Lesson 19: Topic 15 - Cardiac Output Flashcards
why can the heart beat on its own?
it has a pacemaker
if we take our heart out, how fast will it beat?
about 100BPM
what is cardiac output?
multiplying heart rate by stroke volume
when is the ventricle fully filled?
end diastolic volume
when is the ventricle fully empty?
end systolic volume
what is stroke volume?
essentially how much volume can be pushed out of the ventricle
essential how does increased parasympathetic activity vs increase sympathetic activity (and epinephrine) affect HR?
- increased parasympathetic HR = lower HR
- increased sympathetic HR = higher HR
all are extrinsic control
what does extrinsic control mean?
things external to the heart
what increases stroke volume?
extrinsic = sympathetic nervous activity
intrinsic control of cardiac muscle cells which is going in increase end-diastolic volume (so obviously it will increase stroke volume)
what does intrinsic control mean?
things inside the heart
if we increase sympathetic nervous activity, it directly increases stroke volume. but how does in indirectly further increase stroke volume?
it increases venous return (intrinsic) which increases end diastolic volume which will then increase stroke volume
what is the difference in action potentials in pacemaker cells vs cardiac muscle cells?
Pacemakers:
- autorhythmic cells
- non-contractile
- HR regulation
Cardiac Muscle:
- non-autorhythmic cells
- contractile
- SV regulation
why are the SA and AV node action potentials autorhythmic?
because they have pacemaker potential
how does the cardiac muscle control when the heart is going to contract and generate first?
through the SA and the AV node
why is the SA and AV node non-contractile
because their main purpose is to control electrical activity in the heart
how does cardiac muscle dictate stroke volume?
because when the cardiac muscle contracts, it distributes blood throughout the whole body
what drives pacemaker potential?
increasing permeability to calcium through the t-type calcium channel
what dictates the HR?
pacemaker activity
how do we change pacemaker activity?
by changing pacemaker potential
if we slow pacemaker potential, what happens to HR?
it lowers
how do we change pacemaker potential?
we change the permeability of the membrane to different ion influxes
if we increase the amount of potassium efflux through the PNS, what happens?
drives the membrane potential negative because positive is leaving
if we make the membrane potential more negative, what effect does this have on the threshold potential?
it gets further away from the threshold potential.
if we are increasing potassium efflux in a pacemaker cell, what affect does this have wrt sodium?
going to decrease sodium influx into the cell so it further makes the cell/membrane potential negative
pacemaker potential is generally determined by?
the t-type channel for calcium
if we decrease the amount of calcium influx through the t-type calcium channel, what happens to membrane potential?
slows pacemaker potential
what happens together to slow the pacemaker potential in time in order to have a negative effect on HR?
- decrease Na+ and Ca2+ influx
- increase K+ efflux
what is threshold potential when there is PNS or SNS control over the heart in pacemaker potential?
no change. always depolarizes at -40mV.
what is the ONLY thing changing through parasympathetic control of the pacemaker cell?
pacemaker potential
how does the PNS get control over the pacemaker?
through increased acetylcholine
what happens if we increase norepinephrine and/or epinephrine in the pacemaker?
(fight or flight)
- heart rate increases because we need to pump more blood throughout the whole body
- we alter pacemaker potential
how do we alter pacemaker potential in the SNS stimulation of our pacemaker?
- increase Na+ influx into the cell (positive ion going to a negative space to make it more positive)
- increase Ca2+ influx into the cell (through t-type calcium channel)
- these both increase the speed at which we reach threshold potential
PNS and SNS only change?
pacemaker potential
what affect does SNS have on HR?
positive (highers it0
what is a key difference between how PNS and SNS affect HR?
PNS uses potassium efflux to bring the membrane potential down and slow it
depends on what is when one of the nervous systems is dominant?
circumstances. both are typically always in use just one may dominate the other
increased PNS activity ________?
- decreases resting membrane potential
- has a negative effect on HR
- increases K+ efflux
what is the key regulator of stroke volume?
cardiac muscle cell
- when it contracts, how much volume gets pushed out of the heart dictates stroke volume
- (end-diastolic volume)
why do we look at end-diastolic volume and not end-systolic volume when looking at stroke volume?
because when the heart is contracting, its in a state of emptiness and there won’t be volume in the ventricle to measure
how can we affect force produced by skeletal muscle?
changing the length of sarcomeres
how do we know if a sarcomere is at optimal length?
if each myosin head can bind/reach an actin head so this optimizes the amount of cross bridges that can form
the more blood we are pumping out of the heart = ___________ stroke volume
the more stroke volume we are going to get
normal resting length of the heart is around what EDV?
140mL
how do we increase stroke volume from the heart?
we stretch it out
how do we stretch the heart out?
increased venous return
- the more blood going through our body increases the amount of blood in our circulation and increases venous return
- atria squeezes this blood into the ventricle and there is going to be more force as we stretch it out due to the optimal actin and myosin overlap
true or false: cardiac muscle does not normally operate within the descending limb of the length-tension curve.
true
- it cannot be overstretched to the point of not being optimal
what does the length of cardiac muscle depend on?
volume of blood in chamber
can we ever reach the full capacity of what the heart is doing?
no, only in very rare occasions
other than venous return being able to affect/increase stroke volume, what else can?
through SNS control of the heart muscle cells
for the same end-diastolic volume, what can epinephrine (SNS) do for stroke volume?
increase it
how is it possible for epinephrine to increase stroke volume more than venous return?
it is not dependent on changes in actin and myosin overlap
- increasing calcium release inside every individual cardiac cell
what dictates calcium release inside each individual cardiac muscle cell from the SNS?
the L-type calcium channel
- the more calcium we get into the cell, the more calcium is going to bind to the ryanodine receptor, the more calcium release we will have in the sarcoplasmic reticulum
if we increase sarcoplasmic reticulum calcium release, what happens to our cardiac force?
we are going to get more force developed per contraction
why do we get more force if we release more calcium?
we get more calcium binding to troponin C, to reveal more open binding sites on actin, which means more myosin heads can bind and more force can be produced
other than making greater force, how else does epinephrine affect stroke volume?
also faster onset of force
- rate of force development is faster. more calcium more rapidly can get into the cell
- we also get faster relaxation
essentially everything is just faster
increased stroke volume is due to?
- increased L-type Ca2+ channel activation
- increased venous return
- increased epinephrine
