Cardiac Cycle & Control Of Cardiac Output

Question 1

What is the normal stroke volume?

Answer 1

70ml

Question 2

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

Answer 2

Chordae tendineae

Question 3

What are the 7 stages to cardiac cycle?

Answer 3

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

Question 4

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

Answer 4

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

Question 5

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

Answer 5

• 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

Question 6

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

Answer 6

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

Question 7

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

Answer 7

Myocytes repolarise and so start to relax

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

Question 8

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

Answer 8

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

Question 9

How is stroke volume calculated

Answer 9

End diastolic volume- end systolic volume

Question 10

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

Answer 10

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

Question 11

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

Answer 11

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

Question 12

How is cardiac output calculated?

Answer 12

Strove volume x heart rate

Question 13

What determines the end diastolic volume of a normal heart?

Answer 13

The venous pressure- if higher there will be more filling

Question 14

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

Answer 14

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.

Question 15

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

Answer 15

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

Question 16

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

Answer 16

67%

Question 17

What determines contractability of the myocytes?

Answer 17

Neurotransmitters, hormones, drugs

Question 18

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

Answer 18

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

Question 19

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

Answer 19

-90-85 mv

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

Question 20

Describe how an action potential is initiated in the SA node

Answer 20

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

Question 21

What type of voltage gated calcium channels open in myocytes?

Answer 21

L type

Question 22

What happens during myocytes depolarisation?

Answer 22

• 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

Question 23

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

Answer 23

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

Question 24

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

Answer 24

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

Question 25

How is Ca2+ returned to SER and extracellular store?

Answer 25

SER by SERCA | Extracellular by NCX and Ca2+ ATPase

Question 26

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

Answer 26

- 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

Question 27

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

Answer 27

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

Question 28

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

Answer 28

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

Question 29

How is hyperkalaemia treated?

Answer 29

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

Question 30

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

Answer 30

parasympathetic | 100mbp

Question 31

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

Answer 31

vagal nerve | M2 receptors at AVN and SAN

Question 32

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

Answer 32

- B1 adrenoreceptors - Myocardium, SAN, AVN - +vs chonotrophic (increase HR) and +ve iniotrophic (increase contractile force)

Question 33

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

Answer 33

medulla oblongata | info from hypothalamus and baroreceptors in aortic arch and carotid sinus

Question 34

How does sympathetic stimulation cause +ve inotropy?

Answer 34

- 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+

Question 35

How does sympathetic stimulation cause +ve chronotropy?

Answer 35

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

Question 36

How does parasympathetic nervous stimulation cause -ve chronotropy?

Answer 36

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

Question 37

Is the vascualture under both sympathetic and parasympathetic control?

Answer 37

Sympathetic only- except erectile tissue

Question 38

What type of adrenoreceptors are found in the vasculature?

Answer 38

a1 but skeletal muscle and coronary arteries also have b2

Question 39

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?

Answer 39

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

Question 40

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

Answer 40

becuase adrenaline has greater affinity for B2

Question 41

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

Answer 41

greater- means blood supply greatest where its needed

Question 42

What is a sympathomimetic?

Answer 42

A drug that mimics the effect of the sympathetic nervous system

Question 43

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?

Answer 43

atenolol- more selective to heart

Question 44

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

Answer 44

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