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[Music] what's up engineers today in this video we're gonna talk about congestive heart failure before we do that though ba-bang guys we are so happy so proud to be at this point right now in this channel that what we have right here this silver play button it is because of you guys and you guys alone we thank you guys are the best fans we thank you for your support your kind comments amazing emails and messages we love you guys so much and again thank you guys this is
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because of you and we thank you so so so much also we got our nice little studio set up today we aren't completely done with it but once we get everything all finished up we'll give you guys a nice little tour of our nice little ninja nerd headquarters alright guys let's go ahead and get started congestive heart failure alright guys so what we're gonna do is we're gonna talk about congestive heart failure super common disease that you guys should be aware of you see it a
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lot in health care like you see it a lot in the hospital you see a lot outpatient you're gonna see it a lot on your exams there's a lot of high-yield points that we're gonna try to get in this this video today all right so first thing that you guys need to know there's different types of heart failure there's what's called systolic heart failure diastolic heart failure there's a left side heart failure which is way more common there's a right side heart failure less common and then we'll talk
1:27
about another one which is called high output cardiac failure so the first one that we're going to discuss here is gonna be systolic heart failure so let's talk about this one first so well the first one we're gonna talk about here is called systolic heart failure HF here okay so systolic heart failure what does that mean okay systolic heart failure means that this heart the ventricles the myocardium isn't able to generate enough stroke volume okay and therefore if
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you're not able to generate enough blood that you can eject out of the ventricles with one heartbeat that's going to drop your cardiac output if you can't push out enough cardiac output your blood pressure might also drop as well now why is this a systolic heart failure what's the reason why the myocardium isn't pumping enough there's a bunch of different reasons okay but again let's go back to this thing here so Stalag heart failure go back to this equation
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forget this equation cardiac output is equal to the heart rate multiplied by your stroke volume you guys thought physiology was over no it's coming back so you guys remember if there's a drop in this is the the stroke volume there's a directly proportional drop within the cardiac output well what a stroke volume depend upon you guys remember the three things that stroke volume depends on so remember stroke volume depends upon three specific things one is preload
2:53
right and we said that whenever use of you increased stroke volume you increase cardiac output right if we increase preload that increases your stroke volume what's preload you guys remember preload is when there's an increase in the stretch of the myocardium in other words there's an increased filling there's increased venous return there's a lot of blood in the heart before it contracts that's preload second thing that stroke volume depends upon is contractility so
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contractility right so contractility if this increases what does that mean that means that they're generating more force if your ventricles can generate a larger force what does that mean for the amount of blood leaving the ventricles it's more so this is directly proportional the only one that is inversely proportional is afterload and afterload is going to be if we actually decrease the afterload you increase the stroke volume what does that mean okay imagine the pressure inside of the aorta
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is really high so someone has hypertension so they have a high pressure here we'll say here we'll put high pressure high BP the ventricle it's gonna have to push and really really generate enough force to push blood out of the left ventricle and into the aorta normal blood pressure is what ideally so normal BP is usually anywhere like 120 over 80 that's what we would like it to be right so 120 is the systolic pressure 80 is the diastolic pressure but what happens if someone actually has a high
4:28
diastolic pressure so now let's say that we increase it from 80 we increased it to 100 so if it's 120 over a hundred are we gonna be able to pump as much blood out look at the pressure gradient it was 40 so the pulse pressure was 40 now it's 20 I'm not gonna be able to push the same volume of blood out with that systolic pressure when I have us diastolic pressure of 100 I have to increase my systolic pressure now so that's the problem whenever you decrease the afterload you decrease this
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diastolic pressure the pressure that you have to overcome to push blood from the ventricles into the aorta right or into the pulmonary circulation depending upon which side you're talking about so a diseases that affects preload diseases that affect contractility and diseases that affect afterload can lead to systolic heart failure let's think about these now let's go with the most common one first contractility this one is you're gonna see most of the diseases
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affecting this so contractility let's think about it if we want to drop our stroke volume so let's now let's flip the arrows now we want to flip the arrows here if that's the case then let's think about this rationally okay if I drop my contractility I drop my stroke volume so if I drop my contractility I drop my stroke volume if I drop my stroke volume I drop my cardiac output that's the stolid heart failure right so I have to drop my contractility what kind of diseases would decrease the
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contractility of my heart well what if someone had a significant myocardial infarction that wiped out a big portion of their myocardium like an anterior mi the anterior portion of your ventricle your left ventricle it controls 60 to 70 percent of your pumping function if you take that out you're going to decrease the contractility of the heart so we can say if someone has a a myocardial infarction particularly in anterior or we can even say lateral MI so these are gonna wipe
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out a significant portion of your pumping function pretty simple right pretty straightforward that would make sense what if someone has a disease that maybe they have an idiopathic what's called dilated cardiomyopathy what dilated cardiomyopathy is is the ventricles they're the muscles really thin it's weak and the chambers are really globular they're really big so because of that it doesn't have the strength it needs to pump out blood so I'm patients who have what's called
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dilated cardio myopathy I like to think about this as a like a really flappy or fly yeah a little flappy heart okay and the reason why I think about it as a flappy heart is it doesn't it's really big it's really cardiomegaly so they have this big big ventricular chambers and a really thin myocardium and it's not able to generate enough force to push blood out that's a simple cause right so that's one reason so these are gonna be some of the big ones here contractility if you have a decrease in
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contractility it could because you had a significant in mind ischemic heart disease is a very very common cause or dilated cardiomyopathy and dilated cardiomyopathy has so many different reasons why people can develop this it could be because of a viral infection it could be a bacterial infection it could be idiopathic causes where we don't know why it could be because they have autoimmune diseases that are actually causing damage to the myocardium maybe because they have
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infiltrated disorders like maybe cancers or sarcoidosis or hemochromatosis different things like that okay it could be because of alcohol sometimes people have drink they drink a lot of alcohol they call it holiday heart syndrome that can also cause dilated cardiomyopathy so there's multiple different reasons why someone can drop their contractility the most common ones that I want you guys remember that are high yield is ischemic heart disease particularly M eyes
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anterior lateral nature and dilated cardiomyopathy let's move to the next one what if we actually increase the preload and we have someone who already has a decrease in contractility whoo that's bad so if I increase the preload right let's think about this you guys are probably gonna be like wait that doesn't make any sense Act why would you do that let's just follow with me for a second let's say that now I increase the preload technically you increase the
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preload what is that supposed to do the stroke volume supposed to increase it right but what if their muscle isn't able to contract well enough to push the volume of blood out what does that mean so like this think about like this guys you have a heart here right okay you put in this heart originally let's say originally you have in here a hundred and forty milliliters right that's your edv okay now this muscle is super weak so let's say that we generate a contraction
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after we generate a contraction okay let's say that afterwards there's still 100 milliliters that wasn't a very good contraction we only pushed out 40 milliliters generally what you want whenever you have an ejection fraction is you want it to be about 1/2 ideally so we would like it to be down to 70 milliliters okay but let's say that it's not it's less than that I only pumped out 40 milliliters I should have pumped out a total of 70 milliliters my ejection fraction is really low now
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let's say on top of that after this heart contracted it's in diastole now I'm gonna bring more blood to it okay this heart's already jacked up I'm gonna fill it up even more during the venous return part now I'm going to bump it from a hundred let's say I bump it up to 150 so now before it contracts it went from 100 it had this venous return so now let's say that there's venous return and before it contracts again look how much blood you have in here so now we're up let's say
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that we're up to about let's say that we increased it to about 150 mils so now you have 150 mils and you just keep accumulating blood so during this venous return where you had 50 milliliters of blood come back you went from 100 right went back to 150 now you're gonna try to pump out let's say that they keep trying to pump out only 40 mils eventually every single time you're just gonna keep accumulating more and more and more blood less blood is getting out of the
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heart and more blood is sitting in the heart that's not gonna help us so think about first second I want you guys to think about for a second if someone already has a damaged heart and we decide to put more blood or keep more blood in their heart that's a good thing to think about as well I keep more blood in their heart less is going out what is going to do this for me what's going to cause more blood to accumulate what if somebody has what's called mitral regurgitation what
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if somebody has a or t'k regurgitation why would that be the case well think about it if I try to contract blood out right I want blood to leave so I want blood to be able to leave from my ventricles and to go up into the aorta well if someone's valve is all jacked up where's it gonna go whenever it's supposed to come back down and snap that Valve shut it's gonna go right back into the ventricle so it's generally you want blood to only go in one direction and
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that's from the left ventricle into the aorta if that valve is damaged though where's the blood gonna go back it's gonna go back into the ventricle because that valves not doing its job so what does that mean then after the person's contracted they're injected some of the blood out they're gonna have blood accumulating into the ventricles but because they it didn't eject enough out because that valve is all jacked up another thing what if whenever they're ejecting blood out into the aorta some
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of the blood goes back into the atria because that mitral valve is not working properly if some of that blood goes back into the atria because it didn't all go out into the aorta some of that blood is gonna trickle back down to the ventricle again so you're not getting enough blood out so if we think about that increase in preload think about it this specifically increase in preload with a decreased contractility okay because if your muscle is actually somewhat able to
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generate enough force you might be fine for a while until eventually this starts actually causing the muscle to become weaker and weaker and weaker so yes initially if there's an increase in preload you're gonna try to increase your actual stroke volume assuming that the heart is okay assuming that it can maintain contractility but over time that's going to take a toll on the heart and eventually the muscles in become weak when that muscle becomes weak and there's a decrease in contractility and
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this increase in preload eventually that's gonna cause there to not be enough blood being ejected out of the heart okay simple stuff now afterload really doesn't apply too much to the systolic heart failure and I'm gonna explain why it's more applicable when it comes to things particularly with diastolic heart failure okay so for right now I want you to remember that the main things for systolic heart failure are going to be an increase in preload with someone who
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already has a decrease in contractility those are going to be the main situations here so these are big things that I want you guys to remember when it comes to conditions particularly such as systolic heart failure okay that is really really important okay so these are the big conditions that I want you guys to remember now when we go to the next disease okay diastolic heart failure this is another one that you're gonna see and let's talk about this one so diastolic
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heart failure okay so what does it mean for someone to have diastolic heart failure well if you guys remember decrease if you have systolic heart failure that what would did we say was the overall overarching theme there was a decrease in cardiac output the outflow the blood ejection was decreased there was a decreased ejection fraction that's important they're not getting enough blood out of the heart okay in this condition the person's ejection fraction might be okay
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they may have a normal ejection fraction or what we call a preserved ejection fraction the issue with this condition is that they're actually not able to fill properly okay so they have a decrease filling activity and I'll explain what that means okay and the second thing is there afterload is high okay so two things that I want you guys to remember for this one so again diastolic heart failure big things that I want you to remember here is that there is first thing is that
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there is actually specifically a decrease in the actual venous return okay so let's talk about that so let's say a decrease in the preload so what does this mean okay well we say normally what would you say a decrease in preload would decrease stroke volume and decrease cardiac output right that's the idea with that let's get a little bit deeper into this in conditions where there's a decreased preload specifically with diastolic heart failure the heart is really
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stiff okay so let's write down some buzzwords here the heart is stiff okay it's fibrotic it's non-compliant okay which means it doesn't want to stretch these are some big words that help you to kind of like remember this diastolic heart failure it's stiff it's fibrotic it's non-compliant it doesn't one stretch what kind of conditions would make the heart not want to stretch properly well let's think about it the muscle is normally pretty distensible right it does like to stretch a little
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bit what if I replace that muscle with fibrous tissue so sometimes the people with ischemic heart disease so again I can come back to this people would decrease preload it could be because they have a schema card disease so you could see patients who have diastolic heart they are secondary to M eyes or you can also see someone with a systolic heart failure secondary to an MI so remember decrease in preload it could be due to a myocardial infarction okay cool well what else what if the muscle is
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infiltrated with a lot of different types of substances that decreases its ability to be able to stretch you know there's a disease called restrictive cardiomyopathy super rare but it can't happen in patients who have what's called amyloidosis where there's a lot of light chains that get deposited into multiple tissues one of them is the heart and because of that it actually loses some of that normal heart tissue which stretches if you lose the stretchability
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what does that mean it doesn't want to distend so another condition that you want to be aware of is called restrictive cardiomyopathy okay restrictive cardiomyopathy disease is like someone has cancer and they get radiation therapy that really messes up the myocardium or they have amyloidosis or they have hemochromatosis where they have a lot of iron that gets deposited into the tissues or what's called sarcoidosis that's another one where you get these non cake-eating granulomas
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they get deposited into different areas of the body so those could be some of the reasons okay so that's one thing decreased preload what's another one here's another thing to think about what's around the myocardium so you have endocardium myocardium and then what's around that pericardium right the pericardium is generally it doesn't want the heart to overfill but it does allow for some extent expansion right what if there's something that's actually causing that pericardium to become so
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thick and so fibrotic so inelastic that even when the heart is filling it doesn't allow for the heart to move at all into the pericardial cavity what is that called constrictive pericarditis what if somebody has pericarditis particularly constrictive pericarditis so constrictive pericarditis that could be one reason another one it could be an acute onset if someone has cardiac tamponade so that would be more of an acute situation okay so if someone that's cardiac tamponade that's not
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gonna allow for any filling whatsoever because you have so much fluid accumulating in the pericardial cavity that it's strangulating the heart not allowing for it to fill properly so that's another one that you can think about as well okay well I told you decrease preload and the other thing that I wanted you to remember here is afterload okay so big thing for systolic is contractility preload big thing for diastolic is preload afterload okay well what's going on with the after load this
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right here is there is an increase in after load okay now let me explain what I mean by this we already talked about what after load is right it's anything that basically basically increases resistance of blood being able to flow from the ventricles into their arteries well what kind of thing could I do out here in this a Horta that would make it harder or make it higher pressure more resistance for blood to go out what if I had hypertension that doubt do it right
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so if I had hypertension if I have really high blood pressure out here that's gonna make this ventricle have to work harder if a ventricle works harder acutely what's gonna happen how do you adapt to an increase in pressure you have to respond to that by making your myocardial cells bigger you make more sarcomeres if you have more sarcomeres the cell gets bigger if this cell is bigger with more sarcomere that's gonna generate more power and that's going to help to
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push blood out so that's going to be something that will happen in the acute end of this later on that my accordion becomes so weak that eventually starts to becoming flabby and then eventually it could lead to a systolic heart failure so sometimes what you want to remember is that diastolic heart failure you can easily progress into it's a Stalag heart failure okay so let's come back to this increase after load what could increase after load hypertension so if someone has hypertension high
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blood pressure so that's why this is the silent killer you got to catch this early in patients okay and treat them to decrease that afterload and decrease their risk of developing CHF okay well what's another thing what if this valve going from the left ventricle into the aorta is really stiff and I want normally what do you want valves to do right so think about this very simply what do you want valves to normally do open nice and easy right so imagine here
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I have left atrium I have left ventricle here I have my aorta and here I have my valves right when I contract this left ventricle I want blood to go straight out with note no issues I don't want it to be difficult for the blood to leave and I don't want blood to come back in right but if I have to push more and more and more just to open that valve a little bit because it's super thick or it's fibrotic for whatever reason I'm gonna have to generate more pressure to
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open that valve up enough what's that called aortic stenosis okay so think about patients who have let's call it a aortic stenosis and this can happen as you get older okay so people get older or they get what's called a rheumatic heart disease and that can cause a lot of issues with this as well sometimes people are actually born it's really weird you can be born with what's called a bicuspid aortic valve and it puts you at a higher risk of developing aortic stenosis all right let's go to
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another situation here if you have another thing here where we talk about an increase in afterload what if somebody has a congenital condition okay called coarctation of the aorta this can happen in Turner syndrome this can happen in a lot of other conditions but what if somebody has what's called a coarctation of the aorta okay of mayoruna what does that mean what the heck is that Zack think about like this let's continue on with this drawing here you got your aorta right and it's
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supposed to go into the aortic arch and it's supposed to look nice and beautiful like that you want it to be nice and nice and beautiful like that but let's say that for some unfortunate child or person here instead of it being beautiful like that there's this area where it just gets really narrowed okay and because of that what's it gonna do so proximal to wherever that little narrowing is what's gonna happen to the pressure proximal to that but what it's gonna increase because I gotta go and
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squirt five liters of blood per minute through that tiny little stinking space that's gonna generate a lot of resistance and that's gonna increase the pressure that's gonna be an issue there so if I cause that little narrowing it's gonna increase the pressure proximal to that that's another reason okay all right beautiful so diastolic heart failure what is the big thing that I want you guys to remember with this one is that this is primarily going to be a heart failure that can progress to
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systolic heart failure which can be due to situations such as a decrease in preload right the heart doesn't want to expand it doesn't want to stretch or it's got so much resistance in the aorta or in the pulmonary circulation we'll talk briefly about that with right-sided heart failure that you have to generate so much force and so the only way to generate a lot of force is to thicken your myocardium there's also one more disease that I want to think about here
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I just want to mention it real quick since we were talking about congenital heart diseases there is another one called hypertrophic obstructive cardiomyopathy okay congenital condition where sometimes patients they have this thick and thick thick thick thick myocardium but sometimes it even causes the interventricular septum to bulge a little bit so now if I have this sucker bulging a little bit I'm gonna have to push blood against across that bulging area and so because
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of that that can also cause some issues I'm not getting enough blood out because I'm gonna have to increase the amount of pressure I have to generate to push blood out of the ventricle against this bulging myocardium that's obstructing my aortic outlet okay so that's another thing that you want to think about alright so these are some of the big things for systolic diastolic heart failure systolic what I want you to remember is their big buzzwords here I kind of talked about it is that their
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their flob their flappy okay their dilated okay things like that I want you to remember that their flappy their dilated they're just really thin myocardium this one thick myocardium stiff fibrotic non-compliant this one's super compliant oh that's another good thing super compliant okay so it stretches a lot okay this one does not stretch beautiful all right so now guys what we're gonna do is we're gonna move on to right-sided heart failure it's pretty much the same thing that we talked about
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was the Stalag and diastolic heart failure and then we're gonna come back up to this in just a second I just want to mainly focus on the stroke volume I want to talk about how heart rate can basically affect systolic and diastolic but let's keep on with this whole stroke volume aspect so right-sided heart failure not as common to develop on its own but you can develop it you can develop it acutely you can develop it chronically however it's more common for
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someone to have left-sided heart failure lead to right-side heart failure and we'll explain why when we get into more of the pathophysiology and symptomatology okay for right now I want you guys to understand that right-sided heart failure it can develop from other reasons besides EFT side heart failure it's just more common to develop from left side heart failure so what are some of the things that could cause it well let's think about this what is something
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that could increase the afterload okay so let's think about this something that's going to increase the afterload what can do that well if I increase the afterload it has to be something that's going to be increasing the pressure in the pulmonary circulation okay well what do that or it could be my pulmonary valve system right what if my pulmonary valve is really really stiff and doesn't want to open for whatever reason so it could be from someone who has like
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pulmonic stenosis not a super common condition but you can develop it someone who has rheumatic heart disease right that could be a condition something that can also develop what if the pulmonary vasculature there's an idiopathic reason we don't know why but their vessels are constricted okay and they have pulmonary hypertension so someone has pulmonary hypertension that could be a reason why someone can develop bright sided heart failure over time right what if that
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pulmonary hypertension though you got to go back to this there's multiple reasons why someone can develop pulmonary hypertension right so one of the things is it could be because somebody has maybe they have a PE right what if somebody has a clot right what if they have a clot in their pulmonary circulation and that clot and the Perm pulmonary circulation is causing an increase in the pressure proximal to that actual clot the pressure is gonna build up here right you're gonna try to
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shunt it into other small arterioles but if you actually have a decent-sized clot you're gonna actually have this you know obstruction of blood flow and pressure is going to build up proximal to that that could also be a reason why someone could develop right-sided heart failure so but a good kind of goes along with pulmonary hypertension but just for the sake of it let's keep it consistent and just say as a separate cause it could be due to a pulmonary embolism but again
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realize that there's different stages of pulmonary hypertension and different causes of pulmonary hypertension and a pulmonary embolism can be one of those causes another thing that can cause pulmonary hypertension again but we're gonna just try to keep it separate here for a second is let's say that someone has underlying lung disease right specifically let's say that they have COPD so they have COPD or they have severe bronchiectasis or asthma anything that's basically gonna cause there to be
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a decrease oxygenation process here so now think about diseases like someone who has like COPD asthma right to go back to that VQ ratio normally that's equal to 0.8 now if someone has COPD asthma some type of an underlying lung disease you're going to decrease the ventilation to that area right and as a response to that what does your body do if you have like an alveoli here right and that alveoli is not getting enough ventilation are you going to allow for not enough blood flow
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to go to that area or are you going to constrict that vessel and send it to another alveoli that might have more oxygenation you're going to constrict these little vasculature going to this one and send it to a different area but here's the problem what if so many alveoli are damaged that even if you do try to constrict these vessels and send it somewhere else it's going to go to another area which is also hypo ventilated it's going to constrict and there's going to be so
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much vasoconstriction the pulmonary vasculature that it's going to cause the pressure proximal to that to increase so if so many of these actual pulmonary arterial are constricting the pressure proximal to that will build up that is called cor pulmonale okay and that's usually whenever someone has COPD or underlying lung disease that causes intense vasoconstriction of the pulmonary vasculature increasing the pressure proximal to that and that can lead to heart failure okay so that is
30:35
called cor pulmonale and again that's usually due to an underlying like COPD so someone who has chronic bronchitis emphysema okay now let's think about other situations what if somebody has a an increase in the preload and that increase in the preload over time obviously initially the myocardium might be able to sustain that and be able to contract and push enough blood out but over time what do we say it happens if you increase the preload over and over and over and over
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time the myocardium hypertrophy x' over time that hypertrophy starts decreasing the muscle starts getting really really weak and it loses its contractility it kind of goes back to this concept here what could be disease that increases the preload and eventually over time decreases the contractility and can lead to heart failure what if somebody has pulmonary valve regurgitation that could do it right because then the blood supposed to just go into the pulmonary vasculature
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where's it gonna go back down into the ventricle and it's gonna cause that ventricle to expand and expand and expand what if the tricuspid valve is regurge implied and some of that goes up into the right atrium and then it eventually comes back down and I'm stuck with again more volume of blood and my ventricle isn't strong enough to push all that blood out that could also be other causes so I also want you to remember an increase in preload and what can that be due to that could be due to
32:05
tricuspid regurgitation not a super common process you can see it in patients with IV drug users and they have Staphylococcus aureus that actually causes infective endocarditis of that valve and that valve starts actually degenerating and that can lead to it and again another one which is called pulmonary valve regurgitation and that's also not very common but again if you do develop certain diseases that cause that valve that did to generate blood can come back into the ventricles okay
32:36
another thing and this is something that's actually really important to remember what if somebody has a decrease in contractility and this is sometimes something that you can forget and if this smile card iam alright what if they got it in MI what did somebody develop a myocardial infarction on just this side here so they develop some fibrotic tissue and it's just in this area here what kind of em I would only damage the right ventricle in inferior mi right so
33:09
if someone develops a inferior mi right what shows up in two three a VF if you guys remember from your EKG so if someone develops an inferior mi that can also take out your right ventricle as well and that could cause some problems another one that I didn't really mention but again it's not super common but you can see it sometimes in viral infections you can see it an infiltrate of diseases it also could be idiopathic there also could be autoimmune damage is myocarditis so myocarditis is also
33:41
whenever the myocardium is inflamed due to whatever pathological process it loses his ability to contract and if you decrease the contractility you're not pushing enough blood out and again that could also be another cause for heart failure I didn't really mention it in there it's not super common but don't forget about it myocarditis okay so this pretty much talks about our right-sided right-sided heart failure and again remember what I told you this could be
34:10
some of the reasons why someone develops right-sided heart failure but what did I tell you is the more common cause left-side heart failure left-side heart failure is usually gonna be one of the more common causes where someone's heart is failing and that leads to a backup of fluid and blood into the pulmonary circulation causing pulmonary hypertension and then subsequently right-sided heart failure again pulmonary hypertension has multiple different causes that can be idiopathic
34:34
alright it could be due to pulmonary embolism it could be due to an underlying lung disease or it could be due the left-sided heart disease okay so that's important to remember for that situation there could be miscellaneous causes as well so that's our right-sided heart failure last thing I want to talk about before we talk about some of the heart rate things that can also affect heart failure is if someone has not super common but again it can be on your exams it's called high output heart
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failure now here's something you need to realize these things that can cause high output heart failure don't usually cause heart failure on its own so what do I mean by that we're going to talk about some of the causes and they're kind of odd but it'll make sense but usually this occurs with an underlying
35:30
cardiovascular disease okay so someone has an underlying cardiovascular disease whether it be diabetes whether it be sleep apnea whether they smoke whether they have hypertension with a FC ad there's some reason why they develop heart failure it's not just disease causes it they have to have some underlying cardiovascular disease for it to precipitate what do I mean so let's say that the heart is already kind of damaged maybe not super bad but it has some underlying disease and I increase
36:03
the demand now if you guys remember there's you always kind of see like these little things in books you have like you know kind of like a little Wang thing here what happens is the heart the myocardium right it depends upon oxygen supply and oxygen demand right in order for it to function it kind of has to have a nice little equal balance of these two okay let's say that now because this heart is damaged and they have certain underlying diseases that increase the oxygen demand but the
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oxygen supply to the heart is not enough to meet the oxygen demand it's not equal now so let's say that for some reason this just isn't enough there isn't enough oxygen supply why because the person has an underlying cardiovascular disease that we're not going to like go into crazy detail about we just know that they have it but we have an increase in oxygen demand what kind of diseases increase the oxygen demand here's a very simple one and it can actually lead to it anemia what if
37:09
somebody has very severe anemia so if you have very severe anemia what does that do this can lead to hypoxia right you're not delivering enough oxygen to the tissues so what does your body have to do it has to increase the actual cardiac output it has to try to pump more blood out and more blood out that you can deliver enough oxygen to the tissues because your red blood cells are jacked up they're not delivering enough oxygen so now I got to deliver as much blood as I possibly can to compensate
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for that that's one reason what if I have a patient with they have a thiamine deficiency right it's called wet beriberi weird name but wet beriberi this is a thiamine deficiency this can happen in chronic alcoholics so chronic alcoholics who drink tons of alcohol don't really get a lot of nutrients they're deficient in thymine and that can cause an altered mental status like significant confusion it can cause a taxi a' where they kind of have a loss of their balance and being able to kind
38:16
of like stay coordinated and they can have what's called an optimal please aware their six nerve just goes all wonky and okay so they can have some six nerve palsy but another thing that it can do here is let's go back to biochemistry guys yes remember this from glucose glucose eventually gets converted into pyruvate right and then pyruvate gets converted into acetyl co a and then acetyl co a is supposed to go through the Krebs cycle alright well in order for pyruvate to
38:46
get converted into acetyl co if you guys remember you need what's called pyruvate dehydrogenase remember that at an enzyme a coenzyme vitamin b1 which is thymine that enzyme is not gonna work if you don't have find me because you need that coenzyme what happens then if you have glucose being metabolized into pyruvate but pyruvate isn't able to go down into the Krebs cycle you build up a lot of pyruvate where does pyruvate I love one stuff comes together you know I mean
39:15
pyruvate then gets converted into lactic acid what does lactic acid do when it's accumulated in your around your blood vessels what does it do guys it causes vessel it causes dilation so it's gonna lead to vaso dilation if you cause vasodilation you're gonna increase the shunting of blood from the arterial sign of the capillaries to the venous side of the capillaries so that cause is what's called AV shunting if I cause a V shunting think about this I go from the
39:51
arterial side to the venous side really fast how much time is my red blood cells gonna have to drop off oxygen to the tissues not a lot because I'm shunting blood from the arterial side to the venous side because of this lactic acid accumulation if I shunt it from their toyota side to the venous side there's not enough oxygen being delivered to the tissues what does that mean for the heart starts gonna have to pump harder it's gonna have to pump more to deliver more blood
40:15
to the tissues makes no sense so much sense right what if someone has an increased metabolic demand because of they have thyroid thyrotoxicosis okay maybe not thyroid storm but they have very high hyper thyroid levels hyperthyroidism does what it increases your metabolic rate right it increases the oxygen usage to burn calories so what does that do to the tissue it increases their demand of oxygen so now I have to pump a lot of blood as much as I possibly can to those
40:48
tissues so that those tissues get enough oxygen to break down calories to generate muscle contractions to generate heat I'm gonna need to do that now right what about if I overload the volume of the heart what if I get what if someone's pregnant not only are they pregnant and they're increasing their volume overload what do you have you got another little human being there their metabolism is going to go through the roof that can also cause high output cardiac failure as well right so
41:17
peripartum cardiomyopathy is can also develop as well so pregnancy can also be another cause that increases the demand on the heart can cause heart failure if they have underlying CVD another one which actually is really common just show up on exams is called an AV fistula an arteriovenous fistula so sometimes they use this in patients who have getting hemodialysis right and you're basically fusing an artery with a vein okay what happens is as the blood is
41:46
supposed to go down to the tissues right through the artery and then it's gonna it's supposed to come back to a vein right so you want to go artery to vein what happens is is this fistula causes a quick shunting of blood from the arterial side to the venous side high-pressure guess what that does to the resistance on this side it drops the systemic vascular resistance because you're causing a quick shunt if you drop resistance go back to that formula you drop the total peripheral resistance
42:16
remember that formula BP is equal to the cardiac output times the total peripheral resistance if I drop this I drop this how do I have to compensate now I got to increase my cardiac output so now I'm gonna have to increase my cardiac output how do I increase in my cardiac output guys I increase my heart rate and I increase my stroke volume that's increasing the demands on the heart right that makes sense so these are things that you guys got to think about whenever someone has an underlying
42:46
cardiovascular disease and they have other conditions other comorbidities that develop you need to make sure that you watch out for that because they could end up developing heart failure secondarily to that all right last little when talking about we talked a lot about stroke volume and how that relates to cardiac output one thing I didn't mention though is that sometimes people people can have changes in their heart rate they can have arrhythmias and those arrhythmias can
43:10
lead to heart failure not super super common but you got to think about it and it actually does make sense now let's think about this for a second if someone has a high heart rate right they're tachycardic they're tachyarrhythmias maybe a fit maybe a flutter maybe wolff-parkinson-white syndrome maybe a some other type of super ventricular tachycardia like abrt avnrt whatever it is over time or they have v-tach whatever it is they have an increased heart rate what does that do to the the
43:41
diastolic time period if you have an increased heart rate the diastolic time period is going to drop that means that you're not going to get a lot of preload to the ventricles if you don't get a lot of preload to the ventricles you're not going to get enough volume there to generate a good stroke volume right and that stroke volume isn't going to allow for a good cardiac output that's going to be an issue so if you caused them to have a tachyarrhythmia they're not
44:07
getting enough time to properly fill and they're also not getting enough time to properly contract and eject blood out that can lead to heart failure so this one's a double-whammy and it's gonna might hit you guys off for a second but you think about this someone has a tacky arrhythmia that can cause heart failure because you're not giving the hard enough time to go through diastole it's not properly filling if it's not properly filling it's not going to generate enough stroke volume here's the
44:36
other thing if someone has a Brady arrhythmia okay a bradycardia what does that do to this equation here if they have a significant severe heart block let's say they have a Brady arrhythmia okay so they have a Brady arrhythmia maybe they have like a significant heart block of some form okay that's going to drop their heart rate what does that do to the cardiac output it drops the cardiac output what have you do if you drop the cardiac output over time that can drop the blood
45:11
pressure that drops perfusion to the tissues if this happens for a long period of time it can lead to congestive heart failure right so bradycardia you can actually cause a decrease in the heart rate and that can decrease the cardiac output so again double-whammy here it's obviously kind of weird how can two things that are opposite of one another cause heart failure it can't just think about that underlying mechanism here okay that covers our etiology now that we've
45:35
established this strong basis let's move right into the compensation mechanisms and then the symptomatology alright guys so we talked about all the etiological factors and risk factors we even talked about diabetes diabetes is a big risk factor for heart failure obstructive sleep apnea and believe it or not is a big risk factor as well so we talked about a lot of these etiological factors but what I want to do now is put a connection to it okay take how these diseases cause the
46:03
heart not be able to pump properly and then it's gonna make so much sense now how we caught when we talk about the drugs that we use to treat patients with heart failure once we get down this compensation and pathophysiology it's gonna light up you're gonna understand the mechanism of action of these drugs which drugs are the best to treat heart failure it's going to make so much more sense so first thing I want you guys to remember all these diseases that we just talked about just jacked up our
46:30
myocardium right we're gonna focus on left side right now jacked up the myocardium and now the contractility all either regardless the cardiac output is dropping so the patient has a decrease in the cardiac output right that means the volume of blood that's being ejected out every minute is low all right now here's the thing I want you to think about whenever someone has a decrease in the cardiac output that means that there's a drop in the blood pressure now there's specific types of receptors
47:01
located in the carotid sinus you guys remember that was the carotid sinus is responsible for picking up specific types of signals okay and these are signals that are actually going to be whenever someone has a low blood pressure right so you have the carotid sinus and you even have some in the aortic sinus as well now whenever these nerves these little carotid sinus and the order scientists are stimulated from low blood pressure they send signals through the glossopharyngeal nerve in
47:31
the vagus nerve to the medulla in the medulla it activates your cardio acceleration turron your vasomotor center now as a result from that if you activate the cardiac accelerator why because that's sympathetic sympathetic is going to try to increase your heart rate increase your contractility and constrict your vessels all those things we're going to make sense of it are gonna increase your blood pressure because right now the issue here is that decreasing cardiac output technically
48:03
means I have a decrease in blood pressure and that technically means that there is a decrease in tissue perfusion and that's a problem if we're not perfusing our tissues properly they're gonna become my pock sic ischemic eventually come necrotic this is an issue so activate your cardio accelerator and your vasomotor Center that's going to be a part of the sympathetic nervous system now what's gonna happen whenever you stimulate the sympathetic nervous system the first
48:32
thing that's going to happen is you're gonna have these fibers of your cardiac plexus coming down here and it's going to go to a specific area in the heart called the SA node when it goes and acts on the SA node what does that do okay let's say that there's an increase in the stimulation of the SA node if you increase the stimulation of the SA node that's going to increase the heart rate go back to this equation now you have cardiac output equal to heart rate times
48:59
stroke volume you increase the heart rate you increase the cardiac output cardiac output right if you guys remember now blood pressure is equal to the cardiac output times the total peripheral resistance if you increase cardiac output you increase blood pressure that's one way that our body's gonna try to deal with this so whenever our pressure is dropping or we're not perfusing properly one of the big things that happens is the patient becomes tachycardic that's one of the
49:25
things that you'll see on the patient's vials the next thing is you're gonna have these fibers are gonna come down to the myocardium of the heart and you guys know the myocardium of the heart has beta 1 receptors now whenever this actual nerves release some of some norepinephrine epinephrine specifically norepinephrine onto the beta 1 receptors what is that going to do to the actual myocardial cells it's gonna increase their contractility all right if you increase the contractility what does
49:57
that do that increases the stroke volume if you increase the stroke volume you increase the cardiac output if you increase the cardiac output you increase the blood pressure that's another way that our body tries to compensate for that decreased perfusion what's another thing okay other nerves your vasomotor center is going to be sending fibers that go down to your your venous system and your arterial system and they're gonna be releasing norepinephrine onto these
50:25
receptors now again what were these receptors up here that I want you to remember these are beta one for the heart rate and for the contractility these are alpha one which are gonna be on the venous finger muscle did the actual pre capillary sphincters right and then you're gonna have your stereo smooth muscle within the venous system here these are gonna be alpha one receptors now when norepi is released onto these it's going to cause the constriction of these smooth muscle structures if you
50:59
constrict this vessel what do you do to the actual their circumference you decrease it so if I decrease the circumference what does that mean for the resistance I increase the total peripheral resistance if I increase the total peripheral resistance what does that mean for blood pressure that increases it if you constrict the actual venous smooth muscle what does that do remember the venous system is a low pressure system so it's blood flow back to the hearts a lot slower okay that's why our
51:28
veins are blood reservoirs because they have a good portion of our blood volume in them but if we constrict the smooth muscle in those veins we're gonna push the blood up higher right faster so if we cause constriction here what that's gonna do is that's gonna increase the venous return if you increase venous return what does that do that increases preload if you increase preload you increase stroke volume if you increase stroke volume increase cardiac output if
52:01
you increase cardiac output you increase blood pressure all of these things are compensatory mechanisms right what's another thing that happens here well there's actually alpha one receptors also on the actual vessels that are going to the kidney so you're also going to cause smooth muscle constriction of the actual renal arterioles that's going to decrease blood flow to the kidney as well and that's going to drop your glue merula filtration rate as well if you
52:26
drop your glomerular filtration rate you're going to be causing less urine to be made and retaining more fluid and if you do that technically you retain more fluid you increase your venous return and you're technically gonna increase your preload increase your stroke volume so again it's kind of going along with this concept here here's where it gets a little bit more interesting another thing that the sympathetic nervous system does to the kidneys is imagine
52:52
here I take a look a little chunk out of the kidney right and I zoom in on it okay we're gonna zoom in on a nephron okay so if we zoom in on this nephron this is actually gonna be our what does this our Bowman's capsule right so we have our Bowman's capsule here we're gonna have the proximal convoluted tubule descending limb ascending limb distal convoluted tubule collecting duct right and here you're gonna have your efferent arterial so this is where the blood is entering into the glomerular
53:22
capillaries and then here is going to be our efferent arteriole and that's going to be blood leaving de cámaras okay in the eighth farriner tear you're gonna have these specific cells here which are gonna actually have beta 1 receptors and these are called JG cells juxtaglomerular cells if you guys remembered JG cells respond to the actual norepinephrine and secrete a specific chemical called renin what is Rendon do guys I want I'm glad you asked Renan gets put into your venous system
53:59
goes up through your venous system goes from the right heart and goes to your lungs in the lungs you have a specific enzyme ok we're gonna put them right here it's called ace ace is going to take what happens is as Renan is actually going through your vascular system one of the important things to remember here is that the liver actually makes a molecule called angio tense Inogen and what Renan does is is Renan actually converts angiotensinogen and to angiotensin 1 ok and angiotensin 1 is
54:42
actually going to get taken through the venous system ok it's gonna go through the venous system go to the lungs in the angiotensin one is gonna react with the ACE enzyme angiotensin converting enzyme which is gonna convert angiotensin 1 into angiotensin 2 now angiotensin 2 has multiple multiple functions it's literally insane how much this guy does one of the things that he can do here is that he can come over here to your pituitary your posterior pituitary and actually stimulate the posterior
55:17
pituitary to make a hormone called the antidiuretic hormone and we'll talk about what he does maybe a little bit later but basically he increases your water reabsorption if you increase water reabsorption you increase blood volume you increase blood volume you increase venous return increase venous return you increase preload and you increase your stroke volume right it's the same concept here another thing that angiotensin 2 also does is is he can also cause vasoconstriction of your
55:45
arterioles if he causes a basic restriction of the arterials he increases your total peripheral resistance you increase your total peripheral resistance to increase your BP right so many different mechanisms here what else can this guy do he can also come down to your adrenal gland you know your adrenal gland you have your zona glomerulosa right the zona glomerulosa is gonna be up here at the top and it responds to the angiotensin ii and she creates a specific hormone this hormone that it
56:18
makes is called aldosterone now what does aldosterone do aldosterone makes its way to the kidneys and on the actual distal convoluted tubules it what it does is it acts on specific cells that increases sodium reabsorption and water reabsorption and here's the big thing with this if you increase sodium and water reabsorption into the blood what do you do to the blood volume you increase the blood volume if you increase the blood volume what do you do to your venous return you increase your
56:55
venous return if you increase your venous return you increase the preload you increase your stroke volume you increase cardiac output you increase cardiac output you increase blood pressure so it's a very very straightforward concept of how all this stuff happens but here is the problem all of this stuff is happening to compensate for a decrease in the perfusion but why is this an issue because as you try to do all of this here's the thing I want you to remember
57:23
you're trying to increase the heart rate and you're trying to do this that you can increase the cardiac output right what do we say happens if you increase heart rate with someone who has underlying heart disease you're not giving it a lot of time to properly fill and also because you're trying to cause it to contract so often that's going to exacerbate it so you can actually make it worse another thing is is if you increase the vasoconstrictive mechanisms what does that do to the afterload it
57:50
increases it and because of that that's gonna have to make the actual ventricle pump even harder because think about it if you squeeze this vessel here what's gonna happen to all the pressure proximal to this it's gonna build up the pressure and the orders gonna be so darn hide the left ventricles gonna have to work so darn hard to push as much of blood as it possibly can and it's already week you're gonna make it worse if I squeeze this venous system I'm pushing a ton of blood up into the
58:20
actual heart but if the heart is really really weakened you increase the preload what am i doing to it I'm just filling it with so much blood and it's not gonna be able to contract enough to push all that blood out I'm basically drowning the heart with blood it's not strong enough to push all of that increase venous return out and that's another issue okay and by doing this aldosterone this ADH and the angiotensin ii that's just further exacerbating the situation
58:50
it's you're trying to make these things all help to increase perfusion but in the end you're actually making it worse on the heart so that's something I want you to remember this is the compensation mechanisms that your body goes about so here's just a very quick preload into what kind of drugs you would want to give think about it beta blockers alright they would help in this situation ACE inhibitors would inhibit the angiotensin 2 system right all of the
59:20
situations which cause there to be fluid and volume overload diuretics that would also be another great drug drugs that dilate the arterioles and dilate the venules arteriole and vaso Aveeno dilators so it's gonna make so much sense when we go over the mechanisms of action and all these different drugs that are used to treat these patients okay so this is the compensation mechanism I want you to burn this into your brain and really understand this okay alright so last thing I want to talk
59:47
about with congestive heart failure going in kind of finishing off this whole pathophysiology topic stuff is whenever someone has heart failure right there's a lot of symptoms that are basically based on two different things that's if they have a backward flow so let's say backwards failure so in other words the heart is basically the filling up with so much blood and it's not able to inject all that blood out but it starts back flowing into the difference regulations okay we'll talk about those
1:00:16
and then the other one is forward failure and this is basically if you're not able to generate enough cardiac output out into your actual from your left ventricle let's say add into the aorta you're not able to deliver enough blood flow to the brain not able to deliver enough blood flow to the lung is not able to deliver enough blood flow to the GI system to the liver whatever it is those organs can start failing and that can lead to is multi-system organ failure so we'll talk about whenever
1:00:43
you're not able to eject enough blood out of the heart what can happen as a response to that all right so let's talk about a lot of this stuff but what I want us to do for right now is I want us to separate I want you to think about the heart as a left ventricle and then a right ventricle and then we'll talk about how you can have both of these symptoms and what's called by ventricular heart failure so we've been talking about left ventricular heart failure which is more common I'm gonna
1:01:06
talking about right ventricular heart failure remember I told you that sometimes patients can have left ventricular heart failure that leads to right-sided heart failure so they can have by ventricular symptoms and we'll talk about what that is okay so let's first focus on the left heart failure symptoms so here's what I want you to remember here's your left ventricle right so here's our left ventricle for whatever reason that we've talked about already it's not able to pump enough
1:01:31
blood into the aorta so blood is accumulating in this ventricle and as the blood accumulates inside of this ventricle it can start backing up especially if the pump is really really messed up here so as the blood starts backing up into the left atrium it can start backing up into these nice little pulmonary veins as it starts backing up into the pulmonary venous circulation what can start happening as it approaches the capillary beds what's the pressure inside of this pulmonary venous
1:02:03
system now that there's so much blood backing up it's going to be high if there's a high pressure high pressure in the pulmonary veins that's going to lead to some of this actual fluid leaking out into the surrounding interstitial fluid and as that fluid starts leaking out into the surrounding interstitial fluid what do we call all that pulmonary oedema so one of the big big things here is that as the pulmonary venous circulation starts backing up it increases the pulmonary
1:02:38
pressure it increases the pressure in the pulmonary veins eventually that can increase the pressure in the pulmonary capillaries and that can lead to what's called pulmonary edema okay and that is an issue here whenever someone has pulmonary edema they have wet lungs right a lot of fluid can accumulate around that area if you make the actual respiratory membrane really thick and boggy what happens to the ventilation it decreases and if you decrease ventilation you're not going to allow
1:03:15
for enough oxygenation of the blood as it runs through the system what can that lead to hypoxemia so these patients can become hypoxemic so that's another big thing with pulmonary edema remember it thickens that respiratory membrane and alters the gas exchange process if you alter a gas exchange over time that can lead to hypoxemia decrease oxygen levels in the blood so how does people basically symptomatically how can they present well they're going to be short
1:03:45
of breath because they're not properly oxygenating and they're gonna have all this fluid in their lungs so some of the big symptoms that you're gonna see in these patients is they're gonna have what's called dis Nia okay which is basically shortness of breath another thing is they can have a coffee because a lot of this is going to cause irritation to the surrounding bronchioles and other Airways so there can also be a cough more like a dry cough though specifically so you might
1:04:10
have more of a dry cough another thing that you can also see in these patients is that if they're laying flat a lot of that fluid is going to really kind of like lay around the lungs and push on the lungs whether it be a pushing from the back whether it be pushing from the front it's going to be making it very difficult to breathe whenever they're laying flat whether it's they're sleeping or they're just relaxing so they can also have what's called orthopnea so that's where they have a
1:04:40
significant difficulty breathing when they're lying flat on their back so they more prefer to be sitting up you know sitting up or having their bed kind of inclined a little bit because it's easier breathe for them another thing is they can actually wake up at night because they have difficulty breathing that's called paroxysmal nocturnal dyspnea okay so that's another one that you want to think about whenever someone has left-sided heart failure now proximal nocturnal dyspnea dis TIA
1:05:08
Koff orthopnea these are some of your main symptoms that patients are gonna present with also think about it if you have a lot of fluid accumulating around these small bronchioles and you try to breathe it's gonna try to pop those little bronchioles open right whenever you take a deep breath in that can make a specific sound whenever you're all skating the lungs is very important very very important to be able to learn and pick up I suggest trying to take some
1:05:35
time guys and listening to this sound getting used to it recognizing it it's called rails or crackles okay so you want to get used to hearing what's called inspire Tory crackles and again you can hear this in inspiration and expiration usually it's a little bit more significant during inspiration though you want to get used to hearing crackles so crackles is because as you're trying to breathe and all that fluid is accumulating around these smaller bronchioles as you try to
1:06:03
breathe you're trying to pop open those bronchioles and that can produce a crackling sound that could be a very important sign if someone has CHF ooh they have some pulmonary edema I might want to give them some diuretics to pull a lot of the fluid off of them because right now it's causing some significant symptoms that's important okay so big things to pick up on this situation here that's your left-sided stuff and again another thing here is you're increasing
1:06:29
the pressure in the pulmonary veins originally increasing pressure in the pulmonary capillaries and eventually that can also cause increase in the pulmonary pressure of the arteries which can lead to pulmonary hypertension and eventually right-sided heart failure if the right side heart starts failing where is the blood going to back up it's going to back up in two areas it's either gonna back up into the superior vena cava or back up into the inferior vena cava
1:06:55
the blood starts accumulating here and it starts backing up into the superior vena cava the area that it's mainly gonna start becoming more prominent is it's gonna go up the superior vena cava and then when you have here your brachiocephalic here's your right brachiocephalic vein left brachiocephalic vein it's gonna move up into the I J your internal jugular vein right and what happens is the pressure inside of the internal jugular vein is going to be higher because the blood is
1:07:27
backing up into it okay so what they call that is jugular venous distention so whenever someone has jugular venous distention it means that they're having some right-sided heart failure like symptoms and that's causing the blood to back up into that system here's another thing that you can also do remember I told you that the blood will also back up into the inferior vena cava if the blood is backing up in it only can go two ways from the right ventricle right
1:07:54
it can go up the right atrium into the supermoon cave or inferior vena cava what if I take I have the patient laying down now I'm gonna be mean I don't want to but I do it just so I can figure it out I mash on their liver and if I mash on their liver let's say I push hard on enough that I've decreased the actual blood going through the inferior vena cava where's the blood now gonna go and only can go one direction now it's not going to be able to go down here it's
1:08:20
gonna go up and it's gonna cause the pressure inside of the jugular venous system to rise even more that's called hepatic jugular reflux so that's another test that you can also do and write that down here it's called a Patou jugular reflux and basically we look for it to be greater than or equal to three centimeter rise in the jugular venous distention or pressure whenever you mash on someone's liver and the real reason for it is you're dropping the actual blood flow to the portal venous
1:08:53
circulation and they interview Nick Ava and you're causing it to go and build up within the actual the specifically right atrium and the superior vena cava okay so that's one thing that you can also do you can also back down this way if it backs down the inferior vena cava it's gonna start accumulating around the tissues of the liver all right so it's gonna make the liver a little bit big and maybe we can accumulate in the tissues outside of the liver as well so
1:09:19
if it starts accumulating in the liver the liver is gonna get swollen it's gonna get bigger and bigger and bigger what's that called if you get a big liver a Patou megali okay now it can also accumulate some of the fluid outside of the liver and this can be ascites so some of the other things that can happen is as this liver gets so swollen some of the fluid starts leaking out or outside of it that can cause ascites another thing remember the portal venous circulation the portal venous
1:09:50
circulation sometimes what can happen is the blood from the liver can move through the portal venous circulation and it can actually move to the spleen and whenever this happens the spleen can get filled up with a lot of blood and they can get bigger what happens if it gets bigger you get splenomegaly so again that's because the blood is connected from the liver to the spleen via that actual portal venous circulation right so it'll go portal venous circulation splenic vein going to
1:10:20
the spleen and cause the spleen to swell up a little bit and again fluid might accumulate outside of that and that's called ascites what if some of the fluid backs down through the mesenteric circulation right and it accumulates around the actual GI system and you start getting fluid accumulating around the actual GI system your small intestine your large intestines again that could be another situation so they can develop some ascites there okay now here's the thing as you develop a lot of
1:10:50
fluid around these organs what can it do and kind of squeeze on them right and as you squeeze on them it can actually make it difficult for you to be able to maybe move substances through it also might cause substances to back up as well so you might become nauseous you might vomit you might have some abdominal pain and discomfort because all this fluid is pushing on your actual small bound large bowel not likely that you can get an obstruction but again think about it
1:11:16
it's if you have significant amount of fluid pushing on that GI tract it's definitely gonna make it difficult to pass thing long as well okay but again with a lot of ascites you can have nausea you can have some vomiting and some significant abdominal pain as well and also if you have all this fluid accumulation the the the abdomen is going to become kind of really / - Brent and as you tap on them you percuss their abdomen if you have all that fluid around there it's going
1:11:43
to be very dull - percussion okay very very dull another thing you can also do is you can kind of have them laying on their side and you can tap on one side and see if you feel that fluid wave on the other side wherever they're tapping so they call that a fluid wave test okay again you don't have to you can just look to see if there's a lot of protuberance in their belly a lot of dullness to percussion and on imaging you see a lot of ascites as well that could be some of the things that you
1:12:09
could see where else could - put the blood back up not just into the liver and via the portal circulation into the spleen into the small intestine even around the stomach but it can also back up into your actual lower extremities and as this blood starts backing up into the lower extremities it can cause swelling of the legs it can cause calf edema so some calf edema okay but this is generally just your peripheral edema now this edema is very important for you
1:12:40
to remember it can be pitting okay so they're gonna have bilateral edema of the lower extremities and it may have some pitting so what does that mean you can take and push on their skin if you push on their skin wherever that edema is and it leaves kind of like a little dimple there you can kind of an identifiable thing of pitting edema depending upon how long it stays like that and how deep you can stick your finger depends upon this the severity so if it's kind of a plus one you can push
1:13:14
on it maybe it goes less than two millimeters into their skin but it has a brisk return that could be a plus one if I push deeper and it takes a little bit longer maybe it's a plus two if I push really deep and it takes a long time maybe it's a plus three plus four pitting edema so that's another thing that you want to take into consideration when you're examining the patients all of this stuff comes into play so if I have a person who has crackles they have shortness of
1:13:40
breath laying down and their flat they have orthopnea they have jvd I can make it worse by mashing on their liver they have a paddle medley splenomegaly they have nausea vomiting abdominal pain a fluid wave test upper tuber and abdomen bilateral calf edema with possible pitting and I hear crackles on and listening to their lungs that could be all signs of someone having congestive heart failure what's another thing to think about remember I told you that it's not just a backwards failure
1:14:11
what if we're not pushing enough blood out so if I'm not pushing enough blood out going to my extremities what's gonna happen now if I don't get enough blood going to my extremities remember what is blood it's nice and warm right gives warmth that gives color so what's gonna be something if I have a decreased blood flow going to my extremities my extremities are gonna be cool or cold right because I don't have enough blood going to them right and blood carries
1:14:38
with it warmth so I'm gonna have cool extremities so I'm gonna put them up put here extremities cuz this can go for just upper extremity and lower extremities I'm gonna have cool extremities what else would I have blood is not just carrying with it warmth but it's also carrying with it a color so now they're not gonna have that nice you know hue that pinkish hue it's gonna be more pale and appearance another thing is depending upon you know how much if I'm not getting enough blood
1:15:07
to these it to this area here what do we say happens whenever you have a decreased perfusion your sympathetic nervous system kicks on if your sympathetic nervous system kicks on what's one of the ways that your body tries to respond to that you become diaphoretic right so your sympathetic nervous system increases sweating if you become sweaty you can also have this clammy like appearance as well so you might have some clammy hands as well so they can be diaphoretic they're gonna
1:15:35
have cool pale extremities as well that should be important to remember so diaphoretic cool paly extreme pale extremities and again if you don't have enough blood flow going to different organs what could that lead to mold system organ failure as well okay last thing to talk about here if you're really gifted and you have a good ear an amazing stethoscope sometimes you can hear these sounds I wanted to mention them last because again they're not something that unless unless you're a
1:16:04
cardiologist you're gonna probably be hearing you're more likely to just get an echo if you hear a murmur but it's still something I want to talk to you guys about if someone has particularly a systolic heart failure right what do we say we're the big buzzwords they're compliant they're stretchy they basically are flabby or they're dilated okay if I have blood coming into these ventricles through the atria and they're filling and they're filling and they're
1:16:34
filling and they're filling during that filling process if they keep stretching and stretching and stretching sometimes what can happen is they can make a heart sound and that heart sound happens just before the patient has a systolic contraction so the ventricles are in diastole their atria are filling their atria are putting blood from the from the atria to the ventricles the ventricles are filling sometimes the heart can get an extra sound because it's filling filling filling and it kind
1:17:01
of hits up against the actual wall and this heart sound is called an s3 heart sound and this is more common in patients who have what's called systolic heart failure okay and this is identifiable of someone having a very compliant heart okay usually in order to hear this one you got to use the bell of your actual stethoscope and it's actually more likely to be heard if you put them in a left ladder to Cuba decision and listen to the PMI that's another thing if their heart's freaking
1:17:34
big where's it gonna start shifting to if it's getting bigger and bigger and bigger the PMI might move a little bit farther laterally so you might have a displaced PMI as well next thing if the heart's really thick it's fibrotic it's not compliant doesn't want to stretch as the blood is going from the atria into the ventricles and filling them it'll fill fill fill and then it'll hit this point to where it doesn't want to fill anymore and when ever hits the point where he doesn't want to fill
1:18:02
anymore and it's got that point where it's like okay stop it makes a heart sound and that heart sound is called the s for heart sound and this is more common in patients with diastolic heart failure okay so again this is basically whenever someone has a very thick fibrotic non-compliant heart as it fills right it causes this point of where it actually fills and then as it fills fills those fills it stops because it doesn't want to fill anymore and it makes a sound and that's called
1:18:31
your s for heart sound okay so these are all the things that I want you guys to understand when it comes to symptomatology of these patients who have heart failure and now that you guys do know this we should easily be able to talk about the treatment and management of these patients with heart failure our engineers so in this video we talked about congestive heart failure and we talked a lot about it very very common condition something that you should all
1:18:55
really understand you're gonna see it a lot in medicine whether it be on your exams are in the actual wards on in real life I hope this stuff made sense I know we covered a lot of stuff I know it was a really long video and if you guys stuck in throughout the entire thing I can't thank you guys enough I appreciate it so much and I just hope that it all made sense and it really really helped if it did please smash that like button comment down in the comment section and
1:19:18
please subscribe also if you guys get a chance in our description box we have links to our Facebook or Instagram account we also have our email if you guys want to send us messages leave comments whatever we truly appreciate it and we'll do our best to get back to you guys in a timely manner also we do have links to our patreon account if you guys were been willing to even donate a dollar we would really appreciate it helps us to continue to make videos for you guys as enjoyment an engineer's we
1:19:41
love you you guys are awesome best fans in the world until next time
1:19:59
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