Control of force of contraction

Question 1

what must also increase for CO to increase

Answer 1

venous return. how much in how much out

Question 2

what can increase stroke volume

Answer 2

increased force of contraction

Question 3

2 mechanisms that increases force of contraction

Answer 3

1. homeometric mechanism (contractility, aka positive inotropic)
2. heterometric: change in ventricular size = stretches sarcomeres in the myocyte

Question 4

characteristic of homeometric mechanism

Answer 4

• increase in intracellular Ca levels = increase crossbridge formation
• increased RATE of force development
• no change in contraction DURATION
• can be due to extrinsic or intrinsic mechanisms

Question 5

characteristic heterometric mechanism

Answer 5

• no change in contractility ie Ca concentration
• increases ventricular size
• LONGER duration of contraction
• no change in rate of force development

Question 6

what is the rate induced regulation of contraction force

Answer 6

increased HR = reduced systolic and diastolic duration
reduced diastolic duration: less Ca removed from intracellular space by Ca/Na exchanger and Ca ATPase
= accumulation of intracellular Ca and therefore force of contraction

Question 7

explain the indirect regulation of force of contraction by vagal nerve

Answer 7

• NOT DIRECT as no ventricular vagal innervation
• decreased HR = more Ca moved out from intracellular space to ECF = less Ca in cell = weaker contraction

rate induced regulation of contraction force

Question 8

explain how sympathetic innervation to ventricular myocytes increse contractility

Answer 8

NAd = B1 receptor
Adenylyl cyclase activation = increased cAMP level
PKA activation

phosphorylate:
L type Ca Channel = open for longer during plateau phase = more intracellular Ca = more cross bridge

SERCA pump = increase the rate of Ca uptake BACK INTO SR = keep the duration of contraction same

Question 9

describe the Ca-induced Ca release process

Answer 9

L-type Ca channel open in the PLATEAU PHASE of action potential = Ca influx (small intracellular contribution)

Ca binds to ryanodine receptor on sarcoplasmic reticullum (store) = large Ca efflux from store

troponin C bound, tropomyosin moved = myosin binding site on actin revealed

= cross bridge can be formed

Question 10

describe the process of relaxation

Answer 10

when Ca channel closes (time dependent) no more binding site revealed

SERCA - remove intracellular Ca
Diastole: Ca/Na exchange and Ca ATPase remove the ECF source Ca back to extracellular space

Question 11

what is the starlings law of the heart

Answer 11

1. increased VR = increased ventricular filling = stretched = increase force of contraction
2. increased afterload = reduced stoke volume (less ejected) = increased diastolic volume = increased systolic volume = stretched ventricles = increased contration force

Question 12

what are the 3 lengths of sarcomere. where is the natural position of the heart in this

Answer 12

optimum = 100%cross bridge occupied = maximum force generated

overstretched: reduce actin and myosin overlap = reduced CB can be formed

understretched: actin displaced, reduced available site for myosin interaction.
myosin pushed against Z line = distorted

Question 13

heart failure curve

initial compensation explain

Answer 13

depressed curve = easier to reach the tipping point
initial compensation: increase VR, TPR = STRETCHED
but heart weakened cant afford to increase force
= more left more stretched = over the tipping point