cardiac cycle Flashcards
what is systole
Ventricular contraction
Ventricles generate pressure then eject blood into the arteries
what is diastole
Ventricular relaxation
The ventricles fill with blood
what is the 1st phase
systole
what is teh end diastolic volume
maximum blood in the heart just before the ventricle start to contract
End-systolic volume
residual volume left in the heart after contracting
what is teh Stroke volume (mL)
End-diastolic volume - End-systolic volume
how much blood is ejected
what is a clinical indicator of heart function
ejection fraction
how to work it out
stroke volume/End-diastolic volume
normal range of ejection fraction
52 - 72
patient in heart fraction
30 - 35
what is the start of teh cardiac cycle
artial systole
how is the start shown on an ecg
p wave = atrial systole
what does the atrial contraction do
Atria contract to ‘top-up’ the volume of blood in ventricle
what may you hear in the heart of a patient with congestive heart failure, pulmonary embolism or tricuspid incompetence
4th heart sound
next stage
Isovolumetric contraction
what is it shown on ecg
QRS
which is
start of ventricular depolarisation
what is start of ventricular depolarisation
This is the interval between AV valves (tricuspid & mitral) closing and semi-lunar valves (pulmonary & aortic) opening
(ventricular pressure increases near the aortic pressure)
what is the change in volume
no change in volume §
what causes the first heat sound (lub) to occur
closure of AV valves
what sort contractions occur at this point
isometric
what is the next stage
rapid ejection
when does it begin
As ventricles contract pressure within them exceeds pressure in aorta and pulmonary arteries. Semilunar valves open, blood pumped out and the volumes of ventricles decrease.
so what marks the start of this phase
Opening of the aortic & pulmonary valves mark the start of this phase
what is the heart sound in this phase
no heart sound
what is the next stage
Reduced ejection
what does thsi phase signify
This phase marks the end of systole
what causes the semilunar valves to close
Reduced pressure gradient means aortic & pulmonary valves begin to close
As pressures in ventricles fall below that in arteries, blood begins to flow back causing semilunar valves to close
describe the changes to the ventricular volume
Blood flow from ventricles decreases and ventricular volume decreases more slowly
what causes teh t wave
Ventricular muscle cells repolarize producing T wave
what is the next stage
Isovolumetric relaxation
when do the AV valves open
The aortic & pulmonary valves shut, but the AV valves remain closed until ventricular pressure drops below atrial pressure.
what causes the Dichrotic notch
caused by rebound pressure against aortic valve as distended aortic wall relaxes.
what heart sound can be heard
2nd - dub
why
due to closing of the SL valves
what is the rate of pressure decline in the ventricle caused by
rate of relaxation of the muscle fibre
regulated by ca atpases in sr membrane
do volume change
no- isometric
what stage occurs next
Rapid passive filling
when do AV valves open
when ventricular pressure falls below the atrial presuure
what part of ecg
Occurs during isoelectric (flat) ECG between cardiac cycles
no electrical activity
what is the heart sound heard
3rd heart sound – usually abnormal and may signify turbulent ventricular filling
Can be due to severe hypertension or mitral incompetence (mitrial doesn;t close properly)
what is the next stage
Reduced passive filling
aka
This phase can be called diastasis
what happens
ventricle fills more slowly
how mcuh can V without atrial contraction
The ventricles are able to fill considerably without the contraction of the atria.
next stage
starts again atrial systole
how do the pressure change pattern in the right and left side of the heart compare
identical
what is teh differnce in bith sides
Quantitatively, the pressures in the right heart and pulmonary circulation are much lower (peak of systole – 25mmHg in pulmonary artery)
blood difference ejected
Despite lower pressures right ventricle ejects same volume of blood as left (it is simply pumping the same quantity of blood into a lower pressure circuit)!
what is the pulmonary capillary wedge pressure
indirect estimate of left atrial pressure
gives us idea of severity of left ventricular failure
what does an increase in left ventricular pressure cause atrial
increase pulminary oedema
life threating
how to measure the left atrial pressure
use right side of the heart
ventriular bloon right atrium ventricle
what happens when we reach aortic pressure
aortic valvue opens blood expelled from the heart
what is preload
the amount of blood coming back to teh heart stretching the ventricles
how to increase preload
increase in amount of blood returning to the heart
relationship between preload and force
larger preload, larger stretch more force
more blood ejected
what is the afterload
Afterload is the pressure that the heart must work against to eject blood during systole (ventricular contraction
diastolic blood pressure
what does the afterload cause
shorteing of teh muscle fibres
less able to expel blood in teh ventricles
what represents the afterload
The blood pressures in great vessels (aorta and pulmonary artery) represent the AFTERLOAD
what is ESPVR
maximal pressure that can be developed by the ventricle at any given volume
Increases in preload result in
increased stroke volume
what is that known as
This is the Frank-Starling relationship
Increases in afterload result in
decreased stroke volume
afterload increases, the amount of shortening of muscle fibres that occurs decreases
when the after load increases what effect does it have on the aortic valve
Greater pressure required to open aortic valve
afterload is the resistance that is required to be overcome to circulate blood so high pressure aorta = higher pressure in ventricle (i think)
what is cardiac output calculated
Heart rate
*
Stroke volume
what is stroke volume affected by
Preload
Afterload
Contractility
what is Contractility
Contractile capability (or strength of contraction) of the heart
what is it increases by
Sympathetic stimulation
how
Changes Ca2+ delivery to myofilaments
What happens to PV loops during exercise?
(1) Increased VR (vebous return) aided by muscle and respiratory pump increases EDV
2 Main factor: Sympathetic activation of the myocytes increases ventricular contractility, that decreases end-systolic volume.
3 combacted by The increase in arterial pressure that occurs during exercise increases afterload (and can lessen the reduction in end-systolic volume but offset by large increase in contractility)
summary
(4) Combination of increased cardiac contractility and increased VR generate increased SV (and EF) ejection fraction
what is this dependent on
If HR increases to very high rates, diastolic filling time can be reduced and this decreases EDV
what hormone can cause symoathetic innervation
Hormonal: Circulating adrenaline from adrenal gland
nueral
Neural: Noradrenaline released from nerves
how does an increase in preload shown on a pv grapgh
more wide- (more left ventricular volume) (increase size from the left) same pressures
decrease preload
more narrow- less ventricular volume (decrease size from the left)
same pressures
increase afterload
thinner and higher
thinner from the right side is squashed
decrease afterload
normal
excersize
Venous return increases due to venoconstriction and skeletal muscle pump, and contractility is increased via sympathetic nervous system
wider from both sides and higher
what increases afterload
hypertension vasoconstriction
increase preload
higher venous return
