9 Heart Failure - Lecture notes notes PDF

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Heart Failure  Heart Failure o Definition: inability of the heart to maintain sufficient cardiac output to meet metabolic demands of tissues and organs  Something damages the heart and causes myocardial damage, causes the heart not to function as well, causes the body to react in a couple of different ways:  It will release catecholamines, angiotensin, and various inflammatory cytokines à those work together to cause the heart to remodel and will initially hypertrophy (good thing at first) and over time we get fibrosis and apoptosis, some myocardial cells being replaced by scar tissue and some of them dying contributes to more heart damage and more pump dysfunction o Types of heart failure  Systolic vs diastolic  Right-sided vs left-sided o Congestive heart failure  Distention or swelling of veins due to increased pressure within them

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Something damages the heart and causes myocardial damage, causes the heart not to function as well, causes the body to react in a couple of different ways:  It will release catecholamines, angiotensin, and various inflammatory cytokines  those work together to cause the heart to remodel and will initially hypertrophy (good thing at first, makes heart stronger) but over time we get fibrosis and apoptosis  some myocardial cells are being replaced by scar tissue and some of them are dying  contributes to more heart damage and more pump dysfunction o Heart failure is more common in the elderly (85+), deaths from heart failure are increasing, very expensive disorder o Heart failure causes:

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Impaired cardiac function  Cardiomyopathies  MI  Myocarditis  Stenotic valvular disease  Regurgitant valvular disease  Congenital heart defects  Excess works demands- makes heart have to work extra hard  Systemic hypertension  Pulmonary hypertension  Coarctation of the aorta  Thyrotoxicosis  Anemia  AV shunt  SERVA2a – sarcoplasmic reticulum Ca 2+ ATPase  Under expression associated with HF  Treatment with gene therapy in future?  More common in men in younger age, as you get into older age it is more common in women Systolic vs. Diastolic Heart Failure o Systolic dysfunction  Problem during ventricle contraction  Characterized by low EF 50%  Associated with slow or poor relaxation of ventricles during diastole  can’t fill very well  The walls of the ventricles are hypertrophied, are able to pump alright but are not able to relax as well, so there isn’t as much blood filling in  Often associated with aging

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Normal is on the left Systolic dysfunction- Ventricles aren’t able to pump out as much blood due to the weaken condition of the heart Heart as a Two-Pump System

right

heart

lung s

arterie s

vein s o

left heart g

tissue Right sided vs. left sided s

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o Think about where the blood goes from the right heart (to the lungs), where will it back up to (veins and tissues) o Left heart (blood goes out to the body), where will it back up to if it can’t leave (the lungs) Right-sided vs. left-sided failure o Right-sided failure  Right side of the heart can’t do its job  All from blood backing up into the tissues, because it is unable into the right side of the heart and be pumped out normally  Congestion of peripheral tissues  Dependent edema (in feet and lower legs) and ascites  Liver congestion  GI tract congestion  1 type:  Cor Pulmonale= RIGHT SIDED o Right sided heart failure caused by pulmonary hypertension due to lung disease  Caused by lungs o Right side of the heart is pumping against that hypertension for many years  causes right side to fail

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Think about backward and forward effects Thing that happen behind the heart and in front of the heart

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Backward effect: (backing up to body) o Helpful in understanding the difference of right sided of the heart o Hepatomegaly- enlargement of the liver o Distention of jugular veins in the neck- these veins are trying to return blood to the superior vena cava and it’s trying to take blood into the right side of the heart  if there’s blood backed up, those veins will become distended  Forward effects: o Fatigue o Oliguria o Increased heart rate o Faint o Left-sided failure  Decreased cardiac output  Decreased intolerance  Poor peripheral tissue perfusion  Pulmonary congestion  Cyanosis- can’t get enough oxygen in  Pulmonary edema o Blood backs up into pulmonary vessels and increases the hydrostatic pressure  more fluid moving out, fluid in the alveoli  compromises gas exchange

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Cough, orthopnea (not being able to sleep flat), paroxysmal nocturnal dyspnea (sudden shortness of breath during the night)

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For left sided heart failure You don’t see a lot of edema in the lower legs or ascites, person is sitting in the tripod position (when they have trouble breathing) Backward: (lungs is before that=pulmonary issues) o Dyspnea- at rest or on exertion o Crackles in the lungs- when you listen with a stethoscope, air bubbling through water

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Forward: o Low CO o Makes less urine (oliguria) o Basically the same as right sided

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Right-sided- backward effect is going to the liver and the GI tract and peripheral capillaries; forward to the lungs Left-sided- backward effect goes to the lungs; forward goes to the rest of the body

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It is possible to have both types Left-sided can lead to right sided, not usually the other way around  The cough, pulmonary edema, also with the ascites, peripheral edema Compensatory Mechanisms o SNS activation (Sympathetic nervous system) (Baroreceptors activates SNS)  Increased heart rate, increased contractility, arterial vasoconstriction (makes for more afterload for the heart to pump against), renin release (cause fluid retention- body tries to compensate but will actually make things worse)  Results in increased afterload and cardiac workload o RAAS activation (Renin Angiotensin Aldosterone System)  Kidneys release the renin when it’s not getting enough oxygen or enough perfusion  Hypertrophy of the heart- caused by changes in wall tension and myocyte growth  Increased blood volume  Increased preload (helps a little bit), more forceful ejection o Cardiac hypertrophy (overtime)  Improves contractile force (temporarily)  Eventually causes fibrosis and worsening of the heart failure  Little room in the chambers for blood to fill

o (Heart is trying to increase cardiac output through all these mechanisms- for a short time [a few weeks to month] it is helpful but then fibrosis and hypertrophy causes problems

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o The relationship between afterload and stroke volume o With NORMAL heart- as afterload increases, stroke volume goes down a little bit o Moderate- severe heart failure- a little bit of increase in afterload (increase in blood pressure) will cause a huge drop in stroke volume and person may not survive with this change Diagnosing Heart Failure: FACES (to remember the signs and symptoms of heart failure [combines right and left sided]) o Fatigue o Activity limitation o Congestion- in lungs or in abdominal organ o Edema o Shortness of breath NYHA Heart Failure Classes (Leans toward left sided heart failure- more common) o I. Structural heart disease but no S&S or activity limitations  Not aware of signs/symptoms  Little bit of edema, occasional shortness of breath, doesn’t affect ADL o II. Slight limitations of activity; no S&S at rest, dyspnea with moderate activity  Can’t exercise like they used to, notice some swelling of legs o III. Marked limitations of activity; no S&S at rest; dyspnea with mild activity  Shortness of breath with getting up and walking around the house

o IV. Severe activity limitations; S&S present at rest; Sevre dyspnea with any activity  Don’t live very long in this stage...