 heart failure is a condition in which the heart is not able to pump adequate amount of blood which is able to fulfill the body's needs. So basically there is decrease in cardiac output in heart failure and this decrease in cardiac output can occur if the heart function is failing and as you might be aware that heart function basically consists of two fundamental phenomena that is systole where it is contracting and diastole where it is relaxing. Basically in diastole heart filling occurs and in systole the pumping of that filled blood occurs out of the heart. So if the heart is not able to relax properly that is known as diastolic failure and if the heart is not able to pump properly that is known as systolic failure and both are going to lead to decrease in the cardiac output but these terms that is the systolic failure and the diastolic failure have been replaced by newer terms these days where systolic failure is known as heart failure with reduced ejection fraction we will see how it is coming and diastolic failure is basically heart failure with preserved ejection fraction see actually this ejection fraction is a fraction of the blood which is pumped out of the heart so the total amount of blood which is present in the heart at the end of diastole is known as end diastolic volume and out of this the amount which is pumped out of the heart per beat is known as a stroke volume so fraction is basically the ratio of this stroke volume with end diastolic volume and if expressed in percentage it is multiplied by 100. So this fraction normally it is like 50 to 65 percent so that is the normal range if systolic failure occurs that means the heart is not able to pump what happens that this stroke volume actually decreases and this end diastolic volume is normal so you see that this ejection fraction is going to be reduced right because the denominator is normal but the numerator is reduced on the other hand if we see the diastolic failure let me write here if we see the diastolic failure then this end diastolic volume itself reduces because the filling is decreasing right so if filling is less the amount of blood which goes out of the heart will also decrease so stroke volume will also decrease now since both decrease you see ejection fraction is going to be normal so that is preserved ejection fraction so those were certain terms regarding the heart failure systolic failure now known as heart failure with reduced ejection fraction and diastolic failure now known as heart failure with preserved ejection fraction now remember that this systolic failure and diastolic failure can occur either on the right side of the heart that is the right ventricular failure or on the left side of the heart that is the left ventricular failure so left ventricle systolic failure or left ventricle diastolic failure and right ventricle systolic failure and right ventricle diastolic failure and sometimes it is both the ventricles which fail then in that case it is known as biventricular heart failure. So we will come to this left ventricular and right ventricular failure a little bit later. Right now let us see what can be the causes of this systolic heart failure and diastolic heart failure. So first is that in systolic heart failure basically the problem is that the heart is not able to generate enough force so as to pump enough stroke volume. So when that can happen first when there is reduced muscle mass so there is some damage to the muscle cardiac muscle itself that can lead to systolic heart failure as occurs in case of myocardial infarction. Second is in case of dilated cardiomyopathy dilated cardiomyopathy why that is happening that if you know the laplace law. Laplace law says that pressure is equal to tension into two times the wall thickness divided by the radius. Now in dilated cardiomyopathy what happens say suppose this is the normal ventricle size the size of this ventricular cavity increases so you see the radius intraventricular radius increases. Okay so with the same wall tension the pressure generated the intraventricular pressure generated will be lesser so that can be a cause of systolic heart failure and coming to diastolic heart failure where the heart is not able to relax properly so that can happen in case of restrictive cardiomyopathy. So basically we are having the decreased compliance of the ventricles right so they are not able to relax properly hence the feeling of the ventricles is less causing decrease in the cardiac output. Then in cases which cause concentric hypertrophy of the ventricles concentric hypertrophy of the ventricles so what is this concentric hypertrophy actually this occurs in case where the heart needs to generate much more pressure than in physiological conditions so for example in case of hypertension in case of aortic stenosis let me draw say suppose this is the left ventricle though I am talking here again and again about the left ventricle but remember same thing can happen in right ventricle as well we'll just talk about it okay so say suppose this is the left ventricle and this is the aorta suppose there is aortic stenosis that means this aortic valve is not able to open properly during the ventricular system in that case the ventricle has to generate much much more pressure okay so because of this over time if the condition is persisting what will happen that there will be increase in thickness of this ventricular wall right increase thickness of the ventricular wall and with this what is happening you see decrease in the cavity sizes happening right so decrease cavity size will lead to decrease in the filling of the ventricle so that is why concentric hypertrophy leads to diastolic heart failure inability of the heart to fill properly so one where the heart is not relaxing properly because there is some fibrosis the heart muscle has become stiffer and the other is the causes which lead to concentric hypertrophy so I was talking about the left ventricle and right ventricle remember here I gave the example of hypertension and aortic stenosis which will affect the left side of the heart but any cause which is causing pulmonary hypertension that will affect the right side of the heart because the right ventricle is pumping against the pressure in the pulmonary vessels so in that case there will be concentric hypertrophy on the right side of the heart right similarly suppose MI which happens on the right side of the heart then the right side of failure is going to occur point is that depending on that which side of the circulation is getting affected we can get the left-sided heart failure or right sided heart failure so with this let us come to the signs and symptoms what is the physiological basis of these signs and symptoms of heart failure and how it is different in left-sided and right-sided heart failure now to understand the clinical features of the left-sided and right-sided heart failure we should know that clinical features occur because of two reasons one is forward failure forward failure okay and one is backward failure so you see blood is flowing in a series right so if anywhere there is some problem there will be symptoms because the blood is not moving forward and there will be symptoms because blood is getting jammed backwards okay so with this simple concept of forward failure and backward failure let us talk about the clinical features and you see when I'm talking about the clinical features I will not talk about systolic failure and diastolic failure that concept we talk about when we want to know about the causes right because both kind of failures will lead to decrease cardiac output and hence lead to the same problem that is forward failure and backward failure but when we talk about clinical features we talk about the right-sided heart failure and left-sided heart failure because forward for left-sided heart failure will be systemic circulation and backward will be pulmonary circulation on the other hand for right-sided heart failure forward will be pulmonary circulation and backward will be systemic veins isn't it so circulation in the veins so let us see what will be the problems in the left-sided heart failure so we will just focus on the forward and backward of the left side of the heart so you see on the forward side what is happening there is decrease in the cardiac output and decrease cardiac output ultimately will lead to decrease in the systolic blood pressure because cardiac output is the main determinant of systolic blood pressure right so when systolic blood pressure decreases pulse pressure is also going to decrease right so that we will see in forward failure then because systolic blood pressure has decreased there will be activation of the baroreflex okay and this will lead to two things one there will be increase in the heart rate so we will see tachycardia and then there will be vasoconstriction throughout the systemic circulation and this vasoconstriction will lead to cool peripheries okay so cool peripheries will be there then because of decreased blood pressure there will be decreased flow as well so if flow decreases what is going to happen there will be exertional dyspnea okay exertional dyspnea the person will feel breathless when he is doing some work so that will be in the beginning in the latest stages even at rest there might be dyspnea and he will feel fatigued okay also there will be decreased blood flow to various tissues so there will be like a decrease in the renal blood flow this decrease renal blood flow ultimately can cause renal ischemia so they can be renal failure right then they can be decreased liver blood flow so if liver blood flow decreases it can lead to necrosis in the liver and if you have seen my video on hepatic circulation you will see that there are zones in the liver and ischemia affects particular areas of the liver so it leads to basically century lobular necrosis century lobular necrosis so here we are talking about necrosis don't get confused we will talk about hepatome galley also but here we are talking about forward failure right so decrease in renal blood flow decrease in liver blood flow then they can be decreased in the cerebral blood flow as well so it can lead to cerebral ischemia there will be confusion so symptoms of decrease in cerebral blood flow will also be present right now moving on to backward failure so what will be the science of backward failure what is behind the left ventricle first is the left atrium right and further behind the left atrium is the pulmonary circulation so we see features which are for both left atrium and for pulmonary circulation right so what will happen that because the left ventricle is failing left atrium has to do lot of work right and there will be increase in the pressure in the left atrium as well also there will be decrease in the filling of the left ventricle so blood is getting jammed up in the left atrium this ultimately leads to left atrial dilation left atrial dilation and when left atrial dilation occurs two things can occur one chances of atrial fibrillation increase and second there because of the stasis of the blood there can be chances of thrombus formation in this left atrium so that is one thing then other major science and symptoms occur because of the jamming of the blood in the pulmonary circulation so what is happening that because blood is not flowing forward but it is getting jammed up in the pulmonary circulation there is increase in pulmonary capillary pressure okay so this is the blood and here there is the alveoli if the pulmonary capillary pressure increases basically it is the hydrostatic pressure it will cause fluid movement into the interstitial space right and ultimately fluid will move into the alveoli as well so what is this this is development of interstitial edema and pulmonary edema and when this happens you see that diffusion of oxygen is going to become difficult because you see the thickness of the respiratory membrane is increasing so it leads to hypoxia understanding so this is another cause of dyspnea in case of left heart failure so dyspnea is occurring because of decrease in cardiac output and further this is being increased because of the development of pulmonary edema so this leads to exertional dyspnea and also to other science and symptoms that is orthopnea okay what is orthopnea that is breathlessness in the supine position because when the person is standing you see due to gravity venous return is less right it is in the legs on the other hand when the person lies supine what happens there is redistribution of blood and there is increase in the venous return towards the central area so this increases the venous return supine position increases the venous return and ultimately it will lead to more jamming of the blood in the pulmonary circulation because the right ventricle is pumping fine so whole blood is going into the pulmonary circulation thus increasing the pulmonary edema and thus increasing the hypoxia so that leads to breathlessness further right so that is orthopnea another is peroxismal nocturnal dyspnea it is basically similar mechanism is similar as that of orthopnea but it is like a very severe episode acute episode of breathlessness though which occurs in lying position now if we examine a patient with left heart failure we will get certain signs as well so these signs include first is the presence of crackles or rails on auscultation of the chest so that is happening because of the presence of the fluid okay so presence of rails then we may also get prominent S3 and S4 that is because the left atrium is pumping very forcefully to force that extra amount of blood into the left ventricle also S3 and S4 may be heard an auscultation of the chest then on palpation actually if there is a left ventricular hypertrophy we will get left shift of apex beat left and lower shift of apex beat and apex beat will also be sustained so this is the feature of hypertrophy of the heart then because of decrease in the cardiac output what we get is a periodic respiration also that is chain stokes respiration chain stokes respiration this is because the blood is flowing very slowly and what happens the changes in the oxygen and carbon dioxide which are happening in the blood are not very fast communicated to the respiratory center so they are slow to respond so what we get is a periodic breathing for more details on this chain stokes respiration you can watch my video on chemical regulation of respiration there I have talked about somewhat about chain stokes respiration and because of exertional dyspnea we can see signs of labored breathing in the patient that means the use of accessory muscles of respiration right and finally we can also see in pathology we can we can see the macrophages the hemocytorine laden macrophages can appear in pathology why because you see there is so much rise in the pulmonary capillary pressure so sometimes these capillaries may rupture and there may be leakage of blood into the interstitium so whatever macrophages are presented in the alveoli they capture this blood so they become like blood laden so these are basically hemocytorine laden macrophages understanding so these are the various signs and symptoms of left heart failure coming to right heart failure again in right heart failure same thing what we saw in our left heart failure there will be forward failure and there will be backward failure one thing you remember here that one of the most common cause of right heart failure is left heart failure why because whenever there is left heart failure we see that there is increase in the pulmonary capillary pressure so there is pulmonary hypertension development and because of this now right ventricle has to pump very forcefully against this increased pressure in the pulmonary circulation so slowly slowly the right heart also starts to fail right so what are the signs and symptoms of this right heart failure so first we'll talk about backward failure so we saw that this is the right atrium and there is a right ventricle and backward it is basically the systemic veins circulation systemic veins are there so there will be congestion of blood in these systemic veins and what we will get first is increase in JVP jugular venous pressure will rise because you see that what we were talking about left heart failure the backward of right ventricle is right atrium so there will be rise in pressure in the right atrium and JVP is nothing but a reflection of right atrial pressures because here the central venous pressure is also going to increase so there is increase jugular venous pressure then further these veins are going to get congested isn't it they will be jamming of the blood ultimately it will lead to ender hepatomegaly because of the jamming of the blood in the hepatic circulation as well tender hepatomegaly then there will be splenomegaly okay again same thing because jamming of the blood presence of acitus presence of peripheral edema peripheral edema actually also occurs in case of left heart failure that we will see when we are talking about the compensatory mechanisms because there is volume overload and this causes increase in the systemic capillary pressures and there will be more leakage of fluid okay so this peripheral edema we see in left ventricular failure as well that I didn't say before anyways so there will be peripheral edema and this hepatomegaly which I was talking see in left heart failure forward failure we what I said that because of decreased blood flow there can be sentry lobular necrosis may occur because of the ischemia but here there is hepatomegaly because of the congestion and what happens that actually this vein inferior vena keva what happens that lot of central veins from the liver they combine together and they form the hepatic vein which ultimately drains into the inferior vena keva so these central veins of the liver will also be congested okay so there will be jamming of blood here also so it is these areas surrounding these central veins of the liver that we get red brown areas right. red brown so we call it a red brown pariscentral zones red ground perisentral peri is surrounding the central so perisentral and central is the central vein so periscentral zones okay bedground variants allezol why in the periportal region where the portal then is there there refer to normal tan colored right so their ground very central zones and normal tan colored peripheral zones so what we get is something known as nutmeg liver the appearance is like a nutmeg so that is known as nutmeg liver okay. So you do have a look at my video on hepatic circulation to understand this circulation of the liver. So coming back to our forward and backward failure. Backward failure which just discussed forward failure the symptoms will be similar to what we are seeing in the left chart failure because of decrease in the cardiac output because the output from the right ventricle has decreased so the output going into the left ventricle is also less so ultimately the cardiac output will be less so there will be again same things that disneya will be there decrease in systolic blood pressure decrease in pulse pressure and decrease in blood flow to the organs right but one special thing happens you see because the right ventricle is pumping less less circulation is happening to the pulmonary circulation so the jamming of blood which was occurring due to the left ventricle failure now will not occur understanding so when right heart failure develops after the left heart failure okay left heart failure is the cause of right heart failure now the jamming of blood in the pulmonary circulation decreases so that hypoxia which we were talking about there will be decrease in oxygen diffusion that is not going to occur so development of right heart failure after the left heart failure actually decreases the disneya understanding but it's not that the person is improving it is only because the accumulation of fluid in the lungs is decreasing so now what are the compensatory mechanisms which occur in heart failure so first is the compensatory mechanisms occur because of decreased cardiac output so let us write decrease in cardiac output so one thing is decreased cardiac output leads to decrease in systolic blood pressure and hence activation of the baroreflex which in turn is going to cause the increase in the heart rate right increase in myocardial contractility and there will be systemic vasoconstriction so that is one okay so this everything is to increase the systolic blood pressure so that the flow can continue second is the long-term changes which can occur that is the hormonal mechanisms so because of decrease in blood flow there will be decrease in the renal blood flow and hence decrease in the GFR which will lead to activation of the tubular glomeral feedback ultimately causing increase in the release of the renin right and this will lead to increase formation of angiotensin one which will be converted to angiotensin two by angiotensin converting enzyme right so angiotensin one and here is ACE enzyme now this angiotensin two it causes vasoconstriction vasoconstriction okay then it causes release of aldosterone as well so that is responsible for increased sodium reabsorption and there will be increased release of adh as well and both these together will lead to sodium and water reabsorption from the kidneys leading to increase in blood volume okay now this increased blood volume basically will increase the preload to the heart and whenever preload increases there will be increase in the heart contraction isn't it that is what frank styling mechanism says right so by frank styling mechanism there will be increase in the heart contraction right now remember this is compensatory mechanism but it works for only for some time if heart continues failing then this increased preload in fact becomes harmful to the heart and the heart is not able to take up that excess load and it starts failing further because its excess load causes more damage to the heart muscle so this is a second compensatory mechanism third compensatory mechanism is remodeling of the heart very important remodeling of the heart because whatever the pathology is now some changes take place in the heart so as to handle this pathology better however this remodeling further deteriorates the functioning of the heart so this remodeling can include hypertrophy of the heart or there can be dilation of the heart and along with that there is lot of interstitial fibrosis in the heart also and this happens mainly because of the release of this angiotensin so this angiotensin is responsible for remodeling of the heart okay and the final important one is andosterone that is responsible for the remodeling of the heart it is important to know this because we will see that the treatment of heart failure depends on these compensatory mechanisms finally the fourth compensatory mechanism is activation of counteracting vasodilators because you see blood flow is less right and what beroriflex is doing it is causing vasoconstriction so there is release of vasodilators as well and also there is release of some natriuretics so there is atrial natriuretic peptide right so you see here even the sodium and water retention is occurring which is increasing preload but here there are others which are causing vasodilation and are causing sodium excretion as well so that is atrial natriuretic peptide BNP then BGE2 prostaglandin E2 and I2 okay so these are the major compensatory mechanisms which take place in heart failure so if we know this compensatory mechanism so we can very well predict what can be the treatment first is here we are talking about compensated heart failure not decompensated heart failure where somehow that heart failure is occurring but is still systolic blood pressure is being maintained so as to maintain the blood flow so that is compensated heart failure so in that our major goal is to decrease the work of heart decrease the work of heart so that it doesn't fail further and reverse this remodeling so how to decrease the work of heart see work of heart depends on that how much is the preload and how much is the afterload okay work of heart depends on that when preload increases heart has to pump more that means the work of heart is increasing when afterload is increasing then also the heart has to generate more pressure to overcome that afterload so that the blood can flow out so in both cases work of the heart is more and if you see the compensatory mechanism here this vasoconstriction is increasing the afterload right and here increase in blood volume and increase in venous return also happens because this barrel reflects not only causes the arterial vasoconstriction arterial vasoconstriction actually increases the peripheral resistance which causes increase in afterload there is also venoconstriction venoconstriction so that increases the preload so increase in blood volume and the venoconstriction both increase the preload so our target is to decrease the preload and decrease the afterload plus we have to reverse this cardiac remodeling so what should be the treatment decrease in preload we will give diuretics okay then we want veno dilators veno dilators so that the venous return is less so that is done by giving nitrates right then decrease in afterload we want arterial dilators arterial dilators and that is by giving arterial dilators like hydrolazine okay in fact a combination of nitrates and hydrolazine has shown to decrease the mortality in cardiac failure patients then there are others which decrease both preload and decrease afterload right and these are like ACE inhibitors because we are seeing how angiotensin causes vasoconstriction as well and causes increase in the blood volume which increases the preload also so we give ACE inhibitors and angiotensin receptor blockers okay then there are other as well like alpha blockers so we are blocking the sympathetic activity so that the venoconstriction and vasoconstriction doesn't occur understanding so these are hormone blockers and this is to block the baro reflex activity so these are alpha blockers then how to reverse the cardiac remodeling as I told you before that what is responsible for cardiac remodeling it is angiotensin 2 and there is aldosterone which is causing the cardiac remodeling so we block the action of these hormones that is by giving again ACE inhibitors you see how ACE inhibitors are acting they they are decreasing the preload decreasing the afterload and also reversing the cardiac remodeling so ACE inhibitors or angiotensin receptor blockers then there can be aldosterone antagonist also okay aldosterone antagonist then there is another drug that is beta blockers beta blockers can also reverse cardiac remodeling how you see sympathetic activity actually also acts on these JG cells okay JG cells and causes the release of this renin and that is because of the presence of beta 1 receptors there so beta blockers will block these beta 1 receptors on the JG cells and there will be decrease in the release of renin and hence decrease in the formation of angiotensin 2 but remember that these beta blockers are contraindicated in case of decompensated heart failure because same beta blockers which are here acting by decreasing the production of angiotensin 2 in case of a decompensated heart failure there is another action of beta blockers they decrease the heart rate and decrease the heart contraction also because these beta receptors are present on the heart muscle also okay and SA node also so sympathetic activity acts via beta receptors to increase the heart rate and contraction so that also it is decreasing now in chronic it is okay it can work but in decompensated heart failure it becomes unacceptable so it is contraindicated in case of decompensated heart failure now there are newer drugs which can be used in chronic heart failure as well so one is that decrease preload after load then reverse cardiac modeling and the third one is drugs that increase that counteracting vasodilotus which are there which I told you in the compensatory mechanisms let us see once more you see here I told you ANP, BNP, G2, PGI2 so these drugs either increase its activity or prolong its action so actually this BNP there is enzyme neutral endopeptidase which causes the inactivation of BNP so these newer drugs actually inhibit this NLP so that BNP can act longer understanding so that there will be vasodilation all right so that was about compensated or chronic heart failure coming to the treatment of acute heart failure in acute heart failure our main aim is to stabilize the patient so for this what we want is basically increase the contractility of the heart right and second thing we want is decrease the congestive symptoms okay congestive symptoms is basically the symptoms which are occurring due to the fluid overload that is why this heart failure is also known as congestive heart failure because fluid is jamming up everywhere okay so how to increase the contractility of the heart by giving certain drugs like dobutamine how they are acting and all I will not discuss right now for that maybe I'll make another video so dobutamine dopamine is there then cardiac glycosides is there right then there are newer drugs that is the inodilators what are these inodilators inodilators are basically they increase the cardiac contraction and they cause the vasodilation as well then for decreasing the congestive symptoms which are occurring due to fluid accumulation what we need to do we need to decrease the fluid and how to do that by giving the diuretics okay so diuretics will decrease the fluid and hence they will decrease the congestive symptoms by the way just one thing here you see this dobutamine is a beta 1 agonist because we have to increase the cardiac contractility here right and as I told you that for reversing cardiac remodeling we are using beta blockers here we are using beta 1 agonist okay so I hope you like the video we discussed a lot about the different types of heart failure the signs and symptoms of different left heart failure and right heart failure and why they occur we also discussed about the compensatory mechanisms and how treatment is aimed at these compensatory mechanisms which occur in heart failure thanks for watching the video if you liked it do press the like button share the video with others and don't forget to subscribe to the channel physiology open thank you