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CVS
Monday 22nd January 2018
Regulation of Cardiac Output

CO = HR x SV
Main function of organised contraction & relaxation of heart during cardiac cycle so we can eject
blood from heart & also fill heart so it’s ready for next contraction & next relaxation
...
min-1

(at rest, heart beat is 70pm, EDV is 120ml & usually 50ml left at end of ejection phase in heart)
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CO= cardiac output (= flow of blood around cardiovascular system per minute)
HR= heart rate
SV= stroke volume (= Difference between what we fill heart to and what is left at the end)
EDV= end diastolic volume
ESV= end systolic volume
Regulate blood pumping per min by altering heart rate, also can increase EDV or change
systolic volume

Control of Heart rate:
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Image shows: SAN action potential would look like
with no external influences
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Get:
 Steeper slope of pacemaker
potential
 Decrease in threshold
 Cell more depolarised to
start with

All this to
increase
heartrate
...
s
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So… you open more K+ channels & increase K+ efflux making it more
difficult for cells to depolarise during pacemaker potential
o Remember at rest we already have parasympathetic
influence slowing heart rate down from intrinsic pacemaker
rate
 To increase, we can remove parasympathetic
influence as well as bring in more sympathetic
influence
 Balance
 So e
...
when getting up from exercise from rest; to
increase HR, parasympathetic activity decreases &
sympathetic increases
 Analogy of accelerator & brake
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Excitation- contraction coupling:

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Excitation-contraction coupling in cardiac muscle cells
Ca2+ comes into cardiac muscle cells; during plateau phase of action potential
o …talking about: Ventricular or atrial muscle cell action potential (not pace maker
ones bc interesting in contractile cells)
Ca2+ enters via L-type Ca2+ channels found in t-tubules (invaginations inside cells)
o Allows Ca2+ to enter cells v close to apparatus needed to release further Ca2+ and
for contraction of sarcomeres
During action potential: Ca2+ enters; stimulates feet inbetween L-type Ca2+ channels
o These Ca2+ channels called ryanodine receptors or dihydropyrimidine receptors
which are found on sarcoplasmic reticulum of cells
 Where all Ca2+ inside cell stored
o When feet stimulated; ryanodine receptors open; Ca2+ efflux from sarcoplasmic
reticulum
 Increase intracellular conc of Ca2+ in cell
...
Make more cross bridges by releasing
more Ca2+ from SR which affects contractility of cardiac myocyte (or inotropy =
changes in ESV)
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Starlings law of the heart:
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How does this influence SV?
Images= cartoons of ventricle
o At rest= normal filling; fill to EDV of 120ml, eject
70ml & ESV left ~ 50ml
If we need greater SV e
...
during exercise, we can fill/
bring more blood back to heart
o This increases EDV; this stretches ventricles
o Effect of stretch is that heart contracts w/ greater
force of contraction & SV increases by same
amount that EDV increased
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 If ESV has not changed in either
situations; greater forced
contraction ejected a greater
amount of blood so same
amount of blood left over for
ESV
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o Means that if you stretch muscle; sarcomere
length increases, this increases force of contraction
from that muscle
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o Fact that it worked in individual sarcomere
stretched shows it must be intrinsic property of
cardiac muscle
...
(no
more Ca2+ or released inside/ to cell
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o Hypothesis: Stretching cardiac myocyte changes
effective volume of sarcomere such that it
increases local sensitivity of fibres; makes them
thinner so brings them closer
o Hypothesis: actin & myosin get closer together as
stretching happens
“Force of ventricular contraction is dependent on the length
of the ventricular muscle fibres in diastole
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o Graph shows EDV on x-axis; you see as increase EDV (fill ventricle more & stretch
more), contraction force increases
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g
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Regulation of EDV: (venous return & CVP):
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CVP = central venous pressure
Main things affecting EDV:
o Venous return = how much blood brought back to heart
o CVP = pressure of blood at point of which it enters right atrium (confluence of
superior & inferior vena
cava)
Image;
o 1) increase in venous
return increases venous
return; higher filling
pressure for heart so
increases cardiac filling
(from atria into
ventricle) which
increases EDV
o 2) blood coming back
from systemic
circulation mobilised

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veins act as capacitance vessels; we can mobilise blood held inside them to
increase VR & CVR  increase cardiac filling  increase EDV therefore
increase force of contraction & increase right SV
...
)
 Left ventricle stretched
To get changes in left & right SV; think abt factors that influence venous return & CVP
o Another benefit of Starlings law is not only controlling SV but making sure left SV &
right SV equal to eachother (bc both sides of heart contract together)  ensures CO
for both circuits the same
 Important bc e
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L SV stronger than R SV; you would get blood accumulating
in systemic circulation

Factors affecting venous return to right ventricle (RV):
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1) Blood volume
o Depending on how much blood circulating; influences how much in venous
circulation therefore how much returning to R heart
o Increased BV (maybe bc renal failure = failure to modulate vol of blood) leads to
increased VR  extra pressure put on someone’s heart
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g
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Skeletal muscle pump
o Venous side of circulation doesn’t have pump like arterial side of circulation so
rely on other mechanisms to get blood back to heart (e
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respiratory pump)
o Takes advantage of fact that when contracting muscles; bc veins so
compressible; squashing veins pushes blood from inside veins
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Small retrograde movement back
from contraction that will shut valves which stops movement of blood
backwards
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g
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Presence of valves crucial to this
function
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o Takes advantage of pressure changes in thorax
 When breathing in; diaphragm flattens & presses on abdominal contents
including vena cava  increases pressure on inferior vena cava
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This creates pressure
gradient so breathing in basically sucks blood back up to heart
 E
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taking deep breaths when feeling faint to draw blood back up to
heart (RA to fill RV)
Venous tone
o Mechanism to return blood to R side of heart; how constricted / dilated venous
vessels are
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Consider how distensible venous vessels are; less blood in them they’re
flattened
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 So venous tone = important mechanism bc only one that has reflex or
nervous control
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g
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S
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Increased sympathetic activity will evoke
venoconstriction; release of noradrenaline
from sympathetic nerve fibres which
innervate the venous vessels
 Acts on α -1 receptors on smooth
muscle causing contractions therefore
size of lumen to decrease
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 ONLY one with reflex control

Gravity
o V important of venous return to heart; gravity reduces venous return to heart
 All other 4 things; if they increase activity that increase VR to heart
o All above work bc unidirectional valves in veins; blood only moves in one
direction; without them gravity would mega impact ability to immobilise blood
back to heart
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g
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o When lying down, v little effect of gravity bc all of body at same level of heart
o So gravity no increasing hydrostatic pressure by acting on fluids
o Lying down= uniform distribution of blood across body so CVP & VR
maintained @ nice level, allowing filling to occur
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 Not bc all blood drops to feet (not possible bc presence
of valves); just that less of that blood now being
returned to heart
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 CVP (key to determine filling of heart) &
VR fall
 If those fall, then… EDV & SV fall
(SV will fall if EDV does bc
starlings law)
 Preload = any factor which influences how much cardiac muscle cells are stretched
before muscle contraction
o Increases in EDV will increase pre-load on heart
o Increases in VR will increase pre-load bc it increases EDV
o Higher CVP = higher pre-load
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Sympathetic N
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innervation of atrial muscle; increased force of contraction will increase
EDV; greater contribution to filling of heart
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Other factors that affect EDV = Heartrate (>180bpm):
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higher heart rate reduced filling time
does require very high heart rate to get to point where ventricular filling compromised
seen a lot if patient has serious pathological tachycardia
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o Leaves less blood in heart; changing ESV
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 So… when stimulate β receptors with noradrenaline; increase in
cyclic AMP; phosphorylates PKA (protein kinase A) which
phosphorylates L-type Ca2+ channels causing more Ca2+ to open
and more to enter during plateau phase
o Binds to feet of ryanodine receptors; more open so more
Ca2+ released
...

o Called a change in cells
contractility / inotropy
 (sometimes contractility
used to talk about force of
contraction)
 Force of contraction is
related to number of cross
bridges made & ultimately
this determines how much
SV ejected
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(gives shift in Starlings curve)
o Happen as result of Ca2+ handling in cell; things that change in heart failure
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g
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g
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Affected by:
o Peripheral resistance:
 High PR = higher BP makes it more difficult for blood to be ejected into
aorta
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Summary:
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Increase SV by Starlings law of heart, by changing EDV
o No change in ESV by increasing EDV just increase in SV
Also; can change SV by changing contractility so we fill heart to same as resting but eject
more blood (EDV doesn’t change but ESV goes down)
In reality; neither of these happen independently
Regulation of CO
o CO = HR x (EDV – ESV)
 EDV intrinsic factors:
 Pre-load,
 VR/CVP
o Blood volume
o Skeletal muscle pump
o Respiratory pump
o Venous tone
o Gravity
 Atrial contraction
 HR (>180bpm)
 ESV extrinsic factors:
 Contractility/ inotropy
o Sympathetic nerve activity
o Circulating adrenaline / noradrenaline

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