Cardiovascular Mechanics Flashcards

1
Q

How’s does contraction of a singular ventricular cell take place? (Very simple)

A

Electrical event ->

Ca2+ influx, release ->

Contractile event

(Excitation contraction coupling)

(Calcium is very important in cardiac muscle (unlike in skeletal muscle))

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2
Q

What is the structure of a ventricular cell?

A

100 mu m long and 15 wide

T tubules are finger like invagination and of the cell surface

T tubules are 200nm in diameter

They are spaced around 2 mu m apart so that each T tumble lies alongside each Z line of every myofibril

This allows them to carry surface depolarisation deep into the cell

They also have a sarcoplasmic reticulum which acts as the calcium store

46% of the cell is myofibrils, 36% is mitochondria, 4% sarcoplasmic reticulum, 2% nucleus. Other 12%

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3
Q

How do the T tubules interact with the sarcoplasmic reticulum (channels)?

A

The LTCC (l type calcium channels) in the T tubules have to lie very close to Ryanodine receptors (SR calcium release channels) on the SR

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4
Q

How does excitation- contraction coupling in the heart occur (with relation to channels and calcium)?

A

In the T tubules there are many LTCCs (l type calcium channels)

When the cell is depolarised the T tubules carry this deep into the cell

The depolarisation is sensed by the LTCC. This causes it to change conformation and open, allowing calcium from outside the cell to flow down its conc gradient into the cytosol

This calcium binds to ryanodine receptors on the sarcoplasmic reticulum (SR Ca2+ release channels). These are ligand operated channels which open up in response to calcium binding to them

Calcium that is stored In the SR is then released into the cytosol

This calcium then binds to troponin on myofillamnets and activates contraction

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5
Q

How does relaxation of the excitation- contraction coupling in the heart occur (with relation to channels and calcium)?

A

The cytosolic calcium is pumped up against its concentration gradient by the SR Ca2+ ATPase back into the sarcoplasmic reticulum

Here it is ready for release at the next AP

The calcium that initially entered the cell must be effluxed. This occurs during the diastolic interval using the Na+/Ca2+ exchanger

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6
Q

How do the cytoplasmic Ca2+ conc and force of contraction relate?

A

Sigmoid curve

As Ca increases so does force but in an S shape

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7
Q

What is the length tension relation in cardiac muscle?

A

As the cardiac muscle lengthens (is stretched) the peak force produced by it is increased, as well as its baseline force

So longer cardiac muscles have more active force production

There is also some recoil similarly to in elastic bands, so there is also an increase in passive force with muscle length

This is the case in isometric contraction (no shortening)

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8
Q

What is the length tension relation in cardiac Vs skeletal muscle?

A

Cardiac muscle can produce much more passive force as it is more resistant to stretch And less compliant than skeletal muscle

This is due to properties of the extracellular matrix and cytoskeleton

The total force is the sum of active and passive force. However there is an optimum point. When the muscle is stretched beyond this point the total force decreases again as active force decreases

In cardiac muscle, only the ascending limb of this length tension relationship is important as you can’t overstretch cardiac muscle (but you can with skeletal (pulling a muscle))

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9
Q

What are the two forms of contraction used by the heart?

A

Isometric - muscle fibres do not change length but pressure increases in both ventricles

Isotonic - shortening of fibres and blood is ejected from ventricles

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10
Q

What are the preload and afterload?

A

Preload - weight that stretches the muscle before it is stimulated to contract (isometric). Associated with ventricular filling

Afterload - Weight not apparent to muscle in resting state, only encountered when muscle has started to contract (isotonic). Associated with the pressure in the aorta

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11
Q

How are force and preload related?

A

As preload (stretch) is increased, force increases

This is in isometric contraction

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12
Q

How are afterload and shortening of muscle related?

A

As afterload increases, shortening of muscle decreases

This is in isotonic contraction

However if preload is increased (so a larger stretch), more force can be produced in the afterload

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13
Q

What is the in Vivo version of preload?

A

As blood fills the heart during diastole it stretches the resting ventricular walls

This stretch determines the preload on the ventricles before ejection

Preload is dependant on venous return

Measures of preload include end diastolic volume, end diastolic pressure and right atrial pressure

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14
Q

What is the in Vivo version of the afterload?

A

The load against which the left ventricle ejects blood after opening of the aortic valve

Any increase in afterload decreases the amount of isotonic shortening that occurs and increases the velocity of shortening

Measures of afterload include diastolic blood pressure

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15
Q

What is starlings law ( frank starling relationship)?

A

Both frank and starling showed that as filling of the heart increased, the curve of contraction also increases

INCREASED DIASTOLIC FIBRE LENGTH INCREASES VENTRICUKR CONTRACTION

Consequence: ventricles pump greater stroke volume so that, at equilibrium, cardiac output exactly balances the augmented venous return

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16
Q

What causes the frank starling relationship?

A

As the muscle is stretched this changes the number of myofillament cross bridges that interact between actin and myosin

There second reason is that that’s are changes in the Ca2+ sensitivity of the myofillament

17
Q

What is stroke work?

A

Work done by the heart to eject blood under pressure into aorta and pulmonary artery

Stroke work = volume of blood ejected during each stroke multiplied by the pressure at which the blood is ejected

Stroke work = SV x P

Stroke volumes is influenced by preload and afterload. Cardiac Structure can influence the pressure

18
Q

What is the law of laPlace?

A

WHEN THE PRESSURE WITHIN A CYLINDER IS HELD CONSTANT, THE TENSION ON ITS WALLS INCREASES WITH INCREASING RADIUS

Wall tension = pressure in ventricles x radius of vessel

Incorporating wall thickness (h) this can be amended to:

T = (P x R)/h

We want exhale tension in both sides of the heart. But each is working at a different pressure

Therefore in order to create exhale tension the radius can be changed

The radius of curvature in the walls of the left ventricle (higher pressure) is smaller than that in the right ventricles

Failing hearts often become dilated and spherical which increases their wall stress