Week 5 Heart Failure and Cardiomyopathy Flashcards
In a heart with HF
:impaired ventricular contractility, increased afterload, or impaired filling of ventricles can lead to systolic or diastolic dysfunction
Systemic compensation occurs, including increases sympathetic activity, increase in specific hormone circulation, vasoconstriction, ventricular remodeling
Cardiac output
volume of blood ejected from left ventricle each minute
typically 4-6 L/min
CO =
HR x stroke volume
Preload is also called
left ventricle end-diastolic pressure (LVEDP)
Preload measures
stretch on L ventricle at the end of diastole
Increased preload may occur in HF which can
increase cardiac muscle O2 requirement
Many HF medications work to decrease preload
nitrates, diuretics, ACE inhibitors, ARB’s, calcium channels blockers
Afterload
the force against which the L ventricle is contracting to eject blood
Higher afterload =
lower cardiac output
Lower afterload =
higher cardiac output
Aortic pressures and peripheral pressures/resistance can
increase afterload
Increase afterload =
decreased stroke volume = increase blood left in chambers of heart after systole
In HFL elevated afterload leads to
long-term ventricular hypertrophy. While the body initial compensates with other systems, over time this leads to diastolic dysfunction (due to decreased compliance of ventricles – EF preserved) and eventually systolic dysfunction (EF reduced)
Contractility is affect by
HR, afterload, preload, sympathetic/parasympathetic activation
Contractility is decsribed as
the heart’s inherent ability to contract
Contractility is related to the Frank-Starling mechanism
force of cardiac muscle contraction is proportional to resting length of the muscle fibers
Increase preload =
increase contractility = increased stroke volume
Ejection fraction
“A ratio or percentage of the volume of blood ejected out of the ventricles relative to the volume of blood received by the ventricles prior to contraction.”
Normal=60-70%
Reduced ejection fraction – systolic dysfunction
(HFrEF)
impaired contractility, increase afterload
Preserved ejection fraction – diastolic dysfunction
(HFpEF)
impaired ventricular filling
Systemic compensations in HF
Increased blood volume (to increase preload)
Increased sympathetic nervous system activation
Increased HR
Decreased vagal/parasympathetic activation
Increased antidiuretic hormone
Increased renin-angiotensin-aldosterone mechanism activation (RAAS) – regulates blood volume and peripheral resistance
Increased peripheral resistance
HFrEF
CAD**
MI
Valvular regurgitation
Dilated cardiomyopathy
Aortic stenosis HTN
HFpEF
Left ventricular hypertrophy
Fibrosis of heart musculature
MI
Cardiac tamponade
Cardiomyopathies
Class A
at high risk for HF but w/o structural heart disease or symptoms
Class B
structural heart disease but w/o signs and symptoms of HF
Class c
structural heart disease with current or prior symptoms of HF
Class D
Refractory HF requiring specialized interventions
Class I
no limitations of physical activity. Ordinary physical activity does not cause symptoms of HF
Class II
Slight limitation of physical activity. Comfortable at rest but ordinary physical activity results in symptoms of HF
Class III
Marked limitation of activity. Comfortable at rest but less than ordinary activity causes symptoms of HF
Class IV
Unable to carry on any physical activity w/o symptoms of HF or symptoms of HF at rest
HF common presentation
Dyspnea
Orthopnea
Fatigue
JVD
Peripheral edema
Tachycardia
Cachexia
HF prognosis
HF prognosis is generally poor
5-year mortality ranges from 45-60%
Patients with severe HF have a 1-year mortality rate of 60%
Dilated
Dilation of heart chambers, particularly L ventricle
Dilated causes
genetics (40%), toxins (chemo, drugs, alcohol), pregnancy, metabolic conditions involving the thyroid, myocarditis
Dilated patho
L ventricle enlargement leading to decreased contractility and stroke volume
Dilated symptoms similar to HF
dyspnea, orthopnea, edema, fatigue
Restrictive
Stiffness of myocardium resulting in decreased/impaired filling and diastolic dysfunction
Restrictive causes
amyloidosis (protein build-up) and sarcoidosis (inflammatory disease resulting in granulomas)
Caused by increased fibrotic tissues in the heart
Hypertrophic
Thickening of walls of heart chamber
Hypertrophic interesting fact
accounts for 1/3 of sudden cardiac deaths in young athletic population, especially in football and basketball
IOK(-p=[0
Hypertrophic symptoms often present at
a younger age, but some people are asymptomatic
Hypertrophic common symptoms
dyspnea and angina
Valve disease is more common on
L side due to elevated pressures
Risk factors for valve disease
RA, IVDA, smoking, obesity, congenital heart defects, family hx, autoimmune disorders, age
Mitral valve stenosis
most cases caused by rheumatic fever
Mitral valve regurgitation
caused by calcification, rupture of chordae tendinae or papillary muscles
Mitral prolapse
leaflets prolapse into L atrium
Mitral valve presentations
dyspnea, pulm HTN, pulmonary edema, fatigue, weakness
Aortic regurgitation
aortic insufficiency
Aortic regurgitation causes
congenital (2 instead of 3 leaflets to valve), ankylosing spondylitis, Marfan syndrome, HTN, endocarditis, rheumatic disease
Aortic regurgitation common s&s
syncope, angina, SOB, weakness/fatigue
Aortic stenosis
very common in older adults >65 y/o
Aortic stenosis causes
calcification/atherosclerosis or rheumatic disease
Aortic stenosis common s&s
syncope, angina, fatigue, dyspnea, decreased activity tolerance
