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CPP > L11 - arrththymia > Flashcards

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
Q

what determines the time of refractory peroid

A

by the no of available and recovered VG NA channels

26
Q

what does shorter APD lead to

A
  • rapid return to the neg RMP
  • Na channels recover faster
  • shorter refractory peroid
  • re entry circuit
27
Q

what does longer APD lead to

A

NA channels recover more slowly and longer refractory peroid
- but ifits too long, can cause EADs

28
Q

what determines CV

A

charge graident between 2 cells

29
Q

what happens if the depol current is reduced

A
  • longer to reach threshold as the charge gradient is reduced
  • reduces CV and increase risk for ren enrty circuit
30
Q

classes of anti arrhythimic drugs (AADs

A

1,2,3,4

31
Q

what is class 1 AAD

A

VG Na channel blocker s

32
Q

what is class 2 AAD

A

B adrenoreceptor antagonist

-decrease SNS activity

33
Q

what is class 3 AAD

A

VG K channels blocker

34
Q

what is class 4 AAD

A

L type Ca channel blocker

CPP (15 decks)

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