Cardiac Cycle - sounds Flashcards
S4
atrial gallop
stiffened ventricle (usually hypertrophy)
occurs in late diastole
S1
S1= M1 + T1
mitral & tricuspid valves closing
S2
S2 = A2 + P2
aortic & pulmonary valves closing
split during inspiration
S3
vibration in ventricle filling
Supple ventricle = normal in kids
dilated cardiomyopia in adults
stiff aorta
lose compliance
see greater fall in pressure (>130 to 80 drop)
end systolic pressure-volume relationship
maximum pressure that can be developed for any ventricular volume
end diastolic pressure-volume relationship
passive filling of the ventricle
stroke volume =
SV = vol of blood ejected during systole
SV = EDV - ESV
(CO=SV*HR)
normal; 60-100
ejection fraction =
EF = pump efficiency (%) EF = SV / EDV
preload
ventricular stretching prior to contraction
Starling’s law - more filling, more stretch, more contraction, greater CO
ventricular stress
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
afterload
force heart has to overcome to force blood into aorta
wall stress present at peak systolic pressure
very close to aortic pressure
increasing afterload
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
aortic stenosis
narrowing of the aortic valve
increases afterload (due to higher resistence)
generates a sound between S1 and S2
aortic stenosis - compensation
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
inotropy
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)
increase inoptropy
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
autonomic nervous system; pos or neg inotropic
SNS + ionotropic (beta1 adrenergic recep)
PNS - ionotropic
congestive heart failure
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
