4 Section 4 Selected Diseases and Disorders of the Cardiovascular System

Welcome to Lesson 7, Part 4. I’ve got some inspirational quotes for you for today, and some smiles as well. So we’re going to mix it up today and start talking about infections that affect the heart. Actually, we only have time for one because I want to take you to other things that affect the heart as well. So we’re going to talk about infective endocarditis today. And you can tell that the most common culprits that cause this infection are two bacteria streptococcus viridans and staphylococcus aureus. I don’t need you to remember those two bacteria names. if you know it’s bacteria that’s sufficient. Another one that is frequently talked about in the textbook is rheumatic fever. And this one is also caused by Streptococcus, a different strain of it. And you can tell this is a particularly nasty strain of streptococcus. Now our first infection, these bacteria infect the heart by entering the bloodstream and then traveling to the heart. Rheumatic fever is a little different. This streptococcus actually causes an upper respiratory tract infection. So you have strep throat actually. And in Canada of course, if you have strep throat you go to the physician, they swab your throat, they send it to the lab. They then of course, figure out what bacteria you’ve been infected with. And if it’s streptococcus, they’ll probably put you on penicillin or some other antibiotic to make sure that that infection is resolved and goes away. So in Canada rheumatic fever and rheumatic heart disease or not, usually that common. But in other places in the world where perhaps there’s not as easy access to health care or antibiotics. Then you can imagine the scenario playing out where someone has a strep throat infection and it happens and maybe this nasty version. And again, most strep throats are actually not caused by this nasty version. They’re caused by an even different version. Now, we’ve mentioned here. So in Canada, most often it’s not this group A Beta hemolytic streptococcus that gives you a throat infection it’s one that wouldn’t make its way to the heart anyways. Okay, but let’s say you, you live in another country and perhaps help access to health care. It is not as it is in Canada. You are unlucky enough to have the strep throat infection that has this group A beta hemolytic version. And this version, if not treated, if you’re not given penicillin or an antibiotic, then it goes on to cause bigger problems. Specifically the antibodies that actually are designed or become designed against this version. These antibodies are particularly problematic in that they start cross reacting with parts of the body, including the valves of the heart, and they start causing deterioration of heart valves. Okay. So of course, this can lead to long-term and permanent problems. So I’ve given you a taste of it. And if you hear rheumatic fever, rheumatic heart disease, you can picture what’s happening. Like I said, thankfully in Canada it’s not as common just because most people who have strep throat don’t have this nasty version in the first place. And of course, if they have strep throat, they’re going to be treated with antibiotic regardless. So these following steps that may occur if it’s not treated with antibiotic don’t happen and your heart is fine and nothing will happen to it. Okay, so let’s focus on infective endocarditis. And like I said, this one doesn’t start in the throat. This one actually starts in the bloodstream. So I mentioned those two bacteria strains. And you can tell that if you are infected with Streptococcus viridans, that it typically gives rise to less severe signs and symptoms then if you’re infected with Staphylococcus aureus. Now, what happens with either of these microorganisms is they invade the blood. So they enter through a wound, a portal of entry, and they travel the bloodstream. And they all tend to start setting up shop or location on vulnerable parts of the body, which include the heart valves. Because the heart valves are not well vascularized and are therefore, the white blood cells have a hard time defending them. So let’s say the microorganisms land on the valves. They started, of course, deteriorating. The valves and growing and replicating. White blood cells will start coming in but there will be damage. So you’re going to see, of course, inflammation as white blood cells come in. And you’re going to get these growths on the cusps of the valves. And the growths are going to be comprised of basically large fragile masses of fibrin, platelets, blood cells, and of course, those microorganisms are all going to be accumulating on the cusps of the valves. And so one of the diagnostic tools used is this transesophageal echocardiogram. So of course you could do an echocardiogram just through the chest wall. That would be called transthoracic. But of course the rib cage a little bit in the way of the heart. And it’s a longer distance actually than if you were to thread this transesophageal echocardiogram reader into the esophagus you can see is really close to the heart. So you can get really awesome images of the valves. So you of course see that. And I’ll show you an image in a second. And I just want to hopefully make you breath a sigh of relief that most people are not susceptible to this bacteria entering your blood and then causing these big problems on your valves. You tend to be at risk for this happening if you’ve got any kind of abnormality in the valve that puts you at risk. So say you have a congenital defects, one that we perhaps talked about in the last video. Or perhaps that rheumatic fever. You’ve maybe, you’ve moved from another country. And when you were a kid, you were unfortunate to have that rheumatic fever, that group A beta haemolytic Streptococcus cause damage to your valves and so they’re vulnerable to a subsequent infection, perhaps by one of these guys. Or perhaps you know you’ve got some sort of prolapse or perhaps your valves have been replaced by either mechanical valve or perhaps a pig valve. And then, like I said, when it’s an artificial replacement part, the valves, again, they can’t defend themselves as readily, so they become susceptible to places that bacteria will set up, shop and start growing. So the scenario typically plays out and it might be that you’ve gone to get your teeth cleaned up the dentist, right? So they are scaling your teeth. And of course, the dental hygienists, they always tend to nick your gums, right? So you’ve got little bleeding gums and you’ve got this type of bacteria on your skin and sometimes in your mouth. And so they can be opportunistic and then enter those little portals of entry and then start traveling through your blood. And if you’ve got this susceptibility, then they may lodge on those valves and start accumulating this mess, right? So calling in white blood cells, which we know we’re going to activate platelets which are going to accumulate fibrin. And then we’re going to get a mess of blood cells and also dead cells on our valves as well. Facial piercings also put you at risk if you’ve got any kind of abnormality there (in your valves). And this is one of the reasons why you fill in these history forms when you go to the dentist or perhaps your parents did when you were younger and they’ll probably ask you that question. Do you have any have you had any surgery lately? And then do you have any heart replacement valves, etcetera? And if you do what they’re going to do before they do a cleaning on your teeth. They’re going to give you a prophylactic antibiotic, so they’ll give you that beforehand. And then of course, should this happen, that antibiotic is going to get rid of that bacteria before any of this will ever happen. Hopefully this same with anybody who’s getting a piercing done as well, probably fill out a form and hopefully you’ll devulge this type of information and then take an antibiotic prior to getting your tongue pierced or what have you. Another risk factor, of course is immunosuppression, or if you’re older and then of course, intravenous drug users using dirty needles. Again, that would be a basically potentially putting one of these bacteria right into your bloodstream. And if you’ve got this susceptibility, then this could play out. So let’s take a look at one of these images with this really cool echocardiogram. As you can see, we’ve got our left atrium, our left ventricle, and here’s our aorta here. So if we just pull up the description, it’ll tell you that we’ve got a vegetative growth on the aortic valve. It’s pretty big actually. See you can imagine that it’s going to impede blood flow. Okay, so that’s a problem, of course, for cardiac output, it will reduce your stroke volume and cardiac output. And here’s another picture that I found that I thought I would put in. So you can see these vegetative growths on the valves. They’re really messy on the mitral valve in this case. So of course, this potentially would give a sound. These valves probably aren’t closing very well anymore and there might be a bit of regurgitation. There might be a bit of stenosis as well. So you might hear it with a stethoscope because it’s a bacterial infection and you would likely have a fever. And just like any bacterial infection, you might feel tired as your body does this battle. You might not feel like eating. This isn’t anorexia nervosa, it’s not the eating disorder. This is just, you don’t feel like eating when you’re sick because your body is using its resources to battle this infection. Sometimes when you have a nasty infection, you get enlargement of the spleen. That’s where a lot of your immune system cells are, of course housed and become activated. And then unfortunately, septic emboli can fly off of these valves. They’re moving obviously with every heartbeat. And if they fly off these valves, it’s the mitral side. It’s going to fly off the left ventricle up the aorta and then shoot into your systemic circuit and then lodge in tiny capillaries. These Osler nodes are typically found in the fingers or the toes actually. And they’re tender or painful. They’re septic emboli. So they’re basically clusters of bacteria, white blood cells, red blood cells, platelets, fibrin. And they’re just going to jam into a capillary. And of course they are. They’re going to cause some inflammation, pain, all the signs of inflammation, redness, warmth, swelling. Luckily, a person with a healthy immune system is going to start degrading all that mess and getting rid of it, recycling it and of course, healing that area. So typically they don’t last long within a day or two they can be resolved, but still kinda scary. And then with reduced stroke volume and cardiac output, you’re probably thinking, hey, that sounds a lot like congestive heart failure right? So yes, that can occur. So you’re probably thinking, well, do the valves ever fix themselves? and the answer is usually not. So this would be a case where a person is going to need a valve replacement. Ok, here’s that description. So septic emboli from those vegetations can cause vascular occlusion or infection and other areas of the body. So we’ve just shown that with the Osler’s nodes in the dermal capillaries. And like I said, usually resolving within hours to days as macrophages come in and gobble all that mess up. You can do a biopsy from those spots and you can actually figure out what bacteria has is the infection. And it can be a clue as to this person has infective endocarditis. So you might hear something, you might see this biopsy it and also you might remember with DIC or disseminated intravascular coagulation that you can get clots flying through the body in this condition as well. So but usually this is all over the body, not just in the fingers and toes. So that’s another clue, but there’s other things that of course can cause this type of appearance, insect bites, for example. So they’re going to use the biopsy to rule out other causes of this type of event. And then like I said, identify the bacteria. And then of course you’re going to want to treat the cause, right? You’re going to hopefully prescribe antibiotics (if it is bacteria). You can imagine that if it’s sudden that you’re going to have a spiking fever and other signs of bacterial infection, chills, drowsiness. If it’s subacute, then it’s a gradual onset with of course, increasing signs and symptoms and and treatment. Yeah. You want to identify the culprit and then treat with those antimicrobial drugs. If the person is showing signs of congestive heart failure, then you’re going to start treating with congestive heart failure medications. And then of course come up with a plan. Are you going to, you’ll do some imaging, figure out if you’re going to do a (valve) replacement. I’ve got a picture of a tooth and a heart here because in the library, apparently a couple of years ago, at UBC, they had posters. Take care of your teeth and ensure appropriate dental hygiene and you take care of your heart. And my students would ask me, Hey, how’s that possible? Why does good dental hygiene for a happy heart? And so you can kind of tell actually, right? If you’re taking care of your teeth and you’re not getting a lot of gingivitis and other infections within your gums. Then of course, you’re reducing the risks for infective endocarditis for one thing which is great. And it tends to be the thought to that if you’re the type of person that’s taking care of your teeth, you’re probably taking care of other aspects of your body as well. So you’re probably eating a healthy diet and you’re probably doing a bit of exercise. And so there’s this correlation typically between healthy teeth and healthy body in general. Just like, for example, my dad’s a pharmacist and he would always say the best medication that could be prescribed to someone is a dog. And the reason is, as we know already, that a lot of drugs, of course of cons to them, right? There’s never a drug that’s only pros there’s always some cons to drugs. But with the dog, why is the dog the best medicine? Because it gets you out and exercising and hopefully having a healthy lifestyle. So there’s another correlation that people have noticed that if you see someone with a healthy looking dog, that person is probably healthy looking at themselves, right. If the person is not taking care of their dog, maybe as well, maybe they’ve got a fat dog. Maybe their own health is in trouble. So it’s another of these correlation type studies that you might see come up on the news from time to time. So keep that in mind. Best medication is laughter and a dog, probably. Okay, so I want to show you some beautiful valves so you can take a look at those cusps. Nice. Now here’s some more damaged ones with some vegetative growth on them and you can see the incompetence not closing properly. So of course they’re going to put in a mechanical valve or a pig valve. And again, like I was saying, valves are a fairly avascular. So you can put in another species valve and it won’t be rejected, which is pretty cool. In fact, both mechanical valve as well as a pig valve. They last for about 10 to 20 years, both of them. So again, it basically depends on the scenario and the person and the surgeon. And the most current technology as to, which one is used. Let’s carry on and talk about acute pericarditis. Okay, so just flipping gears. Now we can picture what this is. So this is inflammation of the pericardial sac. Now, typically that’s not the first thing that goes wrong with you. You don’t just one day have pericarditis. Usually it occurs because something else has happened first. So when of course, somebody is diagnosed with pericarditis, It’s usually classified by okay. What caused it. And then what type of exudate is building up in the pericardial sac. Okay, so we know that pericarditis means inflammation of the pericardium. And when that happens, unfortunately, the visceral and the parietal pericardial membranes start potentially rubbing on each other, which can of course be painful and it can give a sound so if you are listening through a stethoscope you could hear a friction rub. Now what can cause this? Any type of irritation, of course, is going to cause potentially inflammation to the pericardial membranes, right? So surgery, if it’s close by then of course, that would give rise to inflammation in that zone. If a person had a heart attack and it’s close to the wall of the visceral pericardium. Sure. That would cause inflammation. There’s a lot of damage been done in that zone. Rheumatic fever. So if a person’s had that nasty strep, infection and antibodies have started causing some damage to that heart. You could end up with inflammation in the pericardium. An autoimmune disease such as systemic lupus erythematosus. Unfortunately, this autoimmune disease, I think, is one of the worst in that it can attack almost any cell type in your body. So if it happens to be the case where your immune system is attacking your own heart or the pericardial lining, then of course it will give rise to damage and hence inflammation in that zone, the body’s go-to strategy is always inflammation when in any kind of damage, has been done. If there’s cancer in that zone, we know that kinda irritate regions wherever it is, it can erode blood vessels. And of course, that would stimulate inflammation, kidney damage, maybe the heart itself is fine, but the kidneys are failing. And we haven’t talked about kidneys yet. But you can imagine if the kidneys fail, these are your filters, right? They’re always getting waste out of your body. So if they’re no longer getting waste out of your body, then you’ve got waste traveling through your bloodstream, which can be toxic and really irritating to cells and your heart and those membranes do not like that. So it can give rise to inflammation in different areas of your body for sure. Trauma. So you’re in a car accident, potentially, there’s damage to your chest. Sure. That could give rise to inflammation in that zone, and a viral infection if it happens to enter that space as well. Okay. So you’re going to identify by the cause, what was the cause? Possibly one of these things and then what is the type of fluid that’s filling up the pericardial sac, ok. So that fluid or that effusion might be serous, which means it’s watery, or it might be pus-filled with fibrin in it. That’s a sign of bacterial or viral infection, usually bacterial infection. Or if some blood vessels have been ruptured, there might be blood filling up that space as well. So that might indicate trauma or cancer. And I’m going to set up some videos and I want you to watch them. And I want you to figure out when that person. And actually there’s two videos that show this scenario where pericardial sac is filling with fluid. I want you to figure out what fluid it is, ok and you’re going to see by what fluid they aspirate out of that space. Okay. What colour is it? Okay. So we know that this can be a problem. If fluid starts filling up the pericardial cavity, it starts compressing the heart, which impairs filling, it’s the scenario of cardiac tamponade that we talked about. So if the heart can’t fill, then it can’t generate much of a stroke volume, right? So cardiac output is going to start getting shoddy. Now the right ventricle is typically affected first because the right ventricle muscle is weaker right. Remember the left ventricle is thicker and it can generate more pressure. It’s a stronger muscle. Now, if you have right-sided failure – this is literally right-sided congestive heart failure than we know the signs of right-sided congestive heart failure, distended neck veins. There might be faint heart sounds due to this fluid and pulsus paradoxus may be occurring as well. So here’s another picture of cardiac tamponade. And so you can see step 1 was, Oh no, we’ve got inflammation and fluid is building up in this pericardial cavity. It’s compressing on this wall and the heart can’t fill. And if it can’t fill, then it’s going to have decreased, output to the body. So cardiac output and stroke volume is shoddy. And the other thing too is if that blood can’t leave, then blood can’t enter, right? So we’re going to have decreased blood coming into this heart as well. So you’re going to have backup into the pulmonary circuit. And of course, you can see that if blood can’t leave the pulmonary circuit, then it’s going to be hard to push blood into the pulmonary circuit. And we’re going to have blood building up in our, the right side as well. So we’re going to have that systemic circuit getting congested at the same time. We’ve actually, that happens first because our right side is affected first right. I like this picture actually, it shows you the inflammation and the visceral and parietal pericardial membranes rubbing on each other, giving that friction rub. So what happens is this becomes a long-term problem. Oh no, if it’s chronic, you can imagine that scar tissue could start building up between the pericardial membranes, creating these little adhesions. And that’s problematic because again, we want beautiful fluid in that space lubricating fluid. We don’t want scar tissue, which may of course, disrupt movement of the heart and also cause irritation and rubbing every time the heart contracts. Now, in terms of what could cause chronic pericarditis, any type of prolonged irritation. So, for example, a nasty tuberculosis infection. Remember the lungs are really close to the hearts and TB infection is hard to get rid of. So that might end up causing a lot of fibrous tissues in scarring in that zone. Unfortunately, if you have cancer and you have a lot of radiation treatment done to that zone, it can cause damage inadvertently, of course to this pericardial membrane, leading to a lot of fibrous tissue building up, which potentially is going to lead to chronic pericarditis. And we know the problem is that the heart may become limited in its movement, which means that stroke volume and cardiac output could go down. Another cause we’ve already mentioned this one. So you can picture signs and symptoms obviously would be painful. They’d be the friction rub, potentially dyspnea, especially if there’s pulmonary edema. You would imagine that compensation mechanisms would start taking place. So if cardiac output is down. Remember your medulla oblongata is going to sense that it’s going to be like, whoa, low blood flow, low blood pressure, low oxygen. What are we going to do? We’re going to go into SNS mode and speed up the heart right? And if you’re slightly hypoxic, of course your brain is going to give you those sensations of fatigue, weakness. If you have edema or ascite in the abdominal pelvic cavity, that of course is not comfortable. So obviously you want to treat this and try and prevent it in the first place by treating those primary problems that we listed on the last page. Sometimes they’re going to when they do aspirate that fluid and they’re gonna wanna do that quite quickly to restore, make sure cardiac tamponade doesn’t happen. They’re going to analyze that fluid and find potentially the cause. What kind of infection is it? Analyze what type of bacteria or virus infection it is that would be handy, then treat accordingly. Or if there’s cancer nearby, you might see cancer cells and then. Unfortunately diagnose cancer but at least start treating it asap, which is good. Okay, So hopefully you’ve got a sense of that one, you’ve got a taste of that and we’ll move on to vascular disorders. So we know we talked about atherosclerosis a lot. And of course in Canada, coronary artery disease and hypertension are huge problems. So it’s probably good to talk about hypertension. Now. There’s three types of hypertension, and I just wanted to go through them. Not all of them are related to atherosclerosis. So that’s important to know. And we’ve already talked about that sometimes they call hypertension the silent killer because there can be a gradual onset in terms of signs or symptoms. You can have it and not know, wince. And it’s pretty common, like I said in Canada, apparently, one in three adults have hypertension and 1 in 3 are pre-hypertensive. (XY) Men are more at risk under the age of 55 than women. But after the age of 55, women become more at risk. And estrogen actually is thought to be very heart healthy, happy hormone actually. Estrogen is a bit of a…. it protects our vasculature and nobody really knows why. But of course, unfortunately, after the age of 50, when menopause sets in, estrogen levels start going down. And when that happens, women then become more at risk for hypertension. Genetics is a risk factor and there’s a lot of different genes they are actually linking to your hypertension. So you can see that it’s not necessarily atherosclerotic plaque. Genetics can put you at risk. And its genes to do with Angiotensin 2 and the renin genes ok. So you can imagine, for example, if you have too much renin or too much Angiotensin 2, that, that would induce too much vasoconstriction, right? So they’ve seen that potentially in some families. There’s other genes as well. Now, depending on which number is going up, whether it’s 120 or 80, they’re going to call it systolic or diastolic hypertension. And like I said, there’s three types. There’s primary, secondary, and malignant, which is the worst. It’s what it sounds like because it’s resistance to treatments. Okay, Let’s go through them in order. So primary it’s sometimes called essential hypertension. And the cause is not known. And 90 to 95 percent of all cases fall in this category. So they’re idiopathic, don’t know why. And it’s characterized by someone having a blood pressure consistently above 140 over 90. So this is a resting blood pressure that’s high. And of course you got to adjust for every age. Usually when you’re older, you’re expected to have a slightly higher blood pressure anyways. And like I said, you don’t you you wouldn’t know that you’re you’ve got a high blood pressure maybe unless you’ve been routinely getting your blood pressure done because it’s asymptomatic. So what they see in this instance is you’ve got abnormal vasoconstriction. So just too much vasoconstriction. And that causes problems unfortunately, firstly, it gives rise to high blood pressure and your kidneys, hate it, your kidneys of course are your filter and they want a certain level of blood flow going through them all the time. So when they don’t get that blood flow because your systemic arteries are vasoconstricted, less blood is getting to the kidneys. The kidneys to compensate. They’re like, hey, we want more blood. And so we’re going to actually start secreting renin. And renin actually makes it worse, right? Renin is going to stimulate angiotensin one to be produced. Angiotensin 2 will then of course, end up being produced by ACE and aldosterone and ADH. You’re also going to come into the swing of things. And as a result, we are going to become even more vasoconstricted. And not only that, remember, aldosterone and ADH make you not pee out as much salt and water. So you’re going to accumulate salt and water in your blood. And with this increase in blood volume now, then your blood pressure’s going to go even higher. This compensation strategy is putting you in this vicious cycle of keeping your blood pressure high, or maybe even making it higher. Okay. So of course, we know that over time this creates damage to arterial walls, which of course then becomes sclerotic and hard. They lose their elastic fibers. And when they become hard or more rigid like that, then they’re more prone to tearing and they’re more prone to bulging as well. So an aneurism is a bulge and that bulge, it’s actually going to thin out the blood vessel wall making it again susceptible to a tear. So a very dangerous situation. And we know too that damage can also cause atheromas to start developing. Now, sometimes the first signs start occurring in the areas that need, that are kind of blood hogs. They want, they need a constant supply of blood (or like the retina, have fragile blood vessels that can be damaged by high blood pressure. So the brain, of course, needs a constant supply of blood as does the kidneys and the retina. And so the first signs and symptoms can start occurring in these three places. So if you’re going for a regular eye checkups, your ophthalmologist is actually checking your retina and they’ll see tiny little signs of retinal blood vessels experiencing this. And that might be actually the first clue that you have high blood pressure is these changes in retina capillaries. Ok. And you can imagine that if you’re a super vasoconstricted like this and lots of high blood pressure that some tissues may become ischemic and it might lead to dysfunction of different tissues and even necrosis right? I wanted to put up this picture that I just found that I thought it was really nice was one that shows you what an ophthalmologist might see if you have high blood pressure. So you might see these little bulges or aneurisms in your blood vessels of the retina. You might see these lipid depositions called cottonwoods spots. And then if there’s ischemia, it triggers abnormal growth of blood vessels. And unfortunately this starts impairing your vision. You can see some of these aneurisms have burst and you get little hemorrhages. And that can irritate all of these retinal nerves, right, all your retina is full of rods and cones. All these nerves that pick up signal from your rods and cones potentially get damaged. And that’s actually where the lipid comes from, is from damaged retinal nerves. And retinal nerves don’t replace themselves. So again, it’s contributing to loss of vision unfortunately. Okay? Okay, let’s go to the second category, secondary hypertension. So you can tell that it, it comes from something else right, so caused by…. And the two most common primary causes are kidney disease. So you can tell it’s that phenomenon where renin is overproduced, causing that problem of too much vasoconstriction. Or perhaps a person has an endocrine disease to start with, it’s either a kidney disease to start with or an endocrine disease to start with. And I don’t need you to remember examples of the specific disease. I just wrote them down in case you’ve ever heard of them. And the same with this benign tumor. I don’t need you to remember it. It’s sufficient that you know that it’s just an excess of epinephrine and norepinephrine that are produced. So again, you know, this is part of SNS, fight or flight that causes too much vasoconstriction if it’s in abundance, right? Okay, so with these two things, stimulating vasoconstriction and this also stimulating an increase blood volume. You can imagine these are both leading to hypertension. And unfortunately, both primary and secondary put you at risk for an episode of malignant or resistant hypertension. And this is the scenario that plays out in about 1% of people. And it’s just an emergency situation where all of a sudden you have an uncontrollable, severe and rapid progressive form of hypertension, where you get extreme ischemia to different organs which start failing and you can experience necrosis in those tissues. Nobody’s really sure why these events take place. It’s idiopathic. Sometimes it can occur if there’s a drug or alcohol overdose or withdraw. And it’s characterized by high diastolic pressure. And you can see different signs of hypertension, particularly in the eyes again. So swelling within that zone, papilledema. So this is basically causing cerebral edema. A lot of if you have hypertension in the blood vessels of the brain, there’s a lot of pressure in those blood vessels. They get leaky, right? Just like with pulmonary edema. So you start leaking fluid into your brain and it builds up intracranial pressure. And they always say the eyes are the windows to the brain. So when an ophthalmologist looks through your eyes, you might remember this test if you’ve ever gone for an eye test and they use that instrument that puffs air onto your eyeball and it ricochets off your eyeball. Have you ever noticed that they puff air on your eyeballs. They’re actually measuring the amount of pressure in your eyeball. But it’s also a good sign of the amount of pressure in your brain. So if somebody is very hypertensive, you can start building up edema in the, in both of these zones, which would of course translate into higher and higher pressure. And unfortunately, when you build up a lot of intercranial pressure in your brain, it can start pinching off capillaries, meaning that neurons are no longer getting sufficient blood and therefore oxygen and nutrients. So it’s a very dangerous situation as neurons can start dying. So obviously very irritating to your neurons and your nociceptors are going to start firing and you’re going to have a massive headache. So this condition here, a disease of the brain encephalopathy I’ve just hopefully described that can occur to to hyperperfusion. So again, causing this cerebral edema, this leakiness and the buildup of intercranial pressure. You can imagine the heart doesn’t like this situation either, and it can give rise to temporary deficits of oxygen to the myocardium or prolonged deficits can lead to congestive heart failure and pulmonary edema with all of that pressure causing leaking within the lungs as well. Here’s a flowchart to, to illustrate how this can be a vicious cycle. So the development of hypertension and we’ll go, this is essential hypertension or primary hypertension. And so for whatever reason, a person has too much vasoconstriction. And if they have too much vasoconstriction, then the kidneys hate that. They notice that right away there’s decreased blood flow. And what they do automatically with decreased blood flow is they’re going to secrete renin. They’re going to assume that blood flow is low because of low blood volume. And so they’re going to secrete renin in order to up blood volume and cause systemic vasoconstriction to try and drive more blood flow to the kidney. Unfortunately, we know this makes the problem worse. And also we know renin, of course, causes the secretion of aldosterone and ADH, which increases blood volume. More blood volume again makes for higher pressure. So blood pressure is getting higher and higher. And like we’ve said, it’s starting to cause damage to retinal blood vessels that can cause loss of retinal nerves and blindness. It can damage arterial walls leading to atherosclerosis. It can damage cerebral arteries, which then just like within the retina, can lead to aneurysms and strokes occurring or ischemic strokes to it can make for an increase workload on the heart, right? You’re so hypertensive. Can you imagine how hard the left side of your heart is going to have to try and push to drive blood through those constricted arteries. So can lead to left-sided congestive heart failure. As we saw in our previous video actually. And our kidney blood vessels don’t like this, this high blood pressure damaging them as well. And unfortunately, it is, like I said, a vicious cycle. Now I know we haven’t talked about diabetes, yeah, but high blood sugar that occurs in diabetes can be detrimental to the nephrons in the kidney. And of course, nephrons are wrapped in blood vessels. And that can mean that with damaged blood vessels, remember, damaged blood vessels become more narrow and more constricted. So if a person is diabetic, it can end up with that person becoming hypertensive as this scenario starts to play out. Unfortunately. So you can see that people with diabetes are at risk for all of these things developing. If that diabetes puts that person on this path of hypertension. Okay, So we’ve gone through this already, but I thought I’d put up another picture showing you the same thing, the different parts of the body that are susceptible to hypertension. We talked about risk factors already. So incidence increases with age. Men are more frequently affected than women, particularly under the age of 55. There’s genetic factors and then of course, diet is a huge factor. So salt intake, excessive alcohol intake. Obesity is a risk factor, smoking is a risk factor. We know its vasoconstrictive. Amongst all the other problems it leads to more susceptibility to atherosclerosis as well and prolonged recurrence stress. Now, here’s another picture from your textbook and I thought this was a good one. Again, it shows you the main organs that are affected by hypertension, the organs that hate it. So we talked about the eyes with this retinopathy and I found a nice picture that I thought you like. So it shows a real picture of the retina and it shows you some aneurysms and some bleeding that’s occurring within the retina. And then those fatty deposits from the nerves that are dying in the retina as nerves rupture. Of course, it’s depicted by elevated blood pressure. The kidneys hate it. You might well see the nephrons being affected by low blood flow to the kidneys. So not only are the blood vessels, all the capillaries in the kidneys starting to get messed up. But the nephrons as well (due to ischemia), the heart, again, does not like being ischemic, can lead to episodes of angina or MI. And damage to arterial walls can give rise to an atherosclerosis and we can end up in left-sided congestive heart failure. We can see atherosclerosis in those arteries that are susceptible to it, such as the carotid. Remember the iliacs, the aorta and the cerebral. So again, the cerebral arteries are susceptible and we can end up just like within the retina in these situations of aneurisms. And then those aneurysms bursting giving rise to hemorrhagic stroke. So what can be done? Initial signs are vague. So fatigue, just not feeling great malaise, sometimes a headache in the back of the brain. The key, of course, is to reduce the chances of this happening in the first place, first time by lifestyle changes or making sure that you’re exercising, eating properly. And then of course, if you are diagnosed with hypertension, we already know the drugs that would be effective against that. So hopefully you remember that. Okay. Now an aneurysm, I wanted to show you some good pictures of this. We know the aorta is susceptible, so it’s characterized by dilation and weakening of the arterial wall and then and it’s bulging most often in the abdominal or thoracic aorta. And what we’re going to see is a defect in the middle layer of that blood vessel wall. So remember you’ve got the tunica intima, tunica media and the tunica externa, ok. So here you can tell we’ve got a bulging aortic aneurysm. Here’s another two that are being shown to you. So ascending and descending, I’m never going to ask you to label them. I just wanted to show you pictures. Most common cause atherosclerosis causing causing weakening of the vessel wall. Trauma, of course occasionally can be the cause. Infection such as syphilis and then congenital defects where there’s a weakness in the arterial wall that make it vulnerable to this happening. The signs and symptoms so bruit is an abnormal sound. So sometimes you can hear it if you have got the stethoscope there. Sometimes you can feel it if you’re putting your hands there in that region, palpation can be kind of a warm palpating movement. If it’s close to the esophagus, it can give this person difficulty swallowing, dysphagia. And unfortunately, most often it’s asymptomatic until it’s large enough to rupture. And of course rupture is usually fatal because you can bleed out so quickly, especially if it’s a large hemorrhage, your heart is beating out five liters per minute. So that’s your full blood volume. So within one minute, one liter of or five liters of blood could just dump into your either abdominal pelvic cavity or in thoracic cavity and you would go into organ failure. So signs and symptoms, severe pain when this happens, shock, loss of pulse and organ dysfunction. I want to tell you a story because I have a bit of time. That is a feel-good story and hopefully helps you remember this. And I heard this on the radio. It’s a true story. It took place in the States, and it took place with medical students. And you probably know this, that medical students are of course, taken to the hospital and they actually hire actors to, or they have volunteer actors usually to come in and play out different scenarios. And they usually have an instructor in the hallway watching to see if this medical student is going to ask this person the correct questions, order the correct diagnostic tests, et cetera, and make the correct diagnosis after they’ve talked to their actor patient. Yeah. So this is all coming about and they’d had this old guy coming into the hospital to volunteer for awhile. He just like chatting and he’s a happy guy Anytime Anyhow. So this medical student went in and went through the, you know, the protocol that he is supposed to go through answering the questions. And as he was writing down these items in the chart, he started thinking, Oh, I bet this guy has an aortic aneurysm. It really kinda sounds like it. So he’s supposed to go through the movements and he placed his hands on this man’s abdomen to see if he could feel this. That warm palpating mass. And he did. And of course he freaked out. He thought, No, this can’t be happening. I’m not supposed to be with a real patient. This can’t be real. I’m supposed to be with someone who is pretending. And he dove into the hallway and he said to his instructor, I think this person actually has an aortic aneurysm and the instructor is like Oh, yeah, yeah. No, no, no, no. And so he came in and tested it as well. And sure enough, this old guy did have an aortic aneurysm and they caught it and they of course took this guy to get consulted and of course get it fixed before it ruptured. I mean, if you can imagine, he could have easily been sent home that day and it could have ruptured that night. And it would have been game over for this, this poor old guy. So I just thought it was such a great story. And this young medical student, he makes his first save. And he’s not even a real doctor yet. So hopefully you enjoyed that one. And even today, of course, that doctor has graduated now and that old guy is still comes into the hospital, to volunteer and they’re buddies now and they eat lunch in the cafeteria together sometimes. So it’s a pretty cool story. Alrighty. So these aneurysms can be named if you get all geeky about it. They can be called saccular, just based on the shape, fusiform ok They can be called dissecting and that’s when there’s a tear between the tunica intima and the tunica media. And then blood can actually start pushing its way down and peeling those two tunics apart. And that’s of course quite dangerous as you can see because the walls then even thinner. Okay. Now what they’ll do to diagnose is, well, we’ve already started the diagnosis as you can see, but they’re going to want to take a good image. So whether it’s an x-ray or an ultrasound or a CT scan or an MRI. And they’re going to really assess where it is, of course. And then they’re typically going to put in a graft. And the type of material used as kind of a polyester material, which is amazing to me, but it’s not rejected by your body. So they suture it in. As you can see, there’s different strategies and just depends on where it is though. Perhaps use a catheter to insert it and put it in that way. Or they might actually just cut out this section that is problematic in and put in the graft that way. And then of course, you don’t want this to happen in other areas, the aorta or other places in the body. So you want to obviously treats hypertension if that’s what led to this problem. And yeah, prevent any kind of sudden elevations due to exertion. And you can imagine that these events would cause them. So to wrap up this unit, I was told that I should definitely make sure you knew the difference between the different types of shock. And we’ve talked about these along the way and I thought it would be nice to just put them all in a summary table so you can kind of compare and contrast them. So the first type we looked at was hypovolemic. And you know, this means below, volemic means volume. So you’re like, oh, low blood volume. So maybe we’ve lost blood either through hemorrhaging or perhaps we’ve lost fluid from our blood. Maybe that person has had a severe burn. And remember with a severe burn, you’d have inflammation through ean xtensive region of your body, which might mean that all of a sudden you get a lot of inflammation all over your body. And with inflammation, remember your blood vessels are going to produce a lot of exudate. You’re going to have a lot of edema. So you have a fluid shift. The fluid is shifting out of your blood and into the interstitial spaces. So that would mean that you’re left with a low volume of blood, ok. So that could be the scenario. Third scenario is you’re severely dehydrated. OK could go into hypovolemic shock. This can happen to young athletes on a really, really hot day if they haven’t been (not climatized yet) training if say, it’s the first training days. Sometimes this occurs particularly in places like Texas playing football. Peritonitis. So any kind of inflammation just kind of like the burn situation where you get excessive exudate being produced. So a fluid shift and the same instance with pancreatitis, ok. So hypovolemic is loss of volume in the blood. So of course, that will lead to poor cardiac output. And your organs are getting Whoa. Not enough blood and not enough oxygen, not enough nutrients. And if it’s left without being fix, those organs are going to start failing. So you have to rectify the problem. How are you going to rectify it? You’re going to up this blood volume aren’t you? Okay? You’re going to patch up any kind of hemorrhaging to make sure that you’re not losing more blood to yeah, if that’s the case. Second type, cardiogenic, again, you can tell what causes it based on the name. So genesis we know is means creation of cardio refers to heart. You’re like, Oh, the heart is the problem. It has created this shock. So that means that the heart has become less functional. What could make the heart less functional? Oh shoot, myocardial infarction or some sort of instance that’s caused an arrhythmia. So both of these things we know can reduce stroke volume and reduce cardiac output. What else could reduce cardiac output? Oh no, pulmonary embolus! Remember, if we block our pulmonary circuit with an embolus, then of course blood can’t come back from the lungs to the heart. It’s stuck in the lungs. So if you’ve got poor filling of your heart, then you’re definitely going to have poor output. Cardiac tamponade can reduce cardiac output. Yeah, So what are you going to do? You’re going to treat whatever problem it is. Yeah. The next type, obstructive. So again, as the name implies, Oh, there’s some interference or obstruction in blood flow. So perhaps it’s that cardiac tamponade situation or maybe it’s a big embolus blocking flow through the pulmonary circuit. Now vasogenic. So you think, oh, so genesis of the blood vessels, blood vessels are the problem. And it’s the case where the blood vessels are abnormally vasodilating. They’re dilating too much, that is the problem. So potentially it’s a nerve problem. Remember the nerves from the medulla oblongata are supposed to be able to vasoconstrict when you need to. And if those nerves aren’t working, then those blood vessels could all just vasodilate, right – what if you’ve lost sympathetic tone? When would that happen? Well, it can happen in instances when you’re extremely scared or if you’ve had nerve damage, say through spinal cord injury. Okay Other instances can be when we talk about diabetes, we’ll talk about this. But if you’ve got very low blood sugar, of course your neurons hate that and they can’t function, ok. So then you could lose sympathetic tone totally vasodilate. And if you’re vasodilating, no pressure, no pressure, no flow, your organs hate that. They’re not getting the oxygenated blood they need in order to function properly. Your brain hates that, right? No flow. Your neurons are going to start dying. Anaphylactic shock we talked about and we know what’s happening. It’s an extreme allergic reaction. And as a result, you have systemic vasodilation with a lot of permeability. And we’ve talked about the different allergens that most often give rise to an anaphylactic shock. And the reason you’re systemically vasodilating like this is because you’ve got a massive amount of histamine that’s just been dumped by your mast cells. Okay. So just a huge inflammatory response throughout your body. So lots of vasodilation. Again, if you’re vasodilated, whoa, no pressure, no flow, your organs will start failing. They hate that. Systemic shock. Same idea. Septic of course means you’ve got an infection. So most often bacteria. And because it’s in the blood, it could give rise to a massive inflammatory response. So same idea, just huge dump of this histamine as your white blood cells are trying to battle this bacteria. And again, if you dilate that severely, you lose pressure and you can’t drive flow through your circuit and your organs don’t get that oxygenated blood they need. Now I’ve put star beside each of them because you may see in your textbook that, anytime you’re vasodilated massively like this, leading to shock it is called distributive because you’re not able to distribute the blood that you need to keep your organs alive. So you can see that all three of these are in that category of distributive shock, ok. Okay. So what are you going to do and what are the signs? So the signs and symptoms are really going to be signs of hypoxia. Your tissues are not getting sufficient oxygen. And of course, the medulla oblongata is going to sense that, right, do you remember this chart we looked at? It’s going to sense a low oxygen and it’s going to immediately induce this compensation strategy, right? Both of them, the neural compensation strategy as well as the endocrine compensation strategy. And both of them are systemic. This is a systemic problem. This is not a local problem. So remember with endocrine, you’re like, whoa, not enough blood volume. So it’s going to make you thirsty, right? To try and up your blood volume. Your brain hates low oxygen and it will make you feel anxious, you will get restless, you’ll feel anxiety. And neural is going to induce SNS. Right. So as a result of SNS, you’re going to up your heart rate, right? So you may even be in tachycardia because of low blood flow to your tissues. You may look pale. Your skin might be cool because the blood is going to be pooling in your visceral region. It’s not going to be making it to your, the superficial regions of your body. If blood’s not getting to your kidneys, not sufficient blood is getting to your kidneys. Then your kidneys can’t filter it to make urine. So you won’t be urinating as much, won’t be producing as much urine. If you’re in septic shock, instead of being cool, you might have a fever because that’s usually a go-to response with any type of infection is the pyrogens are released. So you might be feverish actually, but also with a rapid pulse. You might be hyperventilating again because of this hypoxia. Ok, your brain is going to give you some of the first signs and symptoms because your brain when it’s got low oxygen is going to feel it make you feel lethargic. weak, potentially dizzy. You might start to lose consciousness. You’re going to start breathing faster as a results of compensating for low oxygen. And you might be in a state of metabolic acidosis as well due to low oxygen. Remember your cells take on anaerobic cellular respiration and produce a lot of lactic acid. This will increase your respiration rate as well. If you breathe too quickly, remember you’re going to breathe out. If you breathe too quickly, you breathe out a lot of CO2. And if you breathe out a lot of CO2, then remember your carbonic acid levels in your blood go down and you actually might become a little bit alkalosis You might have a little bit of alkalosis in your blood. Just depends if you’re hyperventilating or not, Okay. And then of course, waste can start accumulating in your blood. Your brain doesn’t like that, it doesn’t like low oxygen and you can start losing unresponsiveness, maybe even entering a coma. If the pH of your blood drops below 7.35, it means you’re no longer compensating for being hypoxic. And basically trying to get that CO2 out of your blood. And your brain doesn’t like that, it becomes less responsive. And your kidneys don’t like that and they start going into kidney failure. Okay, with tubular or nephron ischemia and necrosis starting to occur in your kidneys. If your kidneys aren’t working, then you can’t get rid of waste and waste starts accumulating in your blood. So you get too much urea and creatinine, which of course your brain hates. That makes it work even less well. This whole flow chart goes through that same stages as we just went through. So remember with decreased blood pressure, compensation strategies involve SNS, sympathetic nervous system, as well as the renin, angiotensin 2 aldosterone ADH pathways. So as a result, you’re going to have vasoconstriction, which will make you look pale in the superficial tissues, you’re going to retain water and salts. You’re not going to be peeing out as much, you can be vasoconstricting. You’re going to try and retain water just to try and up your blood pressure to keep flow going to your tissues. Unfortunately, if things get worse, your brain is going to start showing signs and symptoms of this. I’ll put up this little blurb at the same time where we’ve got it listed out again. And if you’re not peeing out waste, including excess of hydrogen ions, you may end up getting acidic in the blood. With this comes additional problems that we’d haven’t talked about. If your blood flow is now sluggish due to low blood pressure, it has a tendency to clot. And of course, those thrombi can then block up different capillary beds causing more ischemia. So your organs become less and less functional. The organs that rely on constant supply of oxygen, such as the kidneys, brain, the retina starts suffering. Of course, if you’ve got low blood flow, you’re going to have low blood flow returning to your heart, which of course means low stroke volume and low cardiac output, meaning that you’re in a state of metabolic acidosis. producing a lot of lactic acid, and your brain will become less functional, your organs will become damaged and potentially you end up in organ failure leading to death. Okay, I think I’ve gone through all of those things now. You can see the complications we’ve already talked about. Really, you could just go through them and say complications include kidney damage, lung damage, liver damage, damage to the intestines. If there’s damage to the intestines bacteria from the intestines can start leaking out into your body, giving rise to septicemia. Bacteria can have toxins that make things even worse with sluggish blood flow and with potentially microorganisms in your blood, you may end up. DIC, which throw thrombi by and obstruct more capillaries. Just elevating the problem. Your heart doesn’t like an acidic condition or a low oxygen condition. And if cells are rupturing, if you’ve gotten necrosis in the liver or in the kidneys, you may have too much potassium in your blood. And the heart doesn’t like that either. So you could go into myocardial infarction. Certainly we’ve talked about how your cells and your organs become less functional and can start dying. Okay, so of course you’ve got to treat the primary cause and hopefully this doesn’t progress. I think we’ve talked about everything in this summary table now. So have a look at this and potentially it’s nice piece to study from the osmoreceptors. These are sensing basically though, the solute levels in your blood. So for example, if you’re dehydrated, then you’ll have less water and more solutes. And the medulla oblongata is where the osmoreceptors are. So they’re sensing all the time what your blood volume and blood composition is. So if it senses that you have less water and more solutes, it’s going to tell you that you’re thirsty. Okay, I think everything else we’ve made our way through. So I’ll put up this nice picture. And again, it’s the signs and symptoms as we’ve gone through them. So from the early stages of anxiety to the late stages of organ failure. So again, depending on what type of shock this person is experiencing if it’s hemorrhaging, that of course, you want to try and stop the bleeding. That’s how hypovolemic then you want to up the fluid levels of the blood through IV or potentially a blood transfusion. Anaphylactic shock. We know we’re going to treat with an epipen and antihistamines as well as anti-inflammatories would be very helpful. Septic shock, we want to treat the infection and that of course treat for that massive amount of inflammation that’s taking place. Shock in general, you want to supply supplemental oxygen. And then depending on what type it or shock it is, if it’s through massive vasodilation like anaphylactic shock, then you would want to treat with vasoconstrictors. And then of course you want to try and keep the person comfortable. You hopefully you’ve called 911 and you’re treating the underlying cause. OK. We’ve done plenty, I think for cardiovascular, hopefully I’ve given you a taste of many different things and all the common ones that affect people in Canada as well. So enjoy the rest of your day. I’ve got a brain break for you. I think these are hilarious. I find these on nursing Pinterest sites. I hope you think they’re funny too Here are some more. Diaphoresis means excessive sweating. Thought that was funny. Ok. And I’m going to include some animations now. So I hope you’ll stay tuned because I think they’ll really help explain aspects that we’ve covered in this unit. It’s always neat to see a little animation and it’ll help make things stick a little bit longer and hopefully build memories for exam and well for life, okay? Okay, Take care. Have a great one, and I’ll catch you in the next video. I’ve got some videos I want to show you. I think they’ll help illustrate what we were talking about. I hope you find them helpful. Here, they are. Normally the heart beats regularly at a rate of 60 to 100 beats per minute, triggered by its own electrical conduction system. In tachycardia, the conduction system doesn’t work properly, causing the heart to beat much faster than normal at a rate of more than 100 beats per minute. In contrast to this dysrhythmia or abnormal heart rate, bradycardia can occur. In bradycardia, the heart beats very slowly at a rate of less than 60 beats per minute. If severe, it may require a pacemaker insertion. Normally the heart beats at a regular rate of 60 to 100 beats per minute. Triggered by its own electrical conduction system. When this conduction system is working properly, the sinoatrial or SA node acts as the heart’s natural pacemaker. The SA node generates an electrical impulse that travels to the atrioventricular or AV node, bundle of HIS, right and left bundle branches and purkinje fibers. Each time an impulse reaches the Purkinje fibers, it causes the atria and ventricles to contract, which creates an heartbeat. When problems develop in the heart’s conduction system, the SA node may not work normally. This can cause the heart to beat too quickly. Too slowly, or irregularly. An abnormal heart rate is known as a dysrhythmia. Bradycardia is a dysrhythmia with a heart rate below 60, which can be life-threatening because it is so dangerous. Bradycardia is one of the most common reasons for pacemaker insertion. A pacemaker is a device that restores the heart’s natural rhythm by providing electrical signals to the myocardium. Although different types of pacemakers exists, they all have two main parts. A pulse generator, which is a small box with electrical components and a battery. And one or two leads, which are insulated wires that carry electrical impulses from the pacemaker to the heart. To implant a pacemaker, a surgeon makes a small incision beneath the patient’s clavicle, then guided by X-ray images on a video screen. The surgeon inserts the pacemaker leads into the subclavian vein and threads them towards the heart until one reaches the right atrium. If a second lead is used, the surgeon continues threading it until it reaches the right ventricle. After testing the Leads to make sure they’re working properly. Surgeon connects them to the pulse generator, then places the generator in a small skin pouch created below the clavicle. Finally, the surgeon closes the incision. After implantation, the pacemaker can take over the SA node’s job and keep the heart beating regularly and at the proper rate. Also known as aortic regurgitation. Aortic insufficiency, also known as aortic regurgitation, happens when the aortic semilunar valve leaks. It causes blood to flow backwards from the aorta into the left ventricle. When the left ventricle relaxes. Aortic insufficiency causes a volume overload on the left ventricle with subsequent hypertrophy and dilation of the left ventricle. The left ventricle attempts to compensate for the increased load by increasing its strength of contraction, this may eventually stress the heart to the point of myocardial ischemia. The usual treatment is to surgically replace the aortic semilunar valve. The human heart consists of four chambers and four valves. The valves prevent the backflow or regurgitation of blood between the chambers and the great vessels. The right atrium receives deoxygenated blood from the superior vena cava and the inferior vena cava. The blood pushes open the right atrioventricular or tricuspid valve and enters the right ventricle. The right ventricle pumps blood through the pulmonary semilunar valve into the pulmonary trunk and arteries, which carry it to the lungs for oxygenation. The left atrium receives oxygenated blood from the pulmonary veins. The blood pushes open the left atrioventricular bicuspid or mitral valve and enters the left ventricle. The left ventricle pumps the blood through the aortic semilunar valve into the aorta so it can be transported to the rest of the body. Both the right and left sides of the heart contract at the same time. So the heart is really a combination of two pumps. The blood flow to and from the lungs is called pulmonary circulation. The blood flow to and from the rest of the body is called systemic circulation. Mitral insufficiency, also known as mitral regurgitation, happens when the mitral valve leaks, causing blood to flow backwards from the left ventricle into the left atrium when the left ventricle contracts. Aortic insufficiency, also known as aortic regurgitation, happens when the aortic pulmonary valve leaks. It causes blood to flow backwards from the aorta into the left ventricle. When the left ventricle relaxes. Both of these conditions can result in insufficient volumes of blood being pumped into the systemic circulation, causing a reduced blood supply to the body’s tissues and organs. Blood may also backup within the pulmonary circulatory system, causing pulmonary edema. A potentially life-threatening condition. Sickle cell disease is an inherited disease that causes an abnormality with the hemoglobin in the red blood cell. This abnormality causes the red blood cell to die early and the bone marrow often cannot make enough new red blood cells to counter the early destruction causing anemia. Normally, red blood cells are round and flexible and can move freely throughout your blood vessels. In sickle cell disease, the red blood cells are sickled or C-shaped and are rigid and sticky. The abnormally shaped red blood cells clump together in smaller blood vessels and cause a blockage that decreases or cuts off the blood supply to healthy tissue. This lack of oxygen to the tissue causes severe pain, known as a sickle cell crisis. If left untreated, hypertension can lead to a thickening of arterial walls causing the lumen or blood passage way too narrow in diameter. As a result, the heart must work harder to pump blood through the narrowed arterial openings. In addition, people with hypertension may be more susceptible to stroke. The heart relies on the coronary arteries and their branches for its blood supply. Normally, this blood carries oxygen to the myocardial cells throughout the heart. In a patient with coronary artery disease, however, lipids and other substances can build up within the vessel walls. This atherosclerotic plaque can eventually cause the walls to calcify. It also may block blood flow in the vessel. If blood can’t pass through the blocked vessel, it can’t reach the myocardial cells it normally supplies. Without oxygen. These cells soon die or are damaged. This is how coronary artery disease can lead to myocardial infarction. Angioplasty is a procedure that restores the flow of blood through the coronary arteries that have a narrowed or blocked by atherosclerotic plaque. To perform an angioplasty. A needle is inserted into the femoral artery. Then a guide wire passes through the needle and is gently advance through the arteries to the heart. Next, the needle is removed and a small flexible catheter is slipped over the guide wire and threaded upward. Once the catheter reaches the heart, the catheter tip is positioned inside the affected coronary artery and a contrast dye is injected. Guided by X-ray imaging. The physician identifies any blockages as the arteries fill with dye. Next, a guide wire is advanced and a balloon tipped catheter is slid over it until the balloon reaches the site of the blockage. Rapid balloon inflation and deflation opens the blocked artery. When blood flow has been re-established, the deflated balloon and catheter are withdrawn to maintain artery patency. Some patients also receive an expandable steel mesh tube or stent at the blockage site. If needed, a collapsed stent is placed over the deflated balloon before it is inserted into the artery. When the balloon is inflated, the stent expands and locks into position. Then the balloon catheter are withdrawn. The stent keeps the artery open permanently. Normally the coronary arteries supply blood and oxygen to the heart muscle. In a patient with coronary artery disease, however, atherosclerotic plaque can build up. If too much plaque accumulates, one or more arteries can become blocked, which can prevent oxygen from reaching the heart. This can cause tissue damage and possibly death. To improve blood flow to the heart, a patient may have a coronary artery bypass, graft or CABG of the blocked arteries. In the traditional open heart form of the surgery, a six to eight inch incision is made in the middle of the chest than the sternum is cut-through and the rib cage is moved to examine the heart. Next, one or more healthy graft vessels are selected for the bypass. Commonly used vessels are the internal thoracic or mammary artery in the chest and the saphenous vein in the leg. Alternatively, an arm or wrist artery may be used. Next, the heart is cooled to keep it still using a heart-lung bypass machine and is connected using plastic tubes. One tube carries blood from the body to the bypass machine, which supplies it with oxygen. The other tube pumps the oxygenated blood back to the body. In essence, the blood bypasses the heart and lungs to get to the rest of the body. Now the grafting can begin. The distal end of the internal thoracic artery is dissected and attached to the left anterior descending artery below the blockage. Then sutures are placed at one end of the saphenous vein to the aorta and the other end to the right coronary artery below the blockage. When the graft is in place. Electrical signals are used to restore the heartbeat. Then the patient is disconnected from the heart-lung bypass machine. Finally, the sternum is wired together and the incision is closed with sutures. Instead of the traditional CABG procedure. A patient may also undergo one of two alternative procedures, off pump or beating heart CABG and minimally invasive bypass surgery. In off pump or beating heart CABG. a mechanical device is used to steady the part of the heart where the grafting occurs. a minimally invasive bypass surgery, specially designed instruments are inserted through small incisions in the chest rather than opening the rib cage, as in traditional CABG surgery. All types of coronary artery bypass graft surgery allow freshly oxygenated blood to bypass the blockage and reach the distal heart muscle. The pericardium is a double walled sac that surrounds and protects the heart. Normally, the space between the two walls contains just a few millimeters of fluid, which let the heart move without friction. However, in injury or a disorder can cause excess blood or fluid to accumulate in the pericardium, causing cardiac tamponade. In this dangerous condition, the blood or fluid buildup puts pressure on the heart. As a result, the heart can’t expand completely or pump effectively. Cardiac tamponade is an emergency and requires immediate evacuation by pericardiocentesis. For this procedure, the physician uses an eight inch, 16 or 18 gauge needle and inserts it into the xiphoid region at a 45 degree angle, aiming at toward the left shoulder. Once the needle is in the pericardial space, the physician withdraws the blood or fluid because pericardiocentesis immediately corrects cardiac tamponade. It is the treatment of choice.