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CPT > L9 Arrhythmia > Flashcards

L9 Arrhythmia Flashcards

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1
Q

Torsades de pointes

A
  • due to long QT
  • causes ventricular tachycardia
  • leads to sudden cardiac death due to asystole
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2
Q

Atrial arrhythmia

A
  • SAN not used
  • atria beat up to 300bpm
  • electrical conduction through AVN is quicker so ventricles contract more
  • causes palpitations
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3
Q

P wave

A

Depolarisation of atria

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4
Q

PR interval

A

Conduction through the AVN node

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5
Q

PR segment

A

Conduction through Bundle of His

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6
Q

q deflection

A

Conduction through interventricular septum

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7
Q

QRS

A

Ventricular depolarisation

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8
Q

S deflection

A

Conduction of ventricles up

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9
Q

T wave

A

Ventricular repolarisation

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10
Q

How are arrhythmias caused

A
  • Pacemaker impulse formation - SAN/ AVN
  • contraction impulse conduction - abnormal Bundle of His
  • combination of both

Abnormal impulse generation:

  • automatic rhythms - ectopic beat or enhance normal automaticity
  • triggered rhythms - delayed/early afterdepolarisation

Abnormal conduction:

  • reentry circuits
  • conduction block
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11
Q

Fast cardiac action potential

A

In cardiac myocytes

Phase 0 - Na+ influx causes depolarisation
Phase 1 - Transient K+ efflux
Phase 2 - Ca2+ influx causes cardiac plateau
Phase 3 - K+ efflux - repolarisation
Phase 4 - Na+/K+ ATPase maintains the resting potential

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12
Q

Resting membrane potential in cardiac myocytes

A
  • 90mv
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13
Q

Class 1 drugs

A

Block Na+ channels
Inhibit Na+ influx
Decreased speed of depolarisation, decreasing conduction velocity in tissue

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14
Q

Class 2 drugs

A 
Beta blockers 
Inhibit Ca2+ influx 
Longer calcium plateau 
Prevents phase 4 depolarisation and automaticity 
Good for focal arrhythmias
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15
Q

Class 3 drugs

A

Block K+ channels
Inhibits K+ efflux
Longer time for repolarisation- extended refractory period
QT interval extended - can cause torsardes de pointes
Increases action potential duration

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16
Q

Class 4 drugs

A

Calcium channel blockers
Inhibit calcium influx
Decreases phase 4 spontaneous depolarisation

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17
Q

Slow cardiac action potential

A

In pacemaker cells - SAN/AVN

Phase 0 - Ca2+ influx causing depolarisation
Phase 3 - K+ efflux causing repolarisation
Phase 4 - pacemaker potential - HCN channels activate causing funny currents of sodium influx

  • immediate depolarisation causing automaticity
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18
Q

Specialisation of pacemaker cells

A

Specialised myocytes
Spontaneous depolarisation
Less contractile machinery

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19
Q

Main classes of drugs that act on SAN/AVN

A

Class 2 - beta blockers

Class 4 - calcium channel blockers

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20
Q

Class 4 drugs on SAN

A

Slower conduction velocity as takes longer to depolarise

Increases the refractory period

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21
Q

Salbutamol side effect

A

Beta agonist
Can cause sinus tachycardia as can act on beta1 receptors
Increases calcium influx - increasing conduction velocity

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22
Q

Muscarinic agonists and adenosine

A

Decreased phase 0 depolarisation

Decreased conduction velocity

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23
Q

Wolf Parkinson white syndrome

A
  • accessory pathway in the heart due to Bundle of Kent
  • connects the atria and ventricles
  • reentry circuit over and above the AVN
24
Q

Slow fast reentry

A

50% of the population have slow and fast conduction pathways

  1. An ectopic beat travels via the slow pathway
  2. During its refractory period the rhythm goes back up the other way
  3. Constant loop causes reentry tachycardia
25
Q

Micro reentry in MI

A

MI causes ischaemia and necrosis of heart tissue leading to a scar
Micro reentry can occur in the scar
Causing ventricular arrhythmias - e.g VT

26
Q

Class 1b drugs examples

A

Lidocaine - IV form

Mexiletine - oral form

27
Q

Class 1c drugs examples

A

Flecainide

Propafenone

28
Q

Beta blocker examples

A

Bisoprolol
Metoprolol
Propranolol

29
Q

Class III examples

A

Amiodarone (highest efficacy)

Sotalol

30
Q

Class IV calcium channel blockers

A

Verapamil

Diltiazem

31
Q

Class 1b

A

Mechanism:

  • APD slightly decreased in normal tissue
  • less Na+ influx
  • decreased phase 0 conduction in fast beating of ischaemic tissue
  • slower ventricular contraction

ECG:
- in fast beating or ischaemic patients - longer QRS

Used in: acute ventricular tachycardia especially during ischaemia

Side effects:

  • less pro arrhythmic
  • dizziness and drowsiness
  • abdominal GI upset
32
Q

Class 1c

A

Method:

  • oral - prevention of arrhythmia
  • IV - acute arrhythmia

Mechanism:

  • substantially lower phase 0 - less Na+ influx
  • decreased automaticity
  • increased APD and increased refractory period
Uses: 
- wide spectrum 
- supraventricular arrhythmias - fibrillation and flutter 
- Wolf-Parkinson White syndrome 
- premature ventricular contractions 
ECG: 
- longer PR 
- longer QRS 
- longer QT
33
Q

Sid effects of class 1c

A
  • pro arrhythmia
  • sudden death associated with chronic use and structural hearty disease
  • flutter (1:1 ventricular response)
  • CNS and gastrointestinal effects
34
Q

When can fleconaide be used in structural heart disease patients

A

When the patient has an implantable cardiac defibrillator

35
Q

Class II mechanism

A

Absorption and elimination:

  • propanolol and metoprolol - IV or oral
  • bisoprolol - oral
  • esmolol - IV only (very short acting and short half life)

Effects:
- slower action potential duration in AV node therefore slows conduction velocity

ECG:

  • Increased PR
  • Decreased HR

Uses:

  • sinus and catecholamine dependent tachycardia
  • terminate reentrant arrhythmias at AV node
  • protect ventricles from higher atrial rates in atrial flutter
36
Q

Class II side effects

A

Bronchospasm

Hypotension

37
Q

When should class II not be used

A

In partial AV block or acute heart failure

38
Q

Class III mechanism

A

Taken: oral or IV via central line

Half life: 3 months

Effects:

  • increases the refractory period and APD
  • decreased speed of AV conduction
  • decreases phase 0 and phase 4

Uses:

  • wide spectrum for most arrhythmias
  • especially VT

ECG:

  • longer PR
  • longer QRS
  • longer QT
  • decreased HR
39
Q

Side effects of class III

A 
Pulmonary fibrosis 
Hepatic injury 
Thyroid disease 
Increase LDL cholesterol 
Photosensitivity 
Optic neuritis when stopping medication
40
Q

Sotalol

A

Taken: Orally

ECG:

  • longer QT
  • Lower HR

Uses:
- supraventricular and ventricular tachycardia

Side effects:

  • pro arrhythmia
  • fatigue
  • insomnia
41
Q

Class IV mechanism

A

Verapamil- oral or IV
Diltiazem - oral

Effects:

  • slow conduction at AVN - terminates reentry circuit
  • increases refractory at AVN
  • slow HR as decreases phase 4 slope in SAN

ECG:

  • increase PR
  • Changes heart rate depending on blood pressure

Uses:

  • supraventricular tachycardia
  • re-entrant circuits at AVN
42
Q

Side effects of class IV

A
  • asystole if beta blocker also used with partial AVN block (only give if patient has pacemaker)
  • gastrointestinal problems and constipation

Caution with:

  • hypotension
  • sick sinus
  • decreased cardiac output
43
Q

Adenosine

A

Administration: rapid IV bolus
Half life: very short (seconds)

Mechanism:

  • natural nucleoside that binds to A1 receptors at the AVN, activating K+ currents in the AVN and SAN
  • decreased action potential duration
  • quicker hyperpolarisation
  • decreased HR
  • decreased Ca2+ - increased refractory period at AVN

Effects:
- slows conduction at AVN

Uses:

  • re-entrant supraventricular arrhythmias
  • Diagnosis of coronary artery disease
44
Q

Vernakalant

A

Administration: IV bolus for 10 mins

Mechanism: blocks atrial specific K+ channels

Effects:

  • slows atrial conduction
  • increased potency with higher heart rates

Uses: converts rodent onset AF into sinus rhythm

45
Q

Vernakalant side effects

A

Hypotension
AV block
Sneezing and taste disturbances

46
Q

Ivabradine

A

Administration : oral

Mechanism:
- blocks funny currents in sinus node (no peripheral effect)

Effects:
- slows SAN firing but doesn’t effect BP

Uses:

  • sinus tachycardia
  • reduces heart rate in heart failure and angina
47
Q

Side effects of ivabradine

A
  • flashing lights

- teratogenic

48
Q

Digoxin

A

Mechanism:

  • enhances vagal activity
  • increases K+ efflux and refractory period
  • decreases Ca2+
  • slows AV conduction and HR

Uses:
-reduces ventricularrate in AF and flutter

Contraindication
- renal failure as regally excreted

49
Q

Atropine

A

Mechanism - selective muscarinic antagonist

Effects: blocks vagal activity to speed up AV conduction and increase HR

Uses: treat vagal bradycardia

50
Q

AF drugs

A

Rate control:

  • bisoprolol
  • verapamil
  • diltiazem
  • digoxin

Rhythm control:

  • sotalol
  • flecainide with bisoprolol
  • amiodarone
51
Q

VT drugs

A
  • metoprolol/ bisoprolol
  • lignocaine/ mexilitine
  • amiodarone
52
Q

Wolf Parkinson White syndrome

A

Flecainide - nonstructural or ischaemic heart disease

Amiodarone

53
Q

Re- entrant narrow complex tachycardia drugs

A

Acute (IV)

  • adenosine
  • verapamil
  • flecainide

Chronic:

  • bisoprolol and verapamil
  • sotalol
  • flecainide and procainamide
  • amiodarone
54
Q

Ectopic beat drugs

A

First line - bisoprolol

  • flecainide
  • sotalol
  • amiodarone
55
Q

Sinus tachycardiandrugs

A

Ivabradine
Bisoprolol
Verapamil

CPT (23 decks)

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