Caridac Arrhythmias Flashcards Preview

1st Year Medicine > Caridac Arrhythmias > Flashcards

Flashcards in Caridac Arrhythmias Deck (92):
1

What is an ectopic beat?

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

2

Are ectopic beats dangerous?

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

3

When to ectopic beats more commonly happen?

At night.

4

What are the supra ventricular tachycardias?

Superventricular tachycardia, bradycardia and atrioventricular node arrhythmias

5

What are the supra ventricular tachycardias?

Atrial fibrillation, atrial flutter and ectopic atrial tachycardia.

6

What are the AV node arrhythmias?

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

7

What are the ventricular arrhythmias?

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

8

What can be the clinical causes of arrhythmias?

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

9

What are some abnormal anatomies that can cause arrhythmias?

LVH, accessory pathways and congenital HD.

10

What are some autonomic causes of arrhythmias?

Sympathetic stimulation such as nervousness and exercise.
Increased vagal tone such as bradycardia and heart block.

11

What are some metabolic causes of arrhythmias?

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

12

What are some genetic causes of arrhythmias?

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

13

What are some physiological causes of arrhythmias?

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

14

What is wolf Parkinson white syndrome?

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.

15

What is type A WPW syndrome?

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.

16

What is type B WPW syndrome?

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.

17

What are the symptoms of WPW syndrome?

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

18

What is triggered activity?

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.

19

Whit is triggered activity considered to be the mechanism for?

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

20

What investigations do we do for arrhythmias?

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.

21

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

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

22

What is sinus bradycardia? What can cause it?

Under 60 bpm.
may be physiological e.g. Athletes. Beta blockers can cause it. Also ischaemia which is common in inferior STEMIs.

23

What is the treatment of bradycardia?

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

24

What is tachycardia? What can cause it?

HR of over 100 bpm.
Can be physiological activity e.g. Exercise and drugs.

25

What is the treatment of tachycardia?

Treat underlying cause and give beta blockers.

26

What blood test should be done for arrhythmias?

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

27

What may cause supraventricular tachycardia?

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

28

How do we manage supraventricular tachycardia?

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

29

What is the procedure for cardiac ablation?

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.

30

What can cause AVN conduction disease?

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

31

What is first degree AV block?

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.

32

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

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.

33

What is the treatment of a mobitz 2 heart block?

Permanent ventricular pacemaker may be required.

34

What is third degree AV block?

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

35

What is the treatment of third degree AV block?

Ventricular pacing.

36

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

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.

37

What two different types of pacemakers do we get?

Single chamber - paces atrial or ventricle only.
Dual chamber - paces the atrium and the ventricle simultaneously.

38

When do we use atrial pacemakers?

In isolated SA node disease but normal AV node.

39

When do we use ventricular pacemakers?

AF with slow ventricular rate.

40

When do we use dual chamber pacemakers?

Used for AVN disease.

41

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

Investigate further and consider beta blockers.

42

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

Life threatening but may be haemodynamically stable.
Caused by coronary artery disease or previous MI.

43

What are rare cause of VT?

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

44

What is ventricular fibrillation?
How do we treat it?

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

45

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

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

46

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

Consider adenosine to make a diagnosis.

47

What causes are we looking for in VT?

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

48

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

Sotalol, quinidine, terfenadine and erythromycin.

49

What is the long term treatment for VT?

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

50

What greatly increases the likelihood of AF?

Increasing age.

51

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

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

What is paroxysmal AF?

Lasting less than 48 hours, often recurrent.

53

What is persistent AF?

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

54

What is permanent AF?

Cannot restore NSR by any method.

55

What are diseases associated with AF?

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

56

What is lone AF?

It is idiopathic, has an absence of any heart disease.
Gives a significant stroke rate of over the age of 75.

57

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

Often worse at onset.
Palpitations, pre syncope (dizziness), syncope, chest pain, dyspnoea, sweating and fatigue.

58

What is the mechanism of AF?

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

59

What do we see on an ECG for AF?

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

60

What is AF dependent upon?

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

61

What ventricular rates can we have with AF?

Either slow or fast.

62

What is AF with fast ventricular rate also called?

Pseudo regularisation.

63

What does AF result in?

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

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

AV conduction disease.

65

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

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

66

What are the treatment options for rate control?

Pharmacological drugs to slow down AVN conduction.
Digoxin, Betablockers, verapamil, diltiazem.

67

What does supra ventricular mean?

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

68

What are the treatment options for rhythm control?

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

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?

Na channels
Phase 0
Rhythm control.

70

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?

Beta receptors
Phase 4
Rate control

71

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?

Potassium channels.
Phase 3
Rhythm control

72

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?

Calcium channels
Phase 2
Rate control.

73

What are examples of class I anti arrhythmias?

Lignocaine, quinidine, flecainide and propafenenone.

74

What are examples of class II anti arrhythmias?

Beta blockers e.g. Propranolol.

75

What are examples of class III anti arrhythmias?

Amiodarone, solatol and drondarone.

76

What are examples of class IV anti arrhythmias?

Calcium channel blockers which as verapamil.

77

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

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

What mechanisms lead to torsades de pointes?

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

79

Which patients are at high risk of PE?

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

What are the indications for anti coagulation in AF?

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

81

How do we calculate stroke risk in AF?

CHA2DS2-VASc score.

82

What are the parts of the CHA2DS2-VASc score?

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

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

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

What do we use radiofrequency ablation in AF?

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

Where is the ectopic focus commonly?

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

86

What is atrial flutter?

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

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

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

88

What is the treatment for atrial flutter?

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

89

What does atrial flutter look like on ECG?

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

What are the goals in AF management?

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

91

What is the commonest cause of AF?

Hypertension.

92

What is another name for a malar flush?

Mitral face.