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1st Year Medicine > Caridac Arrhythmias > Flashcards

Caridac Arrhythmias Flashcards

1
Q

What is an ectopic beat?

A

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

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2
Q

Are ectopic beats dangerous?

A

May or may not be depending on how they affect the cardiac output.

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3
Q

When to ectopic beats more commonly happen?

A

At night.

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4
Q

What are the supra ventricular tachycardias?

A

Superventricular tachycardia, bradycardia and atrioventricular node arrhythmias

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5
Q

What are the supra ventricular tachycardias?

A

Atrial fibrillation, atrial flutter and ectopic atrial tachycardia.

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6
Q

What are the AV node arrhythmias?

A

ANV re entry, and accessory pathways such as WPW and AB block first, second or third degree.

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7
Q

What are the ventricular arrhythmias?

A

Premature ventricular complex, ventricular tachycardia, ventricular fibrillation and asystole.

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8
Q

What can be the clinical causes of arrhythmias?

A

Abnormal anatomy, autonomic causes, metabolic, inflammatory, drugs and genetics.

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9
Q

What are some abnormal anatomies that can cause arrhythmias?

A

LVH, accessory pathways and congenital HD.

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10
Q

What are some autonomic causes of arrhythmias?

A

Sympathetic stimulation such as nervousness and exercise.

Increased vagal tone such as bradycardia and heart block.

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11
Q

What are some metabolic causes of arrhythmias?

A

Hyperthyroidism.
Hypoxic myocardium: chronic pulmonary disease and PE.
Ischaemic myocardium: acute MI and angina.
Electrolyte imbalances: imbalances of K, Ca, Mg etc.

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12
Q

What are some genetic causes of arrhythmias?

A

Mutations of cardiac ion channels e.g. The congenital long QT syndrome.

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13
Q

What are some physiological causes of arrhythmias?

A

Previous MI, re entry from an accessory pathway e.g. WPW.

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14
Q

What is wolf Parkinson white syndrome?

A

Congenital abnormality that results in supraventricular tachycardia that uses an atrioventricular accessory tract. Classified into two types according to ECG findings.
Type A and type B.

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15
Q

What is type A WPW syndrome?

A

The delta wave and QRS are mainly upright in the precordial leads. The dominant R wave in lead V1 may be misinterpreted as right bundle branch block.

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16
Q

What is type B WPW syndrome?

A

The delta wave and QRS are mainly negative in leads V1 and V2 and positive in the other precordial leads. Resembling left bundle branch block.

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17
Q

What are the symptoms of WPW syndrome?

A

Palpitations, SOB, dizziness, syncope, sudden cardiac death and worsening of pre existing conditions such as angina.

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18
Q

What is triggered activity?

A

In the terminal phase of AP (phase 3), a small after depolarisation may occur. If it has significant magnitude it can lead to a sustained train of depolarisations called triggered activity.

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19
Q

Whit is triggered activity considered to be the mechanism for?

A

Digoxin toxicity, torsades de pointes in the long QT syndrome and hypokaelaemia.

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20
Q

What investigations do we do for arrhythmias?

A

12 lead, CXR, echo, stress ECG to look for ischaemia or exercise related arrhythmias. 24 holster monitoring - to look for paroxysmal arrhythmias and link symptoms to underlying heart rhythm.
Electrophysiology study - induces arrhythmia and study its mechanisms. Gives an opportunity to treat the arrhythmia by ablation.

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21
Q

Are atrial ectopic beats symptomatic? do they require treatment? What can trigger them?

A

Can by Asymptomatic or give palpitations. Generally no treatment required. Beta blockers may help. Avoid stimulants e.g. Caffeine and cigarettes.

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22
Q

What is sinus bradycardia? What can cause it?

A

Under 60 bpm.

may be physiological e.g. Athletes. Beta blockers can cause it. Also ischaemia which is common in inferior STEMIs.

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23
Q

What is the treatment of bradycardia?

A

Atropine. Pacing if there is haemodynamic compromise e.g. Hypotension of CHF.

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24
Q

What is tachycardia? What can cause it?

A

HR of over 100 bpm.

Can be physiological activity e.g. Exercise and drugs.

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25
Q

What is the treatment of tachycardia?

A

Treat underlying cause and give beta blockers.

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26
Q

What blood test should be done for arrhythmias?

A

FBC, U and Es, glucose, Ca, Mg, TSH.

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27
Q

What may cause supraventricular tachycardia?

A

AV node re entrant tachycardia.
Accessory pathway tachycardia e.g. WPW
Ectopic atrial tachycardia.

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28
Q

How do we manage supraventricular tachycardia?

A 
Acute - vagal manoeuvres, carotid massage, IV adenosine and verapamil.
Chronic - avoid stimulants, radio frequency ablation and anti arrhythmic drugs class 2 or 4.
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29
Q

What is the procedure for cardiac ablation?

A

Explanation and consent, minimal use of sedation (use local), cease ant arrhythmic drugs 3-5 days before. Procedure between 1-2 hours. Catheter through femoral veins. Record ECG during sinus rhythm, tachycardia and pacing manoeuvres. Catheter placed over pathway and tip heated to 55/56 deg.

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30
Q

What can cause AVN conduction disease?

A

Ageing, acute MI, myocarditis, amyloid, beta or calcium channel blockers, aortic valve disease, post aortic valve surgery and genetic.

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31
Q

What is first degree AV block?

A

Not really a block, just a long PR interval over 0.2 seconds. Doesn’t require treatment but follow up is recommended as it may develop.

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32
Q

What is second degree AV block? What are the two types?

A

Intermittent block at the AV node causing dropped beats.
Mobitz 1- progressive lengthening of PR interval eventually resulting in a dropped beat. Usually vagal in origin.
Mobitz 2- pathological, may progress to third degree heart block. Usually 2:1 or 3:1 but may be variable.

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33
Q

What is the treatment of a mobitz 2 heart block?

A

Permanent ventricular pacemaker may be required.

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34
Q

What is third degree AV block?

A

No action potentials from the SA node get through the AV node.

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35
Q

What is the treatment of third degree AV block?

A

Ventricular pacing.

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36
Q

What are the two acute pacing options? What do they involve?

A

Transcutaneous pacer - emergency used until venous access is available. It is painful to the patient.
Trans venous pacer - via the internal jugular, the subclavian or the femoral vein.

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37
Q

What two different types of pacemakers do we get?

A

Single chamber - paces atrial or ventricle only.

Dual chamber - paces the atrium and the ventricle simultaneously.

38
Q

When do we use atrial pacemakers?

A

In isolated SA node disease but normal AV node.

39
Q

When do we use ventricular pacemakers?

A

AF with slow ventricular rate.

40
Q

When do we use dual chamber pacemakers?

A

Used for AVN disease.

41
Q

What should we do if premature ventricular ectopics are worse on exercise?

A

Investigate further and consider beta blockers.

42
Q

What are the symptoms of VT and what usually causes it?

A

Life threatening but may be haemodynamically stable.

Caused by coronary artery disease or previous MI.

43
Q

What are rare cause of VT?

A

Cardiomyopathy, inherited or familial arrhythmia syndromes e.g. Long QT or brugada syndrome.

44
Q

What is ventricular fibrillation?

How do we treat it?

A

Chaotic ventricular electrical activity, which causes the heart to lose the ability to function like a pump.
Needs defibrillation and CPR.

45
Q

What is the acute treatment of VT for both stable and unstable patients?

A

Unstable - DC cardioversion.
Stable - pharmacological cardioversion.
Correct the triggers in both.

46
Q

What should we do if we are unsure if it is VT or something else?

A

Consider adenosine to make a diagnosis.

47
Q

What causes are we looking for in VT?

A

Electrolyte imbalances, ischaemia, hypoxia and medications that prolong the QT interval.

48
Q

What medications prolong the QT interval and so could cause VT?

A

Sotalol, quinidine, terfenadine and erythromycin.

49
Q

What is the long term treatment for VT?

A

Correct ischameia if possible e.g. ReVascularisation.
Anti arrhythmic drugs not to be used.
ICD if life threatening.
Optimise CHF therapies.

50
Q

What greatly increases the likelihood of AF?

A

Increasing age.

51
Q

What is AF? How long does it last? How common is it? Is it symptomatic?

A

Chaotic and disorganised electrical activity causing an irregular heart beat.
Can be paroxysmal, persistent or permanent.
Most common sustained arrhythmia.
Can by symptomatic or Asymptomatic.

52
Q

What is paroxysmal AF?

A

Lasting less than 48 hours, often recurrent.

53
Q

What is persistent AF?

A

Episode lasting over 48 hours, which can still be cardioverted to sinus rhythm. Unlikely to spontaneously revert.

54
Q

What is permanent AF?

A

Cannot restore NSR by any method.

55
Q

What are diseases associated with AF?

A

Hypertension, CHF, sick sinus syndrome, CHD, thyroid disease, familial, valvular disease, alcohol abuse, congenital heart disease and cardiac surgery.

56
Q

What is lone AF?

A

It is idiopathic, has an absence of any heart disease.

Gives a significant stroke rate of over the age of 75.

57
Q

What are the symptoms of AF? When are they worse?

A

Often worse at onset.

Palpitations, pre syncope (dizziness), syncope, chest pain, dyspnoea, sweating and fatigue.

58
Q

What is the mechanism of AF?

A

Multiple wavelets of re entry. Ectopic focus around the pulmonary veins.

59
Q

What do we see on an ECG for AF?

A

Over 300 bpm, irregularly irregular, variable ventricular rate, has an absence of P waves and presence of F waves.

60
Q

What is AF dependent upon?

A

AV node conduction properties, sympathetic and parasympathetic tone and presence of drugs that act on the AV node.

61
Q

What ventricular rates can we have with AF?

A

Either slow or fast.

62
Q

What is AF with fast ventricular rate also called?

A

Pseudo regularisation.

63
Q

What does AF result in?

A

Lost atrial kick and reduced filling times leading to reduced diastole and reduced cardiac output.
Can result in CHF especially in the presence of diastolic dysfunction.

64
Q

What does AF combined with ventricular rates of under 60 bpm suggest?

A

AV conduction disease.

65
Q

What are the different types of management we use for AF?

A

Rhythm control - maintain sinus rhythm predominantly.
Rate control - accept AF but control the ventricular rate.
Anti coags for both approaches.

66
Q

What are the treatment options for rate control?

A

Pharmacological drugs to slow down AVN conduction.

Digoxin, Betablockers, verapamil, diltiazem.

67
Q

What does supra ventricular mean?

A

Origin is above the ventricle e.g. AV node, SA, atrial muscle or HIS origin.

68
Q

What are the treatment options for rhythm control?

A

For restoration of NSR - pharmacological cardioversion with anti arrhythmic drugs. Or direct current cardioversion.
For maintenance of NSR - anti arrhythmic drugs. Catheter ablation of atrial focus or pulmonary veins. Surgery (maze procedure).

69
Q

What channels do class 1 anti arrhythmic drugs block? What phase in action potential does this correlated with? What are their main uses in AF?

A

Na channels
Phase 0
Rhythm control.

70
Q

What channels do class II anti arrhythmic drugs block? What phase in action potential does this correlated with? What are their main uses in AF?

A

Beta receptors
Phase 4
Rate control

71
Q

What channels do class III anti arrhythmic drugs block? What phase in action potential does this correlated with? What are their main uses in AF?

A

Potassium channels.
Phase 3
Rhythm control

72
Q

What channels do class IV anti arrhythmic drugs block? What phase in action potential does this correlated with? What are their main uses in AF?

A

Calcium channels
Phase 2
Rate control.

73
Q

What are examples of class I anti arrhythmias?

A

Lignocaine, quinidine, flecainide and propafenenone.

74
Q

What are examples of class II anti arrhythmias?

A

Beta blockers e.g. Propranolol.

75
Q

What are examples of class III anti arrhythmias?

A

Amiodarone, solatol and drondarone.

76
Q

What are examples of class IV anti arrhythmias?

A

Calcium channel blockers which as verapamil.

77
Q

What is torsades de pointes? How do we recognise it on ECG?

A

Heart rate of 200-250. Irregular rhythm. Can be recognised form a long QT interval and wide QRS. It has a continuously changing QRS morphology.

78
Q

What mechanisms lead to torsades de pointes?

A

Hypokalemia, drug induced prolonged action potential duration and renal impairment.

79
Q

Which patients are at high risk of PE?

A 
Valvular heart disease.
Aged over 75 especially females.
Hypertension.
Heart failure
Previous PE
Coronary artery disease or diabetes over the age of 65.
Thyrotxicosis
80
Q

What are the indications for anti coagulation in AF?

A

Valvular AF, mitral valve disease,

non valvular AF if:over 75, hypertension, previous stroke or thromboembolism. CAD and DM.

81
Q

How do we calculate stroke risk in AF?

A

CHA2DS2-VASc score.

82
Q

What are the parts of the CHA2DS2-VASc score?

A 
CHD or LV dysfunction.
Hypertension.
Age over 75 years.
DM
Stroke
Vascular disease
Age 65-74
Sex - female.

One point for each except after the 2 with 2s in the name.
Higher the score is bigger the risk.

83
Q

What acronym do we use for the bleeding assessment risk? What do the letters mean?

A 
Hypertension
Abnormal renal or liver function
Stroke
Bleeding
Labile INRs
Elderly over the age of 65 years
Drugs or alcohol.

Score over 3 is high risk.

84
Q

What do we use radiofrequency ablation in AF?

A

To maintain SR by ablating AF focus (usually in the pulmonary veins).
For rate control - ablation in the AV node to stop fast conduction in the ventricles.

85
Q

Where is the ectopic focus commonly?

A

In the muscle sleeve sin the Ostia of the pulmonary veins.

86
Q

What is atrial flutter?

A

Rapid and regular form of atrial tachycardia. Usually paroxysmal and sustained by a micro re entrant circuit. The circuit is confined to the right atrium.

87
Q

How long to atrial flutter episodes last and what can they lead to?

A

Seconds to years. Chronic can lead to AF and thromboembolism.

88
Q

What is the treatment for atrial flutter?

A

RF ablation.
Drugs to slow the ventricular rate and restore and maintain sinus rhythm.
Cardioversion.
Warfarin to prevent thrombus.

89
Q

What does atrial flutter look like on ECG?

A 
Rate of 300, ventricular usually 150.
No P waves but saw tooth f wave.
Normal QRS.
Normal conduction but physiologic 2:1
The rhythm is regular but may be variable.
90
Q

What are the goals in AF management?

A

Symptom control, improved cardiac outcomes. Stroke prevention. Treatment of existing disease. Avoid drug toxicities, restore to Simons rhythm.

91
Q

What is the commonest cause of AF?

A

Hypertension.

92
Q

What is another name for a malar flush?

A

Mitral face.

1st Year Medicine (64 decks)

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