cardiac electrophysiology Flashcards

1
Q

A 21 y/omale from Southeast Asia dies in his sleep. Post-mortem molecular autopsy demonstrates a loss-function-mutation in the Voltage Gated Sodium Channel (SCN5a). This will have the following effect on the action potential:

A

phase 0 and 1 since this sodium channel is responsible for phase 0

can result in long QT syndrome when overactivated –> burmuda syndrome

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2
Q

what defines the plateu phase in an action potential

A

L type ca channels

ca coming in and k moving out both slowly

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3
Q

what channels are key for excitatation and contraction

A

L type ca –> ca induced ca release

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4
Q

what is channel and phase and responsible for LQTS 1 and 2 inherited arrhythmias syndromes

A

–IKr(rapid)

–IKs(slow)

phase 3

in KCNQ1, loss of this can cause long QT

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5
Q

what phase and channel is responsible for (Torsadede Pointe) drug induced arrthymias and is tested for when developing new drugs

A

K in phase 3

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6
Q

what activates phase 4 in SA nodal cells

what does phase 4 control

A

hyperpolarization

heart rate

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7
Q

how does going for a run activate the slope of phase 4

A

makes it steeper- faster hr

Catecholamines

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8
Q

name mechanisms to slow SA firing

A
  1. Slows depolarization-
  2. Lowers resting –> opens K
  3. Raises threshold decreases Ca

can slow or stop AV conduction

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9
Q

Blocking the HERG channel will have the following effects on the action potential AND ECG:

A

1.Prolong BOTH Phase III and QT interval

could cause Torsade de Pointe

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10
Q

Anisotropy

A

ordered propogation

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11
Q

what is Arrhythmogenic Right Ventricular Cardiomyopathy

A

Disruption of Desmosomes in Intercalated Disc Causes Heart to Turn into Fat!

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12
Q

How can arsenic cause QTc prolongation

A

trafficking defect, preventing the HERG channel from getting to the sarcolemma (phase III)

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13
Q

what can cause exercise induced tachycardia

A

leaky RyR channel

A.Ca2+influx leads to delayed-after-depolarization mediated triggered arrhythmia

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14
Q

what kind of things could cause a inversion where the repolarization occurs from endo to epi (normal repolarization is epi to endo)

A

pathologic and could be thickening of the heart

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15
Q
A
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16
Q

what would you estimate the rate to be if the p to p covered 5 boxes

A

60

300 150 100 75 60 50

17
Q

what are the 5 questions you ask every ecg

A
  • What is the Rate?
  • What is the Rhythm?
  • What is the Axis?
  • What are the Intervals?
  • Waveform?
18
Q

what would you see in lead 1 if you had left axis deviation due to left ventricular hypertrophy

what if you had right axis deviation due to right ventricular hypertrophy

A

positive in lead 1 but isoelectric in AVR

reverse

19
Q

if the myocardium is thicker than __ mm you increase risk of sudden cardiac death

A

3

20
Q

what does the PR interval represent and how long should it be

A

start of atrial dep to ventricular depolarization

120-200

21
Q

what does the QT interval represent and how long should it be

A

start of ventricular depolarization to the end of ventricular repolarization

should be less than 440 in men and 460 in women

22
Q

what impact would testosterone have on the QT interval

A

shortens it

23
Q

what is the qrs complex and how long should it be

A

qrs –> begining to end of ventricular dep

90-100

advances is more than .12s

24
Q

what kind of things could cause an altered waveform

A

obesity

COPD

effusions

hypothyrodism

kATP and MI could cause ST elevatio

25
Q

which occlusion can be electrially silent

A

LCx

26
Q

where would you see a signal for LCx or diagnal

A

V5/V6

I

AVL

27
Q

where would you see a signal for LAD

septal?

A

V1-V4

septal (V1,V2)

28
Q

where would you see a signal for RCA

A

II, III, aVF

29
Q

why can you see Why can you see the fibrillatorywaves in the ventricle but not atria

A

mass = larger magnitude

30
Q

how do you tell R vs L BBB

A

R –> LAD V1

L –> V6