Electrophysiology II Flashcards

1
Q

SA node

A
  • pacemaker activity
  • normal initiation site of cardiac excitation
  • 60-100/min
  • phase 0, 3, 4
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2
Q

phase 0 of SA

A

rapid depolarization due to Ica voltage dependent L channels

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3
Q

phase 3 of SA

A

-slower repolarization due to inactivation of Ica and activation of delayed V dep K

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4
Q

phase 4/ pacemaker activity

A
  • interaction between Ica T channels, Ik, and If (h)
  • If is net inward current that activates in response to hyperpolarization (when membrane gets back to neg, it sets off)
  • has inward Na and outward K- depolarization in response to hyperpolarization
  • when cell repolarizes, hyperpolarization opens cation channel and Na in and K out- depol
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5
Q

L type calcium channel

A
  • low threshold -40
  • slow inactivation and long lasting
  • large channel size
  • SA pacemaker and AV conduction and excitation contraction coupling
  • contraction of smooth muscle
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6
Q

T type calcium channel

A
  • high threshold -70 (goes open sooner and starts AP)
  • fast inactivation/ doesnt last long
  • small channel size
  • SA node pacemaker and proliferative signaling
  • contraction in smooth muscle
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7
Q

three mechanisms that can slow the SA pacemaker

A
  • decreased rate of depol (K out slower takes longer to get to neg and the If channel to open)
  • diastolic hyperpolarization- more hyperpol means takes more to get to threshold
  • increased threshold-takes longer to get there
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8
Q

ANS regulation of SA node

A

-neuronal PNS and SNS

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9
Q

PNS regulation of SA node

A
  • vagal break
  • vagus nerve, cholinergic (Ach)
  • muscarinic receptor (M2) metabotropic
  • vagus–>Ach released–> Ach activates M2–> activated Gi protein and decreases cAMP which:
  • reduces inward If (less depol)
  • reduces inward Icat (less AP)
  • threshold of Ical more pos (harder to get Ical to open, less Ca in)
  • rate slows down
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10
Q

SNS regulation

A
  • adrenergic, norepi
  • B1 adrenergic receptors, metabotropic
  • B1 receptor activated from norepi–>adenylate cyclase activated–> increase cAMP which:
  • increase If (more depol faster- threshold faster)
  • increases Icat (more Ca in)
  • threshold of Ical more negative (easier to set off AP)
  • increases rate
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11
Q

atropine

A
  • blocks M2- no vagal activation to slow HR, Ach can’t bind

- no drop in HR

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12
Q

propanolol

A
  • B blocker, no SNS sim because norepi can’t bind
  • no speed up
  • not as dramatic as atropine
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13
Q

atropine plus propanolol

A
  • equivalent of removing ANS

- shows how parasympathetic really wins out most of the time over SNS

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14
Q

cardioselective beta blockers

A
  • block B1

- bradycardia

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15
Q

block M2

A

-tachycardia

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16
Q

nerve- inhibit AchE

A

-bradycardia b/c more Ach around to bind and activate M2

17
Q

block uptake of NE

A

-tachycardia (more norepi around to bind to beta)

18
Q

atrial muscle AP

A
  • phases 0-4
  • short plateau because of long Ica and Ikur (ultrarapid)
  • no intrinsic pacemaker
  • ca entry from plateau promotes contraction and refractory period permits filling
19
Q

AV node

A
  • APs similar to SA
  • from SA to AV in 30 ms
  • intrinsic activity of 40/min
  • delay b/n atria and ventricles is 90 ms
  • Ca upstroke
  • SP small
  • slow upstroke
  • few gap junctions
  • conduction velocity low
  • PNS decreases firing rate and conduction V
  • SNS increases firing rate and conduction V, but both really controlled by SA node
20
Q

bundle branches/ purkinje fibers

A
  • highest conduction velocity in heart
  • 4m/s, 80X nodes, 4X muscle
  • AP similar to muscle cells but
  • also have If about 20/ min and irregular
21
Q

ventricular muscle APs

A
  • similar to atrial
  • no intrinsic pacemaker activity
  • orderly, spatiotemporal process
  • from bottom to top
  • coordinated contraction of ventricular muscle cells that produces efficient ejection of blood
  • inside to outside, 3 layers have different APs- see slide
22
Q

coordinated contration

A
  • wave of electrical excitation
  • contraction coupled to electrical excitation
  • heart consists of 2 electrical syncytia
23
Q

propagation of cardiac APs

A
  • gap junctions
  • connexins
  • electrical coupling of cardiac cells
  • need to reach threshold for AP in neighboring cell
  • current flows from A to B and passes AP through gap junction, flows back through membrane as capacitance