Cardiovascular Mechanics Flashcards

1
Q

How does a single ventricular cell contract?

What is the calcium transient effect?

A

Electrical event occurs —> Ca2+ influx, Ca2+ release —> contractile event

In each stimulation there is a rise and fall in cytosolic calcium = calcium transient
Increase just after excitation, then there’s a decrease

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2
Q

How important is calcium for heart contraction?

A

Heart doesn’t contract without external calcium.

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3
Q

Describe single ventricular cell structure
What are T tubules?
What do they do?
What does the sarcoplasmic reticulum do?

A

Ventricular cells 100 micrometers long and 15 micrometers wide

T tubules (transverse tubules) are finger like invaginations of the cell surface. 
T-tubules open up to 200 micrometers in diameter 
Spaced, so that a T tubules lies alongside EACH Z line of every myofibril 
T tubule carries surface depolarisation deep into the cell

Sarcoplasmic reticulum stores calcium in muscle cells

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4
Q
What proportions of the following make up a muscle cell? 
Myofibril 
Mitochondria 
Sarcoplasmic reticulum 
Nucleus 
Other
A
Myofibril - 46%
Mitochondria - 36%
Sarcoplasmic reticulum - 4%
Nucleus - 2%
Other - 12%
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5
Q

Describe excitation coupling in the heart

A

The same amount of calcium entering the muscle leaves the muscle
Depolarisation is sensed by an L type calcium channel, so it alters its conformation and opens up and calcium from the outside of the cell, flows down its conc grad into the cytosol
Calcium can feed myofibrils but mainly binds to the SR (sarcoplasmic reticulum) calcium release channels - ligand operated channels. Open up in response to calcium binding to them.
When the SR calcium release channels open, Calcium is released into the cytosol.
Ca2+ then binds to troponin in the myofilaments and activates contraction.
For relaxation:
Calcium is pumped back up against its conc grad by SR Ca2+ ATPase
(Needs energy), pumps calcium back into the SR, ready to be released at next beat
Same amount of Ca2+ that enters the cell to trigger the release of Ca2+ is removed from the cell during the diastolic interval by protein in the T tubule (sodium calcium exchange system)

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6
Q

What is the relationship between length and tension in cardiac muscle

What is isometric contraction?

A

As muscle length increases, the active force of production - force produced by the muscle increases.

Passive force also increases w length

Isometric contraction is an increase in force without a change in length - no shortening occurring of the muscle cells

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7
Q

How is total force calculated?

What are the differences in length tension relations between cardiac and skeletal muscle and why?

Which part of the cardiac muscle does the length tension relationship apply to?

Why can we not overstretch the cardiac muscle?

A

Total force = Active + passive force

Skeletal muscle is stretchier, doesn’t produce as much passive force as cardiac tissue.
Cardiac muscle is more resistant to stretch and less compliant than skeletal muscle - due to properties of extra cellular matrix and cytoskeleton of the cells.

Only ascending Limb of the relation is important for cardiac muscle

Because the heart is contained within the pericardial sac it can only stretch a certain amount

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8
Q

What are the two forms of contraction of the heart? Define them

A

Isometric contraction - muscle fibres don’t change length but pressure increases in both ventricles

Isotonic - shortening of fibres and blood is ejected from ventricles

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9
Q

What is the preload and afterload?

What happens to the force of contraction as preload changes?

What happens to muscle shortening (isotonic contraction) as the after load changes?

A

Preload - weight that stretches muscle before it is stimulated to contract

Afterload - weight not apparent to muscle in resting state; only encountered when muscle has started to contract

As we increase preload/stretch on the muscle, we increase stretch.

As you increase the afterload, the amount of shortening the muscle undergoes is reduced.

Small preload (shorter muscle lengths) - Less force can be produced 
Larger preload (longer muscle lengths) - More force can be produced
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10
Q

In vivo correlates of preload

A

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

This stretch (filling) determines the preload on the ventricles before ejection

Preload is dependent on venous return

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

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11
Q

In vivo correlates of afterload

A

Afterload is the load against which the left vehicle ejects blood after opening of the aortic valve

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

Measures of afterload include diastolic blood pressure

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12
Q

Define the F-S (frank starling) relationship

Consequences of the F-S relationship?

A

Increased diastolic fibre length increases ventricular contraction

Ventricles pump greater stroke volume so that, at equilibrium, cardiac output exactly balances the augmented venous return.

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13
Q

Why does increased stretch result in increased force? (Two factors)

A

Changes in the number or myofilament cross bridges that interact (more)
- at shorter lengths than optimal the actin filaments overlap on themselves so reducing the number of myosin cross bridges that can be made

-changes in the Ca2+ sensitivity of the myofilaments
Mechanism still unclear
Hypothesis 1: at longer sarcomere lengths the affinity of troponin C (TnC) for Ca2+ is increased due to confrontational change in protein. -
Less Ca2+ required for the same amount of forc

Hypothesis 2: w stretch the space between myosin and actin filaments decreases, w decreasing myofilament lattice spacing, the probability of forming strong binding cross bridges increases.
Produces more force for the same amount of activating calcium

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14
Q

Define stroke work, how do you calculate stroke work?

What factors affect stroke work?

A

Stroke work = work done by heart to eject blood under prsssure into aorta and pulmonary artery

Definition:

Stroke work = vol of blood ejected during each stroke (SV) multiplied by the pressure at which the blood is ejected (P)

SV x P

Preload and afterload influence stroke vol
Cardiac structure affects pressure

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15
Q

What is the Law of LaPlace?

How do you calculate wall tension?

A

Law of la place: when the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius.

Wall tension = pressure in vessel x radius of vessel

T = P x R

Incorporating wall thickness (h), this can be:
T = (PxR)/h

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16
Q

How does the Law or Laplace apply in the heart?

What can happen in failing hearts leading to increased wall stress?

A

Radius of curvature of walls of left ventricle less than that of RV, allowing LV to generate higher pressures w similar wall stress.

Failing hearts often become dilated which increases wall stress