3 Section 3 Selected Diseases and Disorders of the Cardiovascular System

Welcome to Lesson 7, part 3. I sure hope your day is off to a great start I’ve got an inspirational quote to get us started, as well as a bit of a joke. We’re going to talk about angina pectoris. And you might have heard that angina in Greek means strangle and pectoris of course means chest. So we’re talking about chest pain attacks that occur when there is a temporary deficit of oxygen in the myocardium. Now normally, the heart can adapt its blood supply through vasodilation to meet its needs. So for example, if you go for a run, if you’re exercising, you’re heart of course will beat faster. It will contract more forcefully. You’re in fight or flight mode. Your sympathetic nervous system is speeding up the heart and causing it to contract more strongly so that you can sustain that activity, right? Your skeletal muscles will get all of that additional blood flow to support those movements. Now, this is what’s normally supposed to happen. But what if the vessels aren’t able to do that? What if they can’t vasodilate? And I just wanted to remind you of what typically happens in your heart. You got a beautiful young heart. And we looked at this flowchart earlier. So we know that this red pathway is local autoregulation. So when you’re going for a run, we would term that a physical stressor. And of course, your chemoreceptors are going to start sensing lower oxygen levels and higher CO2 levels in the blood. And you might even see a little bit of acid in the blood as well. Those are all stimulants to increase vasodilation, to bring in more blood flow to that heart, to restore homeostasis and ensure that that heart can keep up that faster pace and allow you to sustain that activity. Now, if that’s not happening, it might be because of, you’re probably going to guess atherosclerotic plaque, a very common cause where the lumen of your blood vessels is narrowed. So there’s low flow to the heart tissue and therefore low oxygen. And that heart muscle doesn’t have the oxygen it needs to generate ATP for contraction. So that could be the problem. The other problem might be is maybe one of those coronary arteries has spasmed and that’s exactly what it sounds like. It’s just clenched down randomly. And of course, if it quenches randomly, there will be less flow temporarily to that tissue, lower oxygen. That again, can mean that that person stops the activity. They’re no longer able to complete it. And they may have chest pain. Now, the heart could be fine and you could actually have an attack of angina pectoris. It might be a blood problem. So we know that anemia is a big term. There’s a lot of different anemias. There’s sickle cell anemia, there’s iron deficiency anemia. We know anemia basically means a reduced oxygen carrying capacity of the blood. So it might mean that the hemoglobin is messed up and not able to carry the same load of oxygen. As is the case with Sickle Cell Anemia, the hemoglobin is mutated and actually the whole cell becomes sickle shaped, which actually also impedes the delivery of oxygen to tissues. So all tissues will be affected, including the heart. So in this case, it would be a low oxygen problem that potentially causes this attack. Now the lungs could be the root of the problem. What if the gas exchange surface area is not sufficiently oxygenating the blood? So again, it’s kind of the same problem. You don’t have sufficient oxygen getting to the heart so that it can sustain this activity. 

Now, the other thing that could happen is myocardial hypertrophy. And we learned earlier that when a person’s heart is under duress in pathologic hypertrophy that that heart tends to grow and it’s the thickness of the wall that actually grows in order to try and contract a little bit harder to keep up with the load that it’s been given. Perhaps it’s in a person who’s got high blood pressure. So this poor heart is working harder and harder and hypertrophies, it’s remodelling to try and compensate. And what can happen is the wall will thicken, which of course will be beneficial in supporting this person staying alive in a condition of hypertension. But it could mean that the blood vessels are not keeping up, right there is not sufficient angiogenesis or growth of new blood vessels. So that means that, of course, the myocardium is not getting sufficient oxygen again. Now, I’ve just talked about hypertension. So you can probably picture that when a heart has to work harder, potentially. It’s going to be in a condition when it’s working so hard that it’s not getting the oxygen, it needs to keep up with the demand that’s been put on it. So when someone has an angina pectoris attack, we would say there’s three different patterns that typically take place. And the first is called classic or exertional angina. This is the most common and this is the one you picture and this is the one I like the name exertional because it makes you picture what’s happening. Grandpa has gone out for a run with his buddies. He’s exerting himself and this is when he starts having the chest pain. So you can picture this scenario that because there’s an increase in demand on the heart is beating faster now and hotter. It’s not able to bring enough oxygenated blood to the heart muscle. The second type is variant angina. So this is the vasospasm that I was talking about. So this could be the scenario where gramps is just sitting on the couch, so is completely at rest and all of a sudden has the chest pain because these blood vessels have clenched down. The third type is called unstable angina, and this is the most dangerous. And it just means that the pain becomes more prolonged. So instead of being temporary, it is turning into perhaps a longer bout, possibly leading into an attack or a myocardial infarction. Heart attack, the most probable causes an embolus. So potentially a thrombi, a clot breaking off an atheroma somewhere else in the body, maybe even in one of the coronary arteries flying off and then lodging into a coronary capillary, depriving that part of the myocardium, of oxygenated blood. I love this diagram from one of the textbooks and it’s probably pretty basic. You can picture this. So normally of course, you have enough oxygenated blood coming to your heart to meet demand. So everything’s happy. And when you as a young healthy person go for a run, your coronary arteries vasodilate, and that increased supply of oxygen is brought to the heart and sustains your activity. No problem. Awesome. Now what if this is Grandpa? and poor old grandpa has got atherosclerotic plaque in his coronary arteries. What we might find happen is that even normal activity potentially, Oh, he’s got some pain here. There’s not sufficient oxygen reaching his myocardium and it’s leading to ischemia. If it’s prolonged, it could lead to infarction and death of some of those myocardial cells. So typically what will happen because Gramps is experiencing, pain is he’ll reduce his activity and then he might feel better. The pain will go away because less oxygenated blood is required by his heart to support that reduced activity. Now of course, unfortunately, atherosclerotic plaques tend to get bigger rather than smaller. So this is usually a deteriorating condition and it may be that even doing less and less activity, He’s still is, he starts experiencing more and more pain. So hopefully you can picture that. So I’ve put this little blurb here. Coronary arteries are supposed to vasodilate with stressors such as exercise. But what if they can’t? That’s basically the scenario we’re looking at most of the time. So you’d get these recurrent, intermittent, brief episodes of substernal chest pain. So perhaps everytime Gramps exerts himself a little bit shoveling snow, or perhaps had some bad news, some emotional stress. If you’ve got any kind of stress, your heart rate will naturally pick up. You’ll be in fight or flight mode. And it might be just for a temporary period of time, but it might give Gramps this attack. The attack as you can imagine, vary in severity and duration depending on the cause. But typically if it’s due to a plaque or damage to blood vessel wall, It’s usually the case the attacks become more frequent and longer. Now, hopefully when this starts happening to Gramps he goes to see a doctor and of course doctor will run through those diagnostic tests that we looked at earlier. And he may well be prescribed coronary vasodilators such as nitroglycerin. And we talked about how this mimics the body’s natural nitric oxide, which is a vasodilator. It’s very potent. There’s many ways you can take it. You can take it in a pill form underneath the tongue and it dissolves very quickly into blood vessels that is very helpful. There’s a patch that you can put on your skin as well as an oral spray. So he might be prescribed that and then recommended to take it the next time he starts experiencing something like this. So you can tell it primarily acts on reduction of the systemic resistance, decreasing the heart’s demand for oxygen. If you’re ever out with Gramps and he has an angina pectoris attack. What Gramps should do is find a park bench and sit and he should stay upright if possible. And hopefully he’s brought his nitroglycerin and takes it, whether it’s the pill or the spray or what have you. And you should be checking Gramps’ pulse and breathing. If Gramps’ attack continues, if it’s longer than five minutes or obviously you’re going to follow the doctor’s directions depending on which form of nitroglycerin has been given. But generally, the doctor’s going to say that Gramps should take a second dose if it’s longer than a certain amount of time such as five minutes. So of course, your timing this event and making sure that occurs. And then and the doctor will say potentially after three doses and the pain has lasted. You can see this is long now, ten minutes, you should be calling 9, 11 and getting Gramps to the emergency. Now of course, if Gramps has never had an attack before, then he wouldn’t have gone to the doctor. So he’s not going to be carrying around nitroglycerin.

So obviously if this happens and you suspect that it’s either angina pectoris or myocardial infarction. You have to call the emergency right away because you don’t know you don’t know if it’s angina or if you don’t know it’s something worse which is myocardial infarction, a prolonged period of deprivation of oxygen to the heart. So if grandpa has been diagnosed with angina pectoris, The doctor’s going to say avoid stressors, anything that will get your heart rate up where it will need more oxygen to sustain its activity. Because of course, the more times you put your heart in this condition there is the more potential for heart cells to die if they do become deprived of oxygen for more than three to five minutes. So you don’t want different heart cells die and they don’t replace themselves. So you’re going to avoid stressors. Remember cold weather and hot weather extremes speed up your heart rate. Pollution, eating large meals. So they’ll say eat more frequent smaller meals is easier on the body and of course, carry your nitroglycerin. How would you know if he’s having angina pain? Most often for a (XY) man, it will be an intermittent temporary crushing pain in the chest. Men describe it as being kicked in the chest by a horse, that type of feeling or being sat on by an elephant. And then sometimes there’s that radiating pain down the left arm. Now, our next slide, I thought this was a great figure from one of the textbooks. And of course it shows you this coronary artery disease that can happen, but of course it can happen in different areas of the body, not just the heart, but blood vessels can start becoming occluded with a atheroma in places like the brain. And then we saw that remember the great arteries, the aorta and the iliac arteries are also susceptible to atherosclerotic plaque. So we’ve just gone through this. If there’s a partial occlusion, it can lead to these angina pectoris attacks. You can imagine that if we deteriorate and we fully occlude, that it can lead to myocardial infarction. If this were to occur in the brain, then a partial occlusion can give rise to a mini stroke. You might have heard of a transient ischemic attack or TIA. If it becomes fully occluded, then it can lead to a cerebrovascular accident or a stroke, an ischemic stroke if it happens in the peripheral arteries, so say the aorta, then what we can see, the damage to the blood vessel wall can lead to an aneurism where the blood vessel wall, remember when it becomes damaged it can start bulging and that becomes an aneurism in and a bulgy thinned out wall that’s not elastic and it’s got lots of mess of calcium in. It is quite brittle rarely, and it is susceptible to rupture. And of course, if it’s your aorta, this is fatal a lot of the time. You can imagine how quickly you would bleed out internally if there was a rupture in your aorta. Remember that your whole blood volume is about five liters and your heart pumps out about five liters per minute. And then if this occurs in the iliac arteries, we would, we’re elsewhere in the peripheral system. We would call a peripheral vascular disease. And if it becomes fully occluded, then it can mean that the feet and even the legs, all of a sudden become quite ischemic. Tissue can start dying and it can be susceptible to infection such as gangrene. So it may be that amputation is required to prevent that from happening. So here’s that situation of peripheral vascular disease. It’s most often in the legs that this occurs. And then of course, you would expect that there would be fatigue and weakness in those muscles. They’re deprived of oxygen and it would cause pain. So of course, this pain would usually be associated anytime that muscle needs more oxygen. So during exercise, that’s when you might feel more pain due to muscle ischemia. And of course, nerves that are in the leg are also really reliant on a constant supply of oxygen. So if there’s not sufficient oxygen, you can get tingling, numbness, you can lose sensation, it can be burning. And then of course, if you were to take a pulse, it would be quite weak. And you might even see changes in appearance in the feet and legs. So cyanosis, paleness of the skin, dry and then because that tissue is not maintained itself very well, the skin might be dry, there’ll be less hair follicles and toenails can become thick and hard and even form ridges in them. So telltale signs of ischemia and then of course, any wounds would be slow to heal. So treatment, of course, avoiding it in the first place is the best thing to do is to try and avoid as much atherosclerotic plaque building up as possible through the lifetime, and that’s largely through diet and exercise. One of the things you can do if you have diabetes is to make sure that it’s well controlled, that you’re following the medications that you’re supposed to because high blood glucose levels damages blood vessel walls, which sets the stage for atherosclerotic plaque development, of course, being overweight or obese and having high levels of lipid in your blood also lend themselves to atherosclerotic plaques. So diet is, a healthy diet is recommended if a person is at risk for thrombosis or thromboembolism then anticoagulants and platelet inhibitors might be prescribed. Remember, smoking is a risk factor for atherosclerotic plaques. So stop smoking, then maintaining dependent positions for the leg. So below the heart, it will obviously improve arterial perfusion in the legs. You might be prescribed vasodilators. And then of course you’re going to be watching and taking care of your legs and feet to ensure that you don’t get any infections. Now in the heart, we talked about bypass grafts. This can also be done in other areas of the body as can angioplasty and endarterectomy as well. Okay, let’s move on to myocardial infarction. So you’ve got the idea in this instance, the coronary artery is totally obstructed. This most often occurs with atherosclerotic plaque.

Although at times, if there is a drug overdose, it can lead to a heart attack actually. And we’ve looked at this scenario where the plaque itself could be the common cause or a thrombi flying off of the plaque can cause myocardial infarction as well. That vasospasm we already talked about. Now we’re not really sure why a blood vessel just randomly clenches down like that. It’s thought that the endothelial cells of the blood vessel wall, potentially are dysfunctional, either the endothelial cells release and produce less nitric oxide upon stimulation by rest and digest. So maybe they just aren’t able to produce nitric oxide anymore. And therefore that’s why they don’t vasodilate or maybe they’ve lost sensitivity to nitric oxide. So there’s still producing nitric oxide, but maybe they don’t have the receptors for it or they’re less sensitive, so they don’t vasodilate. And so instead of vasodilating there way too constricted. Now of course, the seriousness of an MI depends on the size, location, and depth of the infarction. So when we’re saying depth, that means whereabouts in the wall of the heart. And it’s characterized by feelings of heaviness, pressure, burning in the chest. You might have heard of, especially (XX) women feeling nausea and indigestion. In fact, (XX) women are at risk for not knowing that they’re actually having a heart attack. Sometimes they just think, oh, they ate something bad. And that can be a real problem because then of course they don’t go and seek help. Now with less oxygen getting to the brain as a result of the heart functioning as well. Then of course, the brain will feel anxious, fearful, and we talked about this substernal crushing pain, radiating pain down the left arm. And you can see the markings where you can get pain. Shoulder, jaw, neck. And unlike angina, pain is not relieved by rest and nitroglycerin. So this might be what happens to Gramps the third or fourth time he has an angina pectoris attack. So he takes his nitroglycerin and there’s no effect of it. So you’re rushing him to the hospital. An ECG can be really informative. And we know that we were supposed to see a beautiful PQRS and T waves. And you can see that already even within minutes, that our P wave is messed up and so is the QRS wave. So these are signs of ischemia. Please don’t memorize these ECGs. I just wanted to give you a sense as to how well these tools can be used to document what’s happening. So you see this elevated ST portion of the graph. The next stages occur within hours to days and check out our really bad QRS wave. Now, our T wave is inverted. The P wave is minimal. Okay, So this is signs that necrosis does occurred. And hopefully this person recovers and regains the nice P wave, QRS wave and T wave. But you can see that because some cells have died, that our QRS is much lower than it or much shallower than it usually is. Other tests that can be done are blood draws where you look at enzymes released from the necrotic cells. And this can be really informative. I can tell you the extent of the damage, how many heart muscle cells have died, right? Remember those heart muscle cells that have died, they rupture and they release things like this one is creatine phosphokinase. You know this one, creatine phosphokinase is of course supposed to be in the cell. And it converts creatine to creatine phosphate. Now, this one here, lactate dehydrogenase, again is supposed to be in the heart, not in the blood. So when you see it rising in the blood, you know that cells have died. And the more that have entered the blood, the more damage has been done. AST is a liver enzyme that tends to go up when cells are damaged. The other thing that you’ll see is remember there’s a lot of potassium inside cells, so cells are rupturing. Potassium will enter the blood. And that will tell you again the extent of damage. And the problem with this too, if there’s a lot of potassium into the blood that it can lead to the heart starting to undergo dysrhythmias, which then can of course reduce cardiac output, which can be problematic. If cardiac output gets too low, the organs won’t receive oxygenated blood sufficiently and potentially start failing. The other things that are not shown in this graph are myosin. So you know that that’s a heart muscle protein and cardiac troponin. So again, they’re not supposed to be in the blood, but if cells have ruptured, then you’re going to start seeing them. And of course, signs of damage are going to attract white blood cells. So you’re going to see white blood cells ramp up their proliferation. You’ll also see C reactive protein, a marker of inflammation. And again, the more CRP you see, the more damage is implied. Remember ESR stands for Eythrocyte Sedimentation Rate. And remember the faster the Eryhtrocyte Sedimentation Rate, the more inflammation and damage there is in the body. Of course, you’d be interested to see how well oxygenated the blood still is and how much is getting its way to all of your tissues. And remember, you could also do that capillary wedge pressure to see how well the left ventricle is generating pressure. So how well is the left ventricle functioning? contracting? So unfortunately, one in four people die, usually due to cardiac arrhythmias, hypoxia, acidosis that occurs at the time. And if a person is entering cardiogenic shock. So remember shock is defined as basically insufficient cardiac output to support life. So this is a heart problem. It’s failure of the ventricles to contract and deliver sufficient cardiac output. So you might see in this condition that a person has a weak pulse. It might be quite rapid because of course, the medulla, oblongata is going to try and speed up the heart rate to compensate for this low stroke volume. And of course, if the stroke volume and cardiac output isn’t sufficient to support life, it can lead to death. What can happen if the person does survive… If there is damage, of course, and they’re likely is, that this person could end up in either an acute or chronic state of congestive heart failure. And this is just defined as when a heart is no longer able to contract as well as as yours does. So it’s less than a 100 percent. And so it could be fatal obviously, or it could just lead to a chronic deteriorating condition over many years due to the loss of functional myocardial cells. The next thing that’s potentially going to happen as a complication is rupture of the necrotic heart tissue. Of course, this would be devastating. The person survives the initial heart attack. And then three to seven days later when the necrotic tissue is breaking down, all of a sudden the whole wall ruptures and likely that person would die.

The other complication is cardiac tamponade. So we talked about, of course, anytime there’s damage anywhere near the heart, you would expect inflammation and therefore exudate potentially filling up the pericardial sac that will then press on the heart and not allow it to fill properly. If it doesn’t fill properly, then it doesn’t eject a full load. So cardiac output would be down. So again, you’re going to be wanting to monitor for that because this could be fatal as well. And of course, if this is the case, then you’re going to want to puncture this pericardial sac and then aspirate out the fluid to relieve the pressure. Another shoddy thing that could happen. Again, the person survives the initial heart attack, but then succumbs potentially three to seven or even more days later is due to an emboli forming. So of course, anywhere there’s damage. So say there’s damage in this wall here. Then of course platelets are going to come in, right, patch it up, and the platelets of course, they can be a little bit loose, right? And this is a moving organ. So you could get bits of that thrombus flying off. And when they fly off, it just depends, you know, which ventricle they formed in. So let’s say this person has had a left ventricular myocardial infarction. So just like this picture here, and that thrombus is formed in this wall. And then of course eventually it just flies off and it goes out the aorta. And if it goes up to the brain, then it could end up giving this person a stroke. Great. This person survives a heart attack and then maybe 10 days later dies of a stroke. If that thrombus is in the right ventricle. So say the myocardial infarction was in the right side of the heart and if it dislodged and got loose, then you think, okay, well, the right ventricle pumps blood through the pulmonary trunk so that embolus is going to end up in the pulmonary circuit. And it would form a pulmonary embolus, which again could be fatal. The other thing we kind of mentioned up here is the situation of acidosis. And acidosis can occur due to hypoxia of your tissues right. So if your tissues are not getting the oxygen they need because this person’s heart is not functioning during this myocardial infarction. The organs start, of course, reverting to anaerobic cellular respiration and they start producing a lot of lactic acid. And if the pH of the blood goes below 7.35, then tissues including the heart, have a hard time functioning properly. Right. So these are all things that the paramedics, as well as the ER physicians are going to be watching for and trying to provide intervention for. Now, if I were to ask you, you’ve called 911, the paramedics come get Gramps. What are they going to do? Obviously, we know that providing oxygen to all the tissues is a priority. See, you might see supplemental oxygen being delivered. If Gramps feels like an elephant is sitting on him, It’s a lot of pain. So you’re going to want to prescribe or give Gramps, analgesics. And that does two things. Not only does it alleviate the pain, but it also will reduce his stress, right? If he’s not in as much pain, then he won’t be as stressed out. And if you’re not as stressed out than your sympathetic nervous system, it can chill out a little bit. And it can slow down those impulses to try and speed up your heart and try and force your heart to contract harder. Which of course, your heart is having a hard time doing it at this point in time. So that can be beneficial in two ways. And then also if they think that this myocardial infarction was a result of or it could lead to a thrombus forming that might then end up causing an emboli. They might prescribe anticoagulants, but thrombolytics might be used especially if they think an embolus caused this myocardial infarction. And then of course, you’re going to want to treat any kind of dysrhythmias that are noticed or hypertension, and then the congestive heart failure. So we’ve talked about different medications that can lighten up workload on the heart in terms of reducing blood pressure if it’s too high, getting the heart to beat at a more normal pace. So with digoxin, that can be helpful. We talked about all of those things, alpha blockers, beta blockers, calcium channel blockers, these all might be useful tools. And then hopefully Gramps survives in the physician investigates what the initial cause is. And if they find atherosclerotic plaque, then they’re potentially going to plan some sort of intervention, whether it’s bypass surgery or angioplasty. And of course, there’s other things that can be done as well involving lasers to remove plaques. So it just depends where it is. I’ve got a picture on the next slide, tickles through some of those things. And then of course, they’re going to recommend that Gramps improves lifestyle. So making sure there’s regular exercise, healthy diet, and reducing stress. Here’s some of the tools and I’m going to post an animations or video, several videos that I’ve already made. And I’ll put them into our module for you to take a look. It’s… they’re very good, and it shows you each one of these strategies that can be used. So remember we talked about the catheter that can be inserted into a coronary artery. So you can do deliver thrombolytics this way. You can use the catheter to insert a balloon and basically inflate it to push that lumen down and flatten it out. Flatten out that atherosclerotic plaque and sometimes that sufficient, you can just withdraw the balloon and that plaque stays flat. Although if the physician thinks the plaques not going to stay flat, they mean we’ll insert a stent. With this balloon. And if you watch the video, you’ll see how that’s done. It’s really cool. And then of course there’s CABG, Coronary Artery Bypass Grafting that can occur. If someone of course has an MI, then you hopefully know how to use how to do CPR. And of course, some places such as gyms and fitness centers have defibrillators that can be useful as well. They’re really easy to use. I’m sure you’ve seen one. You just follow the directions. Let’s talk about congestive heart failure now, we’ve mentioned it as a possible complication of myocardial infarction. Basically congestive heart failure, is the situation when the heart is unable to pump out sufficient blood to meet metabolic demands of the body. It can be acute, but usually it’s chronic. So you could say that usually it’s because the heart is weaker and therefore its contractility is less than normal and therefore its stroke volume and hence cardiac output is less than normal. So typically, this is a complication of another cardiopulmonary condition, such as that MI situation we just looked at, or potentially a valve in the heart is defective. That’s led to reduced stroke volume and cardiac output. Or there’s an increased demand on the heart from hypertension or lung disease, such as in cor pulmonale, which we looked at a little bit earlier.

Now we’re going to talk about left-sided congestive heart failure as well as right-sided congestive heart failure. And most often, hypertension leads to left sided. And we’ll see that lung disease most often leads to cor pulmonale, and then right-sided congestive heart failure. Now what we’re going to see happen is that person maybe able to get by with daily activities, no problem. But is now exercise intolerant. So it be hard for them to run up 10 flights of stairs, for example. Now, as their heart is weaker than say yours is, you’re going to expect that the brain is going to induce some compensation mechanisms to ensure that cardiac output is sufficient to support life, to make sure all of the organs are getting all of the blood flow that they need. And I’ll take you through these compensation mechanisms. And of course, it’s good because it keeps you alive. But we’re going to see that these compensations actually start aggravating the condition in that they make more workload for the heart and contribute to it deteriorating over time. So let’s look at this flow chart. I know it looks super intense, but we’ll walk our way through it and I think you’ll find it makes sense. So this is how the scenario could play out. We could start with some sort of damage to the heart that’s left it weaker. So it might be a myocardial infarction. It might be a bad infection. In this example, it’s a myocardial infarction of the left ventricle. So we’ve lost some heart muscle. Some of that heart muscle has died, which means that that left ventricle, it doesn’t contract as well as it used to. So stroke volume is down, cardiac output is down. And so of course the brain senses this, right? The brain senses, ewwwww low blood pressure, low oxygen coming to the brain. And we’re basically looking at this portion of our flowchart where our cardiovascular centers are receiving this blood pressure and blood chemistry information. And as a result, are going to stimulate the sympathetic nervous system, right? Let’s increase our heart rate. Let’s increase force of contraction and let’s induce vasoconstriction. This will all help to drive blood flow to ensure that the organs stay oxygenated. So of course it helps you stay alive, but you can tell that by causing systemic vasoconstriction, you are increasing afterload. So you are making a harder workload for your poor old heart. And when you speed up the heart rate and you increase its force of contraction, again, you are also increasing workload for this poor heart. Now of course, if the heartbeats really, really fast in tachyardia, we know that that would be even a worse problem if this were to play out because there’s less filling time. Most often we’re not in a state of tachycardia, but of course that could be possible. Now, this is a long-term condition obviously. So you’re going to find the endocrine mechanism also swings into action as a compensation strategy, right? The kidney senses, they sense ooooo low oxygen and low blood flow. So in response, they’re going to start producing renin. And we know renin is an enzyme that catalyzes the reaction from angiotensinogen to angiotensin 1. We know ACE then converts angiotensin 1 to angiotensin 2. Angiotensin 2 causes more vasoconstriction. So you can see we’re backing up our neural input. And we know that systemic vasoconstriction increases workload for the heart. It increases afterload. The heart has to contract harder to push against that vasoconstricted vasculature. And not only that, but angiotensin 2 also stimulates aldosterone production as well as ADH production. And we know those two work together to increase water and salt retention, which increases blood volume. So it’s helpful in that we’ve got more blood volume. We can hopefully keep our tissues well oxygenated by pushing all this blood through the circuit. But of course, this extra blood volume or increase in blood volume increases preload, which of course means the heart has to contract harder to get that increased load out every time. So again, you can tell that we’re upping the workload for our poor old heart. And as a result, we start seeing pathologic hypertrophy. This heart starts growing in size in a spherical matter. And this is called cardiomegaly. And we know that the heart is going to become less and less and less efficient and we’re deteriorating. And we talked about with an increase in the muscle wall that we actually need a greater blood supply and sometimes that doesn’t keep pace. So it might mean that that heart muscle actually becomes more and more deprived of oxygen which can contribute to it failing. Now just a side note. What do you think the two most common causes of pathologic hypertrophy are in Canada. Hopefully you’re thinking coronary artery disease as well as hypertension. Okay? Now, you can tell that we’re in a downward spiral here. So over time, this heart is growing in size. This poor old left ventricle is going to get weaker and weaker as it is trying to contract faster and harder and faster and harder. And eventually, we’re going to see that the left ventricle weakens so much that it can no longer keep up. It doesn’t fully empty. That means our stroke volume and hence our cardiac output is even lower. And if the amount leaving the heart is low, then you can tell that the blood backs up into the pulmonary circuit. Remember the pulmonary vessels feed oxygenated blood into the left side of the heart right. So here’s the pulmonary circuit. And if the blood can’t leave the left ventricle because the left ventricle is weak, then we can’t fill that left ventricle. So these pulmonary vessels become engorged with blood, you get pulmonary congestion. And as a result, we get pulmonary hypertension, right? A lot of pressure and volume start building up in the pulmonary circuit. And remember that they get very leaky and we’re going to start seeing edema within the lungs. So this person is going to have shortness of breath all of a sudden. Now, of course this is a closed circuit. Your blood circuit is closed, right? So you can imagine that if the pulmonary circuit is engorged, then it’s going to start becoming really hard for the right ventricle to push blood into the pulmonary circuit. So you’re going to see the right ventricle start weakening, right? And eventually it will hypertrophy as well, get more and more weak and it won’t completely empty. So that means you’re going to see blood backing up into the systemic circuit and those vessels become engorged. And when they get engorged, of course, it becomes hypertensive and those blood vessels start leaking and you start seeing edema in the feet and in the legs and in the abdominal pelvic cavity. And we’re going to see that it can impair, Of course, those digestive organs in their function. So you’re going to see that even though in this scenario, we’ve started out with left-sided congestive heart failure. It does progress to right-sided congestive heart failure. So I know we’ve just actually ignored all this bit on the side and I’m hoping you can see what a doctor can do. So the different treatments that are used to try to break the cycle are things like the alpha blockers. Let’s cause some vasodilation. Let’s ease up on this intense afterload. Let’s make things easier for this poor heart. So these are the strategies that will be used. We’ll use alpha blockers, we’ll use vasodilators. Maybe we’ll use calcium blockers to again cause some vasodilation. Also potentially slow down heart rate, as do the beta blockers. We know digoxin is helpful in, again, easing up workflow for the heart, but of course, maintaining sufficient contractions. We know that ACE inhibitors can be good as well as diuretics. Yeah, so these of course are strategies that hopefully you can see help ease up this workload for the heart and just slow down the progression of this congestive heart failure. Okay, I love this figure. It’s such a great review of what we’ve just covered. So why don’t we go through it again because repetition is always good. So left-sided, congestive heart failure. Remember that basically anything that affects the left side of the heart, maybe it’s a myocardial infarction that’s caused damage.

There’s something that’s weakened our left ventricle, that’s step number 1. And as a result, it can’t generate the stroke volume that it used to. Hence the wiggly lines. So less stroke volume, therefore less cardiac output. And of course, if less cardiac output is getting to the brain as well as all of the tissues, including the kidney, then those compensation mechanisms start happening. Remember the medulla oblongata induces SNS which causes vasoconstriction. That’s a problem for our heart because it increases afterload, creates more workload for our heart. SNS also speeds up heart rate and force of contraction, again, making things harder on the heart. Now, when the kidneys sense less blood flow, what they do in response to secrete renin. We know renin activates angiotensinogen into angiotensin 1. Angiotensin 1 is then converted to angiotensin 2 with the ACE enzyme. And we know that that increase in angiotensin 2 does exactly what it sounds like. It increases vasoconstriction. So it backs up what our neural compensation mechanisms started. And we know that that’s a problem in that it’s making more workload for the heart. It’s beneficial in that it’s ensuring that there’s blood flow to all of our tissues. But over the long haul we’re going to see deterioration of our left ventricle as it starts pathologically hypertrophying and becoming more week. We know that angiotensin 2 stimulates the secretion of aldosterone from the adrenal gland, as well as secretion of ADH from the pituitary gland. And both of those work together to increase sodium and water retention in the bloodstream. So the kidney is not peeing out that material anymore. Hence, blood volume goes up, which increases blood pressure, which of course is going to increase the afterload and make more work for the heart. So over time, as I’ve said, the heart can’t keep up, it’s going to become more and more weak. And as a result of not sufficiently emptying, then of course, the blood coming back from the lungs can’t fill the left ventricle as normal. We get this backup of blood into the pulmonary circuit. And it’s not that blood goes backwards, it just means that it can’t actually make its way to the left side of the heart. So these pulmonary capillaries become engorged. We have pulmonary congestion and they become leaky. Hence we get leaking of exudate into the alveoli, which of course is going to make for dyspnea. Now as a result of low cardiac output, our tissues are experiencing less oxygen and nutrients than they would like. So there’s cell function is going down. The brain, of course will show signs of fatigue. And with hypoxia, remember tissues revert to anaerobic cellular respiration produce a lot of lactic acid and that might start building up in our blood. And remember the medulla oblongata is always sensing oxygen levels in the blood as well as acidic levels of the blood. And if oxygen is low and acid is high, that will stimulate increased respiration rate. Again, in a compensation mechanism to try and get as much oxygen to the tissues as possible. And these compensation strategies, like I say, work in that they’re keeping your organs alive. But over time we’re going to see deterioration of the heart. Okay, So we saw these problems here. Backup into the left atrium, then into the pulmonary circuit leading to pulmonary edema. We’ve seen this chest X-ray before with all this white mess in our lungs. So lots of fluid in the alveoli. If we turn to this figure, it’s going to go through right-sided congestive heart failure. So again, a nice review. And in this case, something is impeding the right side of the heart. Maybe it’s a myocardial infarction that’s affected the right ventricle muscle this time and therefore, this right ventricle muscle is weaker and it can’t sufficiently empty. And remember it pushes blood through the pulmonary trunk into the pulmonary circuit. So you can see that wiggly line is trying to indicate less blood is being sent to the pulmonary capillaries, and therefore less blood will make its way back to the left side of the heart. So we’re going to see less blood of course, delivered as stroke volume and cardiac output.

Okay, so of course your organs start sensing that including the kidney. And remember too that if the right ventricle is not sufficiently emptying, it’s gonna be hard to start filling it, right? So we’re going to see backup of blood into the systemic circuit. So through the superior vena cava and the inferior vena cava, these vessels will become engorged. And when they become engorged, they develop higher pressure. And as a result of higher pressure, they start leaking. And we can get leaking of exudate in the brain leading to cerebral edema. This is quite dangerous. It can lead to intercranial pressure increasing. And an increase of volume in the brain means that it’s harder to push blood actually into the capillaries of the brain. Those vessels become pinched off and the neurons then become deprived of blood and oxygen and nutrients. And we know that survive for very long. So this is a dangerous situation if it continues. And then in the legs and feet, we know that we’re going to get potentially swelling as well ascites. So of course the medulla oblongata is sensing the same thing. Poor stroke volume, so low blood flow, low blood pressure, low oxygen, potentially metabolic acidosis again. So it’s good to induce SNS as compensation strategies and the kidneys, of course are going to secrete renin. So the same compensation strategies occur and we know that they’re going to increase workload for our heart. And over time, this heart hypertrophies on the right side, making this muscle more spherical, less efficient, and deteriorating over time. Unfortunately. Now, we talked about this occurring based on damage to the right ventricle, say in an MI. But also, we can see that actually a lung disease can set the place for right-sided congestive heart failure. So with that scenario of cor pulmonale and pulmonale refers to lung, cor refers to heart in Latin. And so in this instance, if you can picture what’s happened is, there’s been some…. the heart is fine, but the lung has got problems. Usually it’s a result of smoking. So this person say has emphysema. And as a result of emphysema, we know that there’s damage to the alveoli and there possibly is tar and whatnot coating the alveoli. We’ve lost gas surface exchange area. And remember that with any kind of lung damage, with loss of gas surface exchange area due to smoking or due to repeat infections. You’re going to damage the capillaries that surround all those beautiful alveolar sacs. Remember the capillaries are really close, so there’ll be typically damaged as well. And when lung capillaries are damaged or well when any capillary is damaged, remember that there’s scarring and shrinkage, right? So the capillaries and vessels become more narrow. And when they become narrow, that increases, of course, pulmonary resistance and it increases pressure. So we become hypertensive in the pulmonary circuit. So then of course, it’s really hard for our poor little right ventricle to try and fill these vessels when they’re under hypertension. So the right ventricle will pathologically hypertrophy as it tries to push blood into those clenched up spaces. And eventually we’re going to see it start failing. Okay, So that could be the scenario. I love this picture as well.

Unfortunately, these are real, so these individuals obviously passed away and they’ve got their hearts cut in front of us here. But it shows you how thick the left ventricle can get. during left-sided congestive heart failure. You can see the cause of left-sided congestive heart failure in this instance, it wasn’t MI on the left side. It was due to hypertension. This person had hypertension. And so you can picture stay the aorta being very clenched. And then that left ventricle working so hard, hard, hard, hard to try and push blood through that clenched up aorta and systemic arteries. And over time failing. And notice too that this person, how does a pacemaker put in? So obviously there had been some problems before they passed away. On this side, wow, look at how big our right ventricle is. So here’s our left ventricle here. It’s wall is still thicker. And remember, normally the left wall is thicker as it generates six to eight times more pressure to drive blood through the systemic circuit. And this wall, it’s still got a bit of actually hypertrophy showing signs of right congestive heart failure. And you can tell that the cause was cor pulmonale. So okay. So let’s go through signs and symptoms and I know we’ve talked about these already, but I wanted to throw up some more pictures because it always helps to remember these things when you’ve got pictures in your mind. So remember with left-sided congestive heart failure, the pulmonary capillaries are engorged, they’re congested, they’ve become hypertensive and they start leaking, exudate it into the alveoli, making for shortness of breath. And remember orthopnea is difficulty breathing when you’re lying down. So probably when you’re sleeping because the fluid accumulates in the lungs. So you sit up and hopefully drain the fluid if you’re in the hospital and maybe you’ve got one of those really cool beds that tilts so you can sleep in more of an upright position to prevent this from happening. And of course, unfortunately, and the other problem with fluid in the lungs is it’s a warm, wet, moist environment which bacteria love. And of course you’ve got bacteria in your mouth and all over your skin so they can become opportunistic and descend, give you bacterial pneumonia, which of course would cause even more damage potentially to the alveoli. Of course, with that fluid there, it’s going to be irritating and it’s going to cause that cough reflex where you try and clear that fluid. So that might be a sign. And then this very serious instance of orthopnea. So paroxysmal nocturnal dyspnea refers to an acute episode where it’s extremely hard to actually catch your breath once you sit up from bed. So most often if this has happened, you’ve probably been given one of those tanks of supplemental oxygen and you’ve got those nasal cannula which are going to help deliver that supplemental oxygen for you, it might be that the capillaries are so damaged that you end up getting a little bit of blood in that exudate and you might see it come up if your coughing up material so hemoptysis. And then so treatment and I’ve mentioned in the supplemental oxygen of course is crucial. Your first step, you always want to make sure that person has oxygen. And then you want to get rid of some of that blood volume to reduce pulmonary hypertension. So diuretics reduce hypertension with some of that other antihypertensive medication that we’ve already looked at. So we’ve got we’ve run through a list of those already. And then bronchodilators are sometimes helpful too. If we carry on and we think, okay, well, what were the signs and symptoms of right-sided again? And we’ll remember, oh, swelling in the feet and legs and bum, oh great. And the veins, so the inferior and the superior veins become congested. So of course, jugular veins may look distended. That means they just look swollen and they protrude from the neck. And then in the abdominal pelvic cavity you’ve got of course, your liver and your spleen, which are very well vascularized and those blood vessels when they become engorged, can again start leaking. And the liver and spleen don’t like that. We’re going to see this is abnormal growth of the liver and spleen. There’s a lot of blood vessels making their way from the intestine directly through to the liver, through the portal circulation. And if there’s back-up problems in the liver, then it could lead to digestive disturbances. We mentioned ascites, a complication that occurs when fluid accumulates in the peritoneal cavity. I love this picture because it goes through all of the signs and symptoms we’ve mentioned for right-sided failure in this case, they’ve noted that the problem was cor pulmonale. So we see weight gain with ascites, not feeling like eating and complaints of GI distress due to these engorged blood vessels in the liver, spleen, and intestinal tract, distended jugular veins, the brain of course, feeling hypoxic and perhaps some pressure in there leading to fatigue, probably a headache.

Okay. If it’s acute than you would see probably a flushed face, the headache that I mentioned. And then when the neurons are disturbed in the brain, of course you have a lot of visual neurons. That might well mean that you have vision issues. I love the summary table and I think you can go through it now we’ve covered almost everything. What I’ll mention is maybe the first bit here where we talked about causes of left sided and causes of right-sided congestive heart failure. And we’ve gone through some of them. So we said, okay, could be an infarction on the left ventricle. Now it also could be aortic valve stenosis, narrowing of the aortic valve. Now if you think about it, if that valve is narrowed, it’s going to be really hard for the left ventricle to push blood through that aortic valve. So again, it would be a strain on the left ventricle and it would hypertrophy pathologically and then start deteriorating hypertension. We talked about this when you’ve got systemic arteries clench down, it makes it for hard work on the left ventricle. So setting the stage for left-sided congestive heart failure, hypothyroidism, thyroid hormone, remember it speeds up the heart and it increases force of contraction. So if you have high levels of thyroid hormone for a long period of time, then that is increasing workload on your heart and it can lead to deterioration. Hopefully a physician has noticed that you’ve got this problem though, and there are medications to, to combat this actually. And surgery strategies as well. On the right side, we talked about the problem might be coming from an infarction. You can guess too that pulmonary valve stenosis. may set the stage for a right-sided congestive heart failure. If that valve is very narrow, it’s going to make it real hard work on our right ventricle to push blood through it. And then we talked about cor pulmonale. And of course, signs of hypoxia will occur in both conditions as a result of decreased cardiac output. All right, so we’ve talked about pulmonary congestion on the left side and systemic congestion on the right side. And then all of these signs and symptoms as a result of feeling hypoxic, not getting enough oxygen. And then the reflexes that occur, the compensations that occur that your brain induces in order for you to still get enough oxygen and nutrients to your organs to keep them functioning. Couple of things we might not have mentioned is polycythemia. Remember the kidneys when they sense low blood flow, they’ll secrete erythropoietin EPO. EPO remember, stimulates an increase in red blood cell production, which helps in that it can then carry more oxygen through your blood. So that would occur. Oliguria means decreased output to the kidneys. Then of course there they’ve got less blood to filter. They’re going to produce less urine. I think we’ve talked about all these other signs and symptoms. So that’s great. I’ve got a question for you and I’ve actually already put the answer up, which is a shame, but hopefully you can picture this and perhaps answer on your own. So the question is this a patient’s test, we’ll show atrial natriuretic peptide levels increasing as this disease progresses in both conditions. And the question is, why, why does that happen? Why is there an increase in atrial natriuretic peptide? So first you gotta remember this is the horrible that works in opposition to aldosterone and ADH. And so you can imagine that as this disease increases with blood volume and blood pressure, accumulating that the right atrium will start sensing whoa, high pressure and high volume in the right atrium. And of course that’s not leaving the right ventricle very well, probably. So that pressure and the volume in the right atrium will trigger an increase in secretion of ANP. I’ve got a scenario for you. I don’t know if you’ve ever watch Grey’s Anatomy? I do from time to time. Just because

I love watching the medical part of it. This is an old one and this is when Christina is showing this old surgeon, she’s trying to teach an old dog new tricks. Basically, she doesn’t want him to be forced into retirement. And so they’re showcasing this Batista stitch. That apparently is cutting edge, which is great. And this is our patient. And what they’re doing is ventricular reduction surgery. And so you might be thinking, Well that’s weird. Why would you want to reduce the ventricular wall in the heart? Surely that would make the heart even weaker. And when they do that, they do that in the condition, in this condition of congestive heart failure when there’s been pathologic hypertrophy. And the heart muscle is outgrown its own blood supply. If they cut a little bit of a flap off of the ventricular wall that’s hypertrophied. It can actually make the heart more effective and more efficient. It goes back to that more beautiful cylinder type structure rather than that abnormal spherical structure. So if I were to tell you, well, maybe you can guess what side congestive heart failure this guy has – was it left sided or right sided? So the clue is while he’s in hospital, his family brings him baked tater tots and I want you to see how greasy and deep fried these tater tots look, these are his favourite food and presumably he’s been eating a lot of them lately. So if you’re thinking about it, hopefully you’re thinking, I wonder if that’s led to a lot of atherosclerotic plaque, maybe that’s made him then hypertensive. I betcha this guy has suffered from left-sided congestive heart failure. If you’re thinking that you were right. So let’s move to the next slide on kids. And you are thinking whoa! This is weird. How do children develop congestive heart failure? Surely they haven’t had a lifetime of eating tater tots, and surely they don’t have emphysema. They haven’t been smoking a pack a day leading to cor pulmonale. So how does this happen? So most often, it’s secondary to a congenital heart defect. So poor little baby is born, and at times of course, organs are misformed as baby is developing in mom’s uterus. And there’s a lot of different causes to congenital heart defects, which we’ll talk about later in the next section. And if the heart is defective, then of course you could imagine, okay, then stroke volume is probably down and that means cardiac output is down. And then you’d be thinking, hey, that’s actually the definition of congestive heart failure. And so the baby is going to experience the same thing. Whoa, their stroke volume is down. That means they’re not delivering sufficient oxygenated blood to baby’s tissues. So it’s likely that baby’s not going to be meeting milestones in terms of growth, growth is going to be slower. We’re going to see difficulties in gaining weight. And the reason, of course, is, is if you don’t have oxygen and a lot of ATP, then you can’t do a lot of mitosis, right? And also digestion takes energy to digest food and break it down and then absorb it. That all takes energy. Now in terms of feeding difficulties if baby is nursing. And baby’s got some pulmonary edema is really hard actually to try and breathe and nurse at the same time. So mom might notice that baby is having a hard time nursing. And same if baby is a little bit older and actually, you know, eating on their own. And then too, if you’re thinking, Oh baby might, or the little guy might have pulmonary edema, then they might have orthopnea. So every time they lay baby down, fluid pools and baby’s lungs and then they wake up because they can’t breathe really well. If they’re having that fluid pooling in their lungs, you might see this little baby or toddler. Presumably they’re strong enough at least six months, they’re strong enough to lift their neck can sit. They might adopt this tripod position where they’re basically leaning forward a little bit in kind of a slight crouch. They may even be in a bit of a squat so they could be on their feet actually in the little tripod position. And nobody knows why but having a bit of a lean forward like this, actually assists in breathing when you’ve got this pulmonary edema, other signs of difficulty breathing with anybody would be cough, rapid grunting, respirations, flared nostrils, wheezing. Of course, you would do some diagnostic tests. You may already see cardiomegaly, so signs of congestive heart failure, as well as you could measure arterial blood gases to see how hypoxic baby is. You might hear sounds that indicate a defect. So a defect could incur involve say, aortic valve stenosis or pulmonary valve stenosis.

Or perhaps there is incompetency in the valve, there’s regurgitation. So if there’s regurgitation then that would reduce stroke volume, right? And we’ll look at some more defects that can give an additional sound, a swooshing or a murmur type sound. So that could be a clue. You could measure the amount of pressure, the central venous pressure or the pulmonary capillary wedge pressure. This is a good indication of how much pressure that left ventricle is able to generate. If it’s not able to generate much pressure, you might think, Oh, there’s something wrong with this heart, right? The left side is weak somehow. There may be some sort of defect that has made it weaker. Of course, signs might include signs of hypoxia such as cyanosis, which is shown there. So if we carry on, this has set the stage nicely for talking about these defects that can give rise to congestive heart failure. So you can tell that it does occur in Canada, eight out of 1000 babies are affected. Most of these defects occur really early during embryogenesis. So remember in the first four weeks, mom might not even know she’s pregnant yet. And it might be that in that time she’s accidentally exposed herself to things that can cause congenital heart defects. So those things include drinking alcohol, some drugs. Different viruses actually can cause congenital heart defects. Some sexually transmitted diseases such as syphilis, can cause structural defects. A lot of these viruses, thankfully, you’ve probably been vaccinated against. So German measles or rubella can cause structural defects, anyhow. So unfortunately, these things do occur and the heart is not the only thing that can be to have a hard time forming during this period if mom is exposed to some sort of element like that, cleft palate can develop, for example, the defects we’re going to talk about are the septal defects, the valvular defects, as well as shunts ok. And we’ve got pictures of all three categories so you can see what’s going on. And we’ll talk about the seriousness of each one. So I’ve listed actually some of the causes here that I’ve just mentioned, including Down’s syndrome. What else did I? As well as diabetes. And with a defect, you’re going to see that again. If the valves don’t close properly, you would expect a swooshing or a murmur sound if there’s a little hole in the heart that would create turbulence that would give us swooshing murmur sound. So that’s a clue for sure. And sure if untreated, you can tell that it could lead to congestive heart failure. Now, depending on how serious it is, it leads to either a cyanotic condition. So that’s the blue baby you might hear about. And in acyanotic condition. So a in biology means without. So without cyanosis, that means it’s a pink baby. So would you would suspect that the pink baby It’s the condition is not as serious or severe as the blue baby. Blue baby is most severe, right? Okay. So let’s take a look at some instances and you’ll be able to tell the seriousness of each case ok. So of course, you would suspect that a stroke volume is down and cardiac output is down because the heart has a defect, then your brain will, just like an adult sense low oxygen and low blood flow. And so it will put a baby into sympathetic nervous system as well as the renin pathway. So as a result, so vasoconstriction of the capillaries within the skin, you’re going to be looking pale, maybe cyanotic, the heart rate speeds up, remember? And it might be that the heart is weak because it’s got a defect. So you might see a very rapid pulse at the apex of the heart. But perhaps the heart is not strong enough to always push that blood down to the wrist. So you might see a pulse deficit, right? Where there’s a difference between the number of heartbeats you count per minute at the apex and the number of heartbeats that you find actually making its way down to the wrist or the ankle. If there’s pulmonary edema, you would expect dyspnea, squatting or that tripod position I talked about. And over time, hypoxia leads to this clubbed fingers. So painless enlargements of the ends of each digit. You would suspect that they’re not going to be exercising.

They’re doing a lot of activity because they don’t have enough oxygen. So again, they won’t be able to tolerate extreme weather changes very well either. Of course, growth and development would be delayed and you’ll have erythropoietin being secreted by the kidneys, leading to an increase in red blood cell production. And of course, once the physician has diagnosed this defect, they’re likely going to do a surgical repair. Although at times it’s not as serious and I’ll show you that in it might actually fix itself. So the first problem that we’ll look at is a septal defects. So if it’s ventricular than you would expect, okay. It’s a hole in the interventricular septum between the left and the right ventricle. So sometimes it’s called a hole in the heart. So it can vary in size and location. Obviously, the bigger it is, though more of a problem it can be. And if it’s not treated, that means if it’s not fixed, not surgically fixed than what you would expect is what’s called a left to right shunt. And the reason it’s called a left to right shunt is because if you were to think, Okay, which way is blood more likely to flow from this way or this way or this way to that way. You would think, okay, the left ventricle is stronger. Remember it’s got a thicker muscle so it can generate six to eight times more pressure than the right side. So because it can generate more pressure, this is a high pressure zone and material always flows from an area of high pressure, an area of low pressure. So it creates this left to right shunt. So what does that mean? It means that we’re losing some oxygenated blood, right? Some oxygenated blood is going to go to the right ventricle and then it’ll be pushed to the pulmonary circuit. Okay. So that means that less oxygenated blood than normal, It’s going to go down the aorta. So that means that we are, we’ve got reduced stroke volume, we’ve got reduced cardiac output, so less blood is making its way to the tissues because it’s all oxygenated. Most often the tissues can hang in there, they’re surviving but we’re not thriving. Okay. And baby is pink. So this is an acyanotic condition unless respiratory condition increases pressure in the right ventricle. So what I mean by that is if you can imagine that more blood is being sent to our pulmonary circuit and that pulmonary circuit potentially is becoming hypertensive and it’s going to become harder for this right ventricle to start filling those engorged vessels. And as a result, pressure might start building up in our right ventricle, in which case the shunt would flip. But most often they are going to fix it while it’s still the left to right shunt ok. So let’s carry on. And again, you could have a hole between the right atrium and the left atrium as well, and the arrows already drawn, but I could probably ask you which direction do you think the shunt would be? And again, the same It’s the same scenario because the left side of the heart has more pressure.

So the shunt is going to be left to right. So basically it means the same thing that there’s going to be slightly less oxygenated blood delivered through the aorta and more of that blood. So a little bit of oxygenated blood is going to mix with the deoxygenated blood on the right side of the heart and get sent to the pulmonary circuit. Okay. So as a results, the systemic circuit is still getting oxygenated. Blood. Stroke volume is down but baby is still pink ok So it’s an acyanotic condition. Okay, so let’s move to valvular defects. So we know we’ve got four valves. And of those four, the most commonly affected are the aortic and pulmonary valves. And, and there’s two main defects, either narrowing, stenosis or incompetency when the valve doesn’t completely close and seal and then blood regurgitate or leaks backwards. So in both those cases we see heart hypertrophy and then failure. There is a word that you might have heard before prolapse, mitral valve prolapse is when the flaps are very enlarged floppy and again, not closing properly. Okay. So typically any kind of defect of the valve is going to lead to a replacement either with a mechanical or a pig valve. I love this cartoon because it shows you what a normal valve should do, open nicely, let blood through and then close, not permitting backflow. Stenosis. The wiggly line means there’s less blood flowing through that narrowed valve, but there’s no regurgitation and incompetent valve. The blood flows freely forward, but it leaks backwards. So you’re going to get that murmur that regurgitation. So in this instance they’re showing you what would happen if you have an aortic valve that stenotic. So you can see that with the squiggly line, There’s going to be less stroke volume, less cardiac output. And this left ventricle is going to have to push harder and harder to try and drive blood through that space. So it’s going to hypertrophy, we’re going to get pathologic hypertrophy. And of course, as a result, we might end up with left-sided congestive heart failure unless the valve is fixed. Now with this little guy, you can see we’ve got a really big problem. In fact, we’ve got four problems. Tetralogy of Fallot and it leads to a blue baby. And so we can tell cyanosis has occurred. It’s quite serious. Let’s go through the four abnormalities. So the first one listed is pulmonary stenosis. So narrowing of that valve. So the right ventricle is going to have a really hard time pushing blood into the pulmonary trunk. As a result, it starts hypertrophying very abnormally. And the other problem you see is this ventral septal defect, this hole in the interventricular septum and the third or, I guess the fourth problem is the dextroposition of the aorta. Dextroposition means that the organ is out of place or that an anatomical structure is out of place. And it’s termed an overriding aorta. It’s really hard to draw it, but basically it’s shifted over a little bit. So basically it’s just right over that hole, actually leads to or helps more blood escape out of the right ventricle and then sneak out through the aorta. So as a result of the stenosis and the hypertrophy, this side of the heart generates the most pressure. So you’re going to see blood flow from an area of high pressure to an area of low pressure. So we’re getting the right to left shunt. And this is dangerous because now we’re sending deoxygenated blood down the aorta to the systemic circuit. So it means there’s even less oxygen reaching baby’s tissues now. Okay, so this is an instance where they’re going to try and do surgical repair and probably put this baby on the transplant list. Okay. So I know that was a quick walk-through, but hopefully we’ve covered a lot of bases and you’ve got a sense as to some of the more common things that happen to hearts in Canada. And I’ve hoped you enjoyed it. We’ve hit a good place to have a brain break, so let’s do that. I hope you have an awesome rest of your day. Hit me up with questions if you’ve got them as you’ve gone through, take care, enjoy the cartoons and I’ll see you in the next video.