Regulation of Stroke Volume and Heart Rate Flashcards
Regulation of heart rate
Neural
Regulation of stroke volume
Preload
Afterload
Neural
Pathological
Sympathetic nervous system regulation of heart rate
Nerves release noradrenaline, circulating adrenaline from adrenal medulla, act on beta1 receptors on sinoatrial node, increases slope of pacemaker potential, increases heart rate = tachycardia
Parasympathetic nervous system regulation of heart rate
Vagus releases ACh, acts of muscarinic receptors on sinoatrial node, hyperpolarises cells and decreases slope of pacemaker potential, decreases heart rate = bradycardia
Starling’s law
The energy of contraction is proportional to the initial length of the cardiac muscle fibre
Result of more blood entering the heart on cardiac muscle fibre length
Increases length
Length of the cardiac muscle fibre is also known as
Preload
Preload is affected by the
End-diastolic volume
Effect of increased venous return (preload) on EDV and stroke volume
Increase EDV and so increased stroke volume
Effect of decrease venous return (preload) on EDV and stroke volume
Decrease EDV and so decrease stroke volume
Afterload
Load against which the muscle tries to contract (building up enough pressure to open aortic valve)
Aortic pressure is affected by
How easy it is for blood to get out through the arterioles - total peripheral resistance
Effect of increased total peripheral resistance on aortic pressure and stroke volume
Increases aortic pressure and so decreases stroke volume as ventricle will have to work harder to push open aortic valve
Afterload is set by
The arterial pressure against which the blood is expelled
Sympathetic nervous system regulation of stroke volume
Nerve release noradrenaline, adrenaline in blood from adrenal medulla, act on beta1 receptors on the myocytes, increases contractility (inotropic effect), gives stronger but shorter contraction, increases stroke volume
Effect of increasing contractility on starling graph
Whole graph moves up and becomes steeper
Effect of parasympathetic nervous system on stroke volume
Little effect - vagus nerve does not innervate ventricular muscle
Effect of hypercalcemia on stroke volume starling curve
Shifts curve up and left (steeper)
Effect of hypocalcemia on stroke volume starling curve
Shifts curve down and right (less steep)
Effect of ischaemia on stroke volume starling curve
Shifts curve down and right (less steep)
How does the heart compensate for a reduced pumping ability
Works around a bigger EDV to achieve same stroke volume as normal
Result of working around a bigger EDV
Lower ejection fraction and reduced exercise capacity
Effect of barbiturates (anaesthetic drugs) on stroke volume starling curve
Shifts curve down and right (less steep)
Cardiac output is determined by
Heart rate x stroke volume
Why does increasing heart rate with an electronic pacemaker decrease stroke volume
Shortens cardiac interval which cuts into the rapid filling time, decreases EDV which decreases preload which decreases stroke volume
Control of cardiac output
Heart rate increases Contractility increases Venous return increases - preload Total peripheral resistance fall - afterload Cardiac output increase 4-6 times
Heart rate is increased via
Decreased vagal tone and increased sympathetic tone
Contractility is increased via
Increased sympathetic tone
Effect of increasing contractility
Alters inotropic state and shortens systole
Venous return (preload) is increased via
Vasoconstriction and skeletal/respiratory pumps
Total peripheral resistance (afterload) is decreased due to
Arteriolar dilation in muscle, skin and heart
Control of cardiac input only works through
Integration - all processes working together to produce a co-ordinated increase in CO
