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Z YEAR 1 BRS cardiology > Cardiovascular Mechanics > Flashcards

Cardiovascular Mechanics Flashcards

1
Q

What are ventricular cells?

A

100 μm long and 15 μm wide

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2
Q

What are T tubules?

A

T-tubules (transverse tubules) are finger-like invaginations from the cell surface

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3
Q

How large are T-tubule openings? How far spaced apart are they?

A

Spaced (approx. 2 μm apart) so that a T-tubule lies alongside each Z-line of every myofibril
Carry surface depolarisation deep into the cell

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4
Q

What makes up cardiac cells?

A
  • Myofibrils (mainly 1)

- Mitochondria (mainly 2)

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5
Q

What is the excitation-contraction coupling in the heart?

A
  1. L type Ca2+ channel opens in response to depolarisation Ca2+ enters due to conc gradient
  2. Some goes to activate myofiliament and most goes to bind to SR Ca2+ release channel
  3. As a result channel undergoes confrontational change as ligand gated
  4. Therefore Ca2+ allowed to flow fromm stores into cytosol and bind to myofiliaments
  5. For relaxation, calcium is pumped back up into SR but SR Ca2+ ATPase and calcium taken up against conc gradient so calcium’s restored in SR, ready to be related for next beat
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6
Q

How do you stop too much calcium as stuff coming in and stuff being stored?

A
  • Exchange system on membrane takes calcium out of cell
  • Na+/Ca2+ changer and same amount that enters leaves
  • Does not use ATP
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7
Q

What happens as gradually increase cytosolic calcium ?

A
  • More and more force produced
  • As more and more myofiliaments activated
  • Sigmoidal relationship with calcium intracellular and force production
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8
Q

What is relationship between length-tension and force in cardiac muscle?

A
  • Active force and baseline (passive) force increase as muscle length increase but happens when isometric (no shortening) contraction
  • More stretch muscle more force produced up to certain point
  • So total force is active and passive force combined
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9
Q

Difference between skeletal and cardiac muscle?

A

-don’t need calcium outside as calcium causes opening
1. Cardiac muscle is more resistant to reach and less compliant than skeletal muscle
2. Due to properties of the extracellular matrix and cytoskeleton
3 .Only ascending limb of the relation is important for cardiac muscle
-Heart does not get overstretch

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10
Q

What is isometric contraction?

A

Muscle fibres do not change length but pressures increase in both ventricles

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11
Q

What is isotonic contraction?

A

Shortening of fibres and blood is ejected from ventricles

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12
Q

What is preload?

A

-Weight that stretches muscle before it is stimulated to contract

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13
Q

What is after load?

A

-Weight not apparent to muscle in resting state only encountered when muscle has started to contract

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14
Q

If large load how much shortening?

A

LESS shortening

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15
Q

What happens to shortening if longer muscle length?

A
  • MORE shortening
  • Decrease in sarcomere length, less preload, less stretch potential so less tension so less actin myosin cross bridges so less contraction potential
  • If increase in preload, increase in active tension
  • If long sarcomere length more active tension
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16
Q

What is the preload of the heart?

A
  1. As blood fills the heart during diastole, it stretches the resting ventricular walls
  2. This stretch (filling) determines the preload on the ventricles before ejection
    - More stretch, so more force
    - Deteminate of preload is amount of blood that comes back to heart
17
Q

What is preload dependent upon?

A

venous return

18
Q

What are the measures of preload?

A

end-diastolic volume, end-diastolic pressure (amount of blood in heartbefore contraction) and right atrial pressure (determines venous return)

19
Q

What is afterload in the heart?

A
  • Afterload is the load against which the left ventricle ejects blood after opening of the aortic valve
  • Pressure against which hear has to work
  • Any increase in afterload decreases the amount of isotonic shortening that occurs and decreases the velocity of shortening.
20
Q

What are measures of afterload?

A

diastolic blood pressure

21
Q

What factors affect contraction of heart?

A
  • Isometric contraction (ventricular filling)

- Isontinic contraction (shooter lengths, longer lengths)

22
Q

What is the frank starling relationship?

A

Observations by Frank (1895) and later by Starling (1914) showed that as filling of the heart increased, the force of contraction also increased

23
Q

What is the definition of FS relationship?

A

Increased diastolic fibre length increases ventricular contraction

24
Q

What are the consequences of the FS relationship?

A

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

25
Q

What is one factor causing FS relationship?

A
  1. Changes in number of my-filament cross bridges that interact
  2. At shooter lengths than optimal the actin filaments overlap on themselves so redoing he number of myosin cross bridges that can be made
26
Q

What is another factors causing FS relationship?

A

Changes in Ca2+ sensitivity of the myofilaments

27
Q

What is the first hypothesis?

A
  1. Ca2+ required for myofilament activation
  2. Troponin C (TnC) is thin filament protein that binds Ca2+
  3. TnC regulates formation of cross-bridges between actin and myosin
  4. At longer sarcomere lengths the affinity of TnC for Ca2+ is increased due to conformational change in protein
  5. Less Ca2+ required for same amount of force
28
Q

What is the second hypothesis?

A
  1. With stretch the spacing between myosin and actin filaments (so-called “lattice spacing”) decreases
  2. With decreasing myofilament lattice spacing, the probability of forming strong binding cross-bridges increases
  3. This produces more force for the same amount of activating calcium
29
Q

What is the definition of stroke work?

A

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

30
Q

What is the equation for stroke work?

A

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

31
Q

What affects SV?

A

preload and aferload

32
Q

What affects P

A

Cardiac structure

33
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

34
Q

What is equation for La place?

A

wall tension = pressure in vessel x radius of vessel
T = P x R
Incorporating wall thickness (h)
T= (PxR)/h

35
Q

How is Law place different?

A
  1. Radius of curvature of walls of LV less than that of RV allowing LV to generate higher pressures with similar wall stress
  2. Wall stress kept low in the giraffe by long, narrow, thick-walled ventricle
  3. In frogs, where pressures are low the ventricle is almost spherical
  4. Failing hearts often become dilated which increases wall stress

Z YEAR 1 BRS cardiology (10 decks)

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