Cardiac Muscle Contraction

Question 1

What does the heart muscle look like?

Answer 1

It is striated due to the regular arrangement of contractile protein

Question 2

what is a gap junction in a cardiac myocyte?

Answer 2

protein channels which form low resistance electrical communication pathways between neighbouring myocytes

Question 3

what is the purpose of the desmosomes within the intercalated discs?

Answer 3

they provide mechanical adhesion between adjacent cardiac cells and ensure the tension one cell develops is transmitted to the next

Question 4

what is a myofibril?

Answer 4

the contractile units of muscle which make up a muscle fibre
they have alternating segments of thick and thin filaments

Question 5

What are the thin filaments in a myofibril?

Answer 5

actin which cause the lighter appearance in the fibres

Question 6

What are the thick filaments in a myofibril?

Answer 6

myosin which cause the darker appearance in fibres

Question 7

what are the actin and myosin arranged into within the myofibril?

Answer 7

sarcomeres

Question 8

what theory explains how muscle shortens and produces force

Answer 8

the sliding filament theory - actin filaments slide on myosin filaments

Question 9

What is the role of Ca++ in the sliding filament theory?

Answer 9

to react with the troponin and move the troponin-tropomyosin complex which blocks the actin binding sites aside. This allows the myosin head to bind to the actin and form a actin myosin crossbridge

Question 10

what is the release of Ca++ from the sarcoplasmic reticulum dependent on in cardiac muscle?

Answer 10

the presence of extra-cellular Ca++

Question 11

What is the trigger of ventricular muscle action potential?

Answer 11

Na+ influx triggers an action potential in and as the repolarisation occurs Ca++ is released into the extracellular through L-type Ca++ channels space causing muscle contraction

Question 12

How does Ca++ in the extracellular space result in muscle contraction?

Answer 12

Ca++ is needed to move the tropomyosin blocking the actin binding sites which are needed so the fibres can slide over each other
Ca++ in the extracellular space triggers more Ca++ to be released from the sarcoplasmic reticulum and hence the muscle contracts as a result of an action potential

Question 13

What happens to the Ca++ in the ventricular muscle when the action potential has passed?

Answer 13

Ca++ influx ceases after the action potential has passed

Ca++-ATPase moves the Ca++ into the sarcoplasmic reticulum again and the heart muscle relaxes

Question 14

How do the fibres actually slide over each other?

Answer 14

• the actin myosin cross bridge triggers a power stroke where the thin filament is pulled inward

Question 15

Describe the refractory period of the cardiac muscle

Answer 15

• in the plateau stage of the AP the Na+ channels are depolarised and closed
• as the repolarisation occurs, the K+ channels are open so depolarisation isn’t possible
• the long refractory period means that tetanic contractions aren’t possible

Question 16

What is the definition of Stroke Volume?

Answer 16

the volume of blood ejected by each ventricle per heart beat

Question 17

Stroke Volume =

Answer 17

End diastolic volume (EDV) - End systolic volume (ESV)

Question 18

what are the intrinsic controls of Stroke volume?

Answer 18

• the cardiac preload, determined by venous return to the heart
• increasing the stretch also increases the affinity of troponin for Ca++

Question 19

what is the cardiac preload?

Answer 19

the diastolic length/ stretch of the myocardial fibres, this is determined in part by the end diastolic volume

Question 20

What is the Frank-Starling Mechanism?

Answer 20

the more the ventricle is filled with blood during diastole (EDV) the greater the stroke volume will be

Question 21

How is optimal fibre length achieved in cardiac muscle?

Answer 21

by stretching the muscle - Frank-Starling mechanism

Question 22

How does the Frank-Starling mechanism match SV in RV & LV?

Answer 22

• venous return increasing to the right atrium, increases EDV of right ventricle
• SV increases into the pulmonary artery
• venous return to the left atrium from the pulmonary vein increase
• EDV of left ventricle increases
• increased SV into the aorta

Question 23

What is the afterload?

Answer 23

the resistance into which the heart is pumping - extra load imposed after the heart has contracted

Question 24

What happens when the afterload increases?

Answer 24

• heart is unable to eject the full SV so EDV increases

- SV then increases due to the Frank-Starling mechanism

Question 25

What is the consequence of continued increased afterload (e.g. untreated hypertension)?

Answer 25

• eventually this will result in ventricular hypertrophy

Question 26

What are the extrinsic factors which influence cardiac muscle contraction?

Answer 26

The nerves and hormones

Question 27

What is the effect of the sympathetic nervous system on cardiac muscle contraction?

Answer 27

The neurotransmitter is noradrenaline, and sympathetic stimulation increases the force of the contraction of the cardiac muscle (sympathetic stimulation also causes a positive chronotropic effect)

Question 28

What is a positive inotropic effect?

Answer 28

increased force of contraction

Question 29

How does the sympathetic stimulation increase the force of muscle contraction?

Answer 29

• Activates the Ca++ channels so greater Ca++ influx
• Cyclic AMP mediates the effect of the sympathetic system
• the peak ventricular pressure increases meaning the pressure change in systole increases and hence the duration of systole is reduced
• the rate of ventricular relaxation increases due to the increased rate of Ca++ pumping and so the duration of diastole is also reduced

Question 30

What is the effect of sympathetic stimulation on the Frank-Starling curve?

Answer 30

the curve shifts to the left as the contractility of the heart at a given EDV rises

Question 31

What is the effect of heart failure on the Frank Starling curve?

Answer 31

the curve shifts to the right

Question 32

What is the effect of the parasympathetic stimulation on ventricular contraction?

Answer 32

there is very little innervation of the ventricles and so there is minimal to no effect on SV, it does however have a major influence on HR

Question 33

What hormones effect the heart’s contractility?

Answer 33

adrenaline and noradrenaline released from the medulla have positive inotropic and chronotropic effects however this is normally minimal compared to the effects of noradrenaline as part of the sympathetic stimulation

Question 34

What is cardiac output?

Answer 34

The volume of blood pumped by each ventricle per minute

Question 35

Cardiac output (CO) =

Answer 35

Stroke volume (SV) x Heart rate (HR)