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CPT > L9 Arrhythmia > Flashcards

L9 Arrhythmia Flashcards

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
Micro reentry in MI
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
Class 1b drugs examples
Lidocaine - IV form | Mexiletine - oral form
27
Class 1c drugs examples
Flecainide | Propafenone
28
Beta blocker examples
Bisoprolol Metoprolol Propranolol
29
Class III examples
Amiodarone (highest efficacy) | Sotalol
30
Class IV calcium channel blockers
Verapamil | Diltiazem
31
Class 1b
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
Class 1c
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
Sid effects of class 1c
- pro arrhythmia - sudden death associated with chronic use and structural hearty disease - flutter (1:1 ventricular response) - CNS and gastrointestinal effects
34
When can fleconaide be used in structural heart disease patients
When the patient has an implantable cardiac defibrillator
35
Class II mechanism
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
Class II side effects
Bronchospasm | Hypotension
37
When should class II not be used
In partial AV block or acute heart failure
38
Class III mechanism
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
Side effects of class III
``` Pulmonary fibrosis Hepatic injury Thyroid disease Increase LDL cholesterol Photosensitivity Optic neuritis when stopping medication ```
40
Sotalol
Taken: Orally ECG: - longer QT - Lower HR Uses: - supraventricular and ventricular tachycardia Side effects: - pro arrhythmia - fatigue - insomnia
41
Class IV mechanism
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
Side effects of class IV
- 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
Adenosine
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
Vernakalant
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
Vernakalant side effects
Hypotension AV block Sneezing and taste disturbances
46
Ivabradine
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
Side effects of ivabradine
- flashing lights | - teratogenic
48
Digoxin
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
Atropine
Mechanism - selective muscarinic antagonist Effects: blocks vagal activity to speed up AV conduction and increase HR Uses: treat vagal bradycardia
50
AF drugs
Rate control: - bisoprolol - verapamil - diltiazem - digoxin Rhythm control: - sotalol - flecainide with bisoprolol - amiodarone
51
VT drugs
- metoprolol/ bisoprolol - lignocaine/ mexilitine - amiodarone
52
Wolf Parkinson White syndrome
Flecainide - nonstructural or ischaemic heart disease | Amiodarone
53
Re- entrant narrow complex tachycardia drugs
Acute (IV) - adenosine - verapamil - flecainide Chronic: - bisoprolol and verapamil - sotalol - flecainide and procainamide - amiodarone
54
Ectopic beat drugs
First line - bisoprolol - flecainide - sotalol - amiodarone
55
Sinus tachycardiandrugs
Ivabradine Bisoprolol Verapamil

CPT (23 decks)

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