Exam #2: Cardiac Excitation-Contraction Coupling Flashcards

1
Q

What is the sequence of electrical events in the heart?

A

SA node → AV node → Bundle of His → Bundle branches (L and R) → Purkinje fibers

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2
Q

What is the purpose of the AV nodal delay?

A

Ensures atrial contraction precedes ventricular contraction, allowing for complete ventricular filling between beats

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3
Q

What is the only step of the pathway that conducts from the atria to ventricles?

A

AV node → Bundle of His

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4
Q

What type of cells use a fast action potential?

A

Conductile cells and Contractile cells

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5
Q

What type of cells use a slow action potential?

A

Pacemaker cells (AV and SA node cells)

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6
Q

What type of ion drives fast action potentials?

A

Na+

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7
Q

What type of ion drives slow action potentials?

A

Ca2+

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8
Q

What ion/channel does the ANS act on?

A

Na+ funny channels

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9
Q

With fast depolarization, what event is responsible for the rapid depolarization (upstroke)? What type of channel?

A

Na+ rapidly flowing into cell (ordinary voltage-gated channels)

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10
Q

With fast depolarization, what event is responsible for the plateau phase? What type of channel?

A

Ca2+ slowly flowing into cell (L-type channels)

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11
Q

With fast depolarization, what event is responsible for the rapid repolarization? What type of channel?

A

K+ rapidly flowing out of cell (ordinary voltage-gated channels)

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12
Q

With fast depolarization, what event is responsible for the return to resting membrane potential? What type of channel?

A

K+ slowly flowing out of cell (leaky channels)

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13
Q

What is the purpose of the plateau phase?

A

It increases the duration of the action potential and allows time for the contraction to occur (time for plateau phase = time for full contraction then relaxation)
- Avoid cardiac tetany

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14
Q

Why is the RMP for cardiac muscle -90 mV instead of the -70 mV?

A

K+ permeability is even higher in cardiac cells (MANY:1 when comparing K+:Na+)

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15
Q

With slow depolarization, what event is responsible for the slow depolarization? What type of channel?

A
  • Na+ slowly flowing into cell (funny channels)

- Ca2+ slowly flowing into cell (L-type channels)

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16
Q

What is another name for the slow depolarization phase in slow APs?

A

Pacemaker potential because this phase sets the HR

17
Q

With slow depolarization, what event is responsible for the rapid depolarization?

A

Ca2+ flowing into cell

18
Q

With slow depolarization, what event is responsible for the rapid repolarization?

A

K+ flowing out of cell

19
Q

What type of muscle is cardiac muscle similar to in terms of excitation-contraction coupling? How is it different?

A

Cardiac muscle is very similar to skeletal muscle EXCEPT:

- Cardiac cells also receive Ca2+ from the ECF via L-type channels

20
Q

What are the three ways by which intracellular Ca2+ is decreased?

A
  • SERCA (most significant)
  • Na+/Ca2+ exchanger - uses Na+/K+ ATPase
  • Sarcolemmal Ca2+ ATPase
21
Q

What is the relationship between tension/contraction, sarcomere length and volume?

A

They are all directly related:

- If sarcomere length increases, tension/contraction increases and volume will also increase

22
Q

How does the SNS affect contractility/inotropy?

A

Positive contractility/inotropy effect

23
Q

How does the PNS affect contractility/inotropy?

A

Negative contractility/inotropy effect

24
Q

What type of receptors are utilized by the SNS with relation to contractility/inotropy? What type of protein are they coupled with and what is their action?

A

SNS = B1 receptors

- Coupled to Gs proteins and AC, which activates cAMP and PKA

25
Q

Which two types of proteins are phosphorylated by cAMP during SNS stimulation? What is the action of each in increasing contractility?

A
  • Sarcolemmal Ca2+ channel: increases Ca2+ release from SR

- Phospholamban: increases Ca2+ uptake and storage into SR (pumps it back into SR)

26
Q

What is the general affect that phospholamban activity has on heart rate

A

Contraction is briefer aka faster relaxation (increased HR)

27
Q

What type of receptors are utilized by the PNS with relation to contractility/inotropy? What type of protein are they coupled with? WHAT part of the heart do they specifically act on?

A

PNS = muscarinic receptors
- Coupled to Gi proteins

Decrease contractility in ATRIA

28
Q

With PNS and muscarinic receptors, when ACh is released, what are the two actions it takes to decrease contractility?

OVERALL, what is the general affect of these two actions combined?

A
  • ACh decreases flow of Ca2+ into the cell during plateau phase (less Ca2+ available for contraction)
  • ACh increases K+ current which shortens the duration of the AP and indirectly (further) decreases flow of Ca2+ into the cell during plateau phase

OVERALL, ACh decreases the amount of Ca2+ entering atrial cells during an AP AND decreases the amount of Ca2+ being released from the SR

29
Q

What is the mechanism behind Na+-K+ ATPase blockers? How does this happen, and what affect does this have?

A

Inhibit Na+/K+ ATPase

  1. No K+ flows in and no Na+ flows out through Na+/K+ ATPase
  2. Na+ accumulates inside cell
  3. Na+ is pumped out of cell via Na+/Ca2+ exchanger, so Ca2+ is pumped into the cell
  4. Increased Ca2+ inside cell = increased contractility
30
Q

What is the mechanism behind calcium-channel blockers (3)?

A
  • Decreased contractility
  • Decreased HR
  • Decreased conduction velocity
31
Q

What is the mechanism behind B-Agonists blockers?

A
  1. Increase cAMP production
  2. Increase protein phosphorylation
  3. Increase Ca2+ influx = Increased contractility