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CVS > Cardiac Cycle & Control Of Cardiac Output > Flashcards

Cardiac Cycle & Control Of Cardiac Output Flashcards

1
Q

What is the normal stroke volume?

A

70ml

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2
Q

What attaches the mitral and tricuspid valves to the papillary muscles?

A

Chordae tendineae

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3
Q

What are the 7 stages to cardiac cycle?

A
  1. Atrial contraction
  2. Isovolumetric contraction
  3. Rapid ejection
  4. Reduced ejection
  5. Isovolumetric relaxation
  6. Rapid filling
  7. Reduced filling
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4
Q

What happens during stage 1- atrial contraction- of the cardiac cycle?

A
  • Atria contract
  • produce A wave on wiggers diagram
  • Accounts for final 10% of ventricular filling
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5
Q

What happens during stage 2- isovolumetric contraction of the cardiac cycle?

A
  • The ventricles contract but the Volume of blood remains the same because the aeortic valve hasn’t opened
  • the mitral valve closes and the ventricles contraction causes a slight inversion into the atria causing atrial pressure to spike slightly ( Cwave)
  • S1 heartsound as mitral valve closes
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6
Q

What happens at stage 3- rapid ejection of the cardiac cycle?

A
  • pressure in ventricle becomes greater than aeorta so aeortic valve opens
  • atrial base pulled downwards causing dip in atrial pressure ( X decent)
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7
Q

What happens at stage 4- reduced ejection of the cardiac cycle?

A

Myocytes repolarise and so start to relax

Atria start to fill more so pressure within them rises (U wave)

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8
Q

What happens during stage 5- isovolumetric relaxation of the cardiac cycle?

A

Aeortic valve closes- causes slight rise in aeortic pressure (dicrotic notch)
Both valves are closed so volume in ventricles not changing

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9
Q

How is stroke volume calculated

A

End diastolic volume- end systolic volume

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10
Q

What happens in stage 6- rapid filling of the cardiac cycle?

A

Mitral valve opens so pressure in the atria decreases as its empties (y- descent)
S3 heartsound sometimes present as ventricles fill

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11
Q

What happens at stage 7- reduced filling of the cardiac cycle?

A

heart relaxes as it fills, the venous pressure will determine rate of filling.

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12
Q

How is cardiac output calculated?

A

Strove volume x heart rate

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13
Q

What determines the end diastolic volume of a normal heart?

A

The venous pressure- if higher there will be more filling

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14
Q

What effect will an decrease in total peripheral resistance have on cardiac output?

A

Fall in total peripheral resistance leads to lower afterload so more blood is ejected (increased SV) so increased cardiac output. Also it will increase venous return so increased preload.

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15
Q

What effect does a fall in venous pressure have on CO?

A

less blood returned to heart = lower preload, lower preload= less contractile force and less diastolic filling= less SV and less CO

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16
Q

What % of end diastolic volume is stroke volume? (Usually)

A

67%

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17
Q

What determines contractability of the myocytes?

A

Neurotransmitters, hormones, drugs

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18
Q

When excerisize is initiated, what is the first mechanism to increase blood flow to heart? What is next?

A

Initially muscle pump and venoconstriciton returns more blood to heart. Then vasodilation (decreased TPR). then increased sympathetic drive increases contractibility

19
Q

What is the resting membrane potential of a myocyte and why?

A

-90-85 mv

very permeable to K+ and not to other ions so mostly outward movement of + charge

20
Q

Describe how an action potential is initiated in the SA node

A
  1. Hyperpolarisation by last action potential opens HCN channels (funny currents), this allows slow Na+ influx so the cell starts to depolarise
  2. When threshold is met, Ca2+ channels open and the cell quickly depolarises
  3. Voltage gates K+ channels open at +2- mv, K+ leaves
  4. at -50mv voltage gates + channels close and HCN channels reopen
21
Q

What type of voltage gated calcium channels open in myocytes?

A

L type

22
Q

What happens during myocytes depolarisation?

A
  • when cell before it depolarises, Na+ channels open causing Na+ influx and fast depolarisation to +20 mv
    2. Then transient K+ effluc causes some repolarisation
    3. L type voltage gates calcium channels open when +5-10 mv, causing platau as influx of Ca balances efflux of K+
    4. Membrane potential slowly drops however, and when threshold met, the Ca2+ channels close an voltage gates K+ channels open causing massive efflux of K+ and depolarisation to resting potential
23
Q

How long does myocyte depolarisation take compared with a neurone or SAN?

A

Neurone- very very fast
SAN- 200 ms
myocytes- 300ms

24
Q

Where does most of the Ca2+ come from during myocyte action potential to cause muscle contraction?

A

The SER-
depolarisation causes voltage gates ca channels to open, this induces Ca2+ release from SER by calcium induced calcium release, as the ca2+ from extracellular activates the RyR receptors

25
Q

How is Ca2+ returned to SER and extracellular store?

A

SER by SERCA

Extracellular by NCX and Ca2+ ATPase

26
Q

How does adrenaline/ noradrenaline cause vasoconstriction of arteries not found in skeletal muscle or heart?

A
  • adrenaline activates q type- g protein (a1 GPCR)
  • causes PIP2–> IP3 and DAG
  • DAG activates PKC which deactivates myoslin light chain phosphylase
  • IP3 (and depolarisation) causes Ca2+ release which binds with calmodulin
  • calmondulin binds with Myosin light chain kinase which phosphylates the myosin head and so activates it so that contraction can take place
27
Q

What effect does hypokalaemia ([K+] <3.5mM) have on action potentials and why?

A

delays repolarisation (lengthens platau)
because pottassium channels inhibited when K+ levels are low- dont need to know why
so less K+ influx, so later repolarisation
increased risk of fibrillation as less stable

28
Q

What effect does hyperkalaemia ([k+ >5.5mM) have on heart action potentials and why?

A

Ek is less negative so resting membrane potnential less negative
leads to slower upstroke as some Na+ channels will be inactivated
initially heart more excitable (easier to reach threshold) but when greater than 6.5 mV, you can get asystole

29
Q

How is hyperkalaemia treated?

A

calcium gluconate

insulin and glucose (insulin increases K+ intake by cells, glucose ensures no hypoglycaemia)

30
Q

At rest, does the sympathetic or parasympathetic or nothing stimulate the heart? If denervates, what speed would the heart beat?

A

parasympathetic

100mbp

31
Q

What parasympathetic nerve supplies heart? Which receptors does it act on?

A

vagal nerve

M2 receptors at AVN and SAN

32
Q

What sympathetic receptors are found in heart, where and what is effect of their stimulation?

A
  • B1 adrenoreceptors
  • Myocardium, SAN, AVN
  • +vs chonotrophic (increase HR) and +ve iniotrophic (increase contractile force)
33
Q

Where is cardiac control center? Where does it receive info from?

A

medulla oblongata

info from hypothalamus and baroreceptors in aortic arch and carotid sinus

34
Q

How does sympathetic stimulation cause +ve inotropy?

A
  • B1 s type adrenoreceptor activated
  • Adenylyl cyclase converts ATP to cAMP
  • this activates cAMP dependant protein kinase
  • this phosphylates VOCC so that more Ca enters when it is stimulated (at platau of myocyte action potential)
  • also increases uptake of Ca2+ into SER at rest (so greater influx later)
  • also increases sensitivity of contraction mechanism to Ca2+
35
Q

How does sympathetic stimulation cause +ve chronotropy?

A

more cAMP means activation of HCN funny current channel so faster uptake of Na+

36
Q

How does parasympathetic nervous stimulation cause -ve chronotropy?

A

it increases K+ conductance and decreases cAMP so funny current lasts longer as more Na+ needed

37
Q

Is the vascualture under both sympathetic and parasympathetic control?

A

Sympathetic only- except erectile tissue

38
Q

What type of adrenoreceptors are found in the vasculature?

A

a1 but skeletal muscle and coronary arteries also have b2

39
Q

Coronary arteries and vessels in skeletal muscles have B2 adrenoreceptors as well as a1 receptors, how does the effect of sympathetic stimulation vary in these vessels to a1 only vessles?

A

in a1 vessels you get vasoconstriction but in B2 vessels you get dilation because cAMP produced increases PKA activity which phosphylates and so inhibits myosin light chain kinase (meaning myosin cannot be phosphylated and so less contraction), as well as opening k+ channels

40
Q

Coronary and skeletal muscle blood vessesl have both a1 and B2 adrenoreceptors, why does the adrenaline have a greater vasodilatory than vasoconstrictive effect here?

A

becuase adrenaline has greater affinity for B2

41
Q

Do metabolites such as Co2, K+ and H+ have a greater or lesser vasodilatroy effect than activating b2?

A

greater- means blood supply greatest where its needed

42
Q

What is a sympathomimetic?

A

A drug that mimics the effect of the sympathetic nervous system

43
Q

Propanolol will decrease BP by antagonising Beta receptors causing decrease in HR and vasodilation. However this can cause bronchoconstriction which is bad for asthmatics, which alternative drug can be used?

A

atenolol- more selective to heart

44
Q

What would be the result of a cholinergic antagonist such as atropine?

A

increases HR, bronchodilation, dilates pupil- opposes parasymapthetic nervous system

CVS (7 decks)

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