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Pathology MD3001 > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

Why can electrical activity only pass via AV node?

A

Due to the AV rings as these are insulating materials

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2
Q

What are the different brasycardic dysrhythmias and what are they caused by?

A

Sinus Bradycardia - Drugs, Vagal activity, Hypothyroidism, Sinus node disease or electrolyte abnormalities.

AV block - Vagal activity, myocardial infarction or electrolyte abnormalities

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3
Q

Describe the different degrees of heart block

A

1st - Lengthening of PR interval,
2nd - Morbitz type 1 (progressive lengthening of PR until P wave blocked and then shorter PR interval again). Morbitz type 2 (Block after 2/3 conducted beats in regular pattern)
3rd - Complete AV dissociation

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4
Q

Describe the locations of the AV blocks

A

1st degree and 1nd degree Morbitz 1 - more associated with atria, from SA to AV node.
2nd degree morbitz 2 and 3rd degree - more ventricular, at AV node

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5
Q

Describe the treatments for bradycardia

A
  • Temporary or permanent pacemakers. However treatment is only needed if symptoms of syncope, prophylactic at time of operations or post Acute MI.
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6
Q

What are the two types of tachycardia

A
  • Narrow complex (<0.12)/ Supraventicular tachycardias

- Broad complex tachycardias (>0.12) (mainly ventricular)

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7
Q

Name examples of narrow complex/supraventricular tachycardias

A
  • Atrial tachycardias
  • Junctional Tachycardias
  • AV node re-entrant tachycardia (AVNRT)
  • Atrioventricular re-entrant tachycardia (AVRT)
  • Atrial flutter
  • Atrial fibrillation.
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8
Q

Name some examples of broad complex tachycardias

A
  • Ventricular Tachycardia (monomorphic and poly morphic VT)
  • Supraventricular tachycardia (SVT) with aberration (tachycardia with left or right bundle branch block)
  • SVT with pre-existing bundle branch block morphology on ECG
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9
Q

Explain the three basic mechanisms for tachycardia

A

1) Ectopic focus - Tissue that has a rapid pacemaker function.
2) Re-entry/circus movement
3) Fibrillation (Independent wavelets of activity)

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10
Q

Describe how circus re-entry may arise

A

As an electrical signal travels, it can come across an island of non conducting tissue. Here it splits into two pathways which have different electrophysiological properties which joins distally. One pathway is slow and has short refractory period and the other is fast and has a long refractory period.
Normally the fast signal travels along to the distal end of slow pathway and the signal meet they can not travel in either way due to both ends being refectory. When you have an ectopic beat then the fast pathway will have finished its refractory period so it travels along there and continues to travel along the circuit, this leads to tachycardia.

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11
Q

Describe the appearance of atrioventricular node re-entry tachycardia and the atrioventricular re-entry tachycardia on ECGs

A

Regular, narrow complex tachycardia but without P wave activity. Usually there is no history of cardiac disease

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12
Q

How are AVNRT and AVRT terminated?

A

With intravenous adenosine as the adenosine causes transient heart block.

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13
Q

What is the WOLFF PARKINSON-WHITE SYNDROME? what does it result in?

A

Pre-excitation of ventricles. Occurs because of AV bypass tract with non-decremental conducting properties. Resulting in shortened PR interval and slurred upstroke and widened QRS

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14
Q

What is the significance of Wolff Parkinsin-White syndrome?

A

It forms the basis for circus movement and AV Re-entry tachycardia.

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15
Q

Describe the possible responses to the adenosine test in narrow complex/ventricular tachycardias

A
  • No effect = Wrong diagnosis.
  • Transient Slowing = atrial flutter or atrial tachycardia. In presence of no P waves = AF.
  • Restoration of sinus rhythm = AVNRT or AVRT
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16
Q

Describe the ECG presentation and clinical presentation of atrial fibrillation

A

ECG - Irregular narrow complex tachycardia with no P waves.
Clinical - Fast ventricular response rate - SOB and hypotension.
Slow conduction - Dizziness and syncope.
Embolism of left atrial thrombus.

17
Q

What are some of the causes of atrial fibrilation?

A
  • Ischaemic heart disease,
  • Hypertensive heart disease,
  • Mitral valve disease,
  • Thyrotoxicosis,
  • Cardiomyopathy,
  • Alcohol,
  • Post bypass,
  • Myocarditis,
  • Accessory pathways,
  • Lone.
18
Q

Describe the management of atrial fibrillation?

A
  • Rate or Rhythm control, normally rate control unless person is symptomatic or acutely presents with clear precipitating cause.
  • Prevention of thrombo-embolism
19
Q

Describe the management of AF via rate or rhythm control

A

Rate control - Drugs to slow AV conduction (rate limiting CCBs, Beta blockers, sometimes digoxin) or AV node ablation and permanent pacemaker.

If not rate then rhythm control - Cardioversion, either electrical DC or chemical (Amiodarone) or Maintenance of sinus rhythm, via class 3 or class 1c drugs or via radiofrequency ablation.

20
Q

Describe the prevention of thrombo-embolism in management of atrial fibrillation?

A

High incidence of cerebrovascular accidents (CVA) in AF so need warfarin or NOACs as aspirin has show little to no beneficial effects. If patient has non-rheumatic AF then prescribing is risk based; if over 65yrs, hypertensive, has previous stroke or scores 2+ on the cha2ds2-vasc score.

21
Q

Describe the clinical significance of ventricular tachycardia

A

Very serious and can quickly degenerate into ventricular fibrillation and death. Often associated with previous LV damage

22
Q

Describe the ventricular tachycardia mechanisms

A
  • Acute LV damage (ischaemia and trauma)
  • Chronic LV damage (Re entry in a scar)
  • Abnormalities of the Na and K channels (channel myopathies), causes changes in intracellular K levels changes cellular action potential.
23
Q

Describe the management of acute VT

A 
If haemodynamically compromised - DC synchronised cardioversion. 
If haemodynamics are ok - IV amiodarone, IV lignocaine or IV class 1 agents.
24
Q

Describe the management of long term of VT

A

Management of underlying cause:

  • Active ischaemia in ischaemic heart disease
  • pulmonary regurgitation post fallot repair
  • HF.

Prevent reoccurrence:

  • Implanted cardioverter defibrillator (ICD),
  • Drugs (BB, class 1, amiodarone
  • Ablation
  • Anti-tachycardia pacemaker (ATP)
25
Q

Describe the management of ventricular fibrillation

A
  • Blow to chest (seldom),
  • DC cardioversion,
  • IV adrenaline and DC cardioversion,
  • Treatment of any acute underlying cause
  • ICD implantation
26
Q

What is Torsade de Pointes?

A

Polymorphic ventricular tachycardia

27
Q

Describe the mechanisms of torsade de pointes

A

Congenital - Ion channelopathy, brugada syndrome, catecholaminergic polymorphic VT, ARVC.

Acquired - Drugs that inhibit the inward rectifying K channel. Drugs that lengthen the QT interval or Slow AF with hypokalaemia.

28
Q

What is Long QT syndrome?

A

Inherited heart rhythm problem where the heart muscle takes longer than normal to recharge between beats. The T waves are very abnormal (BIG)

29
Q

What are some of the risks for drug infuced LQTS

A 
Culprit drugs - Antiarrhythmics, quinidine, sotalol and non antiarrhythmics.
Female
HF
LVH
Digoxin
30
Q

LQTS management?

A

Identifying risk, avoid precipitating events, betablockers, pacemaker or ICD.

Pathology MD3001 (20 decks)

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