regulation of stroke volume and heart rate Flashcards
what 2 things regulate heart rate
symp and parasymp NS
how does the sympathetic NS regulate HR
symp nerves release NA adrenal medulla releases adrenaline these act on beta 1 receptors on SAN increased slope of pacemaker potential increased HR
how does the parasympathetic NS regulate HR
vagus nerve releases Ach which acts on muscarinic receptors on SAN
cells are hyperpolarised
decreased slope of pacemaker potential - cells start further from threshold and take longer to depolarise to threshold
HR decreases
what nerve innervates SAN most heavily
vagus cranial nerve
at rest it is constantly working to slow down HR and keep it at 60-70bpm
HR is said to be under vagal restraint
equation for CO
CO = HR X SV
Effect of increasing HR with an electronic pacemaker
small increase in CO then SV decreases
shortened cardiac interval cuts into the rapid filling phase
reduced EDV, reduced preload, reduced SV
physiological effects to offset reduced SV
- HR increases via decreased vagal tone and increased symp tone
- contractility increases via increased symp tone, alters inotropic state and shortens systole. Stronger but shorter contraction, increased SV
- VR increases via venoconstriction and skeletal/resp pumps, maintaining preload
- TPR falls (arteriolar dilation), reduced afterload
- CO increases 4-6x
physiological regulation of SV
preload
afterload
neural
starling’s law
the energy of contraction is proportional to the initial length of the cardiac muscle fibre
stronger contraction in cardiac muscle = bigger SV
define preload
Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling.
what is preload affected by
EDV
increased venous return = increased EDV and SV (vice versa)
this ensures self-regulation; matches SV of RV and LV so they work in series
define afterload
the load against which the muscle tries to contract i.e. how easy it is to get the blood out through the arterioles - TPR
define total peripheral resistance
TPR
how contracted/dilated all the arterioles are when added together
increased TPR = increased afterload, decreased SV
what happens when TPR increases
aortic pressure will increase
ventricle has to work harder to push open the aortic valve and has less energy left to eject the blood
what vessels set the preload
capacitance vessels set the preload
venoconstriction = increased preload, increased SV, helps the heart
what vessels set the afterload
resistance vessels set the afterload
arteriolar constriction = harder for the blood to get out, increased pressure and afterload
heart has to work harder, reduced SV
neural regulation of SV
symp and parasymp NS
sympathetic NS and SV
symp nerves release NA
adrenal medulla releases adrenaline
these act on beta 1 receptors on myocytes
increased contractility - increased amount of calcium coming into the cell from outside, more released from internal stores
contraction is stronger but shorter as Ca is taken up quicker
parasympathetic NS and SV
little effect on contraction
vagus nerve doesnt innervate ventricular muscle
muscarinic receptors present aren’t activated
pathological regulation of SV
blood Ca levels
ischaemia
barbituates
Starling’s law
hypercalcemia and SV
larger conc grad
more Ca enters when channels are open
stronger contraction
shifts Starling curve up and left
hypocalcemia and SV
smaller conc grad
fewer X bridges form
less steep curve - shifts down and right
ischaemia and SV
obstruction of blood supply to part of the heart can't contract properly smaller overall strength of contraction reduced SV curve shifts down and right
barbiturates and SV
shifts curve down and right
reduced SV
Starling’s law and the pumping ability of the heart
starling’s law lets the heart compensate for a reduced pumping ability by working around a larger EDV (less blood pumped out of the heart so EDV increases)
resting SV is achieved at a higher EDV
lower ejection fraction
reduced exercise capacity
