Force Generation By The Hear

Question 1

describe cardiac muscle (2)

Answer 1

striated

no neuromuscular junction, myocytes are coupled by gap junctions instead

Question 2

what causes striation in cardiac muscle?

Answer 2

regular arrangement of contractile protein

Question 3

what are gap junctions?

Answer 3

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)

Question 4

how are adjacent cardiac cells joined together? what is the need for this?

Answer 4

desmosomes within the intercalated discs

ensures that the tension developed by one cell is transmitted to the next allowing whole heart to contracr

Question 5

what are the contractile units of muscle?

Answer 5

myofibrils

Question 6

describe myofibrils

Answer 6

have alternating segments of thick and thin protein filaments called actin and myocin arranged into sarcomeres

Question 7

describe actin

Answer 7

thin

lighter appearence

Question 8

describe myocin

Answer 8

thick

darker appearence

Question 9

portions of myofibril

Answer 9

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

Question 10

what produces muscle tension in myofibril?

Answer 10

sliding of actin filaments on myocin filaments

Question 11

force generation in the heart depends on what?

Answer 11

ATP dependant interaction between myosin and actin filaments

Question 12

is ATP needed for relaxation of muscle?

Answer 12

yes

Question 13

what is required to switch on cross bridge formation?

Answer 13

calcium

Question 14

how do cross bridges form?

Answer 14

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

Question 15

where is calcium released from before it can help form cross-bridge?

Answer 15

sarcoplasmic reticulum (dependent on the presence of extra-cellular calcium)
calcium travels down T tubules to reach the myofibrils

Question 16

what happens during diastole?

Answer 16

ventricular muscle relaxes
once AP has passed, calcium influx ceases, calcium is taken back up in SR via calcium ATPase
calcium stored in SR

Question 17

what happens during systole?

Answer 17

ventricular muscle contracts
calcium influx through L type calcium channels > calcium induced calcium release from SR > calcium activates contractile machinery

Question 18

describe ventricular AP

Answer 18

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

Question 19

what is the refractory period?

Answer 19

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

Question 20

what happens in the refractory period

Answer 20

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

Question 21

what is stroke volume and how is it calculated?

Answer 21

volume of blood ejected by each ventricle per heart beat

SV = EDV - ESV

Question 22

how is SV regulated?

Answer 22

intrinsic and extrinsic mechanisms

Question 23

intrinsic control of SV?

Answer 23

changes in diastolic length/stretch of myocardial fibres (cardiac pre-load - determined by EDV) cause changes in stroke volume

Question 24

what determines EDV?

Answer 24

venous return to the heart

Question 25

what does the frank starling law of the heart describe?

Answer 25

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)

Question 26

what does the tip of the frank starling curve illustrate?

Answer 26

that maximal force is generated at optimal fibre length

Question 27

how does stretch of cardiac fibres affect contraction?

Answer 27

optimal stretch of fibres = optimal contractile ability

stretch also increases the affinity of troponin for calcium

Question 28

how does optimal muscle fibre length differ in cardiac vs skeletal muscle?

Answer 28

cardiac = optimal length achieved by stretching muscle (frank starling)
skeletal = optimal length achieved at resting length

Question 29

how does frank starling law match SV of right and left ventricle?

Answer 29

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

Question 30

does frank starling mechanism compensate for decreased SV caused by increased afterload?

Answer 30

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

Question 31

what is afterload?

Answer 31

resistance into which the heart is pumping

Question 32

describe extrinsic control of SV

Answer 32

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)

Question 33

how does sympathetic stimulation increase force of contraction?

Answer 33

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

Question 34

how does the increases in peak ventricular pressure affect the frank starling curve?

Answer 34

shifts to the left

causes increased contractility of heart at given EDV

Question 35

how does heart failure affect frank starling curve?

Answer 35

shifts to the right (reduced contractility of heart at given EDV)

Question 36

how does parasympathetic stimulation affect the heart?

Answer 36

very little innervation of ventricles by vagus nerve so little if any affect
has major influence on rat but not force of contraction

Question 37

describe hormonal control of SV

Answer 37

adrenaline and noradrenaline released from adrenal medulla have inotropic and chronotropic effect
effects normally minor compared to effects of noradrenaline from sympathetic nerves

Question 38

what is cardiac output?

Answer 38

volume of blood pumped by each ventricle per min

Question 39

how is CO calculated?

Answer 39

CO = SV X HR

Question 40

normal CO?

Answer 40

around 5L per min (70ml X 70 bpm = 4900ml)