Regulation Of Stroke Volume And Heart Rate Flashcards
Effect of sympathetic nervous system on heart rate
Release noradrenaline and adrenaline from adrenal medulla
They act on B1 receptors on sinoatrial node
Increasing the slope of the pacemaker potential and therefore heart rate goes up
Effect of parasympathetic nervous system on heart rate
The vagus releases ACh which acts on muscarine receptors on the sinoatrial node
This hyperpolarises cells and decreases the slope of the pacemaker potential
Decreasing heart rate
Starling’s law
The energy of contraction is proportional to the initial length of the cardiac muscle fibre (preload)
What is preload
Initial length of cardiac muscle fibre
What is preload
Initial length of cardiac muscle fibres
What affects preload
End diastolic volume (end volume of blood in ventricles)
What affects preload
End diastolic volume (end volume of blood in ventricles)
How does EDV affect preload
If there is lots of blood in the ventricles the fibres are stretched and stroke volume increases to match return and vice versa
What is afterload
The load against which the muscle tries to contract
What affects afterload
The total peripheral resistance (size of arterioles)
Increasing aortic pressure so the ventricle will have to work harder to push open the aortic valve and then less energy will be left to eject blood so stroke volume will decrease
Preload Vs afterload
Preload affected by capacitance vessels
Afterload affected by resistance vessels
Effect of sympathetic nervous system on stroke volume
Noradrenaline and adrenaline act on B1 receptors in myocytes to increase contractibility (ionotropic) to give a stronger but shorter contraction
Parasympathetic nervous system effect on stroke volume
Little effect probably because vagus doesn’t innervate the ventricular muscles
Hypercalcaemia on stroke volume
Curve goes up and left (pumps more with less in it)
Hypocalcemia and ischaemia and barbiturates on stroke volume
Shift curve down and right (doesn’t work as well)