hey it's lma again and this is cardiac two lecture which is going to cover heart failure and other fun things so um let's just talk about the definition of heart failure so pumping action of the heart becomes less powerful so basically that contractile force is going to decrease and if you think about that then you got to think about your cardiac output and that is going to be um well i should say not as effective um towards the end of course it's ineffective but anyway eventually the heart is unable to pump effectively in order to oxidate the tissues of the body so you're going to have a decrease in tissue perfusion related to this this poor pump so with that the blood in the ventricles can back up into the circulatory system so that's going to increase the pressure within the blood vessels that can increase hydrostatic pressure which is going to force fluid from the circulatory system so within the vessels out into the tissues so this isn't good um these are kind of older statistics even now but there's about 5 million people in the u.s that are diagnosed with heart failure about 500 000 new cases yearly it is often in african americans than caucasians i think in hispanics as well just one of the big causes of heart failure is hypertension and so that's one of the main reasons rated death is about 10 after one year of diagnosis and about half of those die within five years of diagnosis this is a really expensive cost it's about 60 billion dollars annually and on an inpatient basis about 23 billion that's it that's a lot of money so when we talk about heart failure there is systolic and diastolic you'll notice that as you are reading charts um this can be diagnosed via echocardiogram but systolic dysfunctions inadequate pumping from the ventricles um most common uh form of failure and um an ejection frac that's his fracture we'll fix that uh fraction uh of less than uh 50 so normal is about 55 to 60 so an ejection fraction is something that is going to be a reflection of your cardiac output how much of this blood is getting out of the heart so 50 less than 50 so at 50 um you're probably not symptomatic at all when you're getting down to 20 25 and even less your cardiac output's so low that you're not even really able to do activities of daily living just don't have the profusion that you need so you can hardly you know walk from the bedroom to the bathroom for instance really common causes are coronary artery disease diabetics of course which they usually die of coronary artery disease diabetic cardiomyopathy alcoholic cardiomyopathy valvular disease so with diastolic heart failure this could be called a stiff heart syndrome so the cart can't fully relax during diastole and so that's going to interrupt the filling of the heart so you can kind of visualize if that heart isn't fully able to fill you're not going to get that volume that you need for your cardiac output it occurs in response to an increase in ventricular afterload so this leads to impaired diastolic filling of the left ventricle so this is a classic type of heart failure caused by high blood pressure severe aortic stenosis hypertensive cardiomyopathy ischemic myocardial disease like mi etc and coronary artery disease so there's categories of heart failure left-sided heart failure typically caused by high blood pressure hypertension coronary artery and valvular disease right-sided heart failure can be caused by left-sided heart failure you can get the global heart failure right ventricular myocardial infarctions or pulmonary hypertension so a lot of pulmonary problems copd for instance will eventually cause right-sided heart failure so this is a high output failure it's caused by increased metabolic needs septicemia and anemia just just you don't really need to know that but just in case you see these words on charts or hear of it you're familiar acute heart failure something happens really quickly and doesn't really happen because of long-standing hypertension this can happen because of a heart attack and myocardial infarction or valvular regurgitation so what's what's happening on a pathophysiological level the cardiac myocytes inadequately adapt and they increase that wall stretch in order to maintain cardiac output so this is where we get that hypertrophy or that cardiac remodeling that's usually following a myocardial injury so again key problems big heart hypertrophy and that remodeling so that um places excessive uh hemodynamic burden on the ventricle so they it's got to try to adapt to maintain that cardiac output so adaptations so the frank starling mechanism you've probably learned this back in biology 227 this is where you have an increased preload in order to sustain cardiac performance so your volume is going to go up myocardial hypertrophy just the mass of the contractile the ventricle then is enhanced and you have activation of some neural uh humoral mechanisms like norepinephrine epinephrine etc so this is where your heart rate and contractile or contractile force is going to go up your renin aldosterone angiotensin system is also going to kick in and although these systems are terrific on a normal basis for compensation they really lead to problems with heart failure so um just to review what's released epinephrine norepinephrine vasoactive substances endothelial one vasopressin all cause vasoconstriction which makes sense right because the body is like hey we're not getting enough cardiac output let's fix this problem so normally it would be terrific but that's going to increase an afterload on the heart and that's going to increase the calcium that's going to augment myocytes and it's going to increase contractility and it will affect myocardial relaxation so essentially this is going to make the heart have to work harder um what happens with the redden angiotensin aldosterone system we've got that increase in aldosterone that's going to lead to more sodium and water makes sense we want the blood pressure to go up it's going to increase that preload and the heart is going to have to work even harder because now you've got increased volume so as we advance with our heart failure how does the body try to compensate for that so a decrease over time of these counter regulatory effects of endogenous vasodilators so things like nitric oxide prostaglandins bradykinins uh an atrial naturetic peptide and a b type natural peptide will all help inhibit renin and aldosterone so um you know one of these one of the ways that we test this is your pro-bnp so do you need to know all of these chemical mediators no but i think you should generally understand that you know the heart is remodeling because of this kind of vicious cycle of first having a poor contractile force the body realizing that i just am not getting the cardiac output that i need to so how can i fix this through vasoconstriction and increasing preload and these mechanisms are just going to increase that workload of the heart and cause more hypertrophy and remodeling so including the sympathetic response so you've got beta receptor stimulation which an increase in heart rate and contractility that also is going to trigger more renin release alpha 1 is going to be stimulated that is going to cause more vasoconstriction increasing the blood pressure it's going to increase the the return of blood to the right side of the heart and that is going to cause less time for ventricular filling so increased contractility requires more oxygen increased blood pressure increases the pressure inside that left ventricle that it must overcome in order to get that blood out to the body so you can see it's quite a kind of sequela of of problems the life the left ventricle doesn't empty normally during systole the left atria pumps harder to get all this blood into the left ventricle that still has blood left in it from not completely emptying blood's going to back up into the pulmonary circulation and into the alveoli increased pulmonary pressure impedes the flow from the right ventricle this causes a backup of pressure that the heart needs to pump even harder to the right atria and eventually that's going to back up into the peripheral circulation so let's talk again specifically about left-sided heart failure and causes so again classic hypertension coronary artery disease valvular disease most often would be mitral or aortic and diseases of the myocardium so whenever you have an increased afterload in the periphery then think left-sided heart failure there's a another slide here i think that oh it's just a drawing and you can see right sided versus left-sided i want you to see on the right-sided failure the word right underneath that caption core pulmonale and this is um probably latin and core means heart and of course pulmonary means lungs and so i need you to remember this term and it is going to be reflective of specifically right-sided failure and it's most often caused by pulmonary so make sure you make a note core pulmonale so left sided failure i think left equals lungs you'll notice most of this the symptoms here on this slide are lung related where right sided is more in the periphery than where you see edema and increased jugular vein distension weight gain etc so as we kind of look at differentiate differentiating left from right sided heart failure i want you to think about specific signs that left failure would be so you know i think when we think about crackles in our lungs um certainly that can be a sign of left ventricular failure but not really specific right you can have crackles in your lungs because of pneumonia or um just other problems so go for the big symptoms that are really specific like orthopedia for instance if a patient comes in and is talking about gosh yeah i just i haven't been able to lay flat for i don't know three weeks i've been in a recliner or you know i have to have four or five pillows in my bed in order to to sleep that's a tell-tale sign of left ventricular failure so some other signs might be now and this would be a really late one and that would be that pink frothy sputum um when they're when they cough that's a a real specific and extreme i guess i would say a sign of left ventricular failure certainly not an early sign other signs can be exertional dyspnea paroxysmal nocturnal dyspnea so this is um remember peroxism just means abrupt onset so in the night all of a sudden you're um having difficulty breathing and that's mostly flat dysmea at rest as well