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Cardiac Output Flashcards

1
Q

What is cardiac output

A

volume of blood ejected by each ventricle per min

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2
Q

what is cardiac output dependent on

A

cardiac output = heart rate x stroke volume

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3
Q

what is stroke volume

A

vol of blood ejected by each ventricle per beat

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4
Q

how much blood on avg do we need to pump per min (avg cardiac output) at rest

A

~5 L/min
depending on size, age etc.

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5
Q

avg heart rate at rest

A

~70 bpm

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6
Q

avg stroke vol at rest

A

~ 70ml of blood per beat

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7
Q

avg cardiac output during exercise

A

~20 L/min

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8
Q

avg heart rate during exercise

A

~ 190 bpm

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9
Q

avg stroke vol during exercise

A

105 ml

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10
Q

how might heart rate and stroke vol differ in an athlete
a) at rest
b) during exercise

A

a) HR is lower (40bpm)
SV is higher (140ml) about double

b) HR is same (190bpm)
SV is higher (210ml) about double

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11
Q

whats the avg weight of the heart?

A

300g

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12
Q

how does the heart size differ in an athlete

A

500g

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13
Q

what 3 factors affect heart rate

A

autonomic innervation
hormones
venous return

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14
Q

what 2 things determine stroke vol

A

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

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15
Q

3 groups of factors that can affect the EDV and ESV

A

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

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16
Q

what affects the preload

A

filling time
venous return

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17
Q

what affects contractility

A

autonomic innervation
hormones

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18
Q

what affects the afterload

A

vascular tone - degree of vasocontriction/vasodilation

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19
Q

definition of chronotropic effects

A

factors that effect heart rate

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20
Q

neural regulation of heart : how do we detect changes in the blood that might trigger change

A

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

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21
Q

what are the 2 types of receptors and where are they in the body

A

chemoreceptors - detect chemical changes - in carotid body and within medulla oblongata

baroreceptors - detect pressure changes - in the walls of aorta and internal carotid artery

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22
Q

what might a chemoreceptor change in the blood

A

the CO2 levels
the pH

23
Q

how do we decrease HR

A
  • 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
24
Q

how do we increase HR

A
  • 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

25
name for pathologically low HR
Bradychardia
26
name for pathologically fast HR
tachycardia
27
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)
28
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
29
What type of channels are the K+ channels in this situation
muacarinic receptosrs
30
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
31
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
32
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
33
what is venous return
flow of blood from periphery back to right atrium
34
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
35
whats another way that the sympathetic nervous system can be activated directly by venous return?
sinoatrial nodes get stretched, increases heart rate further
36
stroke volume: what happens when you increase the EDV
Increase in SV Cuz EDV-ESV= SV
37
what is preload
the degree to which ventricular muscle cells are stretched at the end of diastole
38
contractility
the force produced by ventricular muscle cells during systole at a given preload
39
afterload
force that ventricle needs to overcome to open the semilunar valve and eject blood
40
what is preload directly proportional to ?
EDV depends on the rate of venous return the available ventricular filling time (ie ventricular diastole)
41
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
42
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
43
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
44
what factors affect venous return
posture skeletal muscle pump respiratory pump
45
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
46
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
47
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?)
48
inotropic effects def
things that affect the contractility
49
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
50
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
51
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
52
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
53
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
54
what could a prolonged increase in afterload lead to ?
damage in the myocardium lead to heart failure

Body Systems (21 decks)

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