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CS1 Exam 1 > 3- Mechanisms of Dysrhythmias > Flashcards

3- Mechanisms of Dysrhythmias Flashcards

1
Q

what phases correspond to the absolute refractory period?

A

phase 0,1, and2

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2
Q

time that the cell is unable to respond to another incoming impulse

A

absolute refractory period

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3
Q

relative refractory period phase

A

phase 3

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4
Q

sustained inability to respond to an incoming impulse under normal conditions

A

relative refractory period

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5
Q

why doesn’t the heart tetanize like skeletal muscle?

A

extended absolute refractory period due to calcium channels

AND

no recruting

*everything is all or none

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6
Q

define calcium spark

A

calcium-induced(voltage) calcium release(SR calcium channels)

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7
Q

name of calcium release channels

A

ryanodine receptors

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8
Q

increased activity of SERCA by SNS =

A

calcium taken away to increase relaxation faster ALSO SNS increases rate of calcium release from ryanodine.
Together = increased contractions

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9
Q

classify: abnormal or enhanced automaticity

A

active arrhytmia

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10
Q

classify: triggered activity

A

active arrhythmia

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11
Q

classify: reentrant circuits

A

active arrhythmias

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12
Q

slower than normal

A

sinus bradycardia

faster (>100) would be sinus tachycardia

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13
Q

effect of hypokalemia

A

decreases phase 4 K availabale –> easier depolarization and less time between AP

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14
Q

effect of mild hyperkalemia

A

increased AP

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15
Q

effect of severe hyperkalemia

A

unexcitable, no AP

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16
Q

“triggered activity”

A

delayed or early afterdepolarization

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17
Q

arrhythmia is generated at a time when the cell is fully repolarized

A

DAD

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18
Q

arrhythmia generated during phase 2 or phase 3 depending

A

EAD

19
Q

characteristically extended action potential duration indicates…

A

EAD

20
Q

reduced potassium current –>

A

repolarization takes longer than normal –> prolonged APD

21
Q

increased intracellular calcium –>

A

extended plateau phase and extra calcium can activate an additonal sodium current –> prolonged APD

22
Q

mutation of NCX to increase current during the end of phase 2 –>

A

prolonged APD

23
Q

when can EADs be accentuated..

A

at lower heart rates due to the physiologically natural longer APDs at this point

24
Q

exacerbated by higher HR…

A

DADs

because ther is not sufficient time to reduce intracellular calcium between successive beats

25
Q

a fixed pathway exists which connects atrial tissue to ventricular tissue and in doing so, bypasses the AV node

A

wolff-parkinson-white syndrome

26
Q

how does wolff parkinson white syndrome manifest on ECG

A

shortened PR interval (because the bypass impulse travels faster to ventricles than normally conducted signal)

27
Q

core of inexciteable tissue would be..

A

functional reentract obstacle

28
Q

associated with spiral wae

A

anatomical-define reentrant circuit

29
Q

stable spiral wave originating from one position within the ventricular mass

A

monomorphic ventricular tachycardia

30
Q

meandering or drifting spiral waves throughout the ventricular mass

A

polymorphic tachycardia

31
Q

rely on the principles of electrical anisotropy and spatial inhomogeneities

A

reentrant circuits

32
Q

conduction abnormality as a result of tissue structure

A

passive arrhythmia

33
Q

“source sink”

A

a smaller sink will increase APD and a larger sink will reduce APD and conduction velocity

contributes to anisotropy and inhomogeneity in the propogating wavefront

34
Q

true or false: changing the AP duration will change the refractory period

A

true

35
Q

vagal stimulation would have what effect on HR

A

vagal is parasympathetic so it would derease automaticity and decrease HR –> sinus brady cardia

sympathetic would be the opposite: sinus tachyccardia

36
Q

if both para and symp are stimulate who will win for HR?

A

para

37
Q

how does Ach change automaticity

A

slower

by increasing potassium current

38
Q

how does NE change automaticity

A

faster by increasing calcium and funny current

39
Q

how do hypokalemia and ischemia change automaticity

A

faster becasue of a decreased potassium current

40
Q

what 4 things could cause a prolonged APD?

A
  1. reduced potassium current
  2. increased calcium
  3. increased sodium-calcium exchanger activity
  4. increased late sodium current
41
Q

true or false: only anatomically defined reentrant circuits rely on electrical anisotropy and tissue inhomogeneiteies

A

FALSE

both anatomical and cuntionally defined reentrant ircuits rely on electrical anisotropy and tissue inhomogeneiteies

42
Q

spiral wave

A

functioanlly defined reentrant circuit

43
Q

fixed pathway with excitable gap

A

anatomically defined reentrant circuit

CS1 Exam 1 (13 decks)

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