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MD3001 > Pathophysiology of Arrhythmias > Flashcards

Pathophysiology of Arrhythmias Flashcards

1
Q

What are the main types of arrhythmias?

A

– Bradycardias

– Tachycardias

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2
Q

How are disturbances of the cardiac rhythm diagnosed ?

A

With an ECG

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3
Q

Define decremental conduction. Where is it found ?

A

In AV node, the more frequently the node is stimulated the slower it conducts. Prevents rapid conduction to the ventricle in cases of rapid atrial rhythms, such as atrial fibrillation or atrial flutter.

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4
Q

Define fast conduction. Where is it found ?

A

In His Purkinje system, conduct faster and faster until it stops conducting, when refractory.

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5
Q

Describe the phases of a typical cardiomyocyte AP. Relate this to the AP of a pacemaker cell.

A 
Phase 0 = rapid depolarisation
Phase 1 = partial repolarisation
Phase 2 = plateau 
Phase 3 = repolarisation
Phase 4 = pacemaker potential

Pacemaker cells do not have phases 1 or 2.

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6
Q

What are the main kinds of bradycardias, where classified by location.

A

Sinus bradycardias and AV blocks (latter occurs in or below AV node)

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7
Q

What are the causes of sinus bradycardia ?

A 
SINUS BRADYCARDIA ALWAYS A SECONDARY EVENT, TO: 
– Drugs (e.g. Beta Blockers, Diltazem)
– Vagal activity
– Hypothyroidism
– Sinus Node disease
– Electrolyte abnormalities
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8
Q

What are the causes of AV block bradycardia ?

A

– Vagal activity
– Myocardial infarction
– Electrolyte abnormalities
– Degenerative diseases

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9
Q

What are the main kinds of AV blocks ? What is this classification based on?

A

1st, 2nd and 3rd degree AV blocks.

By ECG abnormality

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10
Q

Describe the main feature of 1st degree AV block.

A

– Lengthening of the PR interval

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11
Q

Describe the main feature of 2nd degree AV block.

A

– 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

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12
Q

Describe the main feature of 3rd degree AV block.

A

– Complete AV dissociation (atrial activation (usually from the sinus node) is independent from ventricular activation (originating from the AV junction, His-Purkinje system, or ventricles))

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13
Q

What are the main treatments for bradycardia ?

A

• Pacemakers
– Temporary
– Permanent

• Only if needed, treatment for:
– Symptoms of syncope dizziness
– Prophylactic at time of operations
– Post AMI

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14
Q

What are the main types of tachycardia ? What is this classification based ?

A

Based on ECG

  • Narrow Complex / Supraventricular Tachycardias (whatever is causing it is above AV node and sending it below AV node)
  • Broad Complex Tachycardias (origin is below AV node and therefore arising from ventricle)
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15
Q

What is the main danger with broad complex tachycardias ?

A

Broad complex tachycardias are intrinsically unstable, can move into VF and to death.

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16
Q

Are all broad complex tachycardias VTs ?

A

No, not all broad complex tachycardias are VT

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17
Q

What are the main types of narrow complex / supraventricular tachycardias ?

A

– Atrial Tachycardias (Focus in the atrium)
– Junctional Tachycardias (Arise at junction of the heart)
– AVNRT + AVRT (Involve the AV node intrinsically or AV node and accessory pathway)
– Atrial Flutter (narrow and regular)
– Atrial Fibrillation (narrow but irregular. Could still be AF is broad and irregular)

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18
Q

What are the main types of broad complex tachycardia ?

A

– Ventricular Tachycardia
• Monomorphic (every complex is the same) and polymorphic (complexes are different) VT

– SVT (supraventricular tachycardia) with aberration (= acquired, rate- dependent bundle branch block) (e.g. AVNRT + AVRT ???)

– SVT with a pre-existing BBB morphology on ECG (e.g. SVT of antedromic tachycardia in WPW)

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19
Q

Explain how an SVT with aberration occurs.

A

QRS complex looks narrow but when driven at higher rate, gets rate dependent BBB, so complex widens.

An SVT that comes on as ventricular tachycardia and induces a rate dependent BBB will be broad, this is SVT with aberration.

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20
Q

What are the main basic mechanisms of tachycardia ?

A
  • Ectopic Focus – i.e. tissue with rapid pacemaker function
  • Re-entry / circus movement
  • Fibrillation – independent wavelets of activity
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21
Q

Explain the mechanism of re-entry/circus movement.

A

Following myocardial infarction, dead zones of myocardium cannot conduct electrical impulses. However, because of the syncytial nature of the myocardium, electrical impulses simply flow around the dead zone and activate the remaining healthy myocardium. However, during conditions of ischemia and ischemic injury, ischemic portions of the myocardium will allow action potentials to proceed through them in one direction but not in the opposite direction. This is called unidirectional blockade. If action potentials are able to leak through this damaged area and emerge in the healthy myocardium after that area is past its refractory period, this “reentry” action potential will reactivate the healthy myocardium, sending another action potential generation through the injured tissue path. This process will then repeat again and again in an endless circle. This condition is called a circus rhythm and, as impulses generated from this circus cycle radiate outward through the syncytium, they activate the heart as a whole, at the rate set by the circus rhythm. Such circuits thus become secondary pacemakers. They may involve a few myocardial cells or large portions of the myocardium and often end up pacing the heart at an abnormally high rate

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22
Q

Describe the ECG appearance of AVNRT or AVRT.

A

Regular, narrow complex tachycardia without P waves activity

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23
Q

What are the tachycardias which involve the AV node ?

A

AVNRT and AVRT

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24
Q

What is usually the cardiac history of patients with AVNRT and AVRT ?

A

No history of cardiac disease

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25
Q

Define AVNRT.

A

AVNRT = AV nodal re-entrant tachycardia

– Tachycardia where re-entry circuit is through juxtanodal material

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26
Q

Define AVRT.

A

• AVRT = AV re-entrant tachycardia
– Tachycardia where re-entry is through an accessory pathway
• Revealed accessory pathway means Wolff Parkinson White (if conduct over them in sinus rhythm)
• Concealed accessory pathway means normal non- tachycardia (i.e. the accessory pathway only conducts in a retrograde manner)

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27
Q

What is meant by accessory pathway through which re-entry occurs in AVRT ?

A

His Purkinje material that has breached the AV ring somewhere other than the AV node

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28
Q

Distinguish between revealed and concealed accessory pathway.

A

The accessory pathway through which re-entry occurs in AVRT may either by revealed or concealed.
• Revealed accessory pathway means WPW (if conduct over them in sinus rhythm)
• Concealed accessory pathway means normal non- tachycardia (i.e. the accessory pathway only conducts in a retrograde manner)

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29
Q

How are AVRT and AVNRT terminated ?

A

Using IV adenosine

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30
Q

Define Wolf Parkinson White Syndrome.

A
  • Pre-excitation (of the ventricles)

* Anatomical atrio-ventricular bypass tract with non-decremental conducting properties

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31
Q

What are the ECG findings in WPW Syndrome ?

A

– Shortened PR interval <0.12sec

– Slurred upstroke of QRS and widened QRS complex >0.12sec

32
Q

Is WPW narrow or broad complex ?

A

Narrow complex

33
Q

Define antedromic tachycardia, in WPW.

A

Much less common AVRT in which the circuit is reversed: “antegrade conduction occurs exclusively via the accessory connection and results in a “maximally preexcited” QRS”

34
Q

Given that antedromic tachycardia is the less common form of AVT, what is the more common form of it ?

A

Orthodromic AVRT, in which “anterograde conduction occurs via the AV node with retrograde conduction occurring via the accessory pathway”

35
Q

When is the adenosine test used ?

A

In Narrow Complex / Supraventricular Tachycardias

36
Q

What does the adenosine test consist of ?

A

• i.v. bolus of adenosine (3mg, then 6 mg then 12mg)
• Half life 4.5 secs
• Causes transient and complete AV block
(will stop any tachycardia with re- entry over the AV node i.e. AVNRT and AVRT)
• Observe the response

37
Q

What are the possible responses which can be observed as a result of the adenosine test ? What kind of abnormality does each response point to ?

A

– 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

38
Q

Describe the ECG appearance in AF.

A

Irregular narrow complex tachycardia with no P waves

39
Q

What are the symptoms of AF ?

A

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

40
Q

What are possible causes of AF ?

A 
– Ischaemic Heart Disease
– Hypertensive heart disease 
– Mitral Valve disease
– Thyrotoxicosis
– Cardiomyopathy
– Alcohol
– Post bypass
– Myocarditis
– Accessory pathways
– Lone (no cause)
41
Q

What is the mechanism for AF (cause) ?

A

– Size of Left Atrium (dilated)
• >5 independent wavelets of activity
• Foci of wavelet generation around the insertion of the pulmonary veins

42
Q

Does AF affect any populations more than others ?

A

• Uncommon in children, much more common in large mammals

43
Q

Describe the management objectives of AF.

A

1) Rate Control or Rhythm Control
– Rate control unless
• Symptomatic with high ventricular response rates refractory to treatment
• Acute presentation with clear precipitating cause

2) Prevention of thrombo-embolism (esp. CVA)

44
Q

Identify the specific treatments for rate control in AF.

A

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

45
Q

Identify the specific treatments for rhythm control in AF.

A

• Cardioversion
– Electrical DC cardioversion
– Chemical (e.g. Flecainide, Propafanone, Amiodarone)

• Maintainance of Sinus Rhythm
– Class 3 Sotalol, Amiodarone
– Class 1c Flecainide
– Radiofrequency/cryo ablation (e.g. pulmonary vein ablation with or without atrial lines)

46
Q

Define cardioversion.

A

process of restoring the heart’s normal rhythm by applying a controlled electric shock to the exterior of the chest.

47
Q

Identify the specific treatments for prevention of thrombo-embolism.

A

– Warfarin/NOACs (novel oral anti-coagulants), both reduce stroke risk attributable to AF

48
Q

Why do we want to prescribe treatments of the prevention of thrombo-embolisms in AF ?

A

Because there is a high incidence of CVA (embolic stoke) in AF

49
Q

What are the main causes of stroke/thromboembolism attributable to AF ?

A

Non-rheumatic AF (less common)

Mitral stenosis

50
Q

Why do we not given aspirin as a treatment to prevent thromboembolisms in AF ?

A

Aspirin (300mg a day) has a weak/no beneficial effect

51
Q

How do we decide who gets Warfarin/NOACs in non-rheumatic AF?

A

Risk based: risk of stroke vs risk of anticoagulation

  • Risk of stroke (other than AF) based on age, hypertension, previous stroke
  • Contraindications to anticoagulations (risks include peptic ulcer disease, contact sports, alcoholism)
52
Q

What is CHA2DS2-VASc ?

A

Tool to measure risk of stroke (in order to decide if the person gets warfarin/NOACs in rheumatic AF to prevent thromboembolisms.

53
Q

How may we distinguish between VT and SVT with aberration ?

A

Adenosine test (VT gets no response)

54
Q

Describe the seriousness/progression in time of VT.

A
  • Serious (can degenerate into VF and death + often provokes ischaemia as associated with coronary artery disease)
  • Often fast
55
Q

Why are VTs so serious/can degenerated into VF and death ?

A

Because they have an intrinsically unstable rhythm.

56
Q

What is the ECG appearance of a VT ?

A

Broad complex, no p waves associated with QRS complex

57
Q

What is usually the cardiac history of patients with VT ?

A

• Usually associated with previous LV damage

– MI, hypertensive heart disease, cardiomyopathy, previous heart surgery etc.

58
Q

Distinguish between monomorphic and polymorphic VTs wrt ECG.

A

Monomorphic: usually regular
Polymorphic: irregular (Torsades de Pointes)

59
Q

What questions must we ask when trying to see wether a 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
  • Is there a history of LV damage? – If so statistically a broad complex tachycardia will be VT whatever the ECG looks like

• What is the AV relationship ?
-Independent P waves, fusion or capture beats diagnose VT. Cannon waves in jugular vein pulse also diagnose VT.

60
Q

What is the mechanism for VT (cause) ?

A

1) ACUTE LV DAMAGE
– Ischaemia, trauma
• Specific mechanisms that interfere with cell membrane electrophysiology

2) CHRONIC LV DAMAGE
– (micro) Re-entry around fibrotic areas of non-conduction

3) ABNORMALITIES OF NA AND K CHANNELS (ION CHANNELOPATHIES) = LONG QT INTERVAL SYNDROME
– Changes in intracellular K altering the cellular action potential
• Usually polymorphic VTs (Torsades de Pointes)

61
Q

Describe the management of VT in the short (acute) term.

A

1) ACUTE
• If haemodynamically compromised:
– DC synchronised cardioversion

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

62
Q

Describe the management of VT in the long term.

A

• Management of the cause underlying it, treatment for:
– Active ischaemia in IHD
– Pulmonary regurgitation post Fallot repair – Heart Failure

• Prevention of recurrence
– Implanted cardioverter defibrillator (ICD)
– Drugs Beta blockers, Class 1 agents, Amiodarone
– Ablation
– Anti-tachycardia pacemaker (ATP)

63
Q

What are the main general features of VF ?

A
  • Invariably fatal
  • No detectable cardiac output
  • Often (but not always) preceded by VT
64
Q

What are the ECG features of VF ?

A

Chaotic irregular deflections of varying amplitude

65
Q

What is VF management ? (acutely, and in the long term)

A

ACUTELY:

  • Defibrillation
  • DC cardioversion
  • IV adrenaline + DC cardioversion
  • Treatment of any acute underlying cause

IN THE LONG TERM:
-Implantable cardioverter-defibrillator (ICD) implantation (if patient survives)

66
Q

What is the most likely cause of sudden death with normal heart at autopsy ?

A

Polymorphic Ventricular Tachycardia

67
Q

What are the mechanisms for Torsades de Pointes (causes) ?

A

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

2) ACQUIRED

– Drugs that inhibit inward rectifying K channel
• Erythromycin, antihistamines, antifungal (conazoles), some anti-malarials and some anti-psychotics

– Drugs that lengthen QT interval
• Antiarrhythmics (Amiodarone, sotalol)

– Slow AF with hypokalaemia and long-slow coupling interval

68
Q

What is the distinctive feature of ion channelopathies ?

A

Long QT

69
Q

What is another name for ion channelopathies ?

A

Long QT Interval Syndrome

70
Q

Which phases of the AP change in a long QT interval syndrome ?

A

Phases 2 and 3 (determined by activity in sodium and potassium channels which is where mutations happen)

71
Q

Define Brugada Syndrome.

A

A type of channelopathy in which people with no known heart problems or defects suffer sudden cardiac death or aborted sudden cardiac death. Characterised by Right bundle branch block, with persistent ST-segment elevation.
One of the congenital causes of Torsades de Pointes.

72
Q

What kinds of drugs can induce Torsades ?

A

– Drugs that inhibit inward rectifying K channel (e.g. Erythromycin, antihistamines)
– Drugs that lengthen QT interval (e.g. Antiarrhythmics)

73
Q

Identify some risk factors for drug induced long QT syndrome (ion channelopathies).

A
  • Female gender
  • Heart Failure
  • LVH
  • Hypokalaemia
  • Hypomagnesaemia
  • Digoxin
  • Ca2+ Chan. Blockers
  • Beta blockers
  • Culprit drugs
74
Q

Describe Long QT Syndrome Management.

A
  • Identify risk
  • Avoid precipitating events
  • Beta blockers
  • Pacemaker
  • Implantable cardioverter defibrillator (ICD)
75
Q

Define sudden cardiac death.

A

Unexpected death due to heart problems, which occurs within one hour from the start of any cardiac-related symptoms

76
Q

What are the best tests to diagnose disturbance of the cardiac rhythm ?

A

12 lead ECG

Holter testing

77
Q

Define Holter monitoring.

A

a technique for long-term, continuous usually ambulatory, recording of ECGsignals on magnetic tape for scanning and selection of significant but fleeting changes that might otherwise escape notice.

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