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Cardiovascular > Arrhythmias 1 + 2 > Flashcards

Arrhythmias 1 + 2 Flashcards

1
Q

What is an arrhythmia? What are arrhythmias names according to? (2) Examples? (2)

A
  • Arrhythmia - no rhythm
  • Anatomical site, mechanism
  • Supraventricular (SVT), Ventricular
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2
Q

What is a supraventricular arrhythmia? Ventricular?

A
  • Origin is above the ventricle e.g. SAN, atrial muscle, AV node or HIS
  • Ventricular muscle or fascicles of the conducting system
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3
Q

Types of supraventricular arrhythmias? (2) Examples?

A
  • Supraventicular tachycardia e.g. AF, atrial flutter, ectopic atrial tachycardia
  • Bradycardia e.g. sinus bradycardia, sinus pauses
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4
Q

Types of ventricular arrhythmias? (4)

A
  • Ventricular ectopics or Premature Ventricular Complexes (PVC)
  • Ventricular Tachycardia
  • Ventricular Fibrillation
  • Asystole
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5
Q

Types of AV node arrhythmia? (3)

A
  • AVN re-entry tachycardia
  • AV reciprocating or AV Reentrant tachycardia
  • AV block : 1st degree, 2nd degree, 3rd degree
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6
Q

Clinical causes of arrhythmias? (6)

A
  • Abnormal anatomy (LVH, accessory pathways, congenial HD)
  • Autonomic NS (sympathetic stimulation, increased vagal tone)
  • Metabolic (hypoxia, ischaemia, electrolyte imbalances)
  • Inflammation (viral myocarditis)
  • Drugs (electrophysiologic effects, ANS)
  • Genetic (congenital long QT syndrome)
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7
Q

Electrophysiological mechanisms of arrhythmia? (2)

A
  • Ectopic beats

* Re-entry

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8
Q

What are ectopic beats? Examples? (2)

A

Beats or rhythms that originate in places other than the SA node

  • Altered automaticity e.g. ischaemia, catecholamines
  • Triggered activity, e.g. digoxin, long QT syndrome
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9
Q

What is re-entry? Example?

A

Requires more than one conduction pathway, with different speed of conduction (depolarization) and recovery of excitability (refractoriness)
* accessory pathway tachycardia (Wolf Parkinson White syndrome), previous myocardial infarction, congenital heart disease

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10
Q

Mechanisms of tachycardia? (2) Is tachycardia dangerous?

A
  • Ectopic focus may cause single beats or sustained run of beats, that if faster than sinus rhythm, take over the intrinsic rhythm
  • Re-entry: triggered by an ectopic beat, resulting in a self perpetuating circuit

May or may not be dangerous depending on how CO is affected

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11
Q

What is altered automaticity? How does altered automaticity change heart rate? (3)

A

Cells outside of SA node exhibit spontaneous electrical activity

  • Change threshold
  • Change resting membrane potential
  • Changing phase 4 (pacemaker potential) slope
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12
Q

How does abnormal physiology and pathology cause arrhythmia? (2) Causes of this? (5 + 2)

A

Increases phase 4 slope causing increase in heart rate

  • Hyperthermia
  • Hypoxia
  • Hypercapnia
  • Cardiac dilation
  • Hypokalaemia

Decreases phase 4 slope causing slowed conduction (bradycardia, heart block)

  • Hypothermia
  • Hyperkalaemia
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13
Q

What is triggered acivity?

A

In phase 3 (repolarisation), a small depolarisation called an AFTERDEPOLARISATION may occur, may reach depolarisation threshold and lead to sustained train of depolarisations called TRIGGERED ACTIVITY

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14
Q

Examples of causes of triggered activity? (3)

A
  • Digoxin toxicity,
  • Torsades de Pointes in long QT syndrome
  • hypokalaemia
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15
Q

Do afterdepolarisations always lead to sustained train of depolarisations?

A

No, normally don’t come to anything

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16
Q

What can lead to re-entry? (2) examples?

A
  • Structural abnormalities e.g. accessory pathways, scar from MI, congenital HD
  • Functional abnormalities e.g. ischaemia, drugs
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17
Q

Does scar itself conduct electricity in re-entry circuits?

A

No, scar is electrically inert but splits heart into different electrical pathways

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18
Q

Explain the normal action potential conduction down purkinje fibre to ventricular muscle (4)

A
  • Conduction travels down purkinje fibres into (for simplicity) 2 pathways
  • Conduction speed is the same down both pathways
  • Conduction then meets in the middle and ventricular muscle contracts
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19
Q

Explain how ischaemia causes re-entry arrhythmia (6)

A
  • Ischaemia slows down conduction in one of the pathways
  • Currents will not meet in the middle to cause a single contraction
  • Faster current will cause muscle to contract
  • Slower current will cause an extra beat
  • Current can then travel backwards and re-enter pathway causing re-entrant current and TACHYCARDIA
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20
Q

Symptoms of arrhythmias? (7)

A
  • Palpitations, ”pounding heart”
  • Shortness of breath
  • Dizziness
  • Loss of consciousness; ”Syncope”
  • Faintness: “presyncope”
  • Sudden cardiac death
  • Angina, heart failure
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21
Q

Investigations for arrhythmias? (7)

A
  • 12 lead ECG
  • CXR
  • Echocardiogram
  • Stress ECG
  • 24 hour ECG Holter monitoring
  • Event recorder: (capture the arrhythmia)
  • Electrophysiological (EP) study
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22
Q

What is ECG used for in arrhythmia?

A
  • To assess rhythm
  • Look for signs of revious MI (Q waves)
  • Pre-excitation due to accessory pathway (Wolf Parkinson White syndrome)
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23
Q

What is an accessory pathway? What would indicate pre-excitation on ECG? What can it lead to? Why?

A
  • Extra pathway that crosses atria to ventricle outside of fibrous ring
  • Delta wave (reflects ventricle being depolarised early)
  • Tachycardia
  • Accessory pathway does not pass through AV node so current not slowed down
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24
Q

Purpose of exercise ECG? (2)

A
  • To assess for ischaemia

* Exercise induced arrhythmia

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25
Q

Purpose of 24hr Holter ECG? (2)

A
  • To assess for paroxysmal arrhythmia

* To link symptoms to underlying heart rhythm

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26
Q

Purpose of echocardiography? Examples? (3)

A

To assess for structural heart disease

e. g.
* enlarged atria in AF
* LV dilatation
* Previous MI scar, aneurysm

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27
Q

Purpose of electrophysiological study? (2)

A
  • Trigger the clinical arrhythmia and study its mechanism/pathways
  • Opportunity to treat the arrhythmia by delivering radiofrequency ablation to extra pathway
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28
Q

What is normal sinus arrhythmia? Is it something to be worried about?

A
  • Variation in HR due to reflex change sin vagal tone during respiration i.e. inspiration reduces vagal tone and increases heart rate
  • No, property seen in healthy people
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29
Q

What is sinus bradycardia? Causes? (3) Treatment? (2)

A
  • <60 bpm

Causes

  • Physiological e.g. athlete
  • Drugs (b-bocker)
  • Ischaemia - common in inferior STEMIs

Treatment

  • Atropine if acute e.g. acute MI
  • Pacemaker if haemodynamic compromise e.g. hypotension, CHF, angina, collapse
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30
Q

What is atropine?

A

Anti-vagal which will speed up HR

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31
Q

What is sinus tachycardia? Causes? (2) Treatment? (2)

A
  • > 100 bpm

Causes

  • Physiological e.g. anxiety, fever, hypotension, anaemia
  • Inappropriate e.g. drugs, caffeine

Treatment

  • Treat underlying cause
  • B-blcokers
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32
Q

Symptoms of atrial ectopic beats? (2) Treatment? (2)

A
  • Asymptomatic or palpitations
  • Generally no treatment but b-blockers may help if symptomatic
  • Avoid stimulants e.g. caffeine, cigarettes
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33
Q

Most common cardiovascular rhythm disturbance in paediatrics? Signs on ECG? (3)

A
  • SVT

ECG

  • Tachycardia - almost 300 bpm
  • Non-sinus tachycardia because no P waves present
  • Narrow QRS complex
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34
Q

Causes of regular supraventricular tachycardia? (3)

A
  • AV nodal re-entrant tachycardia (AVNRT)
  • AV reciprocating tachycardia/AV reentrant tachycardia (via an accessory pathway) (AVRT)
  • Ectopic atrial tachycardia (EAT)
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35
Q

What does AVNRT and AVRT use? What is AVRNT? AVRT?

A

AV node

  • AVRNT - circuit within AVN (micro-reentry)
  • AVRT - circuit using AV node and accessory pathway (macro-reentry)
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36
Q

What are types of accessory pathway tachycardia? (3) Features on ECG?

A
  • Pre-excitation - short PR interval
  • Orthodromic AVRT (antegrade conduction through AV node) - normal QRS duration, no delta wave, retrograde P wave AFTER QRS
  • Antidromic AVRT (retrograde conduction through AV node) - wide QRS, delta wave, no P waves (if P wave visible, it is retrograde and occurs just before QRS)
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37
Q

What does a wider QRS indicate?

A

Ventricular conduction slower

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38
Q

What is ectopic atrial tachycardia?

A

Automaticity - tissues other than SA node exhibit spontaneous electrical activity

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39
Q

Acute management of supraventricular tachycardia? (2)

Chronic management? (4)

A

Acute

  • Increase vagal tone e.g. valsalva, carotid massage
  • Slow conduction in AVN e.g. IV adenosine, verapamil

Chronic

  • Avoid stimulants
  • Electrophysiologic study and radiofrequency ablation (first line in young, symptomatic patients) – surgery not given in elderly patients so drugs used instead
  • Beta blockers
  • Antiarrhythmic drugs
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40
Q

What is Radiofrequency Catheter Ablation ?

RFCA) Targets? (2

A

Selective cautery of cardiac tissue to prevent tachycardia
Targets include:
* automatic focus
* part of a re-entry circuit

41
Q

Explain the procedure of electrophysiologic study and RFCA? (3)

A
  • ECG catheters placed in heart via femoral veins
  • Intracardiac ECG recorded during sinus rhythm, tachycardia and pacing manoevers to find location + mechanism of tachycardia
  • Catheter placed over focus/pathway and tip heated to 55-65*C
42
Q

Causes of AVN conduction disease (Heart Block)? (8)

A
  • Ageing process
  • Acute myocardial infarction
  • Myocarditis
  • Infiltrative disease e.g. amyloid
  • Drugs e.g. B-blockers, calcium channel blockers, Digoxin
  • Calcific aortic valve disease
  • Post-aortic valve surgery
  • Genetic : Lenegre’s disease, myotonic dystrophy
43
Q

What is 1st degree A-V (heart) block? ECG sign? Treatment? (3)

A
  • Not really a block - conduction following each P wave takes longer
  • PR interval longer than normal (>0.2 sec i.e. big square)

Treatment

  • No treatment
  • Rule out other pathology
  • Arrange follow-up as more advanced block may develop over time
44
Q

What is 2nd degree A-V block? Types? (2)

A

Intermittent block at the AVN (dropped beats)

  • Mobitz I
  • Mobitz II
45
Q

What is Mobitz I? (2)

A
  • Progressive lengthening in PR interval eventually resulting in dropped beat
  • Usually vagal in origin
46
Q

What is Mobitz II? (2)

Treatment?

A
  • Pathological - may progress to complete heart block (3rd degree)
  • Usually 2:1 or 3:1 (2 P waves for every QRS)
  • Treatment - permanent pacemaker
47
Q

Difference between 3rd degree (complete heart block) and 2nd degree A-V block?

A
  • In 2nd degree, only some APs fail to get through AV node - in 3rd degree, NO APs from atria get through AV node
48
Q

What are the effects of 3rd degree A-V block? (2)
ECG sign?
Treatment?

A
  • Heart either stops (asystole) or enters “escape rhythm” that allows CO and maintains survival
  • Broad QRS - as conduction takes time spreading from gap junction to gap junction
  • Ventricular pacemaker!!
49
Q

What are pacemakers? Where are they positioned?

A
  • Detects abnormal rhythm and delivers shock to return to sinus rhythm
  • RA and RV
50
Q

Types of pacemakers? (2)

A

Single chamber
* paces RA or RV only

Dual chamber

  • Maintains A-V synchrony
  • Used for AVN disease
51
Q

Examples of ventricular arrhythmias? (4)

A
  • Ventricular ectopic or Premature Ventricular Complex (PVC)
  • Ventricular Tachycardia
  • Ventricular Fibrillation
  • Asystole
52
Q

Causes of ventricular ectopics? (3)

A
  • Structural causes: LVH, heart failure, myocarditis
  • Metabolic: Ischaemic heart disease, electrolytes
  • Inherited cardiac conditions
53
Q

When do ventricular ectopics need to be investigated further? What is treatment for ventricular ectopics? (2)

A
  • If worse on exercise need to investigate

Treatment

  • B-blockers
  • Ablation of focus
54
Q

What does it mean if QRS complex is broad? QRS complex narrow?

A
  • Problem in ventricles

* Problem with SA node

55
Q

What is broad complex tachycardia likely to be?

A

Ventricular tachycardia

56
Q

What is VT? Causes? (4)

A

Life threatening but may be haemodynamically stable

Causes

  • Coronary artery disease
  • Previous MI
  • Cardiomyopathy
  • Inherited/familial arrhythmia syndromes e.g. long QT
57
Q

What are most causes of sudden death attributable to?

A

VT and VF

58
Q

What is seen with ventricular tachycardia with haemodynamic compromise?

A

Large, sustained reduction of arterial pressure

59
Q

What is monomorphic VT? Polymorphic VT?

A
  • Morphology of each QRS is the same - fixed circuit

* Morphology constantly changing - multiple circuits, not re-entry (triggered activity or automaticity)

60
Q

What are ECG characteristics of VT? (7)

A
  • QRS complexes are rapid, wide and distorted
  • T waves are large
  • Ventricular rhythm usually regular
  • P waves are usually not visible
  • PR interval is not measurable
  • A-V dissociation may be present
  • V-A conduction may or may not be present
61
Q

What is ventricular fibrillation? Treatment? (2)

A
  • Chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump
  • Defibrillation, Cardiopulmonary resuscitation
62
Q

Acute treatment for VT? (4)

A
  • Direct current cardioversion (DCCV) if unstable
  • If stable: consider pharmacologic cardioversion with AAD
  • If unsure if VT or something else, consider adenosine to make diagnosis
  • Correct triggers/causes (electrolytes, ischaemia, hypoxia, pro-arrhythmic medications)
63
Q

What are pro-arrhythmic medications? Example?

A
  • Drugs that prolong the QT interval

* e.g. Sotalol

64
Q

Long term treatment for VT? (5)

A
  • Correct ischemia if possible (revascularisation)
  • CHF therapies
  • Anti-arrhythmic drugs to date have been shown to be INEFFECTIVE and are associated with worse outcomes!!!!!
  • Implantable cardiovertor defbrillators (ICD) if life threatening
  • VT catheter ablation
65
Q

How is ICD inserted? Dual or single chamber device?

A
  • Through SVC

* Dual chamber

66
Q

What are therapies provided by ICDs? (4)

A
  • Antitachycardia pacing
  • Cardioversion
  • Defibrillation
  • Pacing for bradycardia
67
Q

What is a wide QRS tachycardia with history of CAD/HF? What do most ventricular arrhythmias occur due to? What is the effectiveness of anti-arrhythmic drugs? What is an important part of treatment for VT/VF?

A
  • VT until proven otherwise
  • Structural heart disease (CHF, CAD)
  • ineffective on survival, but are often used together with ICDs to reduce symptoms
  • Optimal management of the underlying condition e.g. CHF, CAD
68
Q

Prevalence and incidence of AF?

A

Increases with age

69
Q

Appearance of AF on ECG? LVH?

A

AF

  • Absence of P waves
  • Irregularly irregular

LVH

  • Very tall R waves
  • ST depression
70
Q

What is atrial fibrillation? Types? (3)

Why is it significant? Presentations?

A
  • Chaotic and disorganized atrial activity causing irregular heart beat
  • Paroxysmal, persistent or permanent
  • Most common sustained arrhythmia
  • Can be symptomatic or asymptomatic
71
Q

Mechanism of AF?

A

Ectopic foci in muscle sleeves in the ostia of the pulmonary veins

72
Q

Termination of AF? (3)

A
  • Pharmacologic cardioversion with anti-arrhythmic drugs (30% effective) e.g. flecainide, sotalol and amiodarone
  • Electrical Cardioversion (90% effective)
  • Spontaneous reversion to sinus rhythm
73
Q

3 types of AF? (3)

A

Paroxysmal

  • Paroxysmal and lasting less than 48 hours
  • Often recurrent

Persistent

  • Lasting greater than 48 hours, can be cardioverted to NSR
  • Unlikely to spontaneously revert to NSR

Permanent
* Inability of pharmacologic or non-pharmacologic methods to restore NSR

74
Q

Associated diseases with AF? (13)

A
  • Hypertension
  • Congestive heart failure
  • Sick sinus syndrome
  • Coronary heart disease
  • Thyroid disease
  • Cardiac Valve disease
  • Congenital heart disease
  • COPD
  • Pneumonia
  • Septicaemia
  • Pericarditis
  • Tumors
  • Vagal cause – high endurance athletes
75
Q

Lifestyle/patient factors associated with AF?

A
  • Obesity
  • Inherited
  • Alcohol abuse
  • Cardiac surgery
76
Q

What is lone (idiopathic) AF? How is it diagnosed? Cause? Why is this dangerous?

A
  • Absence of any heart disease and no evidence of ventricular dysfunction
  • Exclusion
  • Genetic
  • Significant stroke rate if >75 y/o
77
Q

Symptoms of AF? (7) When are they worse?

A

Symptoms

  • Palpitations
  • Pre-syncope (dizziness)
  • Syncope
  • Chest pain
  • Dyspnea
  • Sweatiness
  • Fatigue

Symptoms often worse at onset of AF

78
Q

Appearance of AF on ECG? (5)

A
  • Atrial rate >300 bpm
  • Rhythm - irregularly irregular
  • Ventricular rate - variable
  • Absence of P waves
  • Presence of f waves
79
Q

What does ventricular rate in AF depend on? (3)

A
  • AV node conduction properties
  • Sympathetic and parasympathetic tone
  • Presence of drugs with act on the AV node
80
Q

Is AF a sinus arrhythmia?

A

No, as no underlying sinus beat

81
Q

What is complicated about AF with slow ventricular rate? Treatment?

A
  • May co-exist with periods of fast VR

* Pacemaker req to allow for pharmacologic control of fast VR

82
Q

What is AF with fast ventricular response known as?

A

Pseudo-regularisation

83
Q

What does AF lead to? How? What condition can AF result in?

A
  • Reduced CO
  • Lost ‘atrial kick’ and decreased filling times (reduced diastole)
  • Can result in CCF, esp with diastolic dysfunction
84
Q

What can ventricular rates <60 bpm suggest in AF? Treatment? (2)

A
  • AV conduction disease
  • Caution with anti-arrhythmic and rate-controlling drugs
  • May require permanent pacing
85
Q

What can AF in patients with pre-excitation e.g. Wolf-parkinson-White syndrome result in?

A
  • Ventricular fibrillation and sudden cardiac death
86
Q

Management of AF? (3)

A
  • Rhythm control (maintain sinus rhythm)
  • Rate control (accept AF but control ventricular rate)
  • Anti-coagulation for both approaches if high risk of thromboembolism
87
Q

What treatments are used for rate control in AF? (3) What do they do? What if medications are unsuccessful? (2)

A
  • Digoxin, b-blockers and verapamil/diltiazem
  • Slow down AVN conduction
  • More invasive efforts - electrophysiolgy and ablation
88
Q

What are the 2 goals of rhythm control? What are treatments? (2 + 3)

A

Restoration of NSR and maintenance of NSR

Restoration of NSR

  • Pharmacologic cardioversion (anti-arrhythmic drugs e.g. amiodarone)
  • Direct Current Cardioversion (DCCV)

Maintenance of NSR

  • Anti-arrhythmic drugs
  • Catheter ablation of atrial focus/ pulmonary veins
  • Surgery (Maze procedure)
89
Q

What is electrical cardioversion? What does success depend on?

A
  • Aims at immediate restoration of sinus rhythm

* the time the patient has been in atrial fibrillation

90
Q

What are classes of anti-arrhythmic drugs? (4) Examples?

A
  • Class 1 - reducing Na+ channel current e.g. lignocaine, quinidine, flecainide, propafenone
  • Class II - B-Adrenergic antagonists e.g. propranalol
  • Class III: action potential prolongation e.g. amiodarone, sotalol, DRONEDARONE
  • Class IV - Ca channel antagonists e.g. Verapamil
91
Q

What are AF patients at high risk of thromboembolism? (7)

What is the biggest risk of AF?

A
  • Valvular heart disease
  • Age >75 esp female
  • Hypertension
  • Heart failure
  • Previous thromboembolism/ stroke
  • Coronary artery disease/ diabetes and > 60 years old
  • Thyrotoxicosis

Biggest risk = stroke

92
Q

Indication for anti-coagulation in AF if valvular? Non-valvular? (6)

A

Valvular
* Mitral valve disease - MS and MR

Non-valvular

  • Age >75
  • Hypertension
  • Heart failure
  • Previous stroke/ thromboembolism
  • CAD / DM
  • Diabetes
93
Q

Purpose of radiofrequency ablation in AF? (2)

A
  • To maintain Sinus Rhythm by ablating AF focus (usually in the pulmonary veins)
  • For rate control by ablation of the AVN to stop fast conduction to the ventricles
94
Q

What is atrial flutter? How is atrial flutter sustained? How long to episodes last?

A
  • Rapid and regular form of atrial tachycardia - usually paroxysmal
  • Macro-reentrant circuit
  • Episodes can last from seconds to years
95
Q

What are complications of atrial flutter?

A
  • Chronic atrial flutter usually progresses to atrial fibrillation
  • May result in thrombo-emblism
96
Q

Difference between hearts of patients with paroxysmal atrial flutter and chronic atrial flutter?

A

Patients presenting with paroxysms of atrial flutter often have normal hearts, whereas patients with chronic atrial flutter usually have underlying heart disease

97
Q

Appearance of atrial flutter on ECG? (4)

A
  • Saw-tooth pattern
  • Atria beating fast ~300 bpm
  • AV node cannot conduct that fast (heart block) so 2:1 physiologic pattern
  • Ventricle possibly beating half as fast ~150 bpm
98
Q

Atrial flutter mechanism? Treatment? (4)

A

Counter-clockwise macro-reentrant circuit

  • RF ablation (80-90% long term success)
  • Pharmacologic therapy (slow the ventricular rate, restore sinus rhythm, maintain sinus rhythm once converted)
  • Cardioversion
  • Warfarin for prevention of thromboembolism
99
Q

Goals in AF management? (2)

A
  • Symptom control
  • Improve cardiovascular outcomes e.g. stroke prevention with anti-coagulatns, optimal treatment of underlying CVS disease, lifestyle risk reduction

Cardiovascular (28 decks)

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