Heller Ch. 2 Flashcards

1
Q

What is the RMP of calcium?

A

+100mV (more in interstitial fluid)

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2
Q

What is the RMP of sodium?

A

+70mV (more in interstitial fluid)

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3
Q

What is the RMP of potassium?

A

-90mV (more in intracellular fluid)

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4
Q

What does movement of ions across a membrane cause?

A

A charged membrane…cations move out leaving behind negative proteins

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5
Q

Phase 0 of Fast Response Action Potentials?

A

Sodium permeability rapidly goes UP–>

a sudden DEpolarization

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6
Q

Phase 1 of FRAP?

A

Sodium permeability rapidly goes DOWN and
Potassium permeability goes DOWN–>
a slight REpolarization

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7
Q

Phase 2 of FRAP?

A

Calcium permeability goes UP
Sodium permeability slightly UP and
Potassium permeability stays LOW–>
a PLATEAU

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8
Q

Phase 3 of FRAP?

A

Potassium permeability goes UP
Calcium permeability goes DOWN and
Sodium permeability goes DOWN–>
a REpolarization (Phase 4)

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9
Q

Pacemaker potential cells (Slow-Response Action Potential)?

A

Unstable membranes

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10
Q

Net movement in SRAP cells before AP?

A

Potassium goes DOWN while
Calcium (major) and Sodium (minor) go UP–>
an eventual DEpolarization (action potential)

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11
Q

How is conduction velocity modified?

A

Connexin proteins in gap junctions

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12
Q

Parasympathetic actions through the vagus nerve (ACh):

A

An initial hyperpolarization of the RMP

Slows the rate of spontaneous depolarization of the RMP

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13
Q

How does ACh achieve parasympathetic effects?

A

ACh interacts with muscarinic receptors–>activates Gi
Increases potassium permeability (K[ACh] channels)
Suppresses adenylate cyclase–>decreased cAMP–>reduces inward-going pacemaker current by sodium (i[f] current)

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14
Q

Sympathetic actions (NE):

A

Increases inward currents carried by both sodium (i[f] current) and calcium during the diastolic interval–>increases rate of diastolic depolarization

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15
Q

How does NE achieve sympathetic effects?

A

NE interacts with beta1-adrenergic receptors–> activates Gs
Increases adenylate cyclase–> increases cAMP–> increases open-state probability of the pacemaker sodium current channel (i[f] current)

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16
Q

Define chronotropic:

A

Heart rate

17
Q

Define dromotropic:

A

Conduction velocity

18
Q

Digitalis:

A

Inhibits sodium/potassium pump–>decreased sodium gradient–>non-functional sodium/calcium exchanger–>increased contraction strength/length

19
Q

Ryanodine:

A

Blocks the calcium induced calcium channel

20
Q

Caffeine:

A

Activates the calcium induced calcium channel

21
Q

Contractility:

A

Force at a given length

22
Q

Inotropic:

A

Change in contractility

23
Q

Tension in ventricle?

A

T = intraventricular pressure x internal radius

24
Q
Potassium channel (inward rectifier)
i[K1]
A

Maintains high K+ permeability during phase 4
Decay contributes to diastolic depolarization
Suppression during phases 0-2 contribute to plateau

25
``` Sodium channel (fast) i[Na] ```
Accounts for phase 0 | Inactivation may contribute to phase 1
26
``` Potassium channel (transient outward) i[TO] ```
Contributes to phase 1
27
``` Calcium channel (slow inward, L channels) i[Ca] ```
Primarily responsible for phase 2 Inactivation may contribute to phase 3 Is enhanced by sympathetic stimulation and beta-adrenergic agents
28
``` Potassium channel (delayed rectifier) i[K] ```
Causes phase 3 | May be enhanced by increased intracellular Ca++
29
``` Potassium channel (ATP-sensitive) i[KATP] ```
Increases K+ permeability when ATP is low
30
``` Potassium channel (ACh-activated) i[KACh] ```
Responsible for effects of vagal stimulation Decreases diastolic depolarization and HR Hyperpolarizes RMP Shortens phase 2
31
``` Sodium channel (pacemaker current) i[f] ```
Contributes to the diastolic depolarization Enhanced by sympathetic stimulation and beta-adrenergic agents Suppressed by vagal stimulation