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Arrhythmias Flashcards

1
Q

where is the origin of a supraventricular arrhythmias?

A

above the ventricle

ie SA, atria, AV, HIS

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2
Q

where is the origin of a ventricular arrhythmia?

A

ventricle

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3
Q

what should be the only point of electrical contact between the atria and the ventricles?

A

AV node

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4
Q

what are ectopic beats?

A

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

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5
Q

what are 3 common supraventricular tachycardias?

supraventricular arrhythmias

A

AF
Atrial flutter
ectopic atrial tachycardia

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6
Q

what are 2 common supraventricular bradycardia arrhythmias?

A

sinus bradycardia

sinus pauses

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7
Q

what are 3 common AV node arrhythmias?

A

AVN re-entry
Accessory pathway
AV block

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8
Q

what are 4 common ventricular arrhythmias?

A

premature ventricular complex (PVC)
ventricular tachycardia
ventricular fibrillation
asystole

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9
Q

what causes premature ventricular complexes?

A

ectopic beats originating from the ventricles

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10
Q

how can an accessory pathway arrhythmia be acquired?

A

MI

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11
Q

how can sleep apnoea cause arrhythmias?

A

because patients get hypoxic at night- metabolic cause of arrhythmia

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12
Q

what type of arrhythmia occurs in Wolf Parkinson White syndrome (WPW)?

A

re-entry:

accessory pathway tachycardia

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13
Q

what does hypothermia do to the pacemaker potential slope?

A

decreases slope- negative chronotropic effect

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14
Q

what does hyperthermia do to the pacemaker potential slope?

A

increases slope- positive chronotropic effect

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15
Q

what does hypoxia do to the pacemaker potential slope?

A

increases slope- positive chronotropic effect

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16
Q

what does hypercapnia do to the pacemaker potential slope?

A

increases slope- positive chronotropic effect

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17
Q

why can ischaemia or necrosis increase ectopics?

A

because local areas of ischaemia or necrosis increases automaticity of neighbouring cells

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18
Q

what does hypokalaemia do to the pacemaker potential slope, automaticity and length of repolarisation?

A 
increase pacemaker potential slope
increases automaticity (therefore increases ectopics)
prolongs repolarisation
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19
Q

what does hyperkalaemia do to the pacemaker potential slope and AV conduction?

A

decreases pacemaker potential slope

slows AV node conduction

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20
Q

what is an afterdepolarisation?

A

a small depolarisation after the repolarisation phase of an AP, if this is of sufficient magnistude this will reach threshhold and lead to a full depolarisation- triggered activity

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21
Q

what are the 5 main symptoms of an arrhythmia?

A 
palpitations
SOB
dizziness
syncope
sudden cardiac death
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22
Q

what are the 7 investigations used for a suspected arrhythmias?

A 
12 lead ECG
CXR
echocardiogram
stress ECG
24 hour ECG Holter monitoring
event recorder
Electrophysiological study
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23
Q

what type of heart disease do echocardiograms show?

A

structural heart disease

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24
Q

what is a stress ECG?

A

heart is provoked in a controlled way, ischamia or arrhythmias may only be present when the cardiac demand is higher

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25
what is an event recorder?
a monitor which only turns the recorder on if it detects a change- if the patient feels symptoms it can manually be switched on
26
what is an electrophysiological stufy?
an invasive investigation which deliberately induces a clinical arrhythmia to study mechanism and map the pathway opportunity to treat the arrhythmias by radiofrequency ablation
27
what is pre-excitation?
accessory pathway from atria to ventricles for AP to flow
28
what is the function of a 24 hour Holter ECG?
assesses for paroxysmal arrhythmias | heart rhythm is rarely captured though
29
what vein is the catheter for an electrophysiological study usually put through?
femoral vein
30
if an atrial ectopic beat is asymptomatic how do you treat?
no treatment
31
if an atrial ectopic beat has palpitations how do you treat?
``` beta blockers stimulant avoidance (caffeine, cigarettes) ```
32
what type of STEMI is most likely to cause sinus bradycardia?
inferior MI
33
how do you treat acute sinus bradycardia?
atropine
34
how do you treat sinus bradycardia if it causes haemodynamic compromise?
pacing
35
compare SVT to VT on ECG?
SVT- narrow complex tachycardia | VT- broad complex tachycardia
36
why are SVTs generally more tolerated than VTs?
because there are narrow complexes it means the heart is still pumping in a meaningful way
37
what is the purpose of vagal manoeuvers?
to stop supra-ventricular tachycardias
38
what is the vagal manouevre for infants?
ice water to face
39
what are the vagal manouevres for children?
blow through straw (valsalva manoeuvre) | carotid sinus massage
40
what are the vagal manouevres for adults?
``` carotid sinus massage breath holding coughing NG placement gagreflex anal sweep ```
41
what 3 things may supraventricular tachycardias be due to?
AV nodal re-entrant tachycardia accessory pathway tachycardia (ie WFW) ectopic atrial tachycardia
42
what are the 2 types of re-entry tachycardia?
AV nodal re-entry | accessory pathway
43
where is the accessory pathway circuit in an AV nodal re-entry arrhythmia?
AV node itself
44
what is the acute management of a SVT?
vagal maneuvres IV adenosine IV verapamil
45
what is the chronic management of a SVT?
``` avoid stimulants radiofreq ablation antiarrhythmic drugs (class II or IV) ```
46
what is radioablation of an arrhythmia?
selective cautery of cardiac tissue to prevent tachycardia, targetting either an automatic focus or part of a re-entry circuit
47
what specific valve disease/surgery is most likely to disrupt the AV node?
aortic valve | eg calcification or surgery
48
what is 1st degree AV node block?
PR interval longer than 0.2s
49
what is the treatment of 1st degree AV node block?
none but long term follow up recommended
50
what is 2nd degree AV node block- Mobitz 1?
progressive lengthening of the PR interval, eventually resulting in a dropped beat (vagal in origin)
51
what is 2nd degree AV node block- Mobitz 2?
intermittent dropped beats without lengthening, usually 2:1 or 3:1
52
which mobitz type is more indicative of a pathological cause?
mobitz type 2
53
what is the interventional indication for 2nd degree AV block mobitz type 2?
permanent pacemaker indicated (ventricular pacing)
54
what is 3rd degree AV block?
no APs from atria get through AV node (full block) ventricles and atria contract with no correlation
55
in full heart block, what maintains ventricular rhythm? (and so maintains cardiac output)
escape rhythm | ie starts from somewhere else, not in sinus rhythm
56
what is the interventional indication for 3rd degree AV block?
pacemaker
57
describe the QRS complexes in 3rd degree heart block?
very broad
58
what are the 2 acute pacing options?
transcutaneous pacer | transvenous pacer
59
what are the 2 chamber options of a pacemaker?
``` single chamber (RA or RV) dual chamber (RA and RV) ```
60
what are single RA chamber pacemakers (atrial pacemakers) used for?
isolated SA disease with normal AV node
61
what are single VR chamber pacemakers (ventricular pacemakers) used for?
AF with slow ventricular rate
62
what is the dual chamber pacemaker used for?
AVN disease
63
what is a bad diagnostic sign when investigating a premature ventricular ectopic?
if worse on exercise
64
what drug treatment can be used for premature ventricular ectopics?
B blockers
65
what is ventricular fibrillation?
chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump
66
what is the acute treatment of VT with unstable haemodnamics?
DC cardioversion
67
what is the acute treatment of VT with stable haemodynamics?
pharmacological cardioversion with anti-arrhythmic drugs
68
what is the long term treatment for life threatening VT?
implantable cardiovertor defibrillator
69
what type of pulse is typical of AF?
irregularly irregular pulse
70
what are the 3 types of AF patterns?
paroxysmal persistent permanent (chronic)
71
which pattern of AF is most associated with heart disease?
permanent AF
72
why can pseudonormalisation occur with AF?
because the AF is so fast it looks like normal rhythm
73
what is paroxysmal AF?
occur in (often recurrent) sudden attacks that last less than 48 hours
74
what is persistent AF?
an episode of AF lasting greater than 48 hours, unlikely to spontaneously revert to NSR but can be cardioverted back
75
what is permanent AF?
AF which is unable to be restored to NSR by pharmacological or non pharmacological methods
76
what is lone AF? | idiopathic AF
AF which occurs in the absence of any heart disease and no evidence of dysfunction (a diagnosis of exclusion)
77
what are the 7 main symptoms of AF?
``` palpitations pre-syncope (dizziness) syncope chest pain dyspnoea sweatiness fatigue ```
78
what are the 2 most common mechanisms of AF?
multiple wavelets of re-entry | ectopic focus around pulmonary veins
79
what are 3 ways of reverting AF back to NSR?
spontaneous pharmacological cardioversion (anti-arrhythmic drugs) electrical cardioversion
80
how do you recognise AF on an ECG? | ie what extra or missing waves are there
absence of P waves | presence of f waves
81
what does pre-excitation of the ventricles do the QRS complex?
broadens it
82
what are the 2 management options for controlling AF?
rhythm control | rate control
83
what is the purpose of rhythm control management?
to maintain sinus rhythm
84
what is the purpose of rate control management?
accept AF but control ventricular rate
85
what do you use in high risk AF to prevent thromboembolism?
anti-coagulation | warfarin
86
what are 3 rate controlling anti-arrhytmic drugs?
digoxin beta blockers calcium antagonists (verapamil, diltiazem)
87
what procedures can be done to restore AF to NSR?
direct current cardioversion catheter ablation of atrial focus/pulmonary veins surgery
88
what are class 1 anti-arrhythmic drugs?
Na+ channel inhibitors
89
what are class 1 anti-arrhythmic drugs used for?
rhythm contol
90
what are class 2 anti-arrhythmic drugs?
b-blockers
91
what are class 2 anti-arrhythmic drugs used for?
rate control
92
what are class 3 anti-arrhythmic drugs used for?
K+ chanel inhibitors
93
what are class 3 anti-arrhythmic drugs used for?
rhythm control
94
what are class 4 anti-arrhythmic drugs?
Calicium inhibitiors
95
what are class 4 anti-arrhythmic drugs used for?
rate conrol
96
what type of drugs are flecainide and propafenone?
``` class 1 anti-arrhythmic drugs Na+ channel inhibitors (rhythm controllers) ```
97
what type of drugs are amiodarone and sotalol?
``` class 3 anti-arrhythmic drugs K+ channel inhibitors (rhythm controllers) ```
98
how do you recognise torsades de pointes on an ECG?
``` heart rate of 200-250bpm irregular rhythm long QT interval wide QRS continously changing QRS morphology ```
99
what are the 3 mechanisms leading to torsades de pointes?
``` hypokalemia drug induced- prolongation of the AP duration renal impairment (causing increased drug levels) ```
100
what are the indications for anti-coagulation in AF?
1. valvular disease 2. age >75 3. hypertension 4. heart failure 5. prev stroke/thromboembolism 6. diabetes
101
what is the role of radiofrequence ablation in AF?
either to maintain SR by ablating AF focus or for rate control by ablation of AVN
102
in AF where are the ectopic foci usually found?
in muscle sleeves in the ostia of the pulmonary veins
103
what is atrial flutter?
rapid and regular form of atrial tachycardia (AV only conducts every 2/3 impulse so ventricle rhythm can appear more normal)
104
in atrial flutter what replaces the p wave?
saw tooth F wave
105
what is the mechanism behind atrial flutter?
macro-reentry
106
what is the treatment option with the best success in atrial flutter?
radiofrequency ablation

Cardiovascular RT (12 decks)

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