Force generation by the heart Flashcards
what are striations caused by?
regular arrangements of contractile protein
what are cardiac myocytes electrically coupled with?
gap junctions
what are gap junctions?
protein channels which form low resistance electrical communication pathways between neighbouring myocytes
- they ensure that each electrical excitation reaches all the cardiac myocytes
where are desmosomes found?
within intercalated discs
what is purpose of desmosomes?
provide mechanical adhesion between adjacent cardiac cells
- They ensure that the tension developed by one cell is transmitted to the next
simply what is purpose of gap junctions & desmosomes?
gap junctions = allow spread of action potential
desmosomes = allow adhesion
what is actin?
(thin filaments) causes the lighter appearance in myofibrils & fibers
what is myocyin?
(thick filaments) cause the darker appearance
what are myofibrils?
- they are found inside cardiac muscle cells (like lots of tubes in a muscle fibre)
- contain alternating segments of thick & thin protein filaments
what are sarcomeres?
each myofibril = has several sarcomeres
sarcomere is the area between actin (between light & dark on myofibril)
what is the sliding filament theory?
explanation of how muscle shortens and produces force
= overlap of actin and myosin filaments, shortening the sarcomere
- calcium needs to bind to troponin to change conformation so exposed binding site on actin for myocyin
- myocyin heads cross-bridge and bind to actin which then makes conformational change resulting in the overlap - thin filament pulled inward during contraction
what are the 2 requirements for cross bridging in muscle contraction?
- ATP
- calcium
what is tropomyosin and troponin?
they physically cover myocyin binding site on actin
- when muscle relaxed tropomyosin and troponin cover binding site
(Ca2+ binds to change conformation and uncover)
where does calcium get released from in action potential - so it can bind to troponin and tropomyosin?
- released from sarcoplasmic reticulum
- the release of Ca2+ from SR is dependent on the presence of extra-cellular Ca2+
what happens with calcium once action potential passed?
- Ca2+ influx ceases
- Ca2+ re-sequestered in SR by Ca2+ ATPase & heart muscle relaxes
what is the importance of the long refractory period?
so muscle can’t contract before other contraction finished so not sustained contraction as sustained contraction bad for heart (tetanic contraction)
→because if you could produce another action potential then loop would just keep going and sustained contraction
= by the time it’s ready to produce another action potential - contraction already over so it’s all good to contract again
what is a refractory period?
period following action potential where it isn’t possible to produce another action potential
what is stroke volume?
the volume of blood ejected by each ventricle per heart beat
how to calculate stroke volume?
SV = End Diastolic Volume (EDV) – End Systolic Volume (ESV)
what is stroke volume regulated by?
INTRINSIC and EXTRINSIC mechanisms
what is diastolic length/stretch of myocardial fibers determined by?
the end diastolic volume = the volume of blood within each ventricle at the end of diastole
what determines the cardiac preload?
= end diastolic volume
what is the cardiac preload?
the diastolic length/diastolic stretch of myocardial fibers
= the force that stretches the cardiac muscle prior to contraction
what is relationship between end diastolic volume and venous return?
end diastolic volume is determined by the venous return to the heart (larger EDV means larger cardiac preload)
what is Frank-Starling relationship?
describes the relationship between end diastolic volume and stroke volume (directly proportional)
what does the Frank-Starling mechanism and Starlings law state?
the more the ventricle is filled with blood during diastole (end diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume)
what are 2 factors increased by stretch muscle?
- move toward optimum length (stretch muscle in heart always moves towards optimal length unlike skeletal muscle where there is overstretch)
- increase affinity of troponin for Ca2+
what does starlings law say about stroke volume of RV and LV?
- If venous return to right atrium increases, EDV of right ventricle increases
- Starling’s Law leads to increased SV into pulmonary artery
- Venous return to left atrium from pulmonary vein increases, EDV of left ventricle increases
- Starling’s Law leads to increased SV into aorta
*so saying that increase in right →increase in left too
what is afterload?
the resistance into which heart is pumping
what is the extra load?
imposed AFTER the heart has contracted
what is affect of increased afterload?
- at first, heart unable to eject full SV, so EDV increases
- If increased AFTERLOAD continue to exist (e.g. untreated hypertension), eventually the ventricular muscle mass increases (ventricular hypertrophy) to overcome the resistance
what is positive inotropic effect?
stimulation of sympathetic = increase force of contraction
what is the inotropic effect of noradrenaline on ventricular contraction?
- force of contraction increases (activation of calcium channels = calcium influx)
- effect is mediated by cAMP
- The peak ventricular pressure rises
- Rate of pressure change (dP/dt) during systole increases
- This reduces the duration of systole
- Rate of ventricular relaxation increases (increased rate of Ca2+ pumping)
- this reduced duration of diastole
what is cardiac output?
The volume of blood pumped by each ventricle per minute is known as the Cardiac Output (CO)
what is resting CO in a healthy adult?
approximately 5 litres per minute (70 ml SV x 70 beats per minute = 4900 ml CO)
how do you calculate CO?
CO = SV x HR
does vagal stimulation influence contraction?
NO - influences rate not force of conraction
where are adrenaline & noradrenaline released from?
adrenal medulla - they have inotropic & chronotropic effect
what is inotropic?
modifying the force or speed of contraction of muscles
