot more
[02:04:13] blood flow into the muscles to get you
[02:04:15] ready to run away. So what do beta
[02:04:18] blockers do? Beta blockers block the
[02:04:21] effect of the sympathetic nervous system
[02:04:23] so that you can't increase your heart
[02:04:24] rate. so much you can't increase your
[02:04:27] contractility. You can't increase your
[02:04:29] blood pressure. Why would that work in a
[02:04:32] patient with eskeemic heart disease, a
[02:04:34] patient with coronary artery disease? Of
[02:04:36] course, remember we talked about the
[02:04:39] imbalance between the demand on the
[02:04:41] heart in terms of metabolic supply and
[02:04:44] the supply because of a blocked artery
[02:04:48] there's decreased supply. [snorts] So
[02:04:50] what beta blockers do is by decreasing
[02:04:52] the metabolic demand of the heart they
[02:04:55] reestablish the balance between cardiac
[02:04:58] demand and cardiac nutritional supply,
[02:05:02] oxygen and nutrients.
[02:05:04] They plug into the little receptors in
[02:05:07] the heart that speed up the heart and
[02:05:11] when they do that they stop adrenaline
[02:05:14] from getting into those receptors and
[02:05:16] therefore the heart rate doesn't
[02:05:18] increase even though the sympathetic
[02:05:19] nervous system is pushing. Now it turns
[02:05:22] out that there have been three levels or
[02:05:25] three classes of beta blockers. There
[02:05:28] are ones that are a little more specific
[02:05:29] for the heart. There are some that are a
[02:05:32] little less specific um for the heart
[02:05:34] but more specific for the lung. There
[02:05:37] are some that are a mixture of heart and
[02:05:39] lung and then there are some that are
[02:05:42] either a mixture for heart and lung but
[02:05:44] also dilate blood vessels and therefore
[02:05:46] even accentuate the drop in blood
[02:05:48] pressure. The first group beta 1
[02:05:51] receptor blockers are used for anggina
[02:05:55] and uh particularly also for patients
[02:05:57] with heart failure again where you're
[02:05:59] trying to uh assist the heart a little
[02:06:01] bit by not making such high demands on
[02:06:03] it. The beta 2 receptor blockers are
[02:06:06] used in a a variety of ways also
[02:06:09] sometimes for heart disease sometimes
[02:06:11] for arrhythmias uh and sometimes for
[02:06:13] hypertension. And the beta 3 group uh
[02:06:17] the most recent ones are used for heart
[02:06:19] failure patients. Again, they decrease
[02:06:21] the contractility of the heart. They
[02:06:23] decrease the blood pressure. They
[02:06:25] decrease the work of the heart so that a
[02:06:27] damaged heart can heal a little bit.
[02:06:29] We're going to talk about that some more
[02:06:31] in a moment. Uh I don't expect you to
[02:06:34] read and memorize this list, but here it
[02:06:36] shows you all of the actions of the beta
[02:06:39] 1 and the beta 2 uh blockers. As you can
[02:06:43] see, they have actions throughout the
[02:06:44] body on blood vessels, on the heart, on
[02:06:47] the lungs. And of course, what this
[02:06:49] means is it gives you potential for
[02:06:52] complications. Let's say we have a
[02:06:55] patient with high blood pressure and
[02:06:56] anga, that is the feeling of chest
[02:06:59] discomfort when there's an imbalance
[02:07:01] between blood supply and blood demand.
[02:07:03] We put the patient on beta blocker, but
[02:07:06] we forgot the patient has a history of
[02:07:08] asthma in the past. When we block the
[02:07:10] beta 2 in the lung, we make their asthma
[02:07:13] worse. So, we did something good for the
[02:07:16] heart, but we did something bad for the
[02:07:18] lungs. So, again, this list shows you
[02:07:21] all the different effects of beta
[02:07:24] blockers throughout the body, and a lot
[02:07:26] of them are potential sources for
[02:07:28] complications.
[02:07:31] Here in a little diagram, you see what I
[02:07:34] just said. In the top arrow you can see
[02:07:37] the beta 1 or heart blocking effects
[02:07:40] reduces contractility reduces blood
[02:07:42] pressure um makes the work of the heart
[02:07:45] less. You can also see in the second
[02:07:48] little drawing the lungs. If there's
[02:07:50] beta 2 effects you may increase the
[02:07:53] bronchial constriction that is this
[02:07:56] constriction of the small tubes in the
[02:07:58] lung that lead to asthma. And then you
[02:08:00] [snorts] can see uh down below the beta
[02:08:03] blockers that dilate the blood vessels
[02:08:05] are particularly good uh for heart
[02:08:07] failure. Now let's think for a second
[02:08:09] about the potential of the non-specific
[02:08:12] beta blockers, the one that block both
[02:08:15] both beta 1 and beta 2. These are the
[02:08:18] ones that have the greatest potential
[02:08:20] for causing lung side effects when given
[02:08:24] for the heart. But it turns out that
[02:08:27] selectivity of beta 1 and beta 2, I call
[02:08:30] it semi selectivity because if you take
[02:08:32] a beta 1 selective blocker and you give
[02:08:35] it at a very low dose, it's going to
[02:08:36] mostly block the beta receptors in the
[02:08:38] heart. But if you need to push the dose
[02:08:41] even into moderate levels, there's some
[02:08:43] spillover onto beta 2. So even if you
[02:08:47] are giving a beta 1 blocker to a patient
[02:08:49] with heart disease for anggina or for
[02:08:52] hypertension or for heart failure and
[02:08:55] [clears throat] that patient has a
[02:08:56] tendency to develop asthma when you push
[02:09:00] the dose of that beta blocker into a
[02:09:02] reasonable range, you may well worsen
[02:09:05] their asthma. And almost the only way to
[02:09:06] find that out is to try it and see what
[02:09:08] happens. Particularly if you have a real
[02:09:10] need for that beta blocker. Um and the
[02:09:13] same thing is true. Sometimes we give
[02:09:16] beta 2 stimulants to improve lung
[02:09:19] function by dilating the bronchioles and
[02:09:22] sometimes that results in cardiac
[02:09:23] arhythmias because of spillover in the
[02:09:25] beta 1 area. So again all of these drugs
[02:09:29] are not perfectly selective. They have
[02:09:31] effects throughout the body. And again
[02:09:33] this relates to the art of using these
[02:09:36] drugs because of their potential for
[02:09:38] effects in other parts of the body.
[02:09:42] This complex diagram right here shows
[02:09:45] you all the effects of beta blockers on
[02:09:48] the heart. I'm not going to spend a lot
[02:09:51] of time talking about it. You're welcome
[02:09:53] to look at it at great detail on your
[02:09:55] own, but you can see what happens in the
[02:09:58] heart with beta blockers. They decrease
[02:10:00] contractility. They decrease the heart
[02:10:02] rate. They help to prevent certain kinds
[02:10:06] of electrical short circuits, cardiac
[02:10:08] arrhythmias. Uh we're going to talk
[02:10:10] about that later. particularly atrial
[02:10:12] fibrillation. Um in a sense they quiet
[02:10:15] the heart down in a number of ways. They
[02:10:17] improve the metabolic balance right the
[02:10:20] demand supply relationship within the
[02:10:22] heart that stabilizes the situation in
[02:10:26] patients with es schemic heart disease.
[02:10:28] It helps patients who are hypertensive
[02:10:30] that is have too high blood pressure
[02:10:32] gets them back down into a more normal
[02:10:34] range and it generally quiets down the
[02:10:37] heart. Particularly some individuals are
[02:10:40] prone to marketkedly increase their
[02:10:41] heart rate even [snorts] with small
[02:10:43] disturbances and beta blockers also uh
[02:10:46] very very useful in helping uh in that
[02:10:49] regard.
[02:10:50] Um here you see a summary of the full
[02:10:55] spectrum of cardiovascular effects of
[02:10:57] the beta blockers and their indications.
[02:11:00] Beta blockers are particularly useful
[02:11:03] for anga or for eskeemic heart disease
[02:11:06] for heart failure. Actually, we've seen
[02:11:08] sometimes hearts improve when patients
[02:11:10] have been treated uh with beta blockers
[02:11:12] for heart failure and also for
[02:11:14] hypertension. All very effective and
[02:11:17] then a little less effective for
[02:11:19] controlling arrhythmias and some of the
[02:11:21] other problems. But because anga
[02:11:23] [snorts]
[02:11:24] and heart failure [clears throat] are so
[02:11:25] common, we use a lot of beta blockers.
[02:11:28] Fortunately, almost all of them now are
[02:11:30] generic, so they're relatively
[02:11:32] inexpensive. And usually in moderate
[02:11:35] doses, they're well tolerated. When you
[02:11:37] start to push the doses up, you increase
[02:11:40] the risk for effects in other organ
[02:11:42] systems, and you increase the risk for
[02:11:45] complications.
[02:11:47] So let's talk a little bit about the
[02:11:49] mechanism of benefit of beta blockers in
[02:11:52] eskeemic heart disease. that is
[02:11:54] hardening of the arteries with with
[02:11:55] blockage of blood flow into the heart
[02:11:58] muscle. Well, what we're trying to do is
[02:12:01] rebalance the situation, right? We can
[02:12:03] try and improve blood flow down the
[02:12:06] coronary arteries. We'll talk about a
[02:12:08] strategy to do that in a moment. But the
[02:12:10] most important effect is to try and
[02:12:13] decrease the demand of the heart for
[02:12:15] oxygen and nutrients. We do that by
[02:12:17] dropping the heart rate, by dropping the
[02:12:20] blood pressure, and by dropping
[02:12:21] contractility. So this is all three
[02:12:25] mechanisms work in the patient with es
[02:12:27] schemic heart disease and very often a
[02:12:29] patient who has anga with normal
[02:12:31] activity for example let's say climbing
[02:12:33] a flight of stairs oh they get chest
[02:12:35] discomfort when we give them beta
[02:12:37] blockers their heart rate doesn't
[02:12:39] accelerate as much when they go up the
[02:12:40] stairs their blood pressure doesn't rise
[02:12:42] as much and they don't have anga now
[02:12:44] when they go up the stairs and that's
[02:12:46] the goal as you'll see when we talk
[02:12:48] about eskeemic heart disease we want
[02:12:50] patients who don't have symptoms who can
[02:12:51] lead a norm normal active life as long
[02:12:54] as they're not trying to race up and
[02:12:56] down stairs, but that they can do normal
[02:12:59] daily activities without having anggina.
[02:13:03] Again, here you see a slide quite
[02:13:05] complex listing all of the beneficial
[02:13:08] effects and and some of the potential
[02:13:10] non-beneficial effects of beta blocker
[02:13:13] in a patient with eskeemic heart
[02:13:15] disease. You see the heart rate is down,
[02:13:17] the blood pressure is down.
[02:13:18] Unfortunately uh what happens is
[02:13:21] sometimes because of the decreased
[02:13:22] contractility the heart may dilate a
[02:13:24] little bit and that has a tendency to
[02:13:26] increase myioardial oxygen consumption
[02:13:29] or myioardial oxygen demand for
[02:13:31] nutrients and oxygen but that's a minor
[02:13:34] player in comparison to the decreases in
[02:13:37] the demand that you get from lowering
[02:13:39] heart rate and lowering blood pressure.
[02:13:42] So again, you might want to peruse this
[02:13:44] slide a little in a little more detail
[02:13:46] at your leisure and of course you can
[02:13:48] also read further about this in all the
[02:13:51] standard textbooks of cardiology and
[02:13:53] some of the references which we give at
[02:13:55] the end of this lecture. Now what about
[02:13:57] the so-called anti-arithmic effects of
[02:14:01] beta blockers? We haven't talked a lot
[02:14:03] about arrhythmias. I remember I showed
[02:14:05] you the cardiogram with the Pwave, the
[02:14:07] QRS and the T. Pwave being the atrial
[02:14:10] deolarization, electrical deolarization,
[02:14:12] the QRS being the ventricular one. And
[02:14:15] that's the normal sequence of electrical
[02:14:17] activity passing through the heart. It
[02:14:20] turns out particularly in older
[02:14:22] individuals and even occasionally in
[02:14:23] some younger individuals, you can have
[02:14:26] electrical what I call electrical short
[02:14:28] circuits in which suddenly the heart
[02:14:30] will start to race or there will be
[02:14:33] abnormal activity in the atria. So you
[02:14:35] lose the Pwave and the heart will race
[02:14:38] in a in a very abnormal way. Remember I
[02:14:40] showed you an electroc cardiogram of a
[02:14:42] patient in atrial fibrillation. Instead
[02:14:45] of the nice regular lubdub lubdub
[02:14:49] lubdub, what you had was dubdub.
[02:14:54] And of course when that happens the
[02:14:56] heart could be going as fast as 150
[02:14:58] beats per minute. Even people with
[02:15:01] normal hearts will feel uncomfortable
[02:15:02] with that. And especially individuals
[02:15:05] who have a lack of blood flow getting
[02:15:07] normal blood flow getting into the heart
[02:15:09] because of coronary artery disease. When
[02:15:11] you increase the heart rate like that,
[02:15:13] it's very likely that they will develop
[02:15:15] an imbalance in the supply demand
[02:15:18] relationship anga and they might even
[02:15:20] have a small heart attack. So we try and
[02:15:23] also control uh the at the arrhythmias
[02:15:26] these atrial arrhythmias and also some
[02:15:29] ventricular arrhythmias. Uh and beta
[02:15:31] blockers often help with that. For
[02:15:33] example, early on in the phase of a
[02:15:35] heart attack, a myioardial inffection,
[02:15:36] the administration of beta blockers
[02:15:38] decreases the chance that the patient
[02:15:40] will have a cardiac arrest. We're going
[02:15:42] to talk a lot about arrhythmias in a
[02:15:44] total unit where we talk about diseases
[02:15:46] of the heart and I'll also be talking
[02:15:48] about some therapy at that time. But
[02:15:50] it's important for you to realize that
[02:15:52] the beta blockers not only help to
[02:15:55] control the supply demand imbalance in
[02:15:57] the heart with es schemic heart disease.
[02:15:59] Not only can they help with high blood
[02:16:01] pressure, but they also can help uh
[02:16:04] control arrhythmias. They're not a
[02:16:06] powerful controller of arrhythmia, but
[02:16:08] they're much more benign than many of
[02:16:10] the other drugs that we use that have a
[02:16:12] lot of side effects. More about that in
[02:16:14] a later lecture. Let's talk about heart
[02:16:17] failure. This is a revolution that's
[02:16:20] occurred in the last 15 to 20 years.
[02:16:23] When I was in training, we were told,
[02:16:25] "Don't ever give a beta blocker to a
[02:16:27] patient with heart failure because it
[02:16:28] depresses the contractility, the oomph
[02:16:31] of the ventricle, and you're going to
[02:16:33] make the heart failure worse." Well, it
[02:16:35] turned out that in Sweden, the doctors
[02:16:37] weren't so convinced that beta blockers
[02:16:39] were a bad idea. And they did a series
[02:16:42] of large clinical trials in which they
[02:16:44] demonstrated that actually early on in
[02:16:47] heart failure, the beta blockers might
[02:16:49] have made things a little worse, but
[02:16:50] long-term many of the hearts remarkably
[02:16:54] improved. Well, this was a revolutionary
[02:16:57] thought. [snorts] Something I'd been
[02:16:58] taught in medical school and training,
[02:17:00] don't ever give a beta blocker to a
[02:17:02] patient with heart failure, was now the
[02:17:04] exact opposite. You better be sure and
[02:17:06] give a beta blocker to a patient with
[02:17:07] heart failure. So, what was the benefit
[02:17:10] there? Well, there were several
[02:17:11] benefits. First of all, again, even if
[02:17:14] the heart failure wasn't due to eskeemic
[02:17:17] heart disease, to lack of blood flow in
[02:17:19] the heart, but was due to sick heart
[02:17:21] cells, by decreasing the work of the
[02:17:23] heart, decreasing the heart rate,
[02:17:25] decreasing the blood pressure, you
[02:17:26] actually allowed some of those heart
[02:17:28] cells to recover. [snorts] In addition,
[02:17:30] by blocking the beta receptors on the
[02:17:33] surface of these heart cells, the
[02:17:35] myioardial cells, it actually caused the
[02:17:38] cells to produce more beta receptors.
[02:17:41] And then there was effect from the
[02:17:44] adrenaline hitting those beta receptors
[02:17:46] that increased the contractility of the
[02:17:48] heart when this was done long term. Um,
[02:17:51] and of course then there was a decrease
[02:17:53] in in arrhythmias as well. All that put
[02:17:56] together beta blockers turned out to be
[02:17:58] a huge benefit in heart failure
[02:18:00] patients. And recently over the last 10
[02:18:02] to 15 years, the beta blockers that also
[02:18:05] dilate blood vessels and therefore lower
[02:18:07] the blood pressure have been shown to be
[02:18:09] the best beta blockers for patients with
[02:18:11] heart failure. I can tell you and when I
[02:18:14] saw this the first time, I thought I
[02:18:17] made a mistake. a patient that had
[02:18:19] terrible heart function six months later
[02:18:21] had normal heart function after being
[02:18:23] put on beta blockers. When this
[02:18:25] happened, I said to myself, I must have
[02:18:28] misremembered. I must have made a
[02:18:30] mistake. It couldn't have been that the
[02:18:32] heart function was that bad early on and
[02:18:34] now became normal. When we checked back,
[02:18:36] it turned out I was absolutely right.
[02:18:39] the heart failure uh state had been
[02:18:42] associated with bad left ventricular
[02:18:44] function initially and it became normal
[02:18:46] after six months and I've now seen that
[02:18:48] happen a number of times in a number of
[02:18:50] patients of course the patients and
[02:18:53] their families are ecstatically happy
[02:18:54] when this happens um but even in people
[02:18:57] who don't totally normalize there's
[02:18:59] often an improvement in heart function
[02:19:01] with beta blockers it's the most
[02:19:03] important advance in heart failure
[02:19:04] therapy in the history of cardiology in
[02:19:07] patients with heart failure beta blocker
[02:19:09] ers are not used globally but are part
[02:19:12] of the initial therapy for most patients
[02:19:14] with heart failure with a reduced
[02:19:16] ejection fraction less than 50% hepheref
[02:19:20] beta blockers are not recommended as
[02:19:22] part of the primary therapy for heart
[02:19:24] failure with a preserved ejection
[02:19:26] fraction of 50% so-called hep trials
[02:19:29] have been done and they have not been
[02:19:32] effective unfortunately they're very
[02:19:34] good for hef not good for hep and the
[02:19:37] same is true for the uh angotensin rein
[02:19:40] blockers um ACE inhibitors and ARB. They
[02:19:44] have been shown not to be helpful in
[02:19:46] patients with hep. You know, they can
[02:19:49] occasionally be used in hep to help uh
[02:19:52] uh treat anggina or hypertension. Um but
[02:19:55] they're but if it's just heft pep alone,
[02:19:58] they're not shown to be beneficial.
[02:20:03] And in fact, if you look at Eugene
[02:20:04] Brownwald, who's probably the number one
[02:20:07] cardiologist in the world and one of my
[02:20:09] mentors and teachers, if you look in his
[02:20:11] textbook, he says beta blocker is our
[02:20:14] first choice, of course, for heart
[02:20:15] failure, of course, for eskeemic heart
[02:20:17] disease. Um, and um for hypertension and
[02:20:20] arrhythmias as well, although
[02:20:22] hypertension and arrhythmias, they're
[02:20:24] sort of in second place, but for anga
[02:20:26] and heart failure, they're number one.
[02:20:29] Hello. Now, I'm going to talk about one
[02:20:30] of my favorite topics, which is basic
[02:20:33] life support for cardiac arrest.
[02:20:36] So, let's start off with a case
[02:20:38] scenario. We have a 58-year-old man.
[02:20:40] He's running along in a sporting event
[02:20:42] and he suddenly drops, becoming pulsless
[02:20:45] and apnic. What do you want to do to
[02:20:48] save his life? We're going to talk about
[02:20:50] the most important interventions that
[02:20:51] you can perform right there on the scene
[02:20:53] that are most likely to improve his
[02:20:55] outcome. We're going to talk about why
[02:20:57] this happened physiologically, what
[02:20:59] might be going on with him, and we're
[02:21:01] going to talk about the supporting
[02:21:02] evidence that helps us know what the
[02:21:04] most effective interventions are.
[02:21:07] So, what is cardiac arrest? The term
[02:21:10] cardiac arrest refers to the abrupt sens
[02:21:13] sessation of effective circulation.
[02:21:16] Basically, it means the heart is
[02:21:17] stopped. It encompasses a lot of
[02:21:19] different underlying diseases and
[02:21:21] conditions. But the final common pathway
[02:21:23] in each case is that the heart is not
[02:21:26] producing the effective circulation of
[02:21:28] blood to the body. So the primary cause
[02:21:31] of cardiac arrest first and foremost is
[02:21:33] coronary eskeeia. The whole world over
[02:21:36] that is the number one cause. But there
[02:21:38] are other things that can lead to
[02:21:39] cardiac arrest as well including
[02:21:41] cardiammyopathies,
[02:21:44] structural heart lesions such as
[02:21:45] valvular disease,
[02:21:47] electrical conduction conduction
[02:21:49] abnormalities such as bugata syndrome or
[02:21:51] other channelopathies,
[02:21:54] metabolic disturbances particularly
[02:21:56] those in electrolytes,
[02:21:58] toxic ingestions. There are a number of
[02:22:00] poisonings that can produce cardiac
[02:22:02] arrest and there are other non-cardiac
[02:22:04] conditions that can lead the heart to
[02:22:06] stop.
[02:22:07] When we look at the epidemiology of
[02:22:09] cardiac arrest in the United States, we
[02:22:11] have about half a million arrests per
[02:22:13] year. Of those, about 60% occur outside
[02:22:17] of the hospital. And for out of hospital
[02:22:20] arrest, there's only about a 10%
[02:22:21] survival rate, although that number does
[02:22:23] go up to 30% for cases which are
[02:22:26] witnessed by bystanders and the victim
[02:22:28] receives rapid CPR.
[02:22:31] About 200,000 of these events or about a
[02:22:34] little more than a third occur inside of
[02:22:36] the hospital. And in the hospital, we
[02:22:38] have a 20% survival rate, which is
[02:22:40] double what we get outside of the
[02:22:42] hospital, but it's still really not
[02:22:43] great. Obviously, that survival is going
[02:22:46] to be affected by the ideology of the
[02:22:48] arrest, the hospital itself, how
[02:22:51] prepared it is to deal with high acuity
[02:22:53] events, and believe it or not, the time
[02:22:55] of day. As far as the epidemiology goes,
[02:22:58] the incidence of cardiac arrest
[02:23:00] increases linearly with age. So as you
[02:23:02] get older, you have a higher and higher
[02:23:03] risk of having an arrest. And 57% or
[02:23:06] almost two-thirds of the patients are
[02:23:08] men.
[02:23:11] When you look at the cardiac rhythm in
[02:23:13] patients with cardiac arrest, about a
[02:23:15] quarter have either ventricular
[02:23:17] fibrillation or ventricular tacicardia,
[02:23:20] which are known as the shockable
[02:23:22] rhythms.
[02:23:24] Among those patients you have about a
[02:23:26] 30% survival rate.
[02:23:28] The remaining rhythms which are
[02:23:30] pulseless electrical activity and ascy
[02:23:33] only produce about a 10% survival rate.
[02:23:36] So there's a big difference in how
[02:23:38] likely you are to survive based on what
[02:23:40] type of rhythm your heart goes into at
[02:23:42] the time of arrest.
[02:23:44] Overall shockable rhythms represent a
[02:23:47] minority of arrests. only about 25% but
[02:23:51] 3/4 of patients who survive have
[02:23:53] shockable rhythms. So you are much much
[02:23:55] more likely to survive a cardiac arrest
[02:23:58] if you have ventricular fibrillation or
[02:24:00] ventricular tacic cardia rather than one
[02:24:02] of the other two arrest rhythms.
[02:24:05] When you see somebody in cardiac arrest,
[02:24:07] they are invariably 100% of the time
[02:24:11] unresponsive, pulseless, and most
[02:24:14] commonly apnic. Although a few will have
[02:24:16] preserved agonal respirations or
[02:24:18] gasping.
[02:24:20] When you're evaluating an unresponsive
[02:24:23] patient, you want to always get help
[02:24:25] right away. Not every patient who's
[02:24:27] unresponsive is in cardiac arrest, but
[02:24:29] you should assume the worst case
[02:24:31] scenario. assume that your patient is in
[02:24:33] cardiac arrest and that you need
[02:24:35] immediate backup. And even if your
[02:24:38] patient doesn't turn out to be in
[02:24:39] cardiac arrest, it's never a bad idea to
[02:24:41] get help because the things that make
[02:24:42] you unresponsive are never good. Once
[02:24:45] you have help on the way, the next
[02:24:47] question you want to ask yourself is,
[02:24:50] does this patient have a pulse?
[02:24:54] This is why in cardiac arrest, we don't
[02:24:56] use the old ABC pneummonic that we
[02:24:59] talked about in prior lectures to assess
[02:25:01] the patient. We use CAB circulation
[02:25:05] first because the first and most
[02:25:07] important question is whether or not
[02:25:08] your patient has a pulse. We want to
[02:25:11] check the pulse for a maximum of 10
[02:25:13] seconds always in the kurateed. And if
[02:25:16] at the end of that time there either is
[02:25:18] no pulse or we have any question as to
[02:25:21] whether or not there's a pulse, we're
[02:25:23] going to go ahead and initiate CPR.
[02:25:26] Only after we've decided whether or not
[02:25:28] a pulse is present are we going to worry
[02:25:30] about airway and breathing. So while
[02:25:32] you're checking the pulse, you can look
[02:25:34] for clinical evidence of respiration.
[02:25:37] Again, sometimes you'll see agonal
[02:25:39] breathing or gasping, and rescuers often
[02:25:41] mistake this for normal breathing, but
[02:25:43] you should never see normal rhythmic
[02:25:46] breathing in a cardiac arrest. If you
[02:25:48] do, you should rethink whether or not
[02:25:50] your patient is really in cardiac
[02:25:52] arrest. So like I said your most
[02:25:54] important question is whether a patient
[02:25:56] has a pulse. We're going to assess that
[02:25:58] by palpating the corateed pulse. The
[02:26:00] reason we go for the corateed is in
[02:26:03] shock. This is the last pulse to go. So
[02:26:05] patients who are hypotensive but still
[02:26:07] do have spontaneous circulation might
[02:26:10] lose their radial or their femoral
[02:26:11] pulses but they're always going to keep
[02:26:13] their kurateed pulse up until the last
[02:26:16] moments before they cease to have
[02:26:17] circulation.
[02:26:19] Once again, you get a max of 10 seconds.
[02:26:23] If you don't clearly detect a pulse in
[02:26:25] that time frame, start CPR. You're never
[02:26:28] going to hurt a patient by performing
[02:26:30] unnecessary CPR, but you will absolutely
[02:26:33] hurt people by withholding CPR when in
[02:26:36] fact they don't have spontaneous
[02:26:38] circulation.
[02:26:40] Now, we're going to talk about the
[02:26:41] second part of cardiac arrest or
[02:26:43] advanced life support.
[02:26:47] So there are three major cardiac arrest
[02:26:49] rhythms that we need to be aware of.
[02:26:51] Ventricular fibrillation and ventricular
[02:26:54] tacic cardia pulseless electrical
[02:26:56] activity and ascy. And we're going to
[02:26:59] talk in some detail about each of those
[02:27:01] three identifying some of the key
[02:27:03] similarities and differences between
[02:27:05] them. Let's start off with VIB and VTAC.
[02:27:09] So these rhythms both represent
[02:27:12] disorganized electrical conduction which
[02:27:14] originates in the ventricles.
[02:27:18] There's a number of different causes for
[02:27:19] ventricular fibrillation and tacicardia
[02:27:22] but they're most strongly associated
[02:27:24] with primary heart disease in particular
[02:27:26] coronary eskeemia. So myioardial
[02:27:29] infarctions etc. However, you can also
[02:27:32] see VIB and VTAC in the setting of
[02:27:35] structural heart disease, inherited
[02:27:37] channelopathies, and other clinical
[02:27:39] situations.
[02:27:41] Least commonly, you see VIB and VTAC
[02:27:44] with systemic metabolic derangements,
[02:27:46] things like electrolyte disturbances,
[02:27:48] autoimmunity, toxic ingestions, but
[02:27:51] that's really quite rare. The vast
[02:27:52] majority of these are caused by heart
[02:27:55] attacks.
[02:27:56] So, here's just a review on ventricular
[02:27:59] fibrillation. Like we said in the last
[02:28:01] lecture, this is one of our two
[02:28:02] shockable rhythms. So this is randomly
[02:28:05] fluctuating, completely disorganized
[02:28:07] electrical activity. No pattern, no QRS
[02:28:11] complexes. The heart is literally just
[02:28:13] going in the chest. It's not actually
[02:28:16] beating, meaning that there's no cardiac
[02:28:19] output whatsoever associated with this
[02:28:22] because the heart's not contracting.
[02:28:24] This rhythm, if it's not terminated, is
[02:28:26] completely incompatible with life.
[02:28:31] By contrast, here's VTAC. So, we
[02:28:33] mentioned this in a prior lecture as
[02:28:35] well, but VTAC is organized. It's just
[02:28:38] bizarre. So, these QRS complexes are big
[02:28:42] and tall and wide, but they are
[02:28:44] organized and they are regular. Now, you
[02:28:48] want to think about VTAC anytime you see
[02:28:51] tacocardia,
[02:28:53] meaning a heart rate of greater than
[02:28:55] 100, most commonly greater than 150.
[02:28:58] That means your QRS complexes are going
[02:29:00] to be coming along more than every 3
[02:29:02] millimeters on your tracing or more than
[02:29:04] every two millimeters in the case of a
[02:29:06] heart rate of 150.
[02:29:10] In this case, again, the QRS is wide, so
[02:29:12] it's got to actually be wider than 3
[02:29:14] millimeters to be considered VTAC, but
[02:29:16] usually it's pretty obvious. These are a
[02:29:18] big, wide, very strange looking
[02:29:21] complexes.
[02:29:22] And patients in VTAC can be completely
[02:29:26] pulseless, apnic and dead. They can be
[02:29:29] completely stable and in some cases
[02:29:31] asymptomatic or they can be anywhere in
[02:29:34] between. So the important thing with
[02:29:35] VTAC is when we talk about it in the
[02:29:38] context of cardiac arrest, we're talking
[02:29:40] specifically about pulseless VTAC,
[02:29:43] meaning we don't want to treat VTAC in a
[02:29:45] patient with a pulse, especially a
[02:29:47] stable patient, the same way as we would
[02:29:50] in a pulseless patient. Clearly a stable
[02:29:52] conscious patient is going to hate if we
[02:29:54] start CPR on them.
[02:29:57] All right. So, single most important
[02:29:59] intervention for VIB and VTAC. We
[02:30:01] alluded to this before, but I want to
[02:30:03] emphasize again. It is to defibrillate.
[02:30:06] Now, the great thing about
[02:30:07] defibrillation is this is such an
[02:30:09] important intervention. We've started
[02:30:11] putting defibrillators in public places
[02:30:13] all over the world. So you can now find
[02:30:15] defibrillators in shopping malls, at
[02:30:18] sports stadiums, in the back seats of
[02:30:20] police cars, all kinds of places around
[02:30:23] the world where first responders can
[02:30:26] access them easily and use them quickly
[02:30:28] to save lives when needed.
[02:30:32] So we're going to go through the VIB and
[02:30:33] VTAC algorithm now in some detail. So,
[02:30:36] first and foremost, when you have a
[02:30:38] cardiac arrest, you're want going to
[02:30:39] want to get help right away, and you're
[02:30:41] going to want to initiate CPR, the
[02:30:43] highest quality CPR you can possibly
[02:30:45] manage. Next priority is to get your
[02:30:48] hands on a defibrillator as quickly as
[02:30:50] you can, and to administer a shock for
[02:30:52] VIB or VTAC. We don't shock other
[02:30:55] rhythms, but for these rhythms,
[02:30:56] electricity is key.
[02:31:00] Your next maneuver is going to be to
[02:31:02] continue CPR for five cycles or two
[02:31:04] minutes before you perform another
[02:31:06] rhythm check. At that point, if you're
[02:31:09] still in a shockable rhythm, you're
[02:31:11] going to administer yet another shock.
[02:31:13] And this is also when you're going to
[02:31:14] give a vasopressor drug like
[02:31:16] epinephrine.
[02:31:18] After that, we're going to continue CPR
[02:31:20] for another five cycles or two minutes
[02:31:22] where once again we check the rhythm, we
[02:31:25] defibrillate if we're still in a
[02:31:26] shockable rhythm. And now we're going to
[02:31:28] think about use of anti-riythmic drugs,
[02:31:30] in particular amiiotarone.
[02:31:38] [music]