Cardiac Output Flashcards
What is cardiac output
volume of blood ejected by each ventricle per min
what is cardiac output dependent on
cardiac output = heart rate x stroke volume
what is stroke volume
vol of blood ejected by each ventricle per beat
how much blood on avg do we need to pump per min (avg cardiac output) at rest
~5 L/min
depending on size, age etc.
avg heart rate at rest
~70 bpm
avg stroke vol at rest
~ 70ml of blood per beat
avg cardiac output during exercise
~20 L/min
avg heart rate during exercise
~ 190 bpm
avg stroke vol during exercise
105 ml
how might heart rate and stroke vol differ in an athlete
a) at rest
b) during exercise
a) HR is lower (40bpm)
SV is higher (140ml) about double
b) HR is same (190bpm)
SV is higher (210ml) about double
whats the avg weight of the heart?
300g
how does the heart size differ in an athlete
500g
what 3 factors affect heart rate
autonomic innervation
hormones
venous return
what 2 things determine stroke vol
end diastolic volume (EDV) = the amount of blood in there at the start of contraction
end systolic volume (ESV) = amount of blood left at end of contraction
if you subtract the two, you get SV
3 groups of factors that can affect the EDV and ESV
Preload - factors that affect how much is being loaded in before systole
Contractility - how much force the heart can produce during the contraction
Afterload - force that opposes the ejection of blood from the ventricle
what affects the preload
filling time
venous return
what affects contractility
autonomic innervation
hormones
what affects the afterload
vascular tone - degree of vasocontriction/vasodilation
definition of chronotropic effects
factors that effect heart rate
neural regulation of heart : how do we detect changes in the blood that might trigger change
CVS and CNS have receptors that can detect changes within the blood and cerebrospinal fluid
this indicates whether heart needs to pump out more or less blood
what are the 2 types of receptors and where are they in the body
chemoreceptors - detect chemical changes - in carotid body and within medulla oblongata
baroreceptors - detect pressure changes - in the walls of aorta and internal carotid artery
what might a chemoreceptor change in the blood
the CO2 levels
the pH
how do we decrease HR
- process called cardiac reflex
- sensory nerves send signal to medulla oblongata in the cardioregulatory centre
(to the cardioinhibitory centre section) - this is connected to parasympathetic nervous system
- via the vagus nerve (=cranial nerve 10)
- using the transmitter acetylcholine
- signal arrives at the pacemaker cells of the heart
- tells heart to slow down
how do we increase HR
- sensory nerves send signal to medulla oblongata in the cardioregulatory centre
(to the cardioacceleratory centre section) - this is connected to sympathetic nervous system
- via the sympathetic ganglia (at levels T1-T4)
- using the transmitter noradrenaline
- signal arrives at the pacemaker cells of the heart
- inc HR
ALSO
sympathetic nerves activate the adrenal medulla
to release noradrenaline and adrenaline into circulation
also increases HR
name for pathologically low HR
Bradychardia
name for pathologically fast HR
tachycardia
describe the ionic control at the SA node
DEPOLARISATION
- Na+ travels in via Hyperpolarization-activated cyclic nucleotide–gated (or HCN) channel
= slow rise in memb potential
- when reaches the action potential threshold, then Ca+ channels open and it travels in
= sharp rise in memb potential
initiates contraction of muscle cells
REPOLATISATION
- K+ travels out via K+ channels
= decrease in memb potential
(see onenote for diagram)
How is ionic control affected at the SA node during activation of the parasympathetic system
The acetylchloine released in detected by muscarinic receptors on the K+ channels
Opens up more K+ channels
So it becomes hyperpolarised (more negative)
And takes longer for depolariaation to happen and reach the action potential
What type of channels are the K+ channels in this situation
muacarinic receptosrs
How is ionic control affected at the SA node during activation of the sympathetic system
Opens up more HCN channels and Ca2+ channels
reduced repolarisation (less of +ve increase needed to reach AP)
Rapid depolarisation and increased heart rate
explain why despite the SA node having an inherent rate of >100bpm, regualr resting bpm is 60-100?
background parasympathetic activity
= VAGAL TONE
reduces HR to 60-100bpm
little/no background sympathetic activity
how does vagal tone differ in athletes
higher vagal tone at rest
reduces HR further down to 30-60bpm
little/no background sympathetic activity
ALSO possibly some difference in ion channels
what is venous return
flow of blood from periphery back to right atrium
how does venous return indirectly affect HR and what is the name of this process
stretch receptors in right atrium
triggered when more blood goes into the right atrium
sends signal to medulla
which activates sympathetic nervous system
increases HR
= BAINBRIDGE REFLEX
whats another way that the sympathetic nervous system can be activated directly by venous return?
sinoatrial nodes get stretched, increases heart rate further
stroke volume: what happens when you increase the EDV
Increase in SV
Cuz EDV-ESV= SV
what is preload
the degree to which ventricular muscle cells are stretched at the end of diastole
contractility
the force produced by ventricular muscle cells during systole at a given preload
afterload
force that ventricle needs to overcome to open the semilunar valve and eject blood
what is preload directly proportional to ?
EDV
depends on the rate of venous return
the available ventricular filling time (ie ventricular diastole)
so what happens if you increase the rate/time of filling the ventricle?
Increases EDV
in turn increases the SV
due to Frank Starling Law
What is frank starling law
(the more you stretch a muscle fibre, the more force it’ll produce when it contracts)
force developed in the muscle fibre is depended on the extent the muscle is stretched
What is frank starling law
(the more you stretch a muscle fibre, the more force it’ll produce when it contracts)
force developed in the muscle fibre is depended on the extent the muscle is stretched
what factors affect venous return
posture
skeletal muscle pump
respiratory pump
how does posture affect venous return
blood pools in legs when standing
= decreased venous return
when laying down, central venous pressure increases -> incereased EDV-> increased stroke vol -> increased pulse pressure
how does the skeletal muscle pump affect venous return
movement of skeletal muscles constricts veins
pushes blood up through veins
veins have valves
the valves superior the the contraction site will open and those inferior will close to prevent backflow
how does the respiratory pump affect venous return
inspiration
decreases intrathoracic pressure (cuz volume is inc)
also increases intraabdominal pressure (cuz space decreases)
inc venous return
(*how inc venous return tho?)
inotropic effects def
things that affect the contractility
what are +ve inotropic effects?
when heart needs to increase cardiac output
(autonomic system effects)
the sympathetic nervous system is activated
this again, affects the SA node to get it to beat faster via noradrenaline
and also directly on the ventricular muscle cells to inc force of contraction
also
(hormonal effects)
e.g. NA, adrenaline, thyroid, glucagon
act directly on recpetors to inc contractility
what are -ve inotropic effects
parasympathetic activity
acts mainly on atrial cells (because there’s not many parasymp nerve fibres innovating the ventricle)
produces less forceful contraction
what are the effects of the symp nervous system on contractility
like mentioned before
increases the amount of Ca2+ entering the cell
= causes more forceful contraction
increases velocity of conduction
basically reduces the delay at the AV node
so systole happens quicker
and allows longer for diastole -> increased filling
how does vascular tone affect the afterload?
vasodilation = less resistance = reduces afterload (less force ventricles need to produce to push out blood)
vasoconstriction = more resistace = increases afterload
or stiff valves (heart disease) = more pressure needed to push open the valves = increases afterload
what can a increased afterload do to the ESV
increases ESV
cuz less blood is pumped out
due to the shorter ejectection period
as it takes longer fot the aortic valves to open
ends up decreasing the SV
see onenote for pressure volume graph
what could a prolonged increase in afterload lead to ?
damage in the myocardium
lead to heart failure
