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Cardiovascular > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What is an arrhythmia?

A

Abnormal heart beat

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2
Q

Where do SVT arrhythmias originate from?

A

Anywhere above the ventricle. SA node atrial muscle, His origin, AV node

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3
Q

Where do ventricular arrythmias originate from?

A

Ventricular muscle (common) or fascicles of the conducting system (uncommon)

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4
Q

Name some common Supraventricular arryhthmias?

A 
Tachycardias = Atrial fibrilation, atrial flutter, ectopic atrial tachycardia
Bradycardia = Sinus bradycardia or sinus pauses
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5
Q

What is a focus?

A

Origin of an arrythmia- any part of the heart that can fire and take over the normal rhythm

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6
Q

Name some common ventricular arrhythmias?

A

Ventricular ectopics or premature ventricular complexes (PVC)
Ventricular tachycardia or ventricular fibrilation (can lead to asystole)

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7
Q

Name some common AV nodal arrhythmias?

A 
AV nodal re-entry tahcycardia (AVNRT)
AV block (1st, 2nd or 3rd degree)
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8
Q

Abnormal anatomy is a cause of arrythmias. What aspects of anatomy can cause arrhythmias?

A

Left ventricular hypertrophy, accessory pathways or congenital heart defects

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9
Q

The autonomic nervous system is a cause of arrythmias. What aspects of the ANS can cause arrhythmias?

A 
Sympathetic stimulation (stress, caffeine, hyperthyroidism)
Increased vagal tone (bradycardia)
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10
Q

Metabolic conditions is a cause of arrythmias. What aspects of the metabolism can cause arrhythmias?

A

Hypoxia: chronic lung disease or PE
Ischemic heart diease: MI or angina
Electrolyte imbalance: K+, Ca++, Mg++

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11
Q

Which infections can cause arrhythmias?

A

Viral myocarditis

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12
Q

Which drugs can cause arrhythmias?

A

Direct electrophysiological agents or via the ANS

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13
Q

How can genetics cause arrhythmias?

A

Mutation of genes encoding for cardiac ion channels (Congenital long QT syndrome)

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14
Q

What is an ectopic beat and what can it leads to?

A

A beat or rhythm which originates outside of the SA node.

It can lead to altered automaticity or triggered activity

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15
Q

What is a re-entrant rhythm and and what are some common causes?

A

Rhythm generated outiside of the SA node which requires more than one conduction pathway with different speeds of conduction (depolarisation) and recovery of excitability (refractoriness)
Accessory pathway tachycardia (WPW syndrome)
Previous MI- scar tissue is inert
Congenital heart disease

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16
Q

How is a re-entry rhythm triggered?

A

By an ectopic beat resulting in a propagating circuit

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17
Q

What is automaticity and which part of the action potential does it usually effect?

A

The cells in the heart develop their own firing cycle and do not respond to the SA node. Can occur in the atria or the ventricles
Phase 4

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18
Q

Normally, why does automaticity come about?

A

Phase 4 (slow depolarisation) becomes faster due to:

1) Ion imbalance
2) Lowered threshold value
3) Increased resting potential

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19
Q

What can increase and decrease phase 4 conduction?

A

Increase: Hyperthermia, Hypoxia, Hypercapnia, Cardiac dilation, Hypokalemia
Decrease: Hypothermia or Hyperkapnia

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20
Q

What is triggered activity and which part of the action potential does it usually effect?

A

Where a small depolarisation, called an after depolarisation, occurs in the terminal phase of the action potential. If this is of sufficient magnitude to reach threshold it can lead to a sustained trail of depolarisation Phase 3

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21
Q

Give some common arrhythmias caused by triggered activity?

A

Torsades de pointes in long QT syndrome, digoxin toxicity

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22
Q

What is syncope?

A

A loss of consciousness due to a fall in BP

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23
Q

Give some common symptoms of arrhythmias?

A

Palpitations, SOB, Dizziness, Sudden Cardiac death, Angina and heart failure, Syncope or presyncope.
Can be assymptomatic and an incidental finding

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24
Q

What investigations are needed if you suspect and arrhythmia?

A 
12 lead ECG
CXR
Exercise ECG
24 hour ambulatory ECG
Event recorder- patient activated ECG
Echocardiogram
Eletrophysiological study- invasive but gives the opportunity to treat using radio frequency ablation
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25
Q

What are you looking for on the ECG?

A

Pathological Q waves- signs of a previous MI
Delta waves- signs of pre-excitation or accessory pathway. Slow rise in PR interval because of cell to cell transmission rather than a conduction pathway.

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26
Q

What condition has a typical delta wave?

A

Wolf Parkinson White syndrome due to the accessory pathway- bundle of Kent

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27
Q

What is sinus bradycardia?

A

Heart rate <60bpm

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28
Q

What is Sinus tachycardia?

A

Hear rate > 100bpm

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29
Q

What are the causes of sinus bradycardia?

A

Causes: physiological in atherletes. Drugs like beta blockers or ischemia in an inferior STEMI

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30
Q

What is the treatment for sinus bradycardia?

A

Treatment: Atropine if acute (antivagal and will speed up the heart. Pacemaker is haemodynamic compromise, hypotention, CCF or angina

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31
Q

What are the causes of sinus tachycardia?

A

Physiological- exercise, stress, anxiety.

Drugs

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32
Q

What is the treatment for sinus tachycardia?

A

Treat the underlying cause as arrhythmias are often a sign of other diseases
Beta blockers

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33
Q

What is sinus arrhythmia?

A

Phasic variation in heart rate with respiration. Heart rate decreases during inspiration due to increased venous return

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34
Q

What is the treatment for sinus arrhythmia?

A

None

This is physiological and common in children and young adults

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35
Q

What are the symptoms of atrial ectopic beats?

A

Assymptomatic or palpitaions

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36
Q

What are the causes of atrial ectopic beats?

A

Usually benign but can be a sign of another disease like COPD

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37
Q

What is the treatment for atrial ectopic beats?

A

Often no treatment but aviod stimulants like caffeine and cigarettes. Beta blockers may help

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38
Q

What are the 3 causes of regular SVT?

A

AVNRT- AV nodal re-entrant tachycardia (re-entry within the AV node/micro re-entry)
AVRT- AV re-entry tachycardia (re-entry via and accessory pathway/macro re-entry)
EAT- Ectopic Atrial Tachycardia

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39
Q

How are regular SVTs treated?

A

Radiofrequency ablation to remove the slow pathway

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40
Q

Give and example of an irregular SVT?

A

Atrial tachycardia- AF and atrial flutter

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41
Q

What is the acute management of an SVT?

A

1) Increase the vagal tone. Valsalva manovre or carotid massage
2) Slow conduction in AV node. IV adenosine or IV Verapamil

42
Q

What is the chronic management of SVT?

A

Aviod stimulants
EP study and radiofrequency ablation (young fit and symptomatic)
Beta blockers and anti arrythmic drugs

43
Q

What is Adenosine, Atropine and Amiodarone used for?

A 
Adenosine = slowing conduction in the AV node in SVT
Atropine = increase conduction by suppressing vagal activity in sinus bradycardia
Amiodarone = used in atrial and ventricular tachycardias
44
Q

WHat is Radiofrequency Catheter Ablation (RFCA)?

A

Selective cautry of cardiac tissue to prevent tachycardia, targeting anautomatic focus or part of a re-entry circuit

45
Q

What is necessary for RFCA?

A

Patient to be conscious throughout

Stop antiarrhythmic drugs to provoke the arrhythmia

46
Q

What is the RFCA procedure?

A

1) ECG catheters placed into heart via femoral veins
2) Intracardiac ECG recored during sinus rhythm, tachycardia and pacing manovres to find location and mechanism of tachycardia
3) Catheter placed over focus/pathway and tip hearted to 55-65 degrees.

47
Q

What are the causes of AV node conduction disease (heart block)?

A 
Ageing 
Acute MI
Myocarditis 
Drugs (beta blockers)
Infiltrative disease (amyloid)
Calcified aotric valve disease
Post aortic valve surgery
Genetic disease (Lenegne's disease, muscular dystrophy)
48
Q

What genetic and infiltrative diseases can cause AV node conduction disease (heart block)?

A 
Genetic disease (Lenegne's disease, muscular dystrophy)
Infiltrative disease (amyloid)
49
Q

What is first degree hear block?

A

Extended PR intervals (>0.2 seconds) due to increased AV nodal delay

50
Q

What is the treatment fro first degree heart block?

A

No treatment required as it’s usually assymptomatic but you can montor for development of more serious heart blocks

51
Q

What is second degree heart block and what are the two types?

A

intermittent block at the AV node +> dropped ventricular beats
Mobitz type 1 = progressive lengthening of the PR interval due to increased vagal tone
Mobitz type 2 = Fixed block AV node conduction of 2:1 or 3:1

52
Q

What is the treatment for second degree heart block?

A

Mobitz type 1 = No treatment just monitoring

Mobitz type 2 = Pathological and i may progress to 3rd degree heart block. Pacemaker required

53
Q

What is third degree heart block?

A

Complete heart block. No action potential from the SA node pass through the AV node => Escape rhythm with broard QRS complex

54
Q

What is the treatment for third degree heart block?

A

Needs a pacemaker

55
Q

What are the two types of pacemaker (one for emergency use)?

A

Transcutaineous pacer: emergency use until venous access is achieved- painful for the patient
Transvenous pacer: via internal jugular vein, subclavian vein or femoral vein.

56
Q

What is the difference between a duel and single chamber pacemaker?

A

Duel chamber: two electrodes used to sense electrical current of the heart and deliver current to the heart. 1 elecrode to RA and one to apex of RV. Used for AV node disease as it maintains AV synchrony
Single chamber: Just one electrode to the right atrium or right ventricle only

57
Q

Give another name for ventricular ectopics?

A

Premature ventricular cmplexes

58
Q

What is a premature ventricular complex (PVC)?

A

Premature beat arising from an ectopic focus in the ventricles => transient reduction in arterial pressure

59
Q

What are some of the causes of premature ventricular complexes?

A

Structural: LV hypertrophy, Heart failure, Myocarditis
Metabolic: Ischemic heart disease
Marker of inherited cardiac conditions

60
Q

What is the treatment for premature ventricular complexes?

A

Beta blockers of ablation of focus

61
Q

What is Ventricular tachycardia (VT)?

A

Re-entrant circuit within the ventricles causing broad QRS complexes

62
Q

What ate the two types of VT?

A

monomorhic VT: Where the circuit is going around a scar or one focus
polymorphic VT: where there is more than one circuit/ multiple foci

63
Q

What is haemodynamic instability?

A

An inability to perfuse organs represented by the clinical features of circulatory shock and severe heart failure

64
Q

Are all patients with VT haemodynamically unstable?

A

No some may be alert

65
Q

What are the causes of VT?

A

Significant heart disease: CAD and previous MIs

Rare causes: Cardiomyopathies, inherited/familial arrhythmia syndromes

66
Q

What are some inherited/familial arrhythmia syndromes?

A

Long QT syndrome or Brugaola syndrome

67
Q

What is Ventricular fibrillation?

A

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

68
Q

What is the acute treatment for ventricular fibrillation?

A

Defibrillation and CPR required

69
Q

What is the acute treatment for VT in a patient who is haemodynamically unstable?

A

Direct current cardioversion (DCCV)

Given a general anasthetic and electrodes put on the chest

70
Q

What is the acute treatment for VT in a patient who is haemodynamically stable?

A

Pharmocalogical cardioversion with antiarrythmic drugs (Amiodarone) while preparing for DCCV if necessary
Look for the underlying cause

71
Q

What is the long term treatment for VT?

A

1) Consider revascularisation for ischemia
2) Optimise CCF therapies
3) Antiarrhythmic drugs long term have been shown to be ineffective and lead to worse outcomes long term
4) Use an implantable cardiac defibrillator (ICD) if life threatening
5) Consider Radiofrequency ablation

72
Q

Why is ICD not good if the patient is conscious and in VT and what is an alternative?

A

Very painful as it gives you a shock.

Use anti tachycardia pacing which is pain free

73
Q

Until proven otherwise what is a wide QRS complex tachycardia with a cardiac history?

A

VT until proven otherwise

74
Q

What causes most ventricular arrhythmias?

A

Structural heart disease: LV hypertrophy or heart failure

75
Q

What is primary electrical disease?

A

VT/VF in structurally normal hearts.

Genetic cause and implications for family members

76
Q

What are the defects of impulse formation?

A

Altered automaticity or triggered activity

77
Q

What are the defects in impulse conduction?

A

Re-entrant rhythms (conduction block or accessory tracts)

78
Q

What is physiological altered automaticity?

A

Modulation of the SA node activity by the ANS (eg sinus tachycardia, sinus arrhythmia)

79
Q

What is pathological altered automaticity?

A

Another pacemaker in the heart overrides the SA node

80
Q

When may pathological altered automaticty occur?

A

1) SA node firing frequency is pathologically low or when conduction from the AV node is impaired => escape beat or rhythm.
2) When another pacemaker fires at a faster rate than the SA node => Ectopic beat or rhythm

81
Q

What is an escape beat?

A

Latent pacemaker initiates impulse (because the heart rate is pathologically slow)

82
Q

What is ectopic beat?

A

Another pacemaker initiates an impulse

83
Q

What are the common causes of ectopic beats?

A

Ischemia, hypokalemia, cardiac dialitaion or increase sympathetic activity

84
Q

What is triggered activity?

A

After depolarisations triggered by a normal action potential

85
Q

What are the 2 types of after depolarisation?

A

1) Early after depolarisation EAD

2) Delayed afterpotential DAD

86
Q

What is an EAD?

A

After depolarisation which occurs during the action potential in:

1) Phase 2 - mediated by Ca++ channels
2) Phase 3 - mediated by Na+ channels

87
Q

What aspects of the ECG are associated with EAD?

A

Prolonged PR interval or prolonged QT interval

88
Q

What is a DAD?

A

After depolarisation which occurs after complete repolarisation caused by a transient inward current involving Na+

89
Q

What is associated with DADs?

A

Ca++ overload provoked by caterchol amines, digoxin and heart failure

90
Q

What is a re-entry rhythm?

A

Self sustaining electrical circuit which stimulate the myocardium repeatedly

91
Q

What is required for a re-entrant rhythm?

A

1) Unidirectional block where forwards conduction is prohibited but backwards conduction allowed
OR
2) Variable conduction velocity/ length of refractory within two pathways

92
Q

Action potentials which collide will extinguish each other. True or false?

A

True

93
Q

What is the most common accessory tract pathway?

A

Bundle of Kent

94
Q

Describable the 2 vagal manovres used in SVT?

A

Carotid massage
Valsalvar manovre: blow out while holding your nose against a fixed volume and count to 10.
These will both increase vagal tone

95
Q

What drug can be used to prevent SVT passing into the ventricles?

A

IV bollus adrenaline 6mg (or varapamil)

96
Q

What drug is given in severe sinus bradycardia?

A

Atropine (anticholinergic drug).

If this doesn’t work give adrenaline or isoprenaline.

97
Q

Treatment of Atrial flutter?

A

Amiodarone or DCCV

98
Q

Treatment for AF within 48 hours of onset?

A

DCCV

99
Q

Treatment for AF after 48 hours of onset?

A

Anticoagulate first as a clot may have formed in the heart and medical management to reduce hear rate- amiodarone/digoxin.
After 6-8 weeks you can DCCV

100
Q

Torsades des points is associated with hypokalemia. True or false?

A

True

101
Q

Bundle brach block can lead to disynchroney of contraction of right and left ventricles. What is the treatment for this?

A

Cardiac resynchronisation therapy (CRT) either with a defibrilator or without

Cardiovascular (24 decks)

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