Test 1: Lecture 1 cardiac intro Flashcards
during diastole the pressure in what part of the heart is equal
mitral and tricuspid valves open
atria and ventricles equal pressure
veins and capillaries also same pressure
increase in pressure will leak back into capillaries causing edema/congestion
maintenance of — pressure in the veins avoids congestion
low
pressures in the ventricle alternate between — and — during systolic and diastolic on the right and left sides
high and low
will have same pressure as what it is connected to
during diastolic= low 8
during systolic= high 120
what is preload
pressure/volume/stretch of ventricle right before it contracts
at the end of diastolic/relaxation
what is frank starling mechanism
more preload(volume in ventricle) will = a larger cardiac output, too a certain point
a diseased heart will increase preload to try to —
improve cardiac output
eventually the pressure in the ventricle (preload) will be so high it will leak back to the capillaries and cause congestion/edema
diseased heart will conserve water and salt to increase preload (volume in heart before contraction)
what is afterload
the pressure/resistance that the heart has to overcome to push blood from ventricles into the body
blood pressure (must be above 80 diastolic to push open valves to the arteries)
afterload= [pressure(radius of ventricle)]/[ wall thickness)]
the thicker the wall the smaller the afterload
the bigger the ventricle the bigger the afterload
how does wall thickness effect afterload
the thicker the ventricle the wall (bigger muscle) = smaller afterload
easier for heart to pump the blood from ventricle into the arteries
At the molecular level, — is a load-independent interaction between calcium ions and the contractile proteins.
contractility
what is atrio-ventricular synchrony
timing of contraction
atria contracts then ventricle, allows for atria to contribute 25% of cardiac output
kidney will cause — in response to low perfusion
retain salt and water
vasoconstriction
cardiac and vascular remodeling
explain red curve
diseased heart
if it pumps to quickly, does not have time to relax and fill = lower stroke volume
inverse force-frequency relationship
increase in — will cause concentric hypertrophy
pressure
increased afterload (HTN, stenosis) leads to increased wall thickness to try to over come it
afterload = P(r)/2h
increase in — will cause eccentric hypertrophy
volume
increased volume will cause heart wall to stretch
mitral valve prolapse
why does concentric hypertrophy occur in heart with HTN
increase pressure will cause increased afterload
body compensates by increasing thickness of wall (h)
P*r/2h
increase in h will return to normal amount of afterload
3 limitations of myocardial hypertrophy
too much muscle = excessive hypertrophy
can’t get blood = ischemia
wall becomes stiff and results in poor diastolic relaxation= can’t relax and decreased volume in ventricle = decreased preload
leads to ischemia, fibrosis and scarring which leads to arrhythmia and diastolic heart failure
what limitations of myocardiac eccentric hypertrophy
increase in wall radius
heart has to work harder to contract = increased oxygen demand
leads to ischemia, fibrosis and ventricular remodeling
what type of peptides does the heart make as an endorcine response
natriuretic
cause excretion of sodium= diuretic
opposite response of RAAS
BNP or ANP
explain RAAS pathway
low kidney perfusion leads to release of renin
Angiotensin II & Aldosterone: Try to support circulation by increasing plasma volume and vasoconstriction
1. Fluid and Na+ retention in
kidney
2. Increase ADH
3. Vasoconstriction of vascular
smooth muscle
4. Increase thirst
5. Increase SNS/NE
6. Increase aldosterone
7. Myocardial hypertrophy
long term sympathetic activation will do what to the heart
long exposure to norepinephrine will damage heart function
↑ Myocardial O2 demand
↑ Afterload
Myocyte necrosis
↑ RAAS/ADH →congestion
Arrhythmias
what triggers heart to make natriuretic peptides?
excess stretch
(too much preload)
heart will make ANP or BNP that tells kidney to excrete sodium→ diuretic
BNP has the opposite effect as —
RAAS= hold onto salt and water
BNP= get rid of salt and water
why does RAAS overcome BNP during CHF
loss of heart tissue= decreased production of BNP
receptors on kidney to BNP are reduced
BNP/ANP is excreted faster then RAAS
SNS and RAAS is faster and stronger
right sided heart failure will lead to
ascites and pleural effusion
