Regulation of stroke volume and heart rate Flashcards
What regulates Heart rate
sympathetic and parasympathetic acting on the SAN
How does the sympathetic NS regulate the heart rate
sympathetic nerves release noradrenaline
(plus circulating adrenaline from adrenal medulla)
both act on ß1-receptors on sinoatrial node
Depolarise to threshold quicker
increases heart rate = tachycardia
How does the parasympathetic NS regulate the heart rate
Travels down vagus and releases ACh
acts on muscarinic receptors on sinoatrial node
hyperpolarises cells and decreases slope of pacemaker potential
decreases heart rate = bradycardia
creates a vagal tone
How is normal heart rate regulated
Myocytes cells of the heart spontaneously depolarise to threshold - 100bmp
What does Starlings law state
the energy of contraction is proportional to the initial length of the cardiac muscle fibre
If you increases the end diastolic volume what effect does this have on the Stroke volume
increased EDV means more blood comes into the heart, causing the heart to increase the amount you pump out i.e. increased stroke volume
Why is the relationship of stroke volume and EDV important
Ensure self regulation therefore the Stroke volume of right and left ventricle is maintained the same
What is after load defined as
the load against which the muscle tries to contract
What is the load in present that affects the cardiac muscles ability to expel the blood from the ventricles
afterload is set by the arterial/aortic pressure being high enough to expel the blood from the ventricles
An increase in the arterial pressure is caused by the
increase in the Total periphery resistance due to arterial constriction
Why does increasing the total periphery resistance decrease the stroke volume
As total periphery resistance, increases total aortic resistance, this means more energy is needed to put aortic valves open, therefore less energy is left to push the blood out the heart = decrease in stroke volume
What blood vessels affect the preload
the capacitance vessels - venues and veins
The stretchability defines how much blood can be transported
What blood vessels affect the after load
The resistance vessels - arterioles
The ability to contract and dilate affects the ability to pump blood
Constricting the capacitance vessels has what affect on the preload
Decreases the preload, as constricts vessels so the capacitance is reduced
How does sympathetic system regulate the stroke volume
releases noradrenaline
(plus circulating adrenaline from adrenal medulla)
Act on ß1-receptors on the myocytes
Increasing the release and uptake of calcium
Therefore increasing contractility so contraction are shorter but stronger (an inotropic effect)
What way does sympathetic system shift the starlings la states graph
Shifts the curve to the left
Why does the parasympathetic system have little effect on the stroke volume
Vagus nerve does not inervate the ventricular muscle therefore cant affect contractility
What are other pathological features thats affect stroke volume
Hypercalcemia
Hypocalcemia
Ischaemia
Barbiturates
What effect does Hypercalcemia have on the starling la states graph and how does this occur
shifts curve up and left
This is due to the increase in calcium, therefore more available for cross bridge, so increase strength of contraction
What is Ischaemia
The reduced pumping ability of the heart
What affect does ischaemia have on the starling la states graph, why does it have this effect
shifts curve down and right
Heart muscle no longer efficient therefore doest properly eject blood causing a decrease in stroke volume
How does the Heart compensate for ischaemia so the stroke volume remains the same
Works with a bigger EDV
What is the results of the heart working with a bigger EDV
Lower ejection fraction SV/EDV
Reduced exercise capacity - cant exercise very well
What affect does barbiturates have on the heart
Shifts the curves down and to the right
