regulation of SV & HR Flashcards
what is involved in the regulation of HR?
neural innervation- sympathetic and parasympathetic nervous systems
what is involved in the regulation of SV?
- preload
- afterload
- neural
- pathological
describe how the sympathetic nervous system regulates HR
- sympathetic nervous system releases noradrenaline & also circulating adrenaline from adrenal medulla
- these act on B1 adrenergic receptors on SA node, which increases the slope of the pacemaker potential
- does this by increasing permeability of Na+ and Ca+, which increase rate of depolarisation and hence less time is taken to reach threshold
- increased HR –> tachycardia
describe how the parasympathetic system regulates HR
- VAGUS NERVE releases acetylcholine which acts on muscarinic receptors on SA node
- decreases slope of pacemaker potential as increase permeability of K+ which hyperpolarises the cells and at the same time reduces permeability of Ca+ so takes much longer to reach threshold
- HR reduces –> bradycardia
describe how preload affects SV
Preload is the degree to which the ventricles are stretched prior to contracting
SV is directly related to the force generated by the cardiac muscle prior to contracting. This is determined by 2 factors:
-initial length of muscle fibres prior to contraction
-contractility of muscle fibres
If EDV increases, length of muscle fibre increases as it becomes more stretched –> inc SV
If EDV decreases –> decreased SV
contractility: ability of the heart to contract at any given fibre length. The more contractile the muscle fibre, the greater the force with which it can eject blood & greater SV
describe how after load affects SV
after load is the load against which the muscle tries to contract
Afterload is affected by arterial pressure which in turn is affected by TPR.
If TPR increases, aortic pressure increases and therefore the ventricles need to work harder to overcome the pressure difference to open the aortic valve. This means they don’t have much energy left to do the actual ejecting of the blood and therefore SV decreases
describe how neural innervation affects SV
- sympathetic mostly - noradrenaline and adrenaline released by adrenal medulla act on B1 receptors on myocytes and increase contractility (positive inotropic effect)
- parasympathetic - little effect - due to lack of innervation of vagus nerve on VENTRICULAR MUSCLE
describe how pathological processes may affect SV
hypercalacaemia - greater extracellular calcium, higher conc gradient, more calcium influx, more cross bridges formed, greater strength of contraction
hypocalacemia- opposite
ischaemia- lack of oxygen to heart muscle so less working muscle - decrease SV
Barbiturates - also decrease
how does the heart compensate for a reduced pumping ability?
increase in EDV - which therefore results in a lower ejection fraction
what is the CO equation?
CO= HR x SV
why does increasing HR with an electronic pacemaker result in initially a small increase in CO & then a decrease in SV?
because it then cuts into the rapid filling phase of the ventricles which results in a lower EDV, decreased preload, decreased SV
what are 5 physiological responses to an increase in heart rate which offset this effect?
-arteriolar constriction to gut, kidneys etc and dilation to skin. dilation > constriction so after load decreases
this is due to increased sympathetic tone & decreased vagal tone
-increased venous return due to skeletal/respiratory muscle pumps & venoconstriction- maintains preload
-CO increases 4-6 times
-increased contractility via sympathetic tone
-TPR falls due to arteriolar dilation in skin, heart & muscle
what does Starling’s law state about length of muscle fibre?
Starling’s law states that the force of contraction is proportional to the initial length of the muscle fibre.
what effect does arteriolar constriction have on SV?
increase after load - decreased SV
what effect does constricting veins have on SV?
increase preload - increased SV
