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MBCHB3 RBF > Lecture 4: Treatment of cardiac rhythm disturbances > Flashcards

Lecture 4: Treatment of cardiac rhythm disturbances Flashcards

1
Q

What are the common causes of tachycardias?

A
  • Automacity / triggered activity
  • Re-entrant mechanisms
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2
Q

What are the common causes of bradycardias?

A

SAN/AVN conduction disorders

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3
Q

How can arrhythmias be characterised?

A
  • Simply-> Complex
  • Bening -> Malignant
  • Structural -> Functional
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4
Q

What are the treatment options for arrhythmias?

A
  • Not curative
  • Must consider SE/Drug interactions
  • Drugs or Devices or Intervention interface
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5
Q

What are the sources of bradycardias?

A
  • Physiological
  • Sinus node
  • AV node
  • Neural mediated
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6
Q

What are the sources of tachycardias?

A
  • Atrial
  • Junctional (SVT)
  • Ventricular
    -> Scar
    -> ‘normal’ hearts
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7
Q

What are the cardiac devices that can be used for rhythm disturbances?

A

1) Single or dual chamber pacing or ICD
2) Rate support:
- AV synchrony
- VV synchrony
3) Other:
- Vasovagal syncope device
- Monitors

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8
Q

Is ectopy a concern? how can it be treated?

A
  • Common, benign
  • Assess and can Tx with;
    -> Beta blocker
    -> Ablation
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9
Q

What are the common treatments of rhythm disturbances?

A
  • Assess
  • Re-assurance
  • Drug therapy
  • Withdraw of drug Rx
  • Manage underlying conditions
  • Device
  • Ablation
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10
Q

What do anti-arrhythmic drugs do?

A
  • Ectopic suppression
  • Alters conduction
  • Alters autonomic tone
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11
Q

What is the vaughn williams classification?

A

Class One: Na channel agents (Predom blocking, 1a,1b,1c)

Class Two: Beta blockers i.e metoprolol, propranolol

Class Three: K channel blockers i.e amiodarone

Class Four: Slow Ca channel blockers i.e verapamil, nifidipine

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12
Q

Describe the class 1a,1b,1c effects:

A

1a: Reduce Vmax, prolong AP. [Onset/Offset rapid]

1b: No vmax effect, shortens AP. [Onset,offset fast]

1c: Reduce Vmax, slow conduction. [Onset/offset slow]

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13
Q

What drugs to the vaughn williams classification miss?

A
  • Adenosine
  • Digoxin
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14
Q

How do anti-arrhythmic drugs work at a physiological level?

A

Anti-arrhythmia
- Cell membrane, ANS, vagal tone

Cell membrane activity effects:
- Conduction velocity, length of refractory period, automacity of the SA or AV node.

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15
Q

What are the effects of altered vagal tone?

A

Increased vagal tone:
- Dec HR, SA automacity, slower conduction through AVN

Decreased vagal tone:
- Inc. HR, SA automacity, increased conduction V through AVN

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16
Q

Describe how class 1a Na channel blockers work:

A

-> Slower depolarisation
-> Prolongs refractoriness
-> Reduces conduction velocity
-> Widens QRS interval

** Consider that it may enhance AVN conduction thus might also need rate lowering drugs

17
Q

What things should you always consider when thinking of arrhythmia treatment?

A
  • AP duration
  • Refractoriness
  • Conduction velocity
18
Q

What do class 1B Na channel blockers do?

A
  • Decrease duration of AP
  • Shortens refractory period
19
Q

What do 1C Na channel blockers do?

A
  • Decrease conduction velocity of AP
  • Little or no effect on refractory period
20
Q

How do class 2 beta blockers work to stop arrhthmias?

A
  • Decreases SNS tone, slows conduction velocity
21
Q

What are the possible side effects of beta blockers? when are they useful?

A
  • Bradycardia (Chronic Tx might require pacing)
  • Fatigue (Start low go slow)
  • Cardioselective B1 or non-cardioselective = differing S/E
  • C/I in asthmatics
  • Good for atrial or ventricular arrhythmia
22
Q

What are the effects of class three K channel blockers?

A
  • Increases duration of AP
  • Increases duration of refractory period

Also effects Na and Ca channels

23
Q

What are the considerations for K channel blockers?

A

-> Toxicity (Cumulative)
-> Can impact defib thresholds
-> May slow but not stop VT
-> Atrial or ventricular arrhythmias also…

24
Q

How do class four Ca channel blockers act?

A
  • Mainly affects SA and AV nodes
  • Not pro-arrhythmic
  • Rate-altering
25
Q

How does digoxin treat arrhythmogenesis?

A
  • Increased PSN activity
  • Slows atrial rate and AV conduction
26
Q

How does adenosine treat arrhythmogenesis?

A
  • AV node block
  • Typically IV admin
27
Q

What are the mechanisms of arrhythmogenesis?

A
  • Prolonged repolarisations
  • Development of EADs -> Torsades
  • Re-entry pathways
  • Structural abnormalities i.e HF
  • Afib is regularly irregular…
28
Q

What is AV node re-entrant tachycardia?

A
  • Ectopic beat in ventricles can conduct back through AVN to atria
  • Structural abnormalities elsewhere can also allow loop formation (ante vs orthodromic tachycardia)
29
Q

How does VT occur?

A
  • Re-entrant or automatic trigger around scar tissue
  • VT invades rest of ventricle
30
Q

What causes the broad complex characteristics?

A
  • Cell-cell activation, not conduction system
  • Atria continue to activate and contract normally
31
Q

How do you manage VT/VF?

A
  • Resus if emergency
  • Treat underlying pathology: Ischeamia, bradycardia, structured disease, metabolic or drug cause
  • Anti-arrhythmias
    -> Class one [+ICD back up]
    -> Class 2+3
  • Device ICD or Pacemaker
  • Ablation
32
Q

Whats the considerations when using amiodorone (K channel blocker)?

A
  • Drug interactions ie warfarin, digoxin
  • Many SE: Myalgias, insomnia, prolonged prothrombin time.
  • Toxicity: Liver, renal failure, pulmonary fibrosis, corneal deposits

MBCHB3 RBF (39 decks)

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