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Physiology 1 : cardiovascular > Cardiac contraction > Flashcards

Cardiac contraction Flashcards

1
Q

What is the duration of an action potential?

A

200-500ms

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2
Q

what is the amount of diastolic Ca2+?

A

100nM

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3
Q

What is the amount of systolic Ca2+?

A

10 μM

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4
Q

What is cell shortening like?

A

sub-maximal (not all or nothing)

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5
Q

When does cell shortening happen?

A

During depolarization ‘plateau’ phase of action potential when ICa is generated

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6
Q

When does cell relaxation happen?

A

During repolarisation of action potential

When Ca2+ signal is reduced

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7
Q

How does electrical excitability contract cardiac myocytes?

A
  • contraction is determined by an increase Ca2+
  • Greater increases Ca2+ = increased force of contraction
  • Intracellular Ca2+ levels increase from 0.1 μM to about 10 μM
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8
Q

What are T tubules?

A

→ Extensions of the cell membrane (sarcolemma) that penetrate into the center of cardiac muscle cells

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9
Q

What is the sarcoplasmic reticulum?

A

→ Membrane bound structure within muscle cells similar to the endoplasmic reticulum in other cells and stores Ca 2+

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10
Q

What is a ryanodine receptor?

A

→ Intracellular Ca2+ channel

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11
Q

What is the process of cardiac contraction?

A

→ Action potential depolarizes T tubules and activates VGCC causing a Ca2+ influx

→ Ca2+ binds to RyR located on the SR - close association with T tubules

→ Release of Ca2+ from the SR - CICR

→Ca2+ binds to troponin and there is displacement of tropomyosin / troponin complex which exposes the active sites on the actin

→Myosin thick filament heads bind to the active sites

→Myosin head ATPase activity releases energy (ATP to ADP) and the filaments slide

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12
Q

What are the myosin-actin binding sites blocked by at rest?

A

→ Troponin-tropomyosin complex

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13
Q

How does a rise in calcium cause the actin-myosin cross bridge to be formed?

A

→Ca2+ displaces troponin-tropomyosin so the actin-myosin binding sites are exposed and an actin-myosin cross bridge is formed

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14
Q

What does a rise in Ca2+ cause?

A

→ More sites exposed
→ More cross-bridges
→ Greater contractility

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15
Q

What is troponin composed of?

A

→ 3 regulatory sub units

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16
Q

What is TnT?

A

→ Troponin T which binds to tropomyosin

17
Q

What is TnI?

A

→ Troponin I which binds to actin filaments

18
Q

What is TnC?

A

→ Troponin C binds Ca2+

19
Q

What does binding of Ca2+ to TnC lead to?

A

→ conformational changes of tropomyosin and the exposure of actin binding sites

20
Q

What are TnI and TnT markers for?

A

→ Plasma markers for cardiac cell death

→ following MI

21
Q

How does relaxation occur?

A

→ Action potential repolarization (K+ ions) repolarize T tubules
→ VGCC close and there is a decrease of Ca2+ influx
→ There is no Ca2+ influx so no CICR
→ Extrusion of Ca2+ from the cell (30%) by the Na+/Ca2+ exchanger
→ Ca2+ uptake into the SR via SR Ca2+ ATPase (SERCA 70%) Ca2+ in SR for next contraction
→ Uptake of Ca2+ in mitochondria
→ Reduction in Ca2+ myosin head ATPase activity releases energy (ATP to ADP)
→ Prevention of contraction mechanism

22
Q

What are drugs used for in relation to contractility?

A

→ used to increase contractility of the heart

→ correct acute chronic heart failure

23
Q

What do sympathetic mimetic drugs do?

A

→ Increase VGCC activity

24
Q

What do cardiac glycosides do and what are they used for ?

A

→ Reduce Ca2+ extrusion

→ used for chronic heart failure

25
Q

What are cardiac glycosides and sympathetic mimetic drugs an example of?

A

→ Positive INOTROPES

26
Q

What does noradrenaline do?

A

→ Acts on B1 adrenoceptors to increase contractility

27
Q

What are the 4 effects of sympathetic stimulation on the heart?

A

→Positive inotropic effect
→ Positive chronotropic effect
→ Positive dromotropic effect
→ Lusitropic effect

28
Q

What is a positive inotropic effect?

A

→ Increased contractility of the heart

29
Q

What is a positive chronotropic effect?

A

→ Increased heart rate

30
Q

What is a positive dromotropic effect?

A

→ Increased conduction through the AV node

31
Q

What is a lusitropic effect?

A

→ Increased rate of relaxation

→ K+ channels + SR Ca2+ ATPase

32
Q

How does digoxin work?

A

→ Inhibits Na+/K+ ATPase
→ Build up of Na+
→ Less Ca2+ extrusion by Na/Ca exchanger
→ More Ca2+ uptake into stores and greater CICR

33
Q

When are dobutamine and dopamine used?

A

→ B1 adrenoceptor stimulants

→ May be used in acute heart failure

34
Q

When is glucagon used?

A

→ Used in patients with acute heart failure who are taking B blockers
→ Stimulates Gs pathway increasing cAMP and PKA activity

35
Q

When is Amrinone used and how does it work ?

A

→ Phosphodiesterase inhibitor
→PDE converts cAMP into AMP
→ PDE inhibition leads to build up of cAMP and phosphorylates VGCC

Physiology 1 : cardiovascular (18 decks)

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