Regulation of Stroke Volume and Heart Rate

autonomic nervous system regulates heart rate

sympathetic NS release noradrenaline plus circulating adrenaline from adrenal medulla, both act on B1 receptors on sinoatrial node, increases slope of the pacemaker potential, increases heart rate = tachycardia

parasympathetic NS, vagus nerve releases acetylcholine, acts on muscarinic receptors on sinoatrial node, hyperpolarises cells and decreases slope of pacemaker potential, decreases heart rate = bradycardia

preload is affected by the end diastolic volume

increased venous return = increased EDV therefore increased stroke volume

decreased venous return = decreased EDV therefore reduced stroke volume

ensures self regulation - matches SV of left and right ventricles

afterload is the load against which the muscle tries to contract

if total peripheral resistances, stroke volume will go down (more energy is “wasted” building up enough pressure to open the aortic valve)

Cardiac output = heart rate x stroke volume

increases heart rate causes small increase in cardiac output but stroke volume starts decreasing

shortened cardiac interval cuts into rapid filling phase, reduced end diastolic volumes reduces preload and according to starling’s law, stroke volume is reduced

Control of cardiac output

HR increases via decreased vagal tone increased sympathetic tone

contractility increases via increased sympathetic tone alter ionotropic state and shortens systole

venous return increases…

total peripheral resistance falls…

cardiac output increases 4-6 times