Force Generation By The Hear Flashcards
describe cardiac muscle (2)
striated
no neuromuscular junction, myocytes are coupled by gap junctions instead
what causes striation in cardiac muscle?
regular arrangement of contractile protein
what are gap junctions?
protein channels which form low resistance electrical communication pathways between myocytes
ensure that each electrical excitation reaches all of the myocytes (all or none law of heart)
how are adjacent cardiac cells joined together? what is the need for this?
desmosomes within the intercalated discs
ensures that the tension developed by one cell is transmitted to the next allowing whole heart to contracr
what are the contractile units of muscle?
myofibrils
describe myofibrils
have alternating segments of thick and thin protein filaments called actin and myocin arranged into sarcomeres
describe actin
thin
lighter appearence
describe myocin
thick
darker appearence
portions of myofibril
sarcomere = from Z line to Z line
Z line = jaggy line where adjacent actin filaments meet
M line = line crossing middle of thick myosin filaments
A band = total length of myosin filament
I band = gap between adjacent myosin filaments
H zone = gap between adjacent actin filaments
what produces muscle tension in myofibril?
sliding of actin filaments on myocin filaments
force generation in the heart depends on what?
ATP dependant interaction between myosin and actin filaments
is ATP needed for relaxation of muscle?
yes
what is required to switch on cross bridge formation?
calcium
how do cross bridges form?
calcium binds to troponin and exposes the active site on actin by pulling troponin-tropomysin complex out the way
myosin head binds to active site forming a cross bridge with actin
myosin head bends during power stroke causing the actin filament to slide and ADP + P is released from myosin head
new molecule of ATP attached to myosin head causing the cross-bridge to detach
ATP hydrolyses of ADP + P causing the myosin head to return to the “cocked” position ready to bind to actin again
where is calcium released from before it can help form cross-bridge?
sarcoplasmic reticulum (dependent on the presence of extra-cellular calcium) calcium travels down T tubules to reach the myofibrils
what happens during diastole?
ventricular muscle relaxes
once AP has passed, calcium influx ceases, calcium is taken back up in SR via calcium ATPase
calcium stored in SR
what happens during systole?
ventricular muscle contracts
calcium influx through L type calcium channels > calcium induced calcium release from SR > calcium activates contractile machinery
describe ventricular AP
sharp vertical Na+ influx
Na channels close and calcium chanels open causing downward slope then plateau phase as Ca influxes through L type calcium channels
Ca channels close and K channels open causing a sharp downward stroke as K effluxes
what is the refractory period?
time following initial upstroke of AP and relaxation of the cardiac muscle where another AP cannot be generated
a long refractory period prevents generation of tetanic contraction
what happens in the refractory period
during plateau phase of ventricular AP the Na channels are in the depolarised closed state so they cant open
during the descending phase of action potential the potassium channels are open and the membrane cannot be depolarised
what is stroke volume and how is it calculated?
volume of blood ejected by each ventricle per heart beat
SV = EDV - ESV
how is SV regulated?
intrinsic and extrinsic mechanisms
intrinsic control of SV?
changes in diastolic length/stretch of myocardial fibres (cardiac pre-load - determined by EDV) cause changes in stroke volume
what determines EDV?
venous return to the heart
what does the frank starling law of the heart describe?
relationship between venous return, EDV and SV
states that the more the ventricle is filled with blood during diastole (EDV), the greater the volume of ejected blood will be in systole (SV)
what does the tip of the frank starling curve illustrate?
that maximal force is generated at optimal fibre length
how does stretch of cardiac fibres affect contraction?
optimal stretch of fibres = optimal contractile ability
stretch also increases the affinity of troponin for calcium
how does optimal muscle fibre length differ in cardiac vs skeletal muscle?
cardiac = optimal length achieved by stretching muscle (frank starling) skeletal = optimal length achieved at resting length
how does frank starling law match SV of right and left ventricle?
venous return to right atrium increases = EDV of right ventricle increases = increased SV from right ventricle
venous return to left atrium increases = EDV of left ventricle increases = increased SV from left ventricle
does frank starling mechanism compensate for decreased SV caused by increased afterload?
partially
if afterload increases, heart is initially unable to eject full SV so EDV increases > frank starling mechanisms raise force of contraction > if increased afterload persists the ventricular muscle mass will eventually increase to overcome resistance
what is afterload?
resistance into which the heart is pumping
describe extrinsic control of SV
involves nerves and hormones
ventricular muscle supplies by sympathetic nerve fibres via noradrenaline
stimulation of sympathetic nerves increases force of contraction (+ve inotropic effect) as well as increases rate of contraction (+ve chronotropic effect)
how does sympathetic stimulation increase force of contraction?
activates Ca channels causing a greater calcium influx (cAMP mediated)
causes increase in peak ventricular pressure > rate of pressure change during systole (dP/dt) increases > reduces duration of diastole > rate of ventricular relaxation increases (increased rate of Ca pumping) > reduced duration of diastole
how does the increases in peak ventricular pressure affect the frank starling curve?
shifts to the left
causes increased contractility of heart at given EDV
how does heart failure affect frank starling curve?
shifts to the right (reduced contractility of heart at given EDV)
how does parasympathetic stimulation affect the heart?
very little innervation of ventricles by vagus nerve so little if any affect
has major influence on rat but not force of contraction
describe hormonal control of SV
adrenaline and noradrenaline released from adrenal medulla have inotropic and chronotropic effect
effects normally minor compared to effects of noradrenaline from sympathetic nerves
what is cardiac output?
volume of blood pumped by each ventricle per min
how is CO calculated?
CO = SV X HR
normal CO?
around 5L per min (70ml X 70 bpm = 4900ml)
