cardiac cycle 2 Flashcards
atrial kick
- spurt of blood that gets spurted into ventricles during atrial systole
- non-pathological hearts don’t really need it because they are already passively filling and should have enough blood for their own systole
- HOWEVER, PATHOLOGIC HEARTS DEFINITELY NEED IT
what occurs during isovolumic contraction in the ventricles?
-both valves are closed but the ventricles are still beginning to contract so you see a large increase in pressure in LV
when does the aortic valve open?
-when the pressure in the LV is higher than that of the aorta
why do we need very dispensible aorta
because such a large amount of blood coming from the LV that it balloons the aorta
what corresponds with the T wave on the ECG
-the end of the declined ejection of the blood from the LV and the closing of the aortic valve
once the LV (or RV) pressure is low enough, we can get an opening of the mitral and tricuspid valves to….
start passive filling again but stays below pressure in atria to keep valves open for filling (rapid to reduced)
as the blood is ejected out into the aorta, when does the AV close?
- remains open even thru reduced ejection because the forward momentum of the blood
- end of reduced ejection occurs when the AV closes
what phase of the cardiac cycle is signified by isovolumic relaxation?
-aortic valve closure
dicrotic notch aka incisura
-uptick of the aortic pressure after the AV closes
-due to backwards pressure wave coming from the periphery
-basically, the wave form is a measure of pulses (ck slides 28-29)
-blood moving into the aorta causes pulse that leads to first peak of the figure…. then as the pulse hits the abdominal aorta and it’s bifurcation, you see a reflection coming back to the aortic root
= DOES NOT HAVE TO DO WITH BLOOD- IT’S ABOUT PULSATION
is the dicrotic notch higher in pathologic or healthy pt? why?
-it is higher in pathologic pt because their arteries are stiffer and they do not cushion the pulse as well as healthy pt
when are the valves open
av valves open during atrial contraction and rapid and decreased ventricular filling
what is going on with the valves during isovolumic contraction
all valves are closed- systole
what is going on with the valves during isovolumic relaxation
-all valves are closed-diastole
what is occurring when the semilunar valves are open
-systole: rapid ventricular ejection and decreased vent. ejection
stroke volume
SV = left ventricular end diastolic volume/ left ventricular end systolic volume
(how much is entering the periphery/Ao)
what are the first and second heart sounds
first- closure of AV valves-low pitch, longer duration
second-closure of pv and av- higher pitch, shorter duration
what is physiological splitting of the heart sounds of s2
- it is a sort of mixing up of heart sounds that makes them run together
- occurs during inspiration due to either delayed closure of the PV or early closure of the aortic v.
what is the mechanism of physiological splitting of s2
-delayed closure of PV: during inspiration- greater venous return to right heart so time it tales to expel blood will be longer so pulm closes a bit later after Aortic
-early AV closure- during inspiration, less blood returns to left heart because its trapped in the lungs so less time to change the pressure and close av
=EITHER WAY, AV BEFORE PV
opening snap
- when MV and TV open- may or may not be when heart of pt has fibrosis or stenosis of the valves and it is difficult for them to open
- ventricular dilation can also contribute to sound
fourth heart sound
- always abnormal
-caused by increase in ventricular pressure at end of atrial systole
-louder with decreased ventricular compliance
=groaning of tired and overworked ventricle
sound 3
- between rapid and reduced filling as the chordae tendinae are stretching and AV ring is pulled taut
diastolic murmur
- sound heard after s2 and before s1
- mv stenosis will produce diastolic murmur
systolic murmur
- after s1 but before s2
- mitral regurge since leaflets done close completely and have blood flow during closed valve stage
Paradoxical splitting
- when get conduction thru one ventricle more than another
- can cause a change in the physiological split in s2
- ex? left bundle branch block causes conduction thru the LV to de delayed- get no split at inhalation and at exhalation, get split where pv closes BEFORE AV
