Heart Failure Flashcards
Heart Failure Basic components
1) Poor forward blood flow = low flow (decr cardiac ouput)
2) Backward buildup of pressure = congestion (incr filling pressures) as a response to low flow
3 factors that affect stroke volume
1) preload (incr sv)
2) afterload (decr sv)
3) inotropy (incr SV)
2 factors affecting CO
1) HR (incr CO)
2) SV (incr CO)
Effect of Preload on Stroke volume vs. Ventricular EDP
increased filling of ventricle, incr ventricular output (SV)
the more LV is filled, the ____
more it will contract
the ____ the more it will contract
more LV is filled
incr ___ produces increased SV and CO for given inotropic state
Preload
incr preload increases ___ and ____ for given inotropic state
SV and CO
Effect of inotropy on SV vs. ventricular EDP curve
shifts curve upwards
Same filling (preload) of LV produces a ___
greater squeeze of contraction
Determinants of inotropy
catecholaminergic/adrenergic stim
calcium
incr inotropy produces increased ___ and ____ for the same preload
SV and CO
incr ____ produces increased SV and CO for the same preload
inotropy
Effect of increased preload on PV loop
increased end diastolic pressure (more filling on the LV)
Effect of increased inotropy on PV loop
increased pressure (height) and decr end systolic volume
pump with greater force and empty more of the LV
effect of increased afterload on PV loop
increased end systolic volume and increased pressure
have to pump with more force against higher resistance and empty LESS of LV
Systolic HF basics
weak/damaged myocardium (thinner walls)
Systolic HF problem
problem with squeeze
decr contraction and decr inotropy
hallmarks of systolic dysfunction
decreased ejection fraction
ventricular enlargement
PV loop with systolic HF
decr top pressure line and shift curve to the right
decr inotropy, decr SV (pump out less) and lower systolic blood pressure b/c less force
incr end diastolic volume b/c walls are thinner
Primary causes of systolic HF
1) direct destruction of heart muscle cells
2) overstressed heart muscle
3) volume overloaded heart muscle
causes of Direct destruction of heart muscle cells
MI viral myocarditis peripartum dilated cardiomyopathy alcohol
causes of Overstressed heart muscle
tachycardia mediated HF
meth use
stress provoked
causes of volume overloaded heart muscle
mitral regurg
high cardiac output
- shunting of blood
- wet beriberi
Diastolic HF basics
stiff/noncompliant heart
Diastolic HF problem
impaired filling
decr lusitropy
hallmark of diastolic HF
normal ejection fraction
ventricular wall thickening
PV loop in diastolic HF
incr bottom pressure line, decr top pressure line, decr end diastolic volume
incr stiffness so need higher baseline pressure to keep stiff wall open
can’t fill as much blood due to thick walls
decr top pressure line due to stiffer walls
causes of diastolic HF
1) High afterload / pressure overload
2) Myocardial thickening / fibrosis
3) External compression
causes of High afterload / pressure overload
longstanding HTN
aortic stenosis
dialysis
causes of mycoardial thickening/fibrosis
HCM
primary restrictive cardiomyopathy
causes of external compression
pericardial fibrosis/constrictive pericarditis
pericardial effusion
Right sided HF
can’t pump blood through lungs adequately
Right sided HF
what causes forward RV HF
decr circulating blood flow
Right sided HF
what causes backward RV HF
incr venous pressure
Primary causes of right sided HF
1) Left sided HF
2) lung disease/pulmonary HTN/RV pressure overload
3) RV volume overload
4) damage to RV myocardium
why does left heart failure cause right heart failure
backward HF stresses right side by incr pulm venous pressures
Do HF forms coexist?
Yes
with fibrosis and ischemia
Body’s compensatory responses to decr cardiac output in heart failure
1) neurohormonal activation
2) frank-starling (incr preload)
3) ventricular hypertrophy and dilation
Normal response to decr cardiac output (JGA route)
1) dehydration or bleeding
2) decr LV filling, decr CO
3) juxtaglomerular apparatus sense low flow and activ renin system
4) incr sodium retention
5) activate vasoconstriction
6) incr volume and incr LV filling
Normal response to decr cardiac output
1) dehydration or bleeding
2) decr LV filling, decr CO
3) baroreceptors sense lower pressure
4) adrenergic activation
5) incr HR and vasoconstriction
6) incr blood volume and incr LV filling
Neurohormonal compensatory mechanism- additional effect
supranormal filling pressures
HF effect on SV vs. ventricular end diastolic pressure curve
shift down
given pressure, less stroke volume
Frank Starling compensation
incr LV filling
incr SV
stroke volume preserved by increasing end diastolic filling and pressure
Vascular remodeling via hypertrophy and dilation
Long term incr in cardiac workload and metab demand
4 things
1) ventricular hypertrophy
2) ventricular dilation
3) myocardial damage/apoptosis
4) myocardial fibrosis
Vascular remodeling via hypertrophy and dilation
Overtime remodeling causes (3)
1) decr contractile force
2) decr dynamic function
2) incr diastolic stiffness
