Cardiac Output (Pt2): Mechanical events and Stroke Volume Flashcards
systole
ventricular contraction and blood ejection
Diastole
ventricular relaxation and blood filling
Do the ventricles have the same SV
yes
what is the cardiac cycle predominately driven by
Pressure changes in the ventricles (minor part played by atrial contraction)
What drives opening/closing of valves
pressure changes in the 4 compartments
Systole: isovolumetric ventricular contraction
AV valves closed
Pressure ventricles>atria
Aortic and pulmonary valves closed
Pressure ventricles
Systole: ventricular ejection
AV valves closed and pressure ventricles > atria
Aortic and pulmonary valves open and pressure ventricles > arteries
Diastole: isovolumetric ventricular relaxation
AV valves closed and pressure ventricles > atria
Aortic and pulmonary valves closed and pressure ventricles < arteries
Diastole: ventricular filling
Negative pressure in ventricles (90%):
AV valves open, pressure ventricles < atria
A and P valves closed and pressure ventricles < arteries
Atrial contraction (10%):
AV valves open
A and P closed
Pressure and volume changes during the cardiac cycle
During systole, BP rising in ventricles, SL valves open and blood passes out
In diastole pressure in arteries gets higher than in the heart, then SL valves close and heart starts relaxing.
As it relaxes, creates a vaccuum in the bottom of the heart, and the low pressure flips open the AV valves
SV=
EDV (end diastolic volume) - ESV (end systolic volume)
heart sounds caused by
closure of heart valves
1st sound
closure of AV valves
onset of systole (contraction)
2nd sound
closure of pulmonary and aortic valves
onset of diastole (relaxation)
Regulation of SV
- filling pressure (reload)- starling’s law of the heart
- arterial pressure opposing ejection (afterload)
- contractility: sympathetic nerves, circulating agents
what is end-diastolic ventricular volume (pre load) determined by
CVP - central venous pressure
What is CVP determined by
skeletal muscle pump (blood squeezed back towards heart leading to incr CVP)
Blood volume (reduced BV leads to reduced CVP)
Gravity (posture)- when standing, gravity leads to pooling in legs and reduces volume and CVP
Sympathetic nerves- contraction of central and peripheral veins leads to incr CVP
Respiratory pump (breathing)- inspiration = incr CVP, expiration = decr CVP
frank starling mechanism
ventricles contract with more force (ie incr stroke volume) if it contains more blood (ie incr end-diastolic ventricular volume)
What is frank starling mechanism determined by
length-tension relationship in the muscle ie greater stretch = more tension developed in the cardiac muscle
What is the main function of the frank starling mechanism
maintains balance between left and RHS of the heart and stops accumulation of blood in lungs
How does F-S stop blood accumulating in the lungs
if incr venous return to right ventricle then incr contraction
more blood to lungs
If incr venous return to left ventricle then incr contraction
Incr stroke volume
Blood doesn’t accumulate in lungs
Contractility
sympathetic only, not para, controls SV
Symp release noradrenaline, activate B1 adrenergic receptors, incr force and speed of cardiac muscle contraction and incr ventricular contraction at any given end-diastolic ventricular volume
arterial pressure opposing ejection
Higher arterial BP, harder heart is to open
Hypertension (high BP) makes it more difficult to open valves and eject blood, leading to heart failure
congestive heart failure
reduced CO
tiredness and shortness of breath
Fluid retention via kidneys to incr CO ( venous return)
systolic dysfunction
coronary heart disease leading to ischaemic heart disease and heart attack
Heart attack damages heart muscle, decr ventricular contractility so lower SV
Diastolic dysfunction
Hypertension
stiffening of ventricular wall - incr ventricular muscle- inr cardiac resistance- incr arterial pressure- high BP/ hypertension
Diastolic dysfunction
Hypertension
stiffening of ventricular wall - incr ventricular muscle- inr cardiac resistance- incr arterial pressure- high BP/ hypertension
Also stiffening leads to decr in end-diastolic ventricular volume, leads to decr in stroke volume