Arrhythmias Flashcards

1
Q

An arrhythmia is described as

A
  • a disturbance in the rate and rhythm of the heart beat
  • tacky-decreased R-R
  • Brady- increased R-R
  • irregular - irregular R-R intervals
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2
Q

Arrhythmias are caused by?

A
  • due to changes or losses of electrical integrity
  • genetic origin (ion channelopathy)
  • hyperT, obesity, off target drug effects
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3
Q

supraventricular Arrhythmias occur?

A

originate higher up the conduction route than the V

* Sinus bradycardia
* Sinus tachycardia
* Atrial tachycardia 
* Atrial Fibrillation
* AV block
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4
Q

ventricular Arrhythmias occur?

A

originate in the V
• Ventricular premature beats
• Ventricular tachycardia
• Ventricular fibrillation

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5
Q

how can they be classified by the mechanism ?

A
  • emergence of triggered ectopic activity (automaticity)
  • Delayed after depolarisations
  • early after depolarisations
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6
Q

disturbances in conduction can occur by?

A
  • AVN conduction block

- re-entry circuit formation

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7
Q

ectopic activity is usually seen at?

A
  • the posterior left atrial wall near the region of the pulmonary vein entrance
  • one or multiple sites in the heart start to generate their own electrical activity
  • Spontaneous action potential generation in sites other than the SAN
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8
Q

DADs are

A
  • inappropriate depolarisation during a diastolic interval
  • opening of sufficient Na channels
  • triggering of AP during diastolic
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9
Q

DADs are caused by?

A
  • cellular overload of ca swamps SR with Ca
  • phasic oscillatory phase is the release of ca from the SR via RyR2 channels
  • oscillatory depolarisation inwards current via NXC channels (na Influx)
  • Ca removal via NXC leading to accumulation of +1 charge due to Na influx
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10
Q

EADs are caused by

A
  • reduced K efflux during repolarisation phase due to defective ion channel
  • prolongation of Q-T interval
  • prolongation of ADP
  • prolongation of ADP allows enough time for L-T channels to recover and reactivate
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11
Q

what causes drug induced EADs?

A
  • HERG channel is a depolarising channel
  • drug enters and blocks channel
  • prolonged repol
  • one or more triggered beat
  • cause torsades and de pointes
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12
Q

what causes AVN conduction block?

A
  • reduced or blocked conduction through AVN
  • slowing of propagation through AVN
  • prolonged P-R interval
  • may miss some QRS complex after P-wave
  • complete lack of association between P/ QRS waves
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13
Q

what is re-entry circuit formation ?

A

is the establishment of one or multiple self sustaining circuits within the heart

  • macro
  • micro
  • can obtain multiple in tje same LA
  • can lead to unidirectional conduction block
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14
Q

what determines the probability of forming a re-entry circuit?

A
  • directed related to wavelength

shorter WL = increased likelihood

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15
Q

ADP determines what ?

A
  • the rate of Na channel recovery and therefore RP length
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16
Q

increased susceptibility to arrhythmia arises when?

A
  • ERP is shorter

- CV is lower

17
Q

a shorter ADP ?

A
  • increases K current and decreases inward Ca current
  • more rapid return to RMP
  • Na channels recover quicker
  • shorter RP
  • increased risk of circuit
18
Q

Drugs that prolong ADP work by?

A
  • blocking VG Na channels
  • fewer available Na channels requires cell to reach a higher vT
  • fewer channels prolongs the ERP (APD)
  • protective
  • can lead to EADs
19
Q

slowing CV is observed as what on an ECG?

A
  • V conduction ,observed as increase in QRS complex duration

- atrial conduction, observed as increase in P-wave duration or P-R interval

20
Q

what happens if depolarising current is reduced ?

A
  • fewer Na channels available
  • smaller charge gradient established
  • due to a lower AP magnitude
    = lower amplitude
  • increases risk of developing a re-entry circuit
21
Q

the amplitude of the AP depends on?

A
  • number of available Na channels
22
Q

speed of which a return to negative RMP is controlled by?

A

the duration of the APD