Cardiac Muscle Contraction Flashcards
What does the heart muscle look like?
It is striated due to the regular arrangement of contractile protein
what is a gap junction in a cardiac myocyte?
protein channels which form low resistance electrical communication pathways between neighbouring myocytes
what is the purpose of the desmosomes within the intercalated discs?
they provide mechanical adhesion between adjacent cardiac cells and ensure the tension one cell develops is transmitted to the next
what is a myofibril?
the contractile units of muscle which make up a muscle fibre
they have alternating segments of thick and thin filaments
What are the thin filaments in a myofibril?
actin which cause the lighter appearance in the fibres
What are the thick filaments in a myofibril?
myosin which cause the darker appearance in fibres
what are the actin and myosin arranged into within the myofibril?
sarcomeres
what theory explains how muscle shortens and produces force
the sliding filament theory - actin filaments slide on myosin filaments
What is the role of Ca++ in the sliding filament theory?
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
what is the release of Ca++ from the sarcoplasmic reticulum dependent on in cardiac muscle?
the presence of extra-cellular Ca++
What is the trigger of ventricular muscle action potential?
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
How does Ca++ in the extracellular space result in muscle contraction?
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
What happens to the Ca++ in the ventricular muscle when the action potential has passed?
Ca++ influx ceases after the action potential has passed
Ca++-ATPase moves the Ca++ into the sarcoplasmic reticulum again and the heart muscle relaxes
How do the fibres actually slide over each other?
- the actin myosin cross bridge triggers a power stroke where the thin filament is pulled inward
Describe the refractory period of the cardiac muscle
- 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
What is the definition of Stroke Volume?
the volume of blood ejected by each ventricle per heart beat
Stroke Volume =
End diastolic volume (EDV) - End systolic volume (ESV)
what are the intrinsic controls of Stroke volume?
- the cardiac preload, determined by venous return to the heart
- increasing the stretch also increases the affinity of troponin for Ca++
what is the cardiac preload?
the diastolic length/ stretch of the myocardial fibres, this is determined in part by the end diastolic volume
What is the Frank-Starling Mechanism?
the more the ventricle is filled with blood during diastole (EDV) the greater the stroke volume will be
How is optimal fibre length achieved in cardiac muscle?
by stretching the muscle - Frank-Starling mechanism
How does the Frank-Starling mechanism match SV in RV & LV?
- 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
What is the afterload?
the resistance into which the heart is pumping - extra load imposed after the heart has contracted
What happens when the afterload increases?
- heart is unable to eject the full SV so EDV increases
- SV then increases due to the Frank-Starling mechanism
What is the consequence of continued increased afterload (e.g. untreated hypertension)?
- eventually this will result in ventricular hypertrophy
What are the extrinsic factors which influence cardiac muscle contraction?
The nerves and hormones
What is the effect of the sympathetic nervous system on cardiac muscle contraction?
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)
What is a positive inotropic effect?
increased force of contraction
How does the sympathetic stimulation increase the force of muscle contraction?
- 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
What is the effect of sympathetic stimulation on the Frank-Starling curve?
the curve shifts to the left as the contractility of the heart at a given EDV rises
What is the effect of heart failure on the Frank Starling curve?
the curve shifts to the right
What is the effect of the parasympathetic stimulation on ventricular contraction?
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
What hormones effect the heart’s contractility?
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
What is cardiac output?
The volume of blood pumped by each ventricle per minute
Cardiac output (CO) =
Stroke volume (SV) x Heart rate (HR)
