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Cardiovascular 2018 > Cardiac Arrhythmia 1 > Flashcards

Cardiac Arrhythmia 1 Flashcards

1
Q

How are arrhythmias generally named?

A

By their anatomical site or chamber of origin

By their mechanism

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2
Q

Where is the origin of a supra-ventricular tachycardia?

A

Above the ventricle i.e. SAN, atrial muscle, AV node or HIS origin

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3
Q

What is the origin of a ventricular arrhythmia?

A

The ventricular muscles (common)

Fasicles of the conducting system (uncommon)

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4
Q

What are the SVT’s?

A

Atrial fibrillation
Atrial flutter
Ectopic atrial tachycardia

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5
Q

What are the different supra-ventricular bradycardias?

A

Sinus bradycardia

Sinus pauses

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6
Q

What are the different ventricular arrhythmias?

A

Ventricular ectopics/premature ventricular complexes

ventricular tachycardia

ventricular fibrillation

asystole

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7
Q

What are the AV nodal arrhythmias?

A

AVN re-entry tachycardia

AV reciprocating or AV reentrant tachycardia

AV block

  • 1st degree
  • 2nd degree
  • 3rd degree
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8
Q

What are the clinical causes of arrhythmia?

A 
Abnormal anatomy
ANS
Metabolic
Inflammation
Drugs
Genetic
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9
Q

What anatomical abnormalities can cause arrhythmia?

A

Left ventricular hypertrophy
Accessory pathways
Congenital HD

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10
Q

What ANS causes can result in arrhythmia?

A

Sympathetic stimulation (stress, exercise, hyperthyroidism)

Increased vagal tone causing bradycardia

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11
Q

What metabolic causes can result in arrhythmia?

A

Hypoxia: COPD, PE
Ischaemic myocardium: acute MI, angina
Electrolyte imbalances: K+, Ca 2+, Mg2+

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12
Q

What inflammatory cause can result in arrhythmia?

A

Viral myocarditis

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13
Q

How do drugs cause arrhythmia?

A

Direct electrophysiologic effects or via ANS

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14
Q

What genetic changes can cause arrhythmia?

A

Mutations of genes encoding cardiac ion channels e.g. the congenital long QT syndrome

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15
Q

What are the electrophysiological causes of arrhythmia?

A

Ectopic beats

Re-entry

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16
Q

What are ectopic beats?

A

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

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17
Q

What are the causes of ectopic beats?

A

Altered automaticity: e.g. ischaemia, catecholamines

Triggered activity: e.g. digoxin, long QT syndrome

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18
Q

What does re-entrant arrhythmia require?

A

Requires more than one conduction pathway, with different speed of conduction (depolarisation) and recovery of excitability (refractoriness)

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19
Q

Name some causes of reentrant arrhythmias?

A

Accessory pathway tachycardia (Wolf Parkinson White Syndrome)

Previous MI

Congenital heart disease

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20
Q

Describe the mechanism of ectopic beats?

A

The ectopic focus may cause single beats or a sustained run of beats, that if faster than sinus rhythm, take over the intrinsic rhythm

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21
Q

Describe the mechanism of reentry?

A

Triggered by an ectopic beat, resulting in a self perpetuating circuit

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22
Q

Is tachycardia dangerous?

A

Depends on the affect on cardiac output

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23
Q

What is altered automaticity?

A

A change in the conduction of the heart

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24
Q

What is the most common sympathetic mechanism of altered automaticity arrhythmia?

A

Change in slope (change in depolarisation), resulting in a change in rate

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25
Q

What increases the phase four slope of cardiac myocytes?

A 
Hyperthermia
Hypoxia
Hypercapnia
Cardiac Dilatation
Hypokalaemia (prolongs repolarisation)
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26
Q

What does increase in the slope of phase four cause?

A

Ectopic beats, increase in HR

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27
Q

What causes a decrease in phase four slope of cardiac myocyte action potential?

A

Hypothermia

Hyperkalaemia

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28
Q

What does a decreased phase four action potential of cardiac myocytes cause?

A

Bradycardia, heart block

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29
Q

What is triggered activity?

A

In the terminal phase of the AP (phase 3), a small depolarisation may occur (after depolarisation), and if of sufficient magnitude may reach depolarisation threshold and lead to a sustained train of depolarisations, termed triggered activity

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30
Q

What is the mechanism underlying digoxin toxicity, long QT syndrome, torsades des pointes, hypokalaemia

A

Triggered activity

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31
Q

What structural abnormalities can result in re-entry?

A

Accessory pathways
Scar from MI
congenital heart disease

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32
Q

What functional changes can cause re-entry?

A

Conditions that depress conduction velocity or shorten refractory period promote functional block e.g. ischaemia, drugs

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33
Q

What are the symptoms of arrhythmia?

A 
Palpitations 'pounding heart'
Shortness of breath
Dizziness
Loss of consciousness 'syncope'
Faintness 'presyncope'
Sudden cardiac death
Angina
HF
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34
Q

What investigations are done to investigate arrhythmia?

A

12 lead ECG (in tachycardia, during SR)

CXR

Echocardiogram

Stress ECG
- look for myocardial ischaemia, exercise related arrythmias

24 hour ECG holter monitoring

Event recorder

Electrophysiological (EP) study
-induce clinical arrhythmia to study mechanism and map arrhythmia

35
Q

What would you look for on the ECG?

A

Rhythm

Signs of

  • previous MI
  • pre-excitation (WPW syndrome)
36
Q

What ECG changes indicate pre-excitation?

A

Short PR
Delta wave
Wide QRS
Secondary ST-T change

37
Q

What would you look for on echocardiography?

A

To assess for structural heart disease e.g.

  • enlarged atria in AF
  • LV dilatation
  • Previous MI scar
  • aneurysm
38
Q

What does an EP study provide?

A

The opportunity to perform radio-frequency ablation to extra pathway

39
Q

Describe a normal sinus arrhythmia

A

Variation in heart rate, due to reflex changes in vagal tone during the respiratory cycle

Inspiration reduces vagal tone and increases HR

40
Q

What is classified as sinus bradycardia?

A

<60bpm

41
Q

What are the causes of sinus bradycardia?

A

Drugs (B-blocker)
Physiological (athlete)
Ischaemia (common in inferior STEMIs)

42
Q

What is the treatment of sinus bradycardia?

A

Atropine (if acute e.g. acute MI)

Pacing if haemodynamic compromise (hypotension, CHF, Angina, collapse)

43
Q

What is classifies as a sinus tachycardia?

A

> 100bpm

44
Q

What are the causes of sinus tachycardia?

A

Physiological (anxiety, fever, hypotension, anaemia)

Inappropriate (drugs, etc)

45
Q

What are the treatments for sinus tachycardia?

A

Treat underlying cause

B-adrenergic blockers

46
Q

What are the symptoms of atrial ectopic beats?

A

Asymptomatic

Palpitations

47
Q

What is the treatment for atrial ectopic beats?

A

Generally none

B-adrenergic blockers may hekp

48
Q

What should be avoided in patients with atrial ectopics?

A

Stimulants- caffeine, cigarettes

49
Q

What are the causes of a regular supraventricular tachycardia?

A

AV nodal re-entrant tachycardia
AV reciprocating tachycardia/AV reentrant tachycardia (via an accessory pathway)
Ectopic atrial tachycardia

50
Q

What is the difference between an AVNRT and AVRT?

A

AVNRT: circuit within the AV node, micro-rentry

AVRT: circuit using the AVN and AP way, macro-reentry

51
Q

What will be seen on the ECG in a antegrade AVRT?

A

Normal QRS

No delta wave

Retrograde P wave after QRS

52
Q

What will be seen on the ECG in a retrograde AVRT?

A

Wide QRS with delta wave

P wave rarely seen

If P wave visible it is retrograde and occurs just before the QRS

53
Q

What is the acute management of a supra-ventricular tachycardia?

A

-Increase vagal tone: valsalva, carotid massage
-If slow conduction in the AV node;
IV adenosine
IV verapamil

54
Q

What is the chronic management of supra-ventricular tachycardias?

A

Avoid stimulants

EP study and radio frequency ablation (first line in young, symptomatic patients)

Beta blockers

Anti-arrhythmic drugs

55
Q

What is radio-frequency ablation?

A

Selective cautery of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit

56
Q

How is radiofrequency ablation performed?

A

ECG Catheters placed in heart via femoral veins.

Intracardiac ECG recorded during sinus rhythm, tachycardia and during pacing manoeuvres to find the location and mechanism of the tachycardia

catheter placed over focus / pathway and tip heated to 55-65C

57
Q

What are the causes of AVN conduction disease (Heart block)?

A 
Ageing
Acute myocardial Infarction
Myocarditis
Infiltrative disease (amyloid)
Drugs 
-B-blockers
-CCBs
Calcific aortic valve disease
Post-aortic valve surgery
Genetic
-lenegre's disease
-myotonic dystrophy
58
Q

Describe 1st degree AV block?

A

Not really ‘block’- conduction following each P wave but it takes longer

59
Q

What would you see on the ECG of 1st degree AV block?

A

PR interval longer than normal (>0.2sec)

60
Q

What is the treatment of 1st degree AV block?

A

None

61
Q

What is the management of 1st degree AV block?

A

Rule out other pathology

Long term follow up recommended as more advanced block may develop

62
Q

Describe 2nd degree AV block?

A

Intermittent block at the AVN (dropped beats)

63
Q

What are the types of 2nd degree AV block?

A

Mobitz type I

Mobitz type II

64
Q

What is mobitz type I?

A

progressive lengthening of the PR interval, eventually resulting in a dropped beat.

65
Q

What is the origin of mobitz type I AV block?

A

Usually vagal in origin

66
Q

What is mobitz type II?

A

Pathological, may progress to complete heart block (3rd degree)

67
Q

How would you identify mobitz type II?

A

Usually an identifiable pattern
-2:1
-3:1
is variable

68
Q

What is recommended in mobitz type II?

A

Permanent pacemaker indicated

69
Q

What are the types of pacemakers?

A

Single chamber
(paces the right atria or right ventricle only)
Dual chamber
(paces the RA and the RV)

70
Q

What does a dual changer pacemaker maintain? When is it used?

A

Maintains A-V synchrony (preserves atrial kick)

Used in AVN disease

71
Q

What are the causes of ventricular ectopics?

A 
Structural
-LVH, heart failure, myocarditis
Metabolic
-Ischaemic heart disease, electrolytes
Inherited
72
Q

What would indicate a ventricular ectopic needs to be further analysed?

A

Worse on exercise

73
Q

What is the treatment of ventricular ectopics?

A

B-blockers

Ablation of focus

74
Q

Describe ventricular tachycardia?

A

Life threatening- may be haemodynamically stable

75
Q

Who gets ventricular tachycardia?

A

Most patients have significant heart disease

  • coronary artery disease
  • a previous MI
76
Q

What are the rarer causes of ventricular tachycardia?

A

Cardiomyopathy
Inherited/familial arrhythmia syndromes
-long QT, brugada syndrome

77
Q

What ECG changes help identify VTs?

A
  • QRS complexes are rapid, wide, and distorted
  • T waves are large with deflections opposite the QRS complexes.
  • ventricular rhythm is 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.
78
Q

Describe ventricular fibrillation?

A

Chaotic ventricular activity which causes the heart to lose the ability to function as a pump

79
Q

What is the treatment of ventricular fibrillation?

A

Defibrillation

Cardiopulmonary resuscitation

80
Q

What is the acute treatment of VT?

A

Direct current cardioversion (DCCV) if unstable.

If stable: consider pharmacologic cardioversion with AAD, in meantime prepare for DCCV.

If unsure if VT or something else, consider adenosine to make a diagnosis.

Correct triggers; Look for causes;
Electrolytes
Ischaemia
Hypoxia 
Pro-arrhythmic medications (eg drugs that prolong the QT interval eg., sotalol).
81
Q

What is the long-term treatment of VT?

A

Correct ischemia if possible (revascularisation)

Optimise 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.

82
Q

What is a wide QRS complex with a history of CAD/HF until proven otherwise?

A

VT

83
Q

Where do most ventricular arrhythmias occur?

A

In the setting of structural heart disease

-CHF, CAD

84
Q

What is the optimum management of VT/VF?

A

treat underlying condition e.g. CHF, CAD are important

Cardiovascular 2018 (39 decks)

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