Cardiac Electrophysiology II Flashcards

(35 cards)

1
Q

What does the SA node function to do? What is a special characteristic of it?

A

It functions as the normal initiation site of cardiac excitation. It exhibits intrinsic pacemaker activity. Rate of AP firing is 60-100/min

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2
Q

What are the phases of APs in the SA node cell?

A

Phases 0, 3, 4

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3
Q

Describe phase 0 (of the SA node)

A

Rapid depolarization; due mostly to I-Ca via V-dep L-type channels

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4
Q

Describe phase 3 (of the SA node)

A

Slower repolarization; due mostly to inactivation of I-Ca plus activation of delayed V-dep I-K

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5
Q

What causes pacemaker activity?

A

The interaction between I-Ca (T-type), I-k, and a special current termed I-f (f for funny). I-f is also known as the pacemaker current.

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6
Q

Why is I-f “funny”?

A

Is is a net inward current that activates in response to hyperpolarization (instead of the usual depolarization) and because it has both an inward Na and an outward K component

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7
Q

Describe Phase 4 (of the SA node)

A

a slow ramping depolarization because of the activation of I-f

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8
Q

A major Ca channel in the heart is L-type, describe this channel

A

Slow inactivation (L for long-lasting). Large channel. Fn’s; SA pacemaker, AV conduction, Excitation-contraction coupling. Low threshold of -40mV

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9
Q

A major Ca channel in the heart is T-type, describe this channel

A

Fast inactivationg (T=transient). Small channel. Fn’s; SA pacemaker, proliferative signaling. High threshold -70mV

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10
Q

What are 3 mechanisms that can slow the SA node pacemaker?

A

1-decreased rate of diastolic hyperpolarization. 2-diastolic hyperpolarization. 3-increased threshold.

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11
Q

How does the ANS regulate the SA node?

A

Neuronal input from both parasympathetic inhibition and sympathetic stimulation.

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12
Q

Describe parasympathetic inhibtion; the Vagal brake on the SA node

A

Vagal activity -> ACh released at heart SA node -> binds to M2 receptors -> activation of Gi and decrease of [cAMP]i. Results; slows heart/ pacemaker rate

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13
Q

Describe the sympathetic stimulation on the SA node

A

Norepinephrine binds to B1-adrenergic receptors: activate Gs -> activate adenylyl cyclase -> increase in [cAMP]i. Increases heart rate/ pacemaker rate

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14
Q

What are the mechanisms of action governing Symp stim of SA node

A

Increases phase 4 steepness by increasing inward I-f. Increases Phase 4 steepness by increaseing inward I-CaT threshold of I-CaL at more negative value

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15
Q

What effect does atropine have on sinus pacemaker rate?

A

Blocks parasympathetic control leading to an elevated HR (60-> 110)

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16
Q

What effect does propanolol have on sinus pacemaker rate?

A

Blocks sympathetic control leading to a decreased HR (60->50)

17
Q

What effect does atropine AND propanolol have on sinus pacemaker rate when combined?

A

Blocks symp and parasymp contol leading to an increased HR (60->100) but less than atropine alone

18
Q

What are the phases of atrial muscle AP?

A

0-4. It is different than the SA node phases

19
Q

Describe phase 0 of atrial muscle AP

A

Rapid depolarization; due mostly to I_Na; overshoots 0mV

20
Q

Describe phase 1 of atrial muscle AP

A

Small, limited repolarization. Activation of I_TO; decreased I_Ca and I_Na

21
Q

Describe phase 2 of atrial muscle AP

A

short plateau of depolarization (~200ms); due to prolonged I_Ca PLUS a I_Kur (ultrarapid) the currents balance each other

22
Q

Describe phase 3 of atrial muscle AP

A

Repolarization; inactivation of I_Ca, increased I_K

23
Q

Describe phase 4 of atrial muscle AP

A

Resting value of Vm due to increased iK_i; no depolarizing ramp nor I_f

24
Q

What are the consequences of phase 2

A

Ca++ entry promotes contraction refractory period permits filling

25
Describe the AV node in terms of AP and stimulation from SA node
AP's are similar to those of the SA node. AP's from SA node arrive in ~30ms. AV node has an intrinsic pacemaker activity with an intrinsic firing rate of ~40/min. The delay stage between atria and ventricles is ~90ms.
26
Describe the AV conduction system
Ca upstroke AP's like SA node. AP magnitude is smaller (<0). Slow upstroke. Relatively few gap junctions. Conduction velocity is low
27
What effect does parasympathetic inhibition have on the AV node?
It decreases the firing rate; decreases conduction velocity
28
What effect does parasympathetic stimulation have on the AV node?
It increases firing rate; increases conduction velocity
29
Describe the bundle branches/ purkinje fibers
They have the highest conduction velocity in the heart (~4ms, ~80X nodes, ~4X muscle) AP's are similar to muscle cells BUT Purkinje fibers also have a pacemaker current I_f. Intrinsic firing rate: <20/min and irregular (tertiary effect)
30
Compare ventricular muscle AP's to those of atrial muscle
They are similar. No intinsic pacemaker activity. Electrical activation of the ventricles is a very orderly, spatiotemporal process
31
Describe the spatiotemporal characteristics of ventricular activation. What effect does it have?
Vantricular apex (bottom) inside to out (endo to epicardium) ---(rapid, via Purkinje fibers)--> ventricular base (top also endo to epi). Effect: coordinated contraction of ventricular muscle cells that produces very efficient ejetion of blood
32
How is coordinated contraction achieved?
1-A wave of electrical excitation. 2-contraction coupled to electical excitation. 3-the heart consists of two electrical syncytia
33
How is the propagation of cardiac AP's achieved from cell to cell?
By direct electrical coupling via gap junctions. They provide the physical basis for the electrical coupling of cardiac cells.
34
Describe the electrical activation of the heart?
1-depolarize atria. 2-depolarize septum from left to right. 3-depolarize anteroseptal region of myocardium toward the apex. 4-depolarize bulk of ventricular myocardium, from endocardium to percardium. 5-depolarize poseterior portion of base of LV. 6-Ventricles are now depolarized
35
Discuss the normal activation sequence in the heart
SA, Atrial myocardium, AV node, AV bundle, Bundle branches, Purkinje network, Ventricular myocardium