Cardiac Electrophysiology II Flashcards

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
Q

Describe the AV node in terms of AP and stimulation from SA node

A

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
Q

Describe the AV conduction system

A

Ca upstroke AP’s like SA node. AP magnitude is smaller (<0). Slow upstroke. Relatively few gap junctions. Conduction velocity is low

27
Q

What effect does parasympathetic inhibition have on the AV node?

A

It decreases the firing rate; decreases conduction velocity

28
Q

What effect does parasympathetic stimulation have on the AV node?

A

It increases firing rate; increases conduction velocity

29
Q

Describe the bundle branches/ purkinje fibers

A

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
Q

Compare ventricular muscle AP’s to those of atrial muscle

A

They are similar. No intinsic pacemaker activity. Electrical activation of the ventricles is a very orderly, spatiotemporal process

31
Q

Describe the spatiotemporal characteristics of ventricular activation. What effect does it have?

A

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
Q

How is coordinated contraction achieved?

A

1-A wave of electrical excitation. 2-contraction coupled to electical excitation. 3-the heart consists of two electrical syncytia

33
Q

How is the propagation of cardiac AP’s achieved from cell to cell?

A

By direct electrical coupling via gap junctions. They provide the physical basis for the electrical coupling of cardiac cells.

34
Q

Describe the electrical activation of the heart?

A

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
Q

Discuss the normal activation sequence in the heart

A

SA, Atrial myocardium, AV node, AV bundle, Bundle branches, Purkinje network, Ventricular myocardium