let's take a quick look at hypertension and go through some of the main antihypertensive drugs. Firstly, let's just recap a lot blood pressures. Blood pressure is the amount of force that the blood places upon the walls of your blood vessels. So when your heart contracts and pushes blood out, that blood has some sort of force behind it. And as it comes out, it's going to put some form of pressure on the walls of your arteries. Now you measure this with a cuff, and you place that cuff put only around the brachial artery. And that's a branch of the aorta. And as the blood comes through, it put some pressure on. Now there's two phases, two predominant phases: the systolic phase. This is one heart contracts and pushes the blood. So that's when the blood is at highest pressure. And then the diastolic phase when the heart relaxes and again Bloods been pushed upon the walls because of the recoil of the annular. And this is the diastolic value. So if you were to

take consistent measurements from a patient when the patient's at rest. What is considered a normal blood pressure? Well, a normal blood pressure is a systolic value of below 120 and a diastolic value below 80 millimeters of mercury. Okay, what if you have consistent measurements above this? Well, if you have measurements between 120 to 129 for the systolic and measurement from 80 to 89 for the diastolic, this is recognized as being pre-hypertension. So, not yet considered hypertension, but it demonstrates that this patient may potentially develop hypertension at some point down the track. What if a patient you get consistent measurements of 140 and above and 90 and above? 140 and above for the systolic, 90 and above for the diastolic, again it's in millimeters of mercury. This is recognized hypertension. So today when we're talking about hypertension, we're talking about consistent measurements of blood pressure taken by the patient taken from

the patient is hypertensive when they're at rest, and these measurements are above 140 and above 90 millimeters of mercury. Normal blood pressure readings are around 120 over 80. And how does this change to anything above? Well, we need to talk about blood pressure in itself and talk about what factors contribute to blood pressure. So there's an equation that tells you what are the contributing factors. Blood pressure is equivalent to cardiac output. Remember, cardiac output is the volume of blood that is being ejected by the heart per minute, multiplied by systemic vascular resistance. Systemic vascular resistance, now systemic vascular resistance is also called peripheral vascular resistance or total peripheral resistance. This is the resistance that blood encounters through blood vessels and basically has to do with the diameter of the blood vessel and the length of the blood vessel. Okay, blood pressure is equivalent to cardiac output, how much blood is being pumped out per minute, times systemic vascular resistance, the resistance that the blood faces as it moves through the lumen of those blood vessels. Let's first focus on

current output what is what defines current output so what are the contributing factors for this well if it's the volume of blood they pumped out per minute then the contributing factors would be stroke volume do you remember what stroke volume is that's the volume of blood being pumped out per contraction and it would also be heart rate which is how many times as the heart beat permanent so kavik output is stroke volume times heart rate stroke volume is about 70 mil so every time that left ventricle contracts pushes out about 70 mils of blood it does this about 70 times in a minute 75 ish times so certainly mils times 72 75 times gives you approximately five liters which means cardiac output is approximately five liters all right systemic vascular resistance this is how I like to think about it if you have a blood vessel you know blood vessels are hollow so you've got a blood vessel and it has quite a large lumen so it's quite painted quite open

compare that to a blood vessel that's contracted and has a small wound. Well, when blood moves through this blood vessel, which one is going to experience greater resistance? Well, it's going to be harder for the blood to move through this one here because it's narrower, okay, which means that this blood vessel has low systemic vascular resistance, and this blood vessel has high systemic vascular resistance, which means that when blood vessels constrict, it results in systemic vascular resistance. And what that means is blood needs to pump harder to get through, which means increased systemic vascular resistance results in increased blood pressure. In actual fact, if you look at all of these factors here and see how they contribute to altering blood pressure, if you increase cardiac output, you'll ultimately increase blood pressure. If you increase the stomach resistance, you'll increase blood pressure. If you increase heart rate, you'll increase blood pressure. If you increase stroke volume, you'll increase blood pressure as well. Now, what are some of the factors that affect stroke volume? So the amount of blood that's pumped up out / contraction.

well that's easy. That has to do with blood volume. And what else? Well, blood belly needs to get out so hard is a contract to contract ility. All right. Well, if we were to look at the major factors affecting blood pressure, you would say that they are blood volume. You would say they are contractility. You would say that they are heart rate. You would say that our systemic vascular resistance, which means now somebody has hypertension, we want to treat their hypertension. We need to give them antihypertensive drugs. What do these drugs do? They will either try and reduce systemic vascular resistance by dilating blood vessels. They will try to reduce heart rate by either stopping the sympathetic nervous innovation, but but predominantly the way the valve done contractility. What for causes muscle to contract calcium influx causes muscle to contract. So by reducing calcium or by reducing blood volume and they can do this by inhibiting the renin-angiotensin-aldosterone system, which you know when it gets stimulated.

increases blood volume or by giving a patient some form of diuretic. Diuretic increases the urine output, again reducing blood volume. So, these are the major factors that contribute to pressure, and these are the factors that ant our potential medication and play around with to alter blood pressure. Now, there's three different types of hypertension: primary hypertension, primary hypertension also known as essential hypertension. We don't necessarily know what the cause is all the time. There's secondary hypertension, which means that the hypertension is secondary to some other underlying cause, which means if you treat the underlying cause, the hypertension disappears. And you also have a malignant hypertension, which is a rapid onset of hypertension, which is associated with organ damage or organ failure. Today, we're just going to focus on essential or primary hypertension and some of the common meds used for that. So, I'm just going to use this little area here to write in common type some antihypertensive drugs, and we'll talk about how they have their effect in this.

system what I'll do is just rewrite that over here kind of get with time systemic vascular resistance. Okay, let's have a look at some of the antihypertensive medications. So first, I want to talk about are what we call the beta blockers. Now, beta blockers, you should know that beta now it can be written like that or it can be written as beta beta blockers. So, your sympathetic nervous system will stimulate certain receptors. So, remember that if you look at a sympathetic neuron that the sympathetic neuron that innervates the target organ, let's just say the heart for example, has to release a neurotransmitter at the synapse. Once the neurotransmitter released at all sympathetic neurons at the target organ at the effect organ, it will either be adrenaline or noradrenaline, which means adrenaline and noradrenaline need to bind to specific adrenaline or more adrenaline receptors called adrenergic receptors. Remember, you've got alpha 1, alpha 2, beta 1, V 2 V.

3 adrenergic receptors. What are the receptors specifically located on the heart? They are the beta 1 receptors, which means that for beta blockers, you can have what we call selective beta 1 beta blockers. So I'll just write selective, selectively beta-1, and examples of selective beta-1 atenolol, atenolol, and also metoprolol. You can see that the beta blockers are the long jogs. Now these are selective, which means they will specifically bind to beta 1 receptors on the heart. Okay, which means what? Well, if they have, if you've got the sympathetic neuron and it's releasing adrenaline. If the adrenaline or origin then binds to this beta 1 specific receptor, what happens to the heart? While the heart rate increases, then the contractility of the heart increases. If adrenaline, adrenaline binds to it, is stimulated. Beta blockers such as atenolol and metoprolol, they will bind to this receptor and then tag it, which means it does not get stimulated.

means heart rate decreases. If you decrease heart rate, you decrease blood pressure and contractility decreases. Decrease contractility, increase blood pressure. These are the selected beta blockers. There's non-selective beta blockers as well. For example, I'll write it over here, the non-selective beta blockers. And the non-selective are propranolol, among medications. And propranolol is nonspecific. Which means, what does that mean? Well, okay, let's look at that beta receptors. I said that you've got beta 1, beta 2, mu 2, 3. And I said beta 1, you find at the heart. Where else do you find beta 1? Except it's also found at the kidneys, well not beta 2. Well, you can find beta 2 on vascular smooth muscle. You can find beta 2 at skeletal muscle. You can find beta 2 at the bronchioles of the lungs as well. But I've been to 3, you find beta 3 in fat cells basically. Now when we look at the selected beta blockers, they bind

specifically to b21 and inhibit the effect of the sympathetic nervous system at the heart, and also at the kidneys, which means less running is released. Remember that will know the non-selective well, that means they block all three. Now they block the heart, that's fine, same effect as beta one blocking fat cells, who cares me too - well what's the major adverse effect that you'll find here if it's blocking activation from the sympathetic nervous system at the lungs. Remember what happens, stimulate your fight or flight system, flight or fright or fight. If you stimulate that system, what happens, the bronchioles of your Airways dilate, you get more air in, more air out, that's good, you can have more oxygen to run away, but if you block that, what happens, the opposite, it constricts. So it's not wise to give non-selective beta blockers patience with already existing reversible airway diseases such as chronic obstructive pulmonary disease, emphysema, and asthma. Okay, let's move on. So the beta block is well, let's

come to look at let's look at a singer's okay firstly what's X ace is angiotensin-converting enzyme. You need to go back and watch the movie or the video on the red and angiotensin aldosterone system or do some reading out and you'll realize that before angiotensin 1 can be converted into angiotensin 2 and enzyme needs to come into play. In order for this to occur, that enzyme is angiotensin converting enzyme. Now what's important about this whole process here? Well, once we make angiotensin 2, angiotensin 2 has a number of different activities in the body. First of all, it's a vasoconstrictor, a potent vasoconstrictor, which means if you can strip blood vessels, what are you doing? You're increasing systemic vascular resistance, increasing blood pressure. But also, angiotensin 2 do it results in the release of aldosterone. Why is that important? Aldosterone promotes sodium reabsorption at the

kidneys back into the blood. More sodium into the blood, more water into the blood, more blood volume, increase blood volume, increase blood pressure. What else? Angiotensin 2 stimulates the release of antidiuretic hormone. What does that do? It tells the kidneys to hold on to water. Again, holding on to water increases blood volume, increases blood pressure. So, angiotensin 2 is released into the body to increase blood volume and blood pressure. Therefore, if you inhibit its production via ACE inhibitors, then what happens is you reduce blood pressure. A common medication is an oral pill, is a common ACE inhibitor. Okay, let's move on. I'll write that over here so I've got more room. Okay, let's look at the angiotensin II receptor antagonists. So, this doesn't need too much explanation because I just spoke about it. You can use ACE inhibitors to stop angiotensin 1 into creating angiotensin 2 or you can use angiotensin 2 receptor antagonist, which means get stopped the

ability of angiotensin 2 to binding to its receptors, which means it stops maser constriction. It stops aldosterone release, stops ADH release, and stops or reduces blood pressure. These are the statins, and a common one is candesartan. So there's a recap: tweeter blockers are the lulz ACE inhibitors, other prills, angiotensin II receptor antagonists are the statins. Let's keep going. What else do we have? We've got calcium channel blockers. Now remember what calcium does. Calcium is one of the most abundant extracellular cations, okay, so that means it's positively charged, as you can see here, and it's located outside the cell. When it enters the cell, it can do a number of different things. It can act as a secondary messenger, so it can tell certain things to happen inside the cell, or it can tell muscles to contract. So if you block calcium from entering myocardium heart muscle cell, you can reduce its ability to contract. It's one thing. The other thing is that

certain cells of the heart, such as the nodal cells (sinoatrial node, atrioventricular node). In order for them to depolarize, they require calcium to come in, which means these calcium channel antagonists or calcium channel blockers. What they can do is they can inhibit or reduce the depolarization event of the AV and SA node, slowing the heart rate down and reducing its contraction. There are three major types of these calcium channel blockers. The first one is nifedipine, more than a feather peanut-like drugs. Alright, these drugs do a couple different things. First, they need to be aware that there's not just one type of calcium term, there's many different types, and they're located in many different parts of the body. In actual fact, one organ may have many different types of calcium channels, which means that these different types of calcium channels have certain specificity and may or will have different effects. For example, nifedipine you find is predominantly found on the vascular smooth muscle. The Philippine, I should say, acts at calcium

channels at the vascular smooth muscle, blocking calcium's effect, reducing ways of constriction resulting in vasodilation, reducing systemic vascular resistance, reducing blood pressure. It also seems to have an effect as an angiotensin II, sorry, aldosterone, as an aldosterone receptor antagonist as well. Once I say that means, well, if you stop aldosterone from evidence effect, you stop sodium is a reabsorption, stopping water absorption, reducing blood volume, which you see blood pressure. What other types of calcium channel blockers do we have? We've got Marama pill. Where did these particular drugs have their effects? Well, they tend to work on calcium channels, so block calcium channels at the nose. So si lo hey, we know, so nodal blockers and what you refer to as conductive tissue. So Marama pill blocks the sodium channels at the nodes and the conductive tissue, reducing arrhythmias. So this is a common 88 arrhythmia medication as well. Okay, what's the last one I want to talk about? Diltiazem. Where does the attires

intend to have its effect at the coronary vascular chart. All right, last thing I want to talk about, don't have too much room here. It is so I'm going to have to get rid of the meter blockers other diuretics. Now the diuretics active the kidneys specifically at the nephrons and predominately reduce sodium reabsorption, which means increases the amount of sodium that gets peed out, which means increases amount of water that follows, increasing the volume that you pay out, reducing blood volume, reducing blood pressure. The most common sort of diuretic that would be used as an antihypertensive medication under fire science. Okay, now why would we use that whether Phibes work first of all at the distal convoluted tubules. Why would we use a loop diuretic, for example, acting at the loop of Henle. Well, they're very potent, very powerful, and they're short-lasting. So you'll find that the thiazide is actually longer-lasting and tend to be more.

effective for as anti-hypertensive medications. They commonly use in conjunction with one of these other medications. Now what does this lie as I do at the distal convoluted tubules stops sodium from being reabsorbed. So if you look at the nephron here at the distal convoluted tubules, you've got cells in the walls here. It's locked sodium from being reabsorbed back into the body, which means sodium stays in this tubular, which means water stays in this tube you'll, which means what gets paid out sodium and water, reducing blood volume. Now all directs our act prior to this area here result in potassium being paid out as well, which means that it's not a potassium-sparing diuretic, which means that potassium may also be paid out as well, so you need to be careful with the potassium levels of the patient this medication. So these are the major drugs this is hypertension. I hope that all made sense. Best alike.

Hypertension & Anti-hypertensive drugs

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