Regulation Of Cardiac Function Flashcards
What is EDV?
End diastolic volume
It is the amount on blood in the ventricles at the end of diastole, just before contraction
A larger volume will produce a greater SV
How do you calculate CO ?
HR * SV
What is ESV ?
End systolic volume
It is the volume of blood left in the ventricles after contraction
A low ESV will produce a greater SV
How do you calculate ejection fraction ?
SV/EDV
At rest only half of the blood is pumped out of the heart
What does EDV depend on ?
The venous return- a larger venous return causes an increase in EDV
Filling time - longer in diastole the more filling time and greater EDV
What is preload ?
It’s the same as EDV
What does ESV depend on ?
Afterload - pressure in the aorta which the ventricle is pumping against - a large pressure in the aorta requires a greater pumping force so a greater pressure will increase ESV
Strength of ventricular contraction - the greater the contraction the smaller the ESV
What happens to cross bridge formation when cardiac muscle stretches ?
It increases the number of cross bridges because resting sarcomeres length is closer to 1.8 micrometers so there is more overlap causing greater force of contraction
What is the frank starling law of the heart ?
as the EDV increases the ventricles stretch more which increases the SV therefore the greater the degree of stretch the greater the force of contraction
It is an intrinsic mechanism for increasing heart
What happens if the right side of the heart of failing to pump blood properly ?
Causes peripheral edema
What happens if the left side of the heart is failing to pump properly?
It causes a build up of blood and fluid at the lungs causing ingestive heart failure causing breathlessness
Why do people with hypertension have to make their hearts work harder ?
Due to hypertension there is a increased after load which means the heart has to overcome and larger pressure and if it doesn’t then ESV is increased which reduces CO and SV
Explain sympathetic stimulation of the heart
Sympathetic post ganglionic fibres release noradrenaline onto the heart and this binds to beta adrenoreceptors causing an increased heart rate and force of contraction leading to increased CO
This is an extrinsic mechanism
What happens when noradrenaline binds to beta-1 receptors on the heart ?
Associated with Gs protein Activated G protein activates adenylate Cyclase This increases cAMP This increases protein kinase A Protein kinase A phosphorylates targets
What are the target proteins which protein kinase A phosphorylates upon activation of beta-1 receptors by noradrenaline ?
1) L-type calcium channels - increase influx of calcium ions
2) RyRs - makes these channels more sensitive to calcium so it increases calcium release from SR.
3) phospholambam - causes faster uptake of calcium into SR so there is more calcium ready to release again
4) troponin-I - decreases its affinity for calcium ions allowing calcium ions to be released more quickly so more calcium ions bind in a shorter period of time