Cardiac Cycle - sounds Flashcards

1
Q

S4

A

atrial gallop
stiffened ventricle (usually hypertrophy)
occurs in late diastole

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2
Q

S1

A

S1= M1 + T1

mitral & tricuspid valves closing

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3
Q

S2

A

S2 = A2 + P2
aortic & pulmonary valves closing
split during inspiration

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4
Q

S3

A

vibration in ventricle filling
Supple ventricle = normal in kids
dilated cardiomyopia in adults

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5
Q

stiff aorta

A

lose compliance

see greater fall in pressure (>130 to 80 drop)

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6
Q

end systolic pressure-volume relationship

A

maximum pressure that can be developed for any ventricular volume

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7
Q

end diastolic pressure-volume relationship

A

passive filling of the ventricle

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8
Q

stroke volume =

A

SV = vol of blood ejected during systole
SV = EDV - ESV
(CO=SV*HR)
normal; 60-100

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9
Q

ejection fraction =

A
EF = pump efficiency (%)
EF = SV / EDV
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10
Q

preload

A

ventricular stretching prior to contraction

Starling’s law - more filling, more stretch, more contraction, greater CO

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11
Q

ventricular stress

A

stress = pressure * radius / 2 h (wall thickness)
inc preload -> inc radius = inc stress
stress = det myocardial O2 demand -> can lead to ischemia and more MIs
so, inc wall thickness (hypertrophy) to compensate

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12
Q

afterload

A

force heart has to overcome to force blood into aorta
wall stress present at peak systolic pressure
very close to aortic pressure

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13
Q

increasing afterload

A

heart must generate higher pressure to open aortic valve
aortic valve also will close at higher pressure
inc afterload = dec fiber shortening velocity = (finite time for shortening - wasted time trying to open aortic valve) dec ejection fraction
so, ESV increases, SV decreases
venous return is added, so EDV inc too
(SV decreases bc ESV inc > EDV)
SUMMARY; inc AL dec SV to dec CO

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14
Q

aortic stenosis

A

narrowing of the aortic valve
increases afterload (due to higher resistence)
generates a sound between S1 and S2

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15
Q

aortic stenosis - compensation

A

dec in SV -> drop in BP

inc EDV limited by ventricular hypertrophy, this hypertrophy can lead to lrg inc in EDpressure assoc w reduced EDVs

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16
Q

inotropy

A

strength of contraction
ability to modulate degree of force generation - Ca induced Ca-release (phase 2) allows for more alteration
Starling curves (x-axis Left Ven EDP, y-axis SV)

17
Q

increase inoptropy

A

shifts ESPBR curve to left
keeps Ca channels open a bit longer (inc Ca that enters cell, inc Ca released by Sr
inc Inotropy; dec ESV - inc SV & inc EF => inc Cardiac Output

18
Q

autonomic nervous system; pos or neg inotropic

A

SNS + ionotropic (beta1 adrenergic recep)

PNS - ionotropic

19
Q

congestive heart failure

A

decreased cardiac output
heart operating on lower Starling curve (lower SV for left vent EDP) dec SV & CO
- blood not pumped out as fast as arrives =>inc in Preload -> Frank-Starling compensation restoring CO
- problem: inc preload -> edema -> fluid in lungs = congestive heart failure