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Cardiovascular Conditions (JBR) > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What is atrial fibrillation?

A

Chaotic, disorganised atrial activity

Irregular atrial rhythm at 300-600 bpm

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2
Q

What mechanism causes atrial fibrillation?

A

Chaotic re-entrant impulse conduction
All meaningful atrial contraction is lost and micro-pathway compare with each other
Ectopic focus around the pulmonary veins

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3
Q

What causes AF?

A 
HF/IHD
Hypertension
MI
PE 
Mitral valve disease
Pneumonia
Hyperparathyroidism
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4
Q

What are associated causes of AF?

A 
Alcohol abuse 
Congenital heart disease
Cardiac surgery
COPD 
Septicaemia
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5
Q

What is paroxysmal AF?

A

<48 hours, often recurrent

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6
Q

What is persistent AF?

A

> 48

Can still be cardioverted to NSR

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7
Q

What is permanent AF?

A

Can’t restore NSR

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8
Q

What are symptoms/signs? (AF)

A 
May be asymptomatic
Chest pain
Palpitations
Dyspnoea
Faintness
Sweatiness
Irregularly irregular pulse
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9
Q

What are investigations? (AF)

A

ECG - absent P waves, irregular QRS complexes, “f”-waves

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10
Q

What are complications of AF?

A

Embolic stroke

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11
Q

What are the three aims of AF treatment?

A

Rate control
Restore NSR
Maintain NSR

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12
Q

Which drugs can be used for rate control? (AF)

A

Digoxin (if HF)
Beta-blocker
Verapamil or diltiazem

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13
Q

What is digoxin?

A

Cardiac glycoside

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14
Q

What is the mechanism of digoxin?

A

Binds (blocks) to alpha subunit of sarcolemma Na/K/ATPase in competition with K
Increase Na-Ca exchange
Increase store of Ca in SR
Increase contractility

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15
Q

What are indirect effects of Digoxin?

A

Increase vagal activity
Slow AV discharge and AV node conduction
Increase refractory period

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16
Q

What are direct effects of digoxin?

A

Shorten AP and refractory period in atrial/ventricular myocytes

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17
Q

Toxic concentrations of digoxin cause?

A

Membrane depolarisations and oscillatory after-potentials

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18
Q

What are side effects of dioxin?

A 
Heart block 
Propensity to cause arrythmias
Nausea
Vomiting
Diarrhoea
Disturbance of colour vision
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19
Q

Why can digoxin cause heart block?

A

Excessive AV node depression

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20
Q

What are methods to restore NSR? (AF)

A

DCCV

AADs

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21
Q

AADs generally inhibit specific ion channels with intention of…?

A

Suppression of abnormal electrical activity

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22
Q

What is the mechanism and effect of Disopyramide?

A

Block/unblock sodium channels at moderate rate

Slow rate of rise of AP and prolong refractory period

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23
Q

What is the mechanism and effect of Flecainide?

A

Slow block/unblock of Na channels

Strongly depress conduction in myocardium and reduce contractility

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24
Q

What is the mechanism and effect of Lignocaine?

A

Block/unblock Na channels at rapid rate

Prevent premature beats

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25
Q

Lignocaine primary affects sodium channels in the area of the myocardium that?

A

Rapidly firs APs due to rapid unbinding (Na channels)

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26
Q

What is the main use of Lignocaine?

A

Post-MI ventricular arrhythmias

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27
Q

What is metoprolol?

A

A beta-adrenoceptor antagonist

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28
Q

What is the mechanism and effect of metoprolol?

A

Decrease rate of depolarisation in SA and AV nodes

Suppress sympathetic drive that may trigger V-tach

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29
Q

What is the mechanism and effect of Amiodarone?

A

Slow depolarisation of AP by block of K channels
Increase AP duration and effective refractory period
Suppress re-entry

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30
Q

Amiodarone is mainly used to treat?

A

SVT and VT

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31
Q

What are side effects of amiodarone?

A

Pulmonary fibrosis
Thyroid disorders
Photosensitive reactions
Peripheral europathy

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32
Q

What is the mechanism and effect of Veramapil?

A

Blocks L-type Ca channels
Slow conduction and prolong refractory period in AV node and bundle of His

Slow conduction in SA/AV nodes & decrease force of cardiac contraction

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33
Q

What is Veramapil used for? (AF)

A

Prophylaxis (adenosine for acute) of atrial fibrillation and flutter

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34
Q

What are methods for NSR maintenance? (AF)

A

AADs
Catheter ablation of ectopic focus (pulmonary veins)
Surgery (Maze procedure)

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35
Q

What is atrial flutter?

A

Rapid and regular form of atrial tachycardia (250-350 bpm)

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36
Q

Atrial flutter is usually _____ with espides lasting?

A

Paroxysmal

Seconds-years

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37
Q

What is the mechanism behind atrial flutter?

A

Macro re-entrant pathways

Circuit confined to the atrium

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38
Q

What are signs and symptoms of Atrial flutter?

A

Palpitations
Dyspnoea
Fast and steady pulse

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39
Q

How is Atrial flutter diagnosed?

A

ECG

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40
Q

How is Atrial flutter treated?

A 
Termiantion (rapid atrial pacing, cardioversion or AADs) 
May convert spontaenously
RF ablation
Warfarin to prevent thromboembolism
Obesity and alcohol reduction
Anticoagulants to reduce stroke risk
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41
Q

What is sinus bradycardia?

A

HR <60 bpm

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42
Q

What can cause sinus bradycardia?

A

Physiological (athletes)
Drugs (beta-blockers)
Ischaemia (common in inferior STEMIs)

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43
Q

how do you treat sinus bradycardia?

A

Atropine

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44
Q

Atropine is an example of a?

A

Non-selective muscarinic ACh receptor antagonis

45
Q

Atropine increases?

46
Q

Atropine is the 1st line management of?

A

Severe symptomatic bradycardia (particularly following MI)

47
Q

In MI atropin is given in?

A

Incremental doses

48
Q

Atropin is used in ________ poisoning?

A

Anticholinesterase

49
Q

What is the effect of ACh activating M2 muscarinic cholinoceptors?

A

Decrease activity of adenylate cycles + opens potassium channels to cause hyper polarisation of SA node

Decreases HR, contractility and conduction in AV node

50
Q

How is sinus bradycardia treated if the patient is harm-dynamically compromised?

51
Q

What causes supraventricular tachycardia?

A

Re-entry involving the AV & SA node or atrial tissue

52
Q

What is SVT?

A

Narrow complex tachycardia

53
Q

Which ECG features distinguish SVT?

A

Rate > 100 bpm

QRS width <120 ms

54
Q

What is the atrial firing rate in SVT?

55
Q

How do you manage acute SVT?

A

Increase vagal tone via valsalva maneouvre +/- carotid massage

56
Q

Which drugs slow conduction in the AV node?

A

(iv) adenosine and veramapil

57
Q

Adenosine activates ______

A

A1-adenosine receptors

58
Q

What is the effect of A1-adenosine receptor activation?

A

opens ACh sensitive K-channels
hyperpolarise AV node briefly
Suppress impulse conduction

59
Q

Adenosine is used to stop _____ SVT

A

paroxysmal

60
Q

Describe Torsade de Points

A

Heart rate of 200-259 bpm
Irregular rhythm
Long QT, wide QRS, continuously changing QRS

61
Q

How do you treat Torsade de Points?

A

Magnesium sulphate

62
Q

What is ventricular fibrillation?

A

Chaotic ventricular activity
No QRS complexes
Random frequency and amplitude
Uncoordinated electrical activity

63
Q

Patients in V-fib may be ________ unstable

A

haemodynamically

64
Q

How do you treat V-Fib?

A

CPR

Defibrillation

65
Q

What is monomorphic ventricular tachycardia?

A

Broad complex rhythm
Rapid rate
Constant QRS morphology

66
Q

What is polymorphic V-tach?

A

Torsade de Points

67
Q

V-tach patients may be _______ unstable

A

haemodynamically

68
Q

How do you treat V-tach?

A

precordial thump if defib not immediately available

DCCV

69
Q

If a patient is V-tach is stable you can consider?

A

AADs

Inmeantime prepare for DCCV

70
Q

How can you confirm diagnosis of V-tach if unsure?

71
Q

How is V-tach treated long-term?

A

Correct ischaemia (revascularisation if possible)
Optimise CHF treatment therapy
ICD if life-threatening
VT catheter ablation

72
Q

What can an ICD do?

A

Terminate VT/VF, anti-tachycardia pacing, cardioversion and defibrillation + pace atria and ventricles for bradycardia

73
Q

What is Wolff-Parkinson White Syndrome?

A

Congenital accessory conductance pathway between atria and ventricles

74
Q

What symptoms/signs are there in WPWS?

A

SVT (may be due to AVRT - AV nodal re-entrant pathway)

Pre-excited AF or pre-excited atrial flutter

75
Q

How do you diagnose WPWS?

A 
ECG - short PR interval, wide QRS
Delta wave (slurred upstroke)
76
Q

How do you treat WPWS?

A

Electrophysiology and radio frequency ablation of accessory pathways

77
Q

What is radio frequency ablation (RFCA)?

A

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

78
Q

What are causes of heart block?

A 
Ageing
Acute MI
Myocarditis
Amyloid
Beta-blockers of CCBs
Post-aortic valve surgery
Calcific aortic valve disease
Lenegre's disease (genetic)
Myotonic dystrophy
79
Q

What is Lenegre’s disease?

A

Idiopathic fibrosis of the cardiac conduction system

80
Q

What is 1st degree Heart block?

A

Prolonged Pr interval - delayed conduction

81
Q

What are complications of first degree heart block?

A

More advanced block may over time

82
Q

How do you manage first degree heart block?

A

Ya don’t

83
Q

What are the two types of second degree heart block?

A

Mobitz Type I and II

84
Q

What is 2nd degree heart block mobitz type 1?

A

Cyclical prolongation of PR interval with eventual dropped beats

85
Q

What are causes of Mobitz type I?

A

Usually increased vagal tone

Others: myocardial ischaemia, side effect of CCB, digitals or beta-blockers

86
Q

What is 2nd degree Heart block Mobitz type II?

A

P wave not always followed by QRS )2:1 or 3:1)

87
Q

What are complications of mobitz type II?

A

May progress to complete heart block

88
Q

How do you manage mobitz type II?

A

Permanent pacemaker indicated

89
Q

What is third degree heart block?

A

Complete heart block
Atrial and ventricular dissociation
Lonely P waves
Chaotic PR intervals

90
Q

How do you manage complete heart block?

A

Ventricular pacing

91
Q

What ECG changes are observed in a right bundle branch block?

A

V1 for M wave and V6 for W wave

92
Q

Why is the cardiac axis unchanged is isolated RBBB?

A

Because left ventricular activation proceeds normally via the left bundle branch

93
Q

What is seen on ECG for LBBB?

A

V6 for M wave and V1 for W wave

94
Q

What is sinus tachycardia?

A

HR > 100 bpm

95
Q

What are causes of sinus tachycardia

A

Physiological (anxiety, fever, hypotension, anaemia)
Drugs
Other

96
Q

How do you treat sinus tachycardia?

A

Underlying cause

Beta-adrenergic bockers

97
Q

What cause Ventricular ectopic beats?

A

Structural (LH/HF/myocarditis), metabolic (IHD; electrolytes) or inherited conditions

98
Q

You should investigate further if ventricular ectopic beats are worse on?

99
Q

How do you treat ventricular ectopic beats?

A

Beta blocker +/- ablation of focus

100
Q

How do beta blockers help to restore sinus rhythm?

A

Decrease excessive sympathetic drive - delay conduction through the AV node (to ventricles) and help restore sinus rhythm

101
Q

What are the side effects of beta-blockers?

A 
Bronchospasm
Aggravation of cardiac failure 
Bradycardia 
Hypoglycaemia (if poorly controlled diabetes) 
Fatigue
Cold extremities
102
Q

Atrial ectopics can be asymptomatic or cause?

A

Palpitations

103
Q

Atrial ectopic are usually not treated but _____ may help. Key to management is?

A 
beta-blockers
Avoiding stimualnts (caffeine / cigarettes)
104
Q

What are the causes of arrhythmias?

A

Afterdepolarisation - triggered activity
Structural
Functional

105
Q

What is given to diagnose AF if it is so fast that it appears regular but there are subtle interval changes?

A

Give adenosine to slow AV conduction and visualise fibrillatory waves in background

106
Q

When should you NOT give a patient adenosine?

A

If they have had a previous heart attack or very brittle/uncontrolled asthma

107
Q

Ventricular fibrillation is always associated with?

A

Loss of consciousness

108
Q

What is defined as a prolonged PR interval?

A

> 200 ms (> 5 small squares)

109
Q

Tall tented T-waves indicate?

A

Hyperkalaemia

Cardiovascular Conditions (JBR) (20 decks)

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