L11 - arrththymia Flashcards

1
Q

what does ECG measure

A

electrical activity

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2
Q

what happens during P wave

A

atrial depol

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3
Q

what happneds during QRS complex

A

ventri depol

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4
Q

what happends during T wave

A

ventri depol

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5
Q

what is R-r interval

A

calculates HR

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6
Q

what is P-R interval

A

from start of atrial depol to the start of ventr depol

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7
Q

what is QRS duration

A

total time of ventric depol

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8
Q

what is Q-T interval

A

from start of ventr depol to the end of ven depol

- used to get info about AP duration (APD)

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9
Q

what is arrythmia

A

disturbnace in the rate or rhythm of the heart beat

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10
Q

what is sinus rhythm

A

normal one

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11
Q

what is tachcardyia

A

has shorter r-r intervals

-has a faster HR

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12
Q

what is bradycardia

A

longer R-R intervals

-slower HR

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13
Q

causes of arrhythimas

A
  • loss of electrical activity
  • genetic associated with environmental
  • can reduce CO
  • most common arryhthimas is atrial fibrilla tion
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14
Q

classification of atthythimas regarding the location

A

superventic- location above the ventricles

ventricular - in the ventricles

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15
Q

classification of atthythimas regarding the mechanisms

A
  • triggered ectopic activity - leading to DADs and EADs

- disturbances in conduction - like AVN conduciton and re entry circuit formation

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16
Q

what is ectopic activiity

A

when other site in the heart (not SAN) start to generate their own heart activity
- most commonly in posteroir left atrial wall

17
Q

causes of ectopic activity

A

DADS - delayed depol EADS - early afterdepol

18
Q

how does DADs leads to ectopic acitvity

A
  • Ca overload in the SR so it leaks out
  • Ca removed by the Na/Ca exchanger so One Ca ion out and 3 Na ion in
  • there is net charge of 1+
  • RMP becomes positive and leads to depol inwards current
19
Q

how does EADS lead to

A
  • caused by a prolongation fo APD with reduced K efflux

- prolongation allows for L type Ca channels to recover and reactivate

20
Q

causes od conduction disturbances in arryhthima

A

AVN conduction block - electrical wave not passed through the AVN
- re entry circuit formation

21
Q

what is re entry circuit formation

A

one or multiple self sustaining circuits in the hearts

22
Q

types of re enrty circuits

A

macro, micro , muiltple micro circuits

- increase HR

23
Q

how are re entry circuits fromed

A
  • when there is a damaged tissue in the heart

- once it repairs, the it causes the circuits to be in loop rather than in one direction

24
Q

factors affecting the formation of re entry circuits

A

slower the conduction velocity
the shorter refractory peroid is
shorter the wavelength ,

the more likely the re entry circuits will be formed

25
what determines the time of refractory peroid
by the no of available and recovered VG NA channels
26
what does shorter APD lead to
- rapid return to the neg RMP - Na channels recover faster - shorter refractory peroid - re entry circuit
27
what does longer APD lead to
NA channels recover more slowly and longer refractory peroid - but ifits too long, can cause EADs
28
what determines CV
charge graident between 2 cells
29
what happens if the depol current is reduced
- longer to reach threshold as the charge gradient is reduced - reduces CV and increase risk for ren enrty circuit
30
classes of anti arrhythimic drugs (AADs
1,2,3,4
31
what is class 1 AAD
VG Na channel blocker s
32
what is class 2 AAD
B adrenoreceptor antagonist | -decrease SNS activity
33
what is class 3 AAD
VG K channels blocker
34
what is class 4 AAD
L type Ca channel blocker