SPR L14 Pathophysiology of Common Arrhythmias Flashcards Preview

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Flashcards in SPR L14 Pathophysiology of Common Arrhythmias Deck (22):
1

Pathophysiology of Common Arrhtymias 

What's covered 

(for general perusal)

  • Pathophysiology of arrhythmias
  • Principles of management of arrhythmias

2

What are the characterisitcs of normal cardiac electrical activity?

  • Automaticity
  • Specialised conduction pathways

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3

How can rhythm be assessed?

•Pulse (rate, rhythm)

•ECG waveforms

4

Describe the following on the ECG Waveform

  1. P
  2. PR Interval
  3. QRS
  4. T
  5. QT Interval

  1. Generation and spread of depolarization through atria
  2. Time taken for conduction of depolarization from SA node through atria and AV node, to ventricles
  3. QRS: Spread of depolarization through bundle of His and Purkinje system within ventricles
  4. ventricular repolarization
  5. Total time for depolarization and repolarization of ventricles

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5

General Causes of Arrthythmias

What do cardiac arrthymthmias result from?

  • Abnormal AP initiation
  • Abnormal AP conduction 

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6

Pathophysiology: Bradycardias

What are they defined as and what are the

extrinsic causes?

intrinsic causes?

< 60 beats per minute

Extrinsic causes (normal SA node)

  • Hypothermia
  • Hypothyroidism
  • Drugs, eg b-blockers
  • Neurally mediated
    • Increased vagal tone (athletes)
    • Carotid sinus syndrome
    • Vasovagal attacks

Intrinsic causes (abnormal SA node)

 

  • Ischaemia/infarction node
  • Degeneration/fibrosis node (sick sinus syndrome)

 

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7

Pathophysiology: bradycardias

  1. ​What is heart block?
  2. What is First degree A-V heart block? What is it characterised by?
  3. Second Degree?
  4. Third Degree?
  5. What is bundle branch block?

  1. disruption of conduction by any cause
  2. First-degree (prolonged PR interval: >0.22s)

  3. intermittent conduction

  4. (complete) AV block

    1. P wave dissociated from QRS (escape rhythm)

      Block proximal to bundle of His: QRS normal width and rate adequate (50-60 bpm)

      Block distal to bundle of His: QRS wide (>0.12s) and bradycardia marked (15-40 bpm)

  5. Prolonged QRS complex (>0.10s)

8

Define First Degree A-V Block

prolonged PR interval: >0.22s

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9

Define Second Degree A-V Block

intermittent conduction

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10

Define Third Degree A-V Block

  • P wave dissociated from QRS (escape rhythm)
    • Block proximal to bundle of His: QRS normal width and rate adequate (50-60 bpm)
    • Block distal to bundle of His: QRS wide (>0.12s) and bradycardia marked (15-40 bpm)

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11

Define Bundle Branch Block

Prolonged QRS complex (>0.10s)

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12

What are the Symptoms of Bradycardia?

Symptoms result from hypotension and reduced cerebral blood flow

  • Dizziness
  • Syncope
  • Stokes-Adams attacks (complete heart block)
  • BBB is usually asymptomatic

13

What are the principles of management of bradycardias?

  • Identify and treat extrinsic causes sinus bradycardia
  • Temporary or permanent pacemaker

 

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14

Pathogenesis: Tachycardias

What are they defined as?

How can they be caused?

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> 100 b.p.m.

  • Accelerated automaticity
    • Sinus tachycardia

      • Exercise

      • Postural orthostatic tachycardia

    • AV nodal rhythms

  • Triggered activity (‘after depolarizations’) 

  • Re-entry (‘circus’) movements

    • Fibre bundle splits and re-joins

    • Anterograde conduction in one limb  blocked

    • Retrograde conduction maintained

    • May reflect reduced conduction velocity or prolonged refractory period 

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15

Pathophysiology: Tachycardias

​SUPRAVENTRICULAR TACHYCARDIAS

  1. Where do these originate?
  2. When is the QRS Complex normal?
  3. Describe 
    1. Abnormal sinus tachycardia

    2. AV junctional tachycardias (paroxysmal SVTs)

    3. Atrial fibrillation

    4. Atrial Flutter

 

  1. in atria or AV junction

  2.  if ventricular conduction normal

  3. Describe

    1. Normal P waves

      Cause should be sought, eg anaemia, hyperthyroidism

    2. 140-240 bpm

      P waves may be absent or occur after QRS

      Causes palpitations, dizziness

      Valsalva manoeuvre (increased vagal tone)

    3. Causes include hypertension, IHD, Heart failure, thyrotoxicosis, rheumatic heart disease, alcohol

      Multiple re-entry circuits in atria

      High frequency atrial activity (300-600 p m)

      No co-ordinated atrial activity: no P waves (f waves)

      Tachycardia (120-180 BPM) with irregularly irregular pulse

    4. Similar causes to fibrillation

      Organised atrial activity (250-350 pm)

      Sawtooth F waves between QRS complexes

      Treatment similar to fibrillation

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16

Pathophysiology: Tachycardias

ATRIAL FIBRILLATION

  1. What are the causes of AF?
  2. Describe the pathophysiology of AF
  3. What are the consequences of AF?
  4. What are the principles of management of AF?

  1. Causes include hypertension, IHD, Heart failure, thyrotoxicosis, rheumatic heart disease, alcohol
  2. Multiple re-entry circuits in atria

High frequency atrial activity (300-600 p m)

No co-ordinated atrial activity: no P waves (f waves)

Tachycardia (120-180 BPM) with irregularly irregular pulse

3. 

  • Maybe asymptomatic (30% cases)
  • Effect on CO results from inadequate ventricular filling   (shortened diastole)
    • Reduced exercise tolerance
    • Deterioration of pre-existing heart failure
  • Relative stasis atrial blood: risk of thromboembolism

4. 

Reduce rate (AV nodal drugs)

  • Digoxin
  • Ca channel blockers
  • b adrenoceptor blockers

Re-establish sinus rhythm

  • Anti-arrhythmic drugs
  • DC cardioversion (synchronised to downslope QRS)

Anticoagulation

  • Warfarin

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17

What are the principles of management of atrial fibrillation?

Reduce rate (AV nodal drugs)

  • Digoxin
  • Ca channel blockers
  • b adrenoceptor blockers

Re-establish sinus rhythm

  • Anti-arrhythmic drugs
  • DC cardioversion (synchronised to downslope QRS)

Anticoagulation

  • Warfarin

18

Pathophysiology: Tachycardias

(still Supraventricular)

What is Atrial Flutter?

  • Organised atrial activity (250-350 pm)
  • Sawtooth F waves between QRS complexes
  • Similar causes and treatment to fibrillation

 

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19

Pathophysiology: Tachycardias

Ventricular tachyarrhythmias

  1. Where do these originate?
  2. Describe the following
    1. Ventricular Fibrillation (picture)
    2. Sustained Ventricular TachyC
    3. Non-Sustained Ventricular TachyC
    4. Ventricular Ectopics 

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  1. In ventricular tissue, Often life-threatening
  2. Describe
    1. Major cause: cardiac ischaemia/infarct

      No effective CO, pulseless (cardiac arrest)

      Requires CPR and electrical defibrillation

    2. (>30s) 

      Dizziness, syncope

      Pulse rate 120-220 bpm

      Abnormal, broad QRS complexes

      May lead to VF, cardiac arrest

      Treatment: Antiarrhythmic drugs (IV) and DC cardioversion

    3. >5 consecutive beats, <30s 

    4. Abnormal, broad QRS complexes (picture)

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20

Principles of management: tachyarrhythmias

Outline the main methods of management

Antiarrhythmic drugs

Radiofrequency catheter ablation

Implantable cardioverter-defibrillator (ICD)

21

Principles of Management: Tachyarrhythmias 

Give details of the following:

  1. Antiarrhythmic drugs (picture)
  2. Radiofrequency catheter ablation
  3. Implantable cardioverter-defibrillator (ICD)

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  1. Act on cardiac action potential

    Suppress excitability/slow conduction

  2. Identify and destroys site of origin of focal tachycardia eg major re-entrant pathway

  3. Identifies ventricular tachycardia or fibrillation

    Delivers synchronised pacing to cardiovert (VT)

     or shock to defibrillate (VF)

22

ECG changes in cardiac ischaemia

What are the classical changes?

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  • Abnormal Q waves
    • Initial downward deflection in ‘QRS’ lasting more than 40 ms in any lead except III and aVR
    • Usually indicates transmural infarct with tissue death (electrically inactive)
  • ST segment elevation (transmural or subepicardial injury)

  • ST depression (subendocardial injury)

  • Reflects changes in baseline due to injury currents

  • Depolarization of normal tissue brings pd to true zero

  • T wave inversion (usually transmural)

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