Electrophysiology Flashcards

1
Q

SA node

A

primary pacemaker of the heart
has highest rate of reaching threshold (70-80 APs/min)

failure–>bradycardia (because AV node would take over and it is slower)

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2
Q

Bachmann’s bundle

A

interatrial tracts that spread depolarization from RA to LA

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3
Q

AV node

A

allows signal to pass from atria to ventricles (only bridge b/w the two)

AN region: transitional zone, longer conduction path
N: midpoint of AV node, slower conduction velocity
NH: transition to bundle of His
—>delay before signal goes to ventricles
**allows for adequate ventricular filling

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4
Q

Wolff Parkinson White (WPW) syndrome

A

some individuals have alternate pathway for atrial–>ventricle conduction

faster AV nodal pathway
slower ventricular depolarization
—> can cause signal to conduct back up the normal pathway–>tachycardia

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5
Q

Purkinje fibers

A

arranged linearly like myocytes: have sarcomeres in the R and L ventricles
**larger diameter= increased conduction velocity

activated endocardial–>epicardial
apex–>Base

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6
Q

Functional Syncytium

A

cells contract in synchrony as a result of gap junction connections

if one cell depolarizes, the rest will follow suit

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7
Q

Extracellular Ca and Cardiac contraction

A

influx of EC Ca is required for additional Ca release from SR
**activates RYR

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8
Q

Relaxation

A

removeal of Ca

  • 3Na1Ca antiporter–>ECF
  • ATP Ca++ pump—>ECF (against ECF)
  • SERCA back to sarcolemma
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9
Q

Pacemaker cell RMP

A

NO resting membrane potential

maximum diastolic potential only (slow depolarization)

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10
Q

Non-pacemaker cell RMP

A

RMP around -90mv (true RMP)

same ion distribution as normal AP

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11
Q

Hypernatremia

A

increased ECF Na increases CG during depolarization–>increased amplitude of AP depolarization

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12
Q

Slow response fibers

A

No RMP, lower threshold potential (-40mV)

  • smaller amplitude depolarization
  • Slower conduction velocity

slower upstroke (phase 0)

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13
Q

Fast response

A

have RMP, which is more negative threshold (-70mV), higher amplitude depolarization

very fast upstroke (phase 0)

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14
Q

Na current

A

phase 0 (rapid depol) in fast AP cells

Rapidly activate when membrane depolarizes
IG gates close at +30mV–>phase 1
but some channels remain open and prolongs plateau

Na current–.increased conduction velocity

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15
Q

Ca current

A

depolarization (phase 0) in slow AP channels
Small role in pacemaker phase (phase 4)
plateau in fast response cells
triggers contraction in all cardiomyocytes

*Slower conduction velocity due to smaller Ca current

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16
Q

K current

A

repolarization in all cardiomyocytes

In SA/AV K current decreased negative diastolic voltage to assist with pacemaker activity (phase 4)

17
Q

pacemaker funny current

A

responsible for slow depolarization in SA and AV
-mostly Na influx–> pacemaker potential
Phase 4

18
Q

Purkinje fiber

A

Normally a fast response fiber
but can also become pacemaker cells (very slow)
can have funny current

19
Q

Conduction velocity

A

depends on

1) amplitude of AP (affected by Na ECF)
- -> increase amplitude= increase ability to depolarize adjacent membrane
2) Slope of depolarization

20
Q

Hyperkalemia and conduction velocity

A

Small persistent depolarization (to -50)–> closes IG gates on may Na channels–> fewer channels able to respond–> smaller amplitude AP–> decrease conduction velocity

can be caused by CAD/MI ischemia–> decrease Na+K+ ATPase–> exs ECF Na and Exs ECF K–>rhythm disruption
-MI also releases K+

21
Q

effective refractory period

A

aka absolute refractory

  • IG gates closed after fast response depolarization
  • phase 0–> midPhase 3

reopen after repolarization

22
Q

relative refractory

A

can initiate another AP
mid-phase 3–> end phase 3

if a subsequent AP comes in, the later in the RP= greater amplitude of its upstroke

can limit ectopic beats

23
Q

Ectopic foci

A

abnormal impulse that takes a different conduction path and setup its own pacemaker rhythm –> arrhythmias and fibrillation (circus movements)

ex: WPW syndrome

24
Q

Long QT syndrome

A

prolonged action potential
still in some degree of refractory when another AP comes in–>causes oscillation of moderate depolarization/repolarization

25
Q

Early afterdepolarization (EAD)

A

low slope, low amplitude
abnormal depolarization in late phase 2 or in phase 3
Long QT
more abnormal

26
Q

Reentry

A

set up a new circuit that it completely out of order

generate APs that do not follow normal pathways (out of order)
cause premature contractions
–>prolonged QRS (PVCs)

27
Q

Factors promoting reentry

A

***—>increase likelihood that you comeback to node by the time the cell has recovered

1) lengthened conduction pathway: dilated heart chambers, atrial enlargement etc
2) decrease conduction velocity: hyperkalemia, ischemia, Purkinje block
3) Shorten refractory period (drugs, epi)

28
Q

Funny current

A

opens at more negative (hyperpolarized voltages)

causes Na influx

29
Q

Hyperkalmeia and HR

A

slowes HR by affecting driving force for K efflux

–> slows phase 4 repolarization–>delay in reaching hyperpolarization