CVS 2 - Mechanical properties of the heart 1 Flashcards
What is needed for contraction of a single ventricular cell?
External calcium as you have CICR
Skeletal muscle can contract in solution which has no calcium
What is the approximate size of a ventricular myocyte and T tubules?
15 x 100 micrometres for cell
T tubule 200 nm diameter
Describe the excitation-contraction coupling of the heart including the receptors involved.
Depolarisation causes the opening of L-type calcium channels situated on the myocyte membrane. This leads to influx of calcium into the myocyte. The calcium then binds to the Ryanodine receptor on the SR membrane and leads to the release of calcium from the SR –> this is Calcium Induced Calcium Release (CICR). This calcium causes the myofilament contraction.
SERCA then takes the calcium used for the contraction from the cytoplasm back into the SR. The Na/Ca exchanger pumps out as much calcium as entered the cell in the first place.
What is the shape of the force-calcium relationship?
Sigmoidal
What concentration of calcium is sufficient to generate maximum contraction?
10 micromolar
Compare the length-tension relationship in skeletal and cardiac muscle.
Cardiac muscle is much more resistant to stretch and exerts a lot more passive force
What happens to force when muscle is stretched?
Amount of active force increases as muscle gets longer. Relationship is called the active force production
Active force is parabolic relationship (kind of)
If overstretched, active force declines
What is passive force?
Passive recoil force from stretching due to elastic nature of the tissue - linear relationship
What are the two forms of contraction of the heart?
Isometric - no shortening but pressure in both ventricles increases
Isotonic - shortening of fibres and blood ejected from ventricles
What is Preload?
The weight that stretches the muscle before it is stimulated to contract
What is afterload?
The weight that the muscle encounters after it contracts. Not visible when the muscle is not contracting
What is the effect of increasing preload?
Increasing preload increases the force exerted by the muscle fibres
What are the effects of increasing afterload?
Increasing afterload decreases the amount of shortening of muscle fibres so their force and decreases the velocity of shortening of the fibres.
–> weaker and slower contraction
What are the in vivo correlates of preload?
End diastolic volume (this is the venous return to the heart that stretches the muscle fibres) as blood fills the ventricules during the relaxation phase of the cardiac cycle (diastole) it stretches the resting ventricular walls –> stretch=preload
Dependent on venous return to the heart
More blood filles–> more preload –> more force
What are the in vivo correlates of afterload?
The load against which the left ventricle ejects blood after opening of the aortic valve –> pressure agains the aortic valve us not seen until it opens = afterload = diastolic pressure
So simple measure of afterload is DBP
Any increase in afterload decreases the amount of shortening that occurs which decreases force and velocity of contraction
What is Frank-Starling’s law?
Increase in diastolic fibre length increases ventricular contraction.
What is the consequence of Starling’s law?
Ventricles pump greater stroke volume so that at equilibrium CO exactly balances the augmented venous return
(blood going in balanced by blood going out)
Starling’s law is caused by what two factors?
Changes in the number of myofilament cross-bridges (if too short they overlap and too stretched there fewer cross bridges)
Changes in the calcium sensitivity of the myofilaments with increased length
What is Stroke Work?
Work done by heart to eject blood under pressure into aorta and pulmonary artery
Stroke work = SV x P
Volume of blood ejected with each stroke x pressure at which blood is ejected
State the law of Laplace
When the pressure within a cylinder is held constant, the tension on its walls (wall stress) increases with increasing radius
T = P x R
E.g Left and right ventricle have similar wall stress (=T). However LV has smaller radius than RV (smaller R) meaning it can generate higher pressures (P has is bigger because T is the same but R is smaller). Generating high pressure in aorta is essential to go to whole body.
Wall stress is like ‘pulling pressure’ what pulls the walls apart
So a heart failing often becomes dilated which increases wall stress
Also thickness of wall has an impact: the bigger, the less tension there is so LV has thicker walls to reduce tension and hence can increase pressure.
