The Cardiac Cycle-MBBS1-2022-handout.pdf

Hello my name is Professor Mike Shattock and welcome to my lecture on The Cardiac Cycle. As you can see on the left, this presentation will be divided into two short lectures with a gap in between. You can navigate directly to the start of each mini-lecture using the chapter markers that appear if y...

Hello my name is Professor Mike Shattock and welcome to my lecture on The Cardiac Cycle. As you can see on the left, this presentation will be divided into two short lectures with a gap in between. You can navigate directly to the start of each mini-lecture using the chapter markers that appear if you hover your cursor over the top left corner of the video window. In the first lecture will talk about the ECG and the electrical events and how these correlate with mechanical contraction. In the second lecture we will talk about how the mechanical contraction of the heart genetrates the peripheral pulse in both the arterial and venous circulations. Finally, we will briefly describe the heart sounds that can be heard by ausculation - that is, listening at the body surface usually using a stethescope. 1 What you can see here is the lecture plan for both lectures. We have previously learned about the ECG in my lecture on the Initiation of the Heartbeat. Will briefly review the waves of the ECG before moving on to describe how that electrical excitation activates contraction and the changes in pressures and volumes measured in the chambers of the heart. We'll talk about how those pressures and volumes change as we move around the contractile cycle and how the heart operates as a pump. Finally, in this first lecture, will describe what are known as pressure- volume loops. More about these later. In the second lecture we will go on to talk about the peripheral pulse and the heart sounds. 2 I have already covered this in my lecture on the Initiation of the Heart Beat. So, this slide is just to remind you of the sequence of the ECG and how the ECG waves correspond to the different underlying mechanical events of the cardiac cycle. Here you can see, in a sequence of events, the ECG regenerating and the wave of excitation spreading down the heart through the ventricles, round up through the free walls, and giving us that PQRS and T pattern should now be familiar to you. The waves and what they represent are labelled on the right hand side of this slide – take a moment to remind yourself of these. 3 Before we think about the pressure and volume changes in the ventricles, we need to just be reminded or some of the anatomy - specifically the names of the valves that separate the different chambers and the outflow tracts. In this diagram you can see the two main valves between the upper chambers of the heart and the lower chambers of the heart. On the right hand side all of the diagram (or the left hand side of the heart) you can see the valve that connects the left atrium to the left ventricle - this is labelled the mitral valve. It's also sometimes known as a bicuspid or left atrioventricular valve - the clue is in the name - it's called bicuspid because it has two leaflets, but it's most commonly called the mitral valve and you'll see it referred to as such and in many textbooks. In this lecture we will talk about it as the mitral valve. On the right side of the heart (the left side of your diagram) you can see the valve between the right atrium and the right ventricle. This has three leaflets and so is called the tricuspid valve. It's also sometimes referred to as the right atrioventricular valve but is most commonly is referred to as the tricuspid valve - so that's what we will call it in these lectures. There are two other valves you need to think about. These are the valves on the outflow tracts from the ventricles. The outflow from the left ventricle flows into the aorta through the aortic valve and the outflow from the right ventricle flows into the pulmonary artery through the pulmonary valve. Both of these valves are semi-lunar valves - we will refer to them as the pulmonary valve and the aortic valve. All these valves share one common feature and that's written on the right hand side of the slide. Healthy valves have very little resistance to flow. So what 4 that means is that a small pressure gradient across them is sufficient for them to open. You only need a few mmHg pressure difference between one side of the valve and the other and the valve can be pushed open. If there's a few mmHg difference in the opposite direction, the valve snaps shut. They are very easy to open a very easy to close. This is an important feature of the valves - healthy valves only need a very small pressure gradient across them for them to open or close. You'll see why that's important later in this lecture. ‹#› This shows a 2-D echocardiogram. Echocardiograms are generated by placing an ultrasonic probe on the surface of the body. In this case the probe is placed near the tip of the sternum pointing up into the thorax. The segment shown in white is interrogated by the echo software and blood moving towards the probe in this segment is coloured red and blood moving away from the probe is coloured blue. Mitral regurgitation would show up as a blue jet from LV to LA. Note: there is no mitral regurgitation in this example. You can see the opening of the atrio-ventricular valves (mitral and tricuspid). Recall that the opening and shutting of the valves in the heart is not due to muscle contraction, it’s simply due to pressure differentials and, only a small pressure gradient is necessary to open a valve. The atrioventricular valves are quite floppy, but they are anchored to the walls of the ventricles by the papillary muscles and chordae tendineae so they don’t blow back into the atria when the pressures in the ventricles rises during systole. They do however bulge back into the atria during systole, and this creates an additional atrial pressure wave that can be visualised externally as it causes a pulse of blood into the jugular vein that can be seen at the neck (see later in the lecture). Damage to these anchoring structures, for example after an MI, can result in an atrioventricular valve everting back into an atrium, so during systole you get some blood being pumped backwards, in the wrong direction and this can be visualised on echo as described above. 5 Let's think about what the pressure and volumes are changing and how they change in the course of a complete contractile cycle. At the top here you can see I've labelled the different phases of the contractile cycle as Diastole and Systole. You should be familiar with the idea that Diastole is the gap in between beats and Systole is the contractile phase. What we've marked here is the various pressures in the various chambers and the major vessel leading out of the left ventricle - the aorta. We're going to consider the pressures in the left side of the heart (the left atrium and the left ventricle). In the diastolic phase (in the gap between beats) you can see that the aortic pressure is falling and aortic pressure At this stage the left atrial pressure (marked with the number one) is actually higher than the left ventricular pressure (which is in the purple colour). So if you look at where the Point #1 is on the diagram, you can see that the left atrial pressure (in brown) is just slightly higher than the left ventricular pressure (purple). So, as we said in the previous slide, that means the valve will push open the atrial pressure is higher than the ventricular pressure and so the valve is open and blood will flow from the left atrium into the left ventricle. You can see in the volume trace below (dark blue colour) that the volume in the left ventricle at this point is is very high. So, 6 the ventricle is almost full of blood at this point. At Point #1, on the ECG you can see the P wave - when the P wave occurs the left atrium contracts. This gives a little kick which gives us extra filling of the left ventricle as the final bit of blood is pushed into it by the atrial contraction. At Point #2 you see the left atrium contracts and that's called the atrial kick. ‹#› Let's think about what the pressure and volumes are changing and how they change in the course of a complete contractile cycle. At the top here you can see I've labelled the different phases of the contractile cycle as Diastole and Systole. You should be familiar with the idea that Diastole is the gap in between beats and Systole is the contractile phase. What we've marked here is the various pressures in the various chambers and the major vessel leading out of the left ventricle - the aorta. We're going to consider the pressures in the left side of the heart (the left atrium and the left ventricle). In the diastolic phase (in the gap between beats) you can see that the aortic pressure is falling and aortic pressure At this stage the left atrial pressure (marked with the number one) is actually higher than the left ventricular pressure (which is in the purple colour). So if you look at where the Point #1 is on the diagram, you can see that the left atrial pressure (in brown) is just slightly higher than the left ventricular pressure (purple). So, as we said in the previous slide, that means the valve will push open the atrial pressure is higher than the ventricular pressure and so the valve is open and blood will flow from the left atrium into the left ventricle. You can see in the volume trace below (dark blue colour) that the volume in the left ventricle at this point is is very high. So, 7 the ventricle is almost full of blood at this point. At Point #1, on the ECG you can see the P wave - when the P wave occurs the left atrium contracts. This gives a little kick which gives us extra filling of the left ventricle as the final bit of blood is pushed into it by the atrial contraction. At Point #2 you see the left atrium contracts and that's called the atrial kick. ‹#› At this point the ventricle is now full of blood and ready to contract. At Point #3 the electrical excitation the QRS complex of the ECG can be seen and the wave of excitation spreads through the left ventricle called causing it to contract. If you look at the purple trace in the top panel, you can see that this contraction raises the pressure in the left ventricle and the pressure starts to rise very steeply but, because the aortic valve is still closed at this point, this phase is called the isovolumic contraction ('iso' meaning 'the same', and 'volume' obviously meaning volume). So, at Point #4 we have a phase of isovolumic contraction - the pressure rises in the ventricle but the volume doesn't change. You can see that (marked in red) on the volume trace (blue). This period of isovolumic contraction comes to an end when the left ventricular pressure goes higher than the aortic pressure (remember what we said before a small change in pressure either side of the valve will open the valve). So at the point that the left ventricular pressure exceeds the aortic pressure, the aortic valve opens (at Point #5). The moment the aortic valve opens the ventricle can start to empty and the pressure is high in it - so it pushes the blood out through the aortic valve. You can see on the left ventricular volume trace (in blue) the fall in volume as blood is ejected out of the left ventricle. This phase therefore (marked as Point #6 on this diagram) is called ventricular ejection. 8 At Point #7 the left ventricular pressure starts to fall as the ventricle stops contracting. Left ventricular pressure continues to fall until it falls below the level of the aortic pressure. At that point (Point #8 marked on the diagram), the left ventricular pressure is lower than the the aortic pressure and so the aortic valve snaps shut. When it snaps shut it gives a little bump in their aortic pressure trace which is called the dichotic notch. We can see that dichotic notch in arterial pressure measurements made both directly in their aorta and further round in the peripheral circulation. It is a very characteristic feature of arterial pressure - that little notch where the aortic valve has snapped shut. With the aortic valve shut, the ventricle continues to relax but, because the valve is shut, the volume is not changing. So we have this period of isovolumic relaxation (which you can see marked on the trace). If you look at the blue left ventricular volume trace, you can see the volume is not changing but the pressure is falling very steeply in the left ventricle. This period of isovolumic relaxation comes to an end when the left ventricular pressure falls below the left atrial pressure trace (if you look at the purple line (marked Point #9), it falls very steeply until it goes below the brown line). At that point, the left ventricular pressure is now lower than the left atrial 9 pressure and so the mitral valve opens. At that point blood can again flow from the left atrium into the left ventricle and the left ventricle can start to refill. If you look at the blue trace, you can see the left ventricular volume now going up very steeply as blood flows from the left atrium into the left ventricle. Note: in the diagram at the bottom left of this slide, if you review this slide, you can see this diagram has maps onto the pressure and volume changes showing when the valves are open and closed. You can see at this point the mitral valve is open and blood is flowing from the left atrium into the left ventricle and the left ventricular volume is going back up as it refills with blood. If you replay this slide, this picture should show you pictorially how the valves are opening and closing at the different stages. ‹#› We can put a catheter into the left ventricle of the heart in the Cardiology Catheter Lab. We can measure the pressure and volume changes that occur in a single cardiac cycle. This generates what's called a pressure-volume loop. You can see one in this slide. On the X-axis we have left ventricular volume and on the Y-axis we have left ventricular pressure. Every time the heart beats, we will go round one of these loops. So, let's talk our way around this loop starting in the bottom left hand corner. In the bottom left, the ventricle is essentially empty. It is fully contracted and we are at a point which is called the End Systolic Point. At this point, the end-systolic volume (ESV) (as you can see in the diagram) is about 50 millilitres. So, the ventrcicle never completely empties of blood- even at peak contraction there's still a little bit of blood left in the ventricle. We will talk about that in the next slide. That blood that's left is about 50 millilitres. So, as the heart starts to relax we enter this period of ventricular filling where the volume in the ventricle goes up. After the mitral valve is opened, blood flows from the left atrium into the left ventricle - filling the left ventricle and taking the volume from about 50 ml up to about 120 ml. When we get to about 120 ml, the ventricle is now full and we reach the end-diastolic volume (EDV). At that point, with the ventricle 10 full, the mitral valve closes because the left ventricular pressure is now above the left atrial pressure. The wave of excitation then spreads to the left ventricle and the left ventricle contracts and we enter this period of isovolumic contraction. You can see here that the volume remains at about 120 ml - hence it's called isovolumic and the pressure rises from about 20 mmHg up to about 80 mmHg. Now you will recall that your diastolic blood pressure the pressure in your aorta usually sits at around 80 mmHg. So when the left ventricular pressure gets above 80 mmHg, the aortic valve will open. The aortic valve is pushed open at around about 80 mmHg and the heart enters this period of ejection - blood is pushed out of the left ventricle and into the systemic circulation. The left ventricle empties and goes from about 120 ml to about 50 ml. In that top part of the pressure-volume loop at the peak, the pressure reaches its systolic maximum in the aorta which is about 120 mmHg. Again, you'll recall that your peak systolic blood pressure is about 120 mmHg (and your diastolic blood pressure is about 80 mmHg). So the peak of the loop the pressure in the ventricle is about 120 mmHg. When the ventricle starts to relax, the pressure starts to fall in the top part of that loop and it continues to fall until the pressure in the left ventricle falls below the pressure in the aorta and the aortic valve snaps shut (at the top left hand corner pressure volume loop). Now the ventricle is essentially empty and we enter this phase of isovolumic relaxation where the volume stays the same but the pressure falls (from around 100 to about 20 mmHg). That completes one pressure volume loop. Every time the heart contracts, it goes round this loop once. We can insert a catheter into the left ventricle and measure these pressures and volumes and it gives us really useful information about both the contractile phase and the relaxation phase of the cardiac cycle. The sort of things we can measure are shown in the next slide. ‹#› The first most obvious thing we can measure is the stroke volume. Stroke volume is the difference between the end -diastolic volume and the end-systolic volume. That is, how much blood is in the heart when it's full (ie about 120 ml) and how much blood is left over when we have finished the contraction (in this case about 50 ml). So, the difference between 120 and 50 is about 70 ml - that's the width of the pressure volume loop. By measuring the width of the loop, we get a measure of stroke volume. The other thing we can measure is stroke work - this is how much work the heart does moving blood into the peripheral circulation. It is measured by measuring the area of a pressure-volume loop - if the heart is working harder the loop is larger, if the heart is working less hard it is smaller. So we can measure an index of how much work the heart is doing by measuring the area of a pressure volume loop. On the right hand side here you can see some of the other things we can measure. We've listed stroke volume here at the top (which is the end diastolic volume minus the end systolic volume) which in this case is about 70 ml. The unit of stroke volume is millilitres. We can also measure something very important called ejection fraction. That's the fraction of blood that is in the heart at end diastole (when it is full) that is ejected with each beat. So we take 11 the stroke volume (the end-diastolic volume minus the end-systolic volume) and divide it by the end-diastolic volume, (x 100) to give us a percentage. That is the percentage of blood that fills the ventricle that is ejected with each beat. In red on the right hand side you can see the calculation for the example of the loop that we've shown on the left hand side. So, in this case, the equation is ((120 - 50) / 120) * 100. This gives us an answer of 58%. So, 58% of the blood that is in the ventricle when it is full is ejected with each beat. This is a really useful index because people with heart failure will have ejection fractions which are low (30-35%). Anybody with an ejection fraction of greater than say 55 up to about 75% would be normal. So 58% ejection fraction is perfectly normal. If you had an ejection fraction of 35% you would be in severe heart failure. This is a very useful index. As we said you can measure stroke work (and the units are often wrong in the literature) but can be variously mmHg cm 3 or other units (ie Joules). You will see different units quoted in the literature but it doesn't matter massively as very often this might be used as a relative change for any given situation. We can also measure functions of systolic behaviour or systolic function or contractility (how strongly the heart is contracting) or indeed how well it is relaxing in between beats which would be called diastolic function. We can get measures of what we would call compliance or stiffness (how stiff the ventricle is) and again these are really useful indices when we're dealing with patients with heart failure. ‹#› 12 Welcome back to the 2nd mini-lecture in the series on the Cardiac Cycle. In the first lecture we considered the electrical and mechanical events underlying the contraction cycle. In this second lecture lecture be we're going to describe arterial and venous pulses and understand the factors that affect them. Finally, we will describe the various types of heart sound and explain what causes them. 13 Before we think about pressure pulses we need to review the effects of gravity. Any column of liquid exerts a hydrostatic pressure. The higher the column, the greater the pressure. You can see that illustrated on the left hand side of the slide When thinking about blood, for every 30 cm of height, a column of blood will exert a pressure 23.4 mmHg. Why is 30cm a relevant number? It’s the approximate height of your brain above your heart! So, the pressure at the heart is approximately 23.4 mmHg HIGHER than that at the brain. So, if you look at thr right hand side of the slide, you can see that when you have a mean arterial pressure (MAP) of about 100 mmHg at the level of the heart, the blood pressure at your head is about 77 mmHg. This is true when you are standing on the earth with the force of gravity equal to 1G. As an interesting digression: Pilots flying fast jets are subjected to higher G forces. So, from what you now know, you can estimate how many G it will take to reduce your head-level MAP to zero (i.e. no perfusion of your brain!). For every 1G we will lose 23.4mmHg pressure at head level. So……… 1G = 77 mmHg 2G = 54 mmHg 3G = 31 mmHg 4G = 8 mmHg 5G = -15 mmHg So somewhere between 3 and 4.25G head level MAP will fall to zero – i.e. no blood flow to the brain. The pilot will pass out within 5 seconds! This is super 14 serious as fast jets can ‘pull’ 9G (and they cost a lot of money when they crash!). ‹#› Here are the pressures in the venous and arterial circulations in a person standing vertically (on earth at 1G!). If you look at the right hand side of the slide we can see the arterial pressures. The dynamic pressures, shown in green, are what the heart WOULD produce if the subject was simply lying down horizontally. At heart level the mean arterial pressure is about 100 mmHg and you can see, in green, that when a subject is lying down the head level and foot level pressures are barely affected by gravity. The slight fall in mean arterial pressure at the extremes is simply due to loss of energy as the pulse wave moves further from the heart. On the right hand side (in blue) you can see the effects of hydrostatic pressure when a person is standing - as we discussed in the previous slide. So the net effect is the dynamic pressure in green minus the hydrostatic pressure. This gives us the total pressures shown in red. Look at our how high our blood pressure is in our feet. Or indeed how relatively low it is in our hand stretched above our head. Now you can appreciate why we quickly get cramp whilst trying to paint a ceiling And you can understand why Michelangelo had to lie down to paint the Sistine Chapel. On the left hand side of the slide you can see the equivalent pressures in the venous circulation. Again you can see the high pressures in our feet and the low pressures above the heart and not only are these pressures low, but in the venous circulation they are negative. So blood returning from the head and upper body to the heart does so through a syphon effect. 15 As we saw in the previous slide, the effects hydrostatics mean that the venous pressures above the heart are low while arterial pressures, and pulse pressures, are high. So the low venous pressure and the effects of hydrostatic pressures, mean that the jugular vein will collapse simply due to the hydrostatic influences about 5cm above the height of the heart. The arterial pressure wave will also change dynamically due to hydrostatics as you move away from the heart. 16 So, lets first think about venous pressures. These are best visualised by the jugular venous pulse (or JVP). This pulse, as you can see here in red, is biphasic and it is low pressure. It can be assessed by viewing the dilation of the jugular veins in the neck. When measured directly, the way in which the biphasic waveform correlates with the cardiac cycle is shown in this slide. Remember, there are no valves between the right atrium and the jugular vein and so any rise in pressure in the right atrium is transmitted efficiently back up the venous tree. The wave itself is divided into a number of components. The a wave is right atrial contraction or right atrial systole. When the atrium contracts, as you can see in the diagram, the pressure wave dissipates back through the jugular vein and appears as the a wave on the jugular venous pulse. The C wave is caused by the transmitted carotid pulse - that is because the carotid artery lies close to the jugular vein in the neck, the carotid arterial pulse is picked up through the tissue by the jvp. The C wave also reflects the ballooning of the tricuspid valve back into the right atrium during right ventricular contraction so this further raises the JVP causing the C wave. You could see the rise in right atrial pressure that slightly precedes the C wave in the blue trace on the upper right. The next phase of the jugular venous pulse is called the X wave, or 17 the X descent. This is related to atrial relaxation. You should note that this technically starts at the start of the a wave but is interrupted by the C wave as the pressure descends. The next component of the jugular venous pulse is called the V wave. The V wave corresponds to right atrial filling during ventricular systole and the further bulging of the tricuspid valve, which is still closed, raising right atrial pressure. As the RA pressure goes up, this again dissipates backwards into the jugular vein and that's shown as the V wave on the JVP. Finally, there is what's called the Y wave or Y descent. This is atrial emptying during ventricular diastole and before the atria contract again. During this phase, the tricuspid valve is open and blood is flowing into the right ventricle, and jvp is falling. From these waves it is clear that because it is a low pressure system it is easily perturbed by other factors. For example, the adjacent carotid pulse is transmitted through the tissue and this contributes to C wave. Similarly, bulging, stenosis or regurgitation of the tricuspid valve will affect the shape and size of the JVP wave. Hence, the jvp is diagnostically very useful as it shows a lot of things going on within the heart itself. ‹#› As we have said, the central venous pressure is quite low, and as a result of gravity the veins a few cm above the heart collapse because the pressure inside them is negative. Blood still runs through them of course, but they are flat. As you move down towards the heart, at some point the pressure is high enough so that veins are rounded, and the height of this point above the heart is a readout of central venous pressure (CVP). This is shown in this slide. You can best see the point of collapse in the internal jugular vein, which runs right under the skin. The pressure waves in the right atrium back up into the jugular vein, so it’s possible to discern them as changes in the collapse point. As we have already described, changes in pressure in the RA occur with different pathologies affecting the tricuspid valve, and also in heart failure, and these can be visualised as changes in the pulse in the internal jugular vein. Why does the patient need to be at an angle? If the patient was upright, the point of collapse would be lower, where the jugular is below the level of the clavicle, and can’t be seen. If the person is lying down, there is no point of collapse! However, with the person lying back at about 45o, with a normal CVP the collapse point is usually about 3cm above the manubriosternal angle, and is in the part of the internal jugular which can be seen. In the handout accompanying this lecture, some of the reasons why 18 the internal jugular vein is preferred to the external are detailed. The internal jugular vein is anatomically closer to the right atrium while the external does not directly drain into the superior vena cava. The internal jugular is valveless and pulsations can be seen. Due to presence of valves in the external jugular, pulsations cannot be seen. Vasoconstriction, secondary to hypotension (as in congestive heart failure), can make the external jugular small and barely visible. The external jugular is superficial and prone to kinking. ‹#› In the two slides, we are going to describe how JVP can be used to diagnose tricuspid abnormalities. In tricuspid stenosis, as shown here, the a wave (1st pulse) is enhanced as RA pressure rises higher during atrial contraction due to the increased resistance of the tricuspid valve. This is the diagnostic feature of tricuspid stenosis. 19 In tricuspid regurgitation, the v wave (2nd pulse) is enhanced as ventricular contraction ejects blood through the incompetent tricuspid valve hence raising RA pressure and jugular pressure in this phase. This starts in the early phase of ventricular contraction (the c wave) at a time when there should be isovolumic ventricular contraction but because the valve is leaky, some volume is squirted back into the atrium (see dotted ventricular contraction trace at the top of the slide). It persists through into the ventricular ejection phase. A Giant or enhanced v wave is called the Lancisi Sign – after the Italian physiologist Giovanni Maria Lancisi (1654-1720) who first recognized this pattern. 20 Having considered the venous pulse, what about the arterial pulse? The arterial pressure pulse is largely monophasic (and high pressure) but the shape of peak and the the descending phase is influenced by factors such as reflected waves, compliance, resonance, interference and damping. You can see a reflected wave here in this example (in green). How large any reflected waves are depend on where you measure the pressure. These reflected waves, are properties of the blood vessels themselves and hence the shape and magnitude of the arterial pulse wave varies at different points along the arterial tree. This is explained in more detail in the next slide. 21 This slide is largely self explanatory. However, it is worth noting that the compliance and physical properties of the vascular network determine the shape of the arterial pulse at different points in the vascular tree. Reflected waves for example, can interfere with the forward compression wave such that the pulse wave is altered – if this interference is summative, the pulse pressure can actually increase in magnitude. Look at the pressure in the aortic arch………there is a little bump near the top of the upstroke. This is where the forward pressure wave meets the reflected wave bouncing off the ‘stretchy’ aorta. This gives the pressure an extra ‘kick’. This ‘kick’ is called augmentation. Sometimes, further down the vascular tree, reflected waves can be out of phase and this can depress the forward pressure wave. This is highly complex AND YOU DO NOT NEED TO UNDERSTAND THIS IN DETAIL…….but, just remember that the shape and size of the arterial pulse differs in different vessels (because of damping, reflection, interference and resonance). You can see how the shape of the arterial pressure pulse changes as you move further away from the heart. 22 Finally, we are going to consider the heart sounds. 23 When animated, this slide plays the normal heart sounds. 24 What you just heard are the two primary heart sounds in a normal heart. These are known as S1 and S2. These are typically described in textbooks as “Lup” “Dub”. These heart sounds are caused by the valves of the heart snapping shut. S1 is the initiation of ventricular systole and is the closure of the atrioventricular valves. It is typically low frequency. The second heart sound S2 is the closure of the semilunar valves in the outflow tracts. The two addition extra heart sounds (S3 and S4) are not usually heard (and we will discus these later). Have another listen and see if you can discern the two distict heart sounds. 25 This slide when animated, repeats the normal heart sounds for a few seconds. 26 This slide illustrates what is know as a ‘gallop rhythm’. I this rhythm you can now hear the S3 and S4 heart sounds associated with the valves snapping open. This is indicative of a raised end-diastolic pressure. Have a listen to a gallop rhythm. 27 This slide when animated plays a gallop rhythm 28 Sometimes, of course, the valves do not shut and open properly and this leads to what are called heart murmurs. These are sounds that you can hear in between the standard heart sounds. These murmurs are caused by turbulence in the blood rather than the valves snapping open and shut. This turbulence can be caused by valvular stenosis or valvular regurgitation and they can occur in systole or they can occur in diastole. 29 Here’s an example of a diastolic murmur caused by mitral stenosis. The narrowing of the mitral valve, causes turbulence when the ventricle fills. Have a listen to this – 30 This slide when animated plays the diastolic murmur associated with mitral stenosis. 31 Another common diastolic murmur is caused by incompetence of the aortic valve. So, when the ventricle is relaxing during diasole, blood flow back through the incopetant aortic valve causing diastolic turbulence. Have a listen to this –. 32  This slide when animated plays the diastolic murmur associated with aortic incompetence. 33 Systolic murmurs typically have the opposite underlying pathology. For example, aortic stenosis causes a systolic murmur as blood wooshes through a narrowed aortic valve. Have a listen - 34 This slide when animated plays the systolic murmur associated with aortic stenosis. 35 Another common systolic murmur is caused by mitral incompetence. So, when the left ventricle is contracting during systole, turbulent blood flows back through the mitral valve into the left atrium. Have a listen to this – 36 This slide when animated plays the systolic murmur associated with mitral incompentence. 37 Finally to summarise what I've told you at the end of this lecture, you have been reminded of the basics of ECG recording. You should understand the relationship between the electrical events and the timing of pressure and volume changes within the chambers of the heart. We have described how by measuring pressures and volumes, pressure-volume loops can be derived which gave useful information about cardiac function. We have described the hydrostatic effects on venous and arterial blood pressures, and how the jugular venous pulse can be used to give information about cardiac function and the circulation. Similarly the profile of the peripheral arterial pulse changes depending on where it is measured and, although we did not cover this changes as we age, suffer from arthersclerosis and as our arteries harden. Finally we have described the various types of heart sound and the underlying causes of some of the principle pathologies that can be detected. Thank you for your attention. 38