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Semester 1 Year 2 > Pathophysiology of arrythmias > Flashcards

Pathophysiology of arrythmias Flashcards

1
Q

How are disturbances in cardiac rhythm diagnosed?

A

ECG

either bradycardia or tachycardias

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2
Q

Discuss the conducting tissue of the heart

A

Obv all cardiac cells form a functional syncytium via desmosomes, but beyond that points of note are:

The SA node (pacemaker)

AV ring (insulating material)

AV node (decremental - the more frequently the node is stimulated the slower it conducts)

His Purkinge tissues (fast conduction)

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3
Q

Have a look at electrolyte changes over an ECG, its kinda cool

A

Nerd

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4
Q

Discuss Bradycardias

A 
• Sinus Bradycardia
– Drugs
-• Beta Blockers, Diltazem
– Vagal activity
– Hypothyroidism
– Sinus Node disease
– Electrolyte abnormalities

• AV Block
– Vagal activity
– Myocardial infarction
– Electrolyte abnormalities

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5
Q

Discuss AV Block

A

• 1st Degree
– Lengthening of the PR interval

• 2nd Degree
– Mobitz Type 1 (Wenckebach block).
• Progressive lengthening of PR interval until P wave blocked and then PR short again
– Mobitz Type 2
• Block after 2 or 3 conducted beats in regular pattern

• 3rd Degree AV block
– Complete AV dissociation

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6
Q

What are the treatments for bradycardia

A

• Pacemakers
– Temporary
– Permanent

• Only if needed
– Symptoms of syncope dizziness
– Prophylactic at time of operations
– Post AMI

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7
Q

What are the types of tachycardias

A
  • Narrow Complex / Supraventricular Tachycardias

* Broad Complex Tachycardias

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8
Q

Discuss Narrow complex/supraventricular tachycardias

A 
– Atrial Tachycardias
– Junctional Tachycardias 
– AVNRT + AVRT
– Atrial Flutter
– Atrial Fibrillation
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9
Q

Discuss broad complex tachycardia

A

– Ventricular Tachycardia
• Monomorphic and polymorphic VT
• Fascicular (RBBB and LAD and not very wide)
• RVOT (LBBB and RAD)
– SVT with aberration (= acquired, rate- dependent bundle branch block)

– SVT with a pre-existing BBB morphology on
ECG

– SVT of antedromic tachycardia in WPW

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10
Q

What are the basic mechanisms of tachycardias

A
  • Ectopic Focus – i.e. tissue with rapid pacemaker function
  • Re-entry / circus movement
  • Fibrillation – independent wavelets of activity
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11
Q

Discuss tachycardias involving the AV node

A

• Narrow complex, usually no P waves, usually very fast, and no history of cardiac disease

• AVNRT = AV nodal re-entrant tachycardia
– Tachycardia where re-entry circuit is through juxtanodal material

• AVRT = AV re-entrant tachycardia
– Tachycardia where re-entry is through an accessory pathway
• Revealed accessory pathway means WPW 12 lead ECG
• Concealed accessory pathway means normal non- tachycardia 12 lead ECG (i.e. the accessory pathway only conducts in a retrograde manner)

• All are terminated by i.v. adenosine

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12
Q

Discuss Wolff-Parkinson-White syndrome

A

First of all, what a cool name, it is:

  • Pre-excitation (of the ventricles)
  • Anatomical atrio-ventricular bypass tract with non-decremental conducting properties

• Results in
– Shortened PR interval <0.12sec
– Slurred upstroke of QRS and widened QRS complex >0.12sec

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13
Q

What is the adenosine test in narrow complex / supraventricular tachycardias

A

Remember adenosine woman? Pretty sure this is that

  • i.v. bolus of adenosine (3mg, then 6 mg then 12mg)
  • Half life 4.5 secs
  • Causes transient and complete AV block

Adenosine will stop any tachycardia with re- entry over the AV node i.e. AVNRT and AVRT

• Responses:
– No effect. = Wrong diagnosis. Sinus Tachy in case of narrow complex or VT in case of broad complex
– Transient slowing with (=atrial flutter or atrial tachycardia) or without revealed P waves (= AF)
– Restoration of sinus rhythm AVNRT or AVRT

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14
Q

Discuss atrial fibrillation

A
  • Very common
  • Irregular narrow complex tachycardia with no P waves

• Symptoms
– Fast ventricular response rate – SOB, hypotension – Slow conduction – dizziness and syncope
– Embolism of left atrial thrombus (CVA)

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15
Q

What causes atrial fibrillation

A 
– Ischaemic Heart Disease
– Hypertensive heart disease 
– Mitral Valve disease
– Thyrotoxicosis
– Cardiomyopathy
– Alcohol
– Post bypass
– Myocarditis
– Accessory pathways
– Lone (no cause)
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16
Q

What are the mechanisms of atrial fibrillation

A

– Size of Left Atrium

  • Uncommon in children, much more common in large mammals
  • > 5 independent wavelets of activity
  • Foci of wavelet generation around the insertion of the pulmonary veins
17
Q

Discuss management of atrial fibrillation

A
  • Rate control or rhythm control ?
  • Prevention of thrombo-embolism (esp. CVA)

• Who gets which?
– Rate control unless
• Symptomatic with high ventricular response rates refractory to treatment
• Acute presentation with clear precipitating cause

– Rate control
• Drugs to slow AV conduction
– Diltiazem, Verapamil, Beta blockers, (Digoxin)
• AV node ablation and permanent pacemaker

– Rhythm control
• Cardioversion
– Electrical DC cardioversion
– Chemical – Flecainide, Propafanone, Amiodarone
• Maintainance of Sinus Rhythm – Class 3 Sotalol, Amiodarone
– Class 1c Flecainide
– Radio frequency/cryo ablation
» Pulmonary Vein ablation with or without atrial lines

• Prevention of thrombo-embolism (esp. CVA)
– High incidence of CVA (embolic stoke) in AF
• First noticed in mitral stenosis
– Warfarin/NOACs therapy became standard
• Non-rheumatic AF
– Less than MS but still very significant
– Warfarin/NOACs causes a 66-70% reduction in stroke risk attributable to AF
– Aspirin (300mg a day) has a weak/no beneficial effect

– Who gets Warfarin/NOACs in non-rheumatic AF? Risk based
• Appreciable risk of stoke other than AF – Age (>65yr)
– Hypertension
– Previous stroke – CHA2DS2-VASc

• No contraindiactions to anticoagulation
– Peptic ulcer disease, Contact sports, alcoholism etc.

18
Q

What atrial fibrillation pts should get anticoagulants

A

Those with a CHA2DS2-VASc score of 2 or more

19
Q

Discuss ventricular tachycardia

A

• Serious
Ventricular Tachycardia
– Often fast
– Can degenerate into VF (and death)
• Inherently Unstable rhythm
• Often provokes ischaemia as associated with CAD
• Usually associated with previous LV damage
– MI, hypertensive heart disease, cardiomyopathy, previous heart surgery etc

20
Q

How to tell if broad complex tachycardia is VT or SVT with aberration

A
  • Is the distinction important? - If fast and the patient unwell the treatment is the same DC cardioversion
  • Width of QRS – >140msec VT
  • If RBBB: RSR’, R’>R favours SVT

• AV relationship
– Independent P waves, fusion or capture beats diagnose VT. Cannon waves in JVP

• NB these are not invariable as there is quite often 1:1 retrograde conduction

• Irregular
– Nearly always AF

• Is there a history of LV damage? – If so statistically a broad complex tachycardia will be VT whatever the ECG looks like

21
Q

Discuss ventricular tachycardia mechanisms

A

• AcuteLVdamage
– Ischaemia, trauma
• Specific mechanisms that interfere with cell membrane electrophysiology

• Chronic LV damage
– (micro) Re-entry around fibrotic areas of non- conduction

• Abnormalities of the Na and K channels (Ion channelopathies) = Long QT interval syndrome
– Changes in intracellular K altering the cellular action potential
• Usually polymorphic

22
Q

Discuss management of acute VT

A

• If haemodynamically compromised: – DC synchronised cardioversion

• Haemodynamics OK
– i.v.Amiodarone
– i.v. lignocaine (only to works in acute ischaemia)
– i.v.Class 1 agents (procainamide)

23
Q

Discuss management of VT long term

A

• Management of the cause underlying it:
– Active ischaemia in IHD
– Pulmonary regurgitation post Fallot repair – Heart Failure
• Prevention of recurrence
– Implanted cardioverter defibrillator (ICD)
– Drugs Beta blockers, Class 1 agents (?prognosis),, Amiodarone
– Ablation
– Anti-tachycardia pacemaker (ATP)

24
Q

Discuss ventricular fibrillation

A
  • Invariably fatal
  • ECG chaotic often fine movements
  • No detectable cardiac output
  • Often (but not always) preceded by VT
  • Blow to the chest
  • DC cardioversion
  • IV adrenaline + DC cardioversion
  • Treatment of any acute underlying cause
  • ICD implanation
25
Q

What is Torsade de Pointes - polymorphic ventricular tachycardia

A
  • Tachycardia that can degenerate and cause death

* Cause of sudden death with normal heart at autopsy

26
Q

What are the mechanisms of Torsade de Pointes

A

• Congenital
– Ion channelopathy, Brugarda, Catacholaminergic Polymorphic VT, ARVC
• Plus a provocation – adrenalin, facial immersion, exercise, hypokalaemia

• Acquired
– Drugs that inhibit inward rectifying K channel
• Erythromycin, antihistamines, antifungal (..conazoles), some anti-malarials and some anti-psychotics
– Drugs that lengthen QT inetrval
• Antiarrhythmics, Amiodarone, sotalol
– Slow AF with hypokalaemia and long-slow coupling interval

27
Q

Discuss long QT syndrome diagnosis

A
  • 1in5,000
  • Family history of sudden death
  • Death is associated with adrenergic setting
  • <1 point low prob.
  • 2-3 intermediate
  • 4 or more high
28
Q

What is brugada syndrome?

A

a genetic disorder in which the electrical activity within the heart is abnormal.[2] It increases the risk of abnormal heart rhythms and sudden cardiac death due to serious abnormal heart rhythms such as ventricular fibrillation or polymorphic ventricular tachycardia.

29
Q

Discuss drug-induced Torsad

A

• Many drugs which may be linked by effects on inward rectifying Potassium channel
• Pause-dependent initiation
Its Torsade de Pointes

30
Q

What are some risk factors for drug-induced LQTS

A 
• Female gender 66%
• Heart Failure 25%
• LVH 14%
• Hypokalaemia 18%
• Hypomagnesaemia 9%
• Digoxin 29%
• Ca2+ Chan. Blockers 14%
• Beta blockers 11%
• Culprit drugs
– Antiarrhythmics 77% 
– Quinidine 32% 
– Sotalol 17% 
– Non-antiarrhythmics 23%
31
Q

LQT Syndrome Management

A
  • Identify risk
  • Avoid precipitating events
  • Betablockers
  • Pacemaker
  • ICD
32
Q

Conclusions

A
  • The 12 lead ECG and Holter testing allow the precise diagnosis of disturbance of the cardiac rhythm
  • Cardiac rhythm disturbances are potentially fatal and require specialist treatment
  • Both drugs and device therapy are involved in the management of cardiac rhythm disturbance

Semester 1 Year 2 (69 decks)

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