Regulation of Stroke volume Flashcards
Describe the regulation of HR - SNS
Sympathetic Nervous system
- S. Nerves releases noradrenaline + adrenal medulla releases adrenaline into blood
- both act an B1 receptors on Sinoatrial node
- increases HR = tachycardia
Describe the regulation of HR - PNS
Parasymathtic Nervous System
- vagus releases Ach
- acts on muscarinic receptors on SA node
- hyperpolarises cells and decreases slope of PM potential
- decreases HR - Bradycardia
What is starling’s law?
-states the energy of contraction is porportional to the initial length of the cardiac muscle fibre
Describe the effect of preload on SV
- preload affected by EDV
- A high EDV(amount of blood that fills ventricles before systole), the stronger contraction, hence the stronger the SV as actin and myosin are at optimal lengths for contraction ( SL)
- increased venous return increases EDV, increasing SV
Describe the effect of afterload on SV
- After load is the load in which ventricles are trying to contract against
- There is a high aortic pressure ( due to high total peripheral) resistance[arteriolar constriction) which means ventricles need to work harder(it will have less energy to do so) to open up aortic valve so less blood will be pumped out
- Afterload is dependent on Total peripheral resistance. If TPR increases, SV will decrease( more energy is wasted building up sufficient pressure to open aortic valve)
Preload vs Afterload - what vessels affect them?
Preload affected by:
- venules/vins
- capitance vessels
Afterload affected by:
- arterioles
- resistance vessels
State the factors that affect SV
- SNS
- PNS
- Preload
- Afterload
Cardiac output calculation
HR x SV
- CO affected by all of the factors)
Describe the regulation of SV - SNS/PNS
SNS
- noradrenaline and circulating adrenaline act on B1 receptors on the myocytes
- this increases contractility ( an inotropic effect[anything that affects strength of contraction]) giving a stronger, but shorter contraction
PNS
- litte effect on strength of contraction
- vagus nerve does not innervate ventricular muscle
What does contractibility mean?
-ability of heart to contract ; change
The effect of Hypercalcemia, hypocalcemia and isachemia on SV ( Starling’s curve)
Hypercalcemia
- positive inotropic effect
- shifts curve upwards and to the left
- this means a smaller EDV can generate a higher SV
- remember high calcium will allow more cross bridge formation > stronger strength of contraction
Hypocalcemia
- negative inotropic effect
- shifts curve downards and to the right
- a higher EDV generates a smaller SV
- isachemia or drugssuch as barbatituates
LVEDV is the amount of blood in ventricles just before systole
Starling’s law - compensation
- SL lets the heart compensate for a reduced pumping ability around a bigger EDV resulting in lower ejection fraction, and reduced excercise capacity
- In a heart attack, muscle loss in LV > less SV > more EDV?
EDV will increas as right ventricle is still functioning ( more blood entering vs pumping on eft side )
LECTURE RECORDING
Effect of inceasing HR with electronic pacemaker on CO, SV and why
- CO increases but SV decreases
- this is beacause the shortened cardiac interval cuts into the rapid filling phase
- essentially less filling phase?
- reduced end diastolic volume reduces preload and by SL’, reduces SV
Control of CO during excercise
HR increase
- via decreased Vagal tone
- increased sympathetic tone
Contractibility increases
- via increased sympathetic tone
- alters inotropic state + decreases systole
Venous return increases(preload)
- via venoconstriction.
- skeletal/respiratory pumps
- maintains preload
Total peripheral resistance falls afterload)
- due to arteriolar dilation in the muscle ( that is requiring blood), skin, and heart
- reduces afterload
CO increase 4-6 times
Vasoconstriction vs venoconstriction
Vasoconstriction decreases BF in vessels wheras venoconstriction will increase BF
