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Body Systems > Cardiac Output > Flashcards

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
Q

name for pathologically low HR

A

Bradychardia

26
Q

name for pathologically fast HR

A

tachycardia

27
Q

describe the ionic control at the SA node

A

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
Q

How is ionic control affected at the SA node during activation of the parasympathetic system

A

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
Q

What type of channels are the K+ channels in this situation

A

muacarinic receptosrs

30
Q

How is ionic control affected at the SA node during activation of the sympathetic system

A

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
Q

explain why despite the SA node having an inherent rate of >100bpm, regualr resting bpm is 60-100?

A

background parasympathetic activity
= VAGAL TONE
reduces HR to 60-100bpm

little/no background sympathetic activity

32
Q

how does vagal tone differ in athletes

A

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
Q

what is venous return

A

flow of blood from periphery back to right atrium

34
Q

how does venous return indirectly affect HR and what is the name of this process

A

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
Q

whats another way that the sympathetic nervous system can be activated directly by venous return?

A

sinoatrial nodes get stretched, increases heart rate further

36
Q

stroke volume: what happens when you increase the EDV

A

Increase in SV

Cuz EDV-ESV= SV

37
Q

what is preload

A

the degree to which ventricular muscle cells are stretched at the end of diastole

38
Q

contractility

A

the force produced by ventricular muscle cells during systole at a given preload

39
Q

afterload

A

force that ventricle needs to overcome to open the semilunar valve and eject blood

40
Q

what is preload directly proportional to ?

A

EDV
depends on the rate of venous return
the available ventricular filling time (ie ventricular diastole)

41
Q

so what happens if you increase the rate/time of filling the ventricle?

A

Increases EDV

in turn increases the SV
due to Frank Starling Law

42
Q

What is frank starling law

A

(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
Q

What is frank starling law

A

(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
Q

what factors affect venous return

A

posture

skeletal muscle pump

respiratory pump

45
Q

how does posture affect venous return

A

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
Q

how does the skeletal muscle pump affect venous return

A

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
Q

how does the respiratory pump affect venous return

A

inspiration
decreases intrathoracic pressure (cuz volume is inc)
also increases intraabdominal pressure (cuz space decreases)

inc venous return

(*how inc venous return tho?)

48
Q

inotropic effects def

A

things that affect the contractility

49
Q

what are +ve inotropic effects?

A

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
Q

what are -ve inotropic effects

A

parasympathetic activity

acts mainly on atrial cells (because there’s not many parasymp nerve fibres innovating the ventricle)

produces less forceful contraction

51
Q

what are the effects of the symp nervous system on contractility

A

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
Q

how does vascular tone affect the afterload?

A

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
Q

what can a increased afterload do to the ESV

A

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
Q

what could a prolonged increase in afterload lead to ?

A

damage in the myocardium
lead to heart failure

Body Systems (21 decks)

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