Arrhythmias Flashcards
1
Q
What are arrhythmias?
A
Disturbances in heart rate or rhythm that can be caused by changes in impulse formation or impulse conduction
2
Q
Where do supraventricular arrhythmias arise?
A
In the atria or AV node
3
Q
Where do ventricular arrhythmias arise?
A
In the ventricles
4
Q
What do alterations in impulse formation involve?
A
Changes in automaticity, triggered activity
5
Q
What do abnormalities in impulse conduction arise from?
A
Re-entry, conduction block, accessory tracts
6
Q
Rate of pacemaking in the AV node
A
50-60bpm
7
Q
Rate of pacemaking in the purkinje fibres
A
30-40bpm
8
Q
Overdrive suppression
A
The SA node pacemaking is the highest and is dominant over other latent pacemakers
9
Q
What happens if overdrive suppression is lost?
A
That triggers the latent pacemakers to take over
10
Q
What can cause loss of overdrive suppression?
A
SA node firing frequency is pathologically low, conduction of impulse from SA node is impaired, if a latent pacemaker fires at an intrinsic rate faster if SA node despite SA node functioning normally, as a response to tissue damage
11
Q
Ectopic beat
A
A heartbeat due to an impulse generated somewhere in the heart outside the AV node. A series of these can generate an ectopic rhythm
12
Q
What things can cause an ectopic rhythm?
A
Ischaemia, hypokalaemia, increased sympathetic activity, fibre stretch
13
Q
Afterdepolarisations
A
When a normal action potential triggers abnormal oscillations in the membrane potential
14
Q
Two types of afterdepolarisations
A
Early afterdepolarisations and delayed afterdepolarisation
15
Q
When do early afterdepolarisations occur?
A
During the inciting action potential within late phase 2 (terminal plateau) and early phase 3 (partial repolarisation occurring)
16
Q
What are early afterdepolarisations occurring in late phase 2 mediated by?
A
Calcium channels when sodium channels are still closed
17
Q
What are early afterdepolarisations occurring in early phase 3 mediated by?
A
Sodium channels
18
Q
When are early afterdepolarisations most likely to occur?
A
When heart rate is low
19
Q
What are early afterdepolarisations associated with?
A
Purkinje fibres, prolongation of the action potential and drugs that prolong the QT interval
20
Q
When do delayed afterdepolarisations occur?
A
After complete repolarisation
21
Q
What are delayed afterdepolarisations caused by?
A
Large increases in calcium
22
Q
How do large increases in calcium result in delayed afterdepolarisations?
A
Excessive calcium results in oscillatory release of calcium from sarcoplasmic reticulum and a transient inward current that occurs in phase 4
23
Q
When are delayed afterdepolarisations most likely to occur?
A
When the heart rate is fast
24
Q
What can delayed afteredepolarisations be triggered by?
A
Drugs that increase the calcium influx or release of calcium from the sarcoplasmic reticulum (e.g. digoxin)
25
Defects in impulse conduction causing arrhythmias
Re-entry, conduction block (through AV node)
26
What do re-entry arrhythmias involve?
A self sustaining electrical circuit that stimulates an area of the myocardium repeatedly/rapidly
27
What does the re-entrant circuit require?
Unidirectional block and slowed retrograde conduction velocity
28
What does unidirectional block involve?
Anterograde conduction is prohibited and retrograde conduction is allowed (action potential goes back through in the 'wrong' direction in the damaged cells)
29
First degree conduction block:
- What happens in this?
- What will be seen on an ECG?
- The tissue conducts all impulses but more slowly than usual
- Long PR interval seen on ECG (>0.2s)
30
2 types of second degree conduction block
Mobitz type I, Mobitz type II
31
Describe mobitz type I conduction block
The PR interval gradually increases from cycle to cycle until AV node fails and a ventricular beat is missed
32
Describe mobitz type II conduction block
The PR interval is constant but every nth ventricular depolarisation is missing
33
Describe complete conduction block (aka third degree conduction block)
Atria and ventricles beat independently governed by their own pacemakers. Ventricular pacemaker is now the Purkinje fibres – fire relatively slowly and unreliably – manifest as bradycardia and low cardiac output
34
Example of accessory tract pathway
Bundle of Kent
35
What is an accessory tract pathway?
An electrical pathway in parallel to the AV node
36
Describe speed of impulse in Bundle of Kent vs AV node
Impulse through Bundle of Kent is conducted more quickly than the AV node
37
What happens in the ventricles with an accessory pathway
Ventricles receive impulses from both the normal and accessory pathways – can set up the condition for a re-entrant loop predisposing to tachyarrhythmias
38
What do anti-arrhythmic drugs generally do?
Inhibit specific ion channels with the intention of suppressing abnormal electrical activity
39
Vaughn Williams classification of anti-arrhythmic drugs:
- Ia - target and example
- Ib - target and example
- Ic - target and example
- II - target and example
- III - target and example
- IV - target and example
- Ia = Voltage-activated Na+ channel, e.g. Disopyramide
- Ib = Voltage-activated Na+ channel, e.g. Lignocaine
- Ic = Voltage-activated Na+ channel, e.g. Flecainide
- II = beta-adrenoceptor (antagonist), e.g. Metroprolol
- III = Voltage-activated K+ channels, e.g. Amiodarone
- IV = Voltage-activated Ca2+ channels, e.g. Verapamil
40
Action of class Ia anti-arrhythmic drugs
Associate with and dissociate from Na+ channels at a moderate rate. Slow rate of rise of AP and prolong refractory period
41
Action of class Ib anti-arrhthymic drugs
Associate with and dissociate from Na+ channels at a rapid rate. Prevent premature beats
42
Action of class Ic anti-arrhythmic drugs
Associate with and dissociate from Na+ channels at a slow rate. Depress conduction
43
Action of class II anti-arrhythmic drugs
Decrease rate of depolarization in SA and AV nodes
44
Action of class III anti-arrhythmic drugs
Prolong AP duration increasing refractory period
45
Action of class IV anti-arrhythmic drugs
Slow conduction in SA and AV nodes. Decrease force of cardiac contraction
46
When do class I anti-arrhythmic drugs dissociate from the sodium channel?
In the resting rate
47
Which anti-arrhythmic drugs would you use to treat arrhythmias in the atria?
Classes IC, III
48
Which anti-arrhythmic drugs would you use to treat arrhythmias in the ventricles
Classes IA, IB, II
49
Which anti-arrhythmic drugs would you use to treat arrhythmias in the AV node
Adenosine, digoxin, classes II, IV
50
Which anti-arrhythmic drugs would you use to treat arrhythmias in the atria and ventricles as well as AV accessory tract pathways
Amiodarone, sotalol, classes IA, IC
51
What does adenosine do?
Activates A1-adenosine receptors coupled to Gi/o
52
What does digoxin do?
Stimulates vagal activity
53
What does verapamil do?
Blocks L-type voltage-activated calcium channels
54
Supraventricular tachycardia types
Atrial fibrillation, atrial flutter, ectopic atrial tachycardia
55
Ventricular arrhythmia types
Ventricular ectopics, ventricular tachycardia, ventricular fibrillation, asystole
56
Clinical causes of arrythmias
Abnormal anatomy, autonomic nervous system, metabolic, inflammatory, drugs, genetic
57
Causes of tachycardic arrhythmias
Hyperthermia, hypoxia, hypercapnia, cardiac dilation, hypokalaemia
58
Causes of bradycardic arrhythmias
Hypothermia, hypokalaemia
59
Symptoms of arrhythmia
Palpitations, SOB, dizziness, loss of consciousness, faintness, sudden cardiac death, angina, heart failure
60
Investigations for arrhythmia and their effects
ECG, CXR, echocardiogram, stress ECG, 24 hour ECG, event recorder, electrophysiological study
61
What do sinus arrhythmias involve?
Variations in heart rate, due to reflex changes in vagal tone during the respiratory cycle. Part of ECG is slow and part of the ECG shows faster. This is commonly seen in younger people/younger adults
62
Sinus bradycardia:
- What is it?
- Causes
- Treatment
- Sinus rhythm with heart rate <60bpm
- Causes can be physiological i.e. athletes, drugs can cause it and it can be caused by ischaemia
- Treatment is atropine or pacing if haemodynamic compromise.
63
Sinus tachycardia:
- What is it?
- Causes
- Treatment
- Sinus rhythm with heart rate >100bpm
- Physiological (anxiety, fear, hypotension, anaemia), can also be caused by drugs
- Treatment is to treat underlying cause and beta-blockers
64
Atrial ectopic beats:
| - Treatment
No treatment if asymptomatic, beta-blockers may help, avoid stimulants (caffeine, cigarettes)
65
Regular supraventricular tachycardia:
- What may it be due to?
- Acute management
- Chronic management
- Due to AV nodal re-entrant tachycardia, AV reciprocating tachycardia, ectopic atrial tachycardia
- Acute - Valsava manœuvre, carotid massage, IV adenosine or IV verapamil
- Chronic - avoid stimulants, radiofrequency ablation, beta blockers, anti-arrhythmic drugs
66
In which patients is radiofrequency ablation first line?
Young, symptomatic patients
67
Radiofrequency catheter ablation
Selective cautery of cardiac of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit
68
Radiofrequency catheter ablation procedure
- ECG catheters placed in heart via femoral veins
- Intra-cardiac ECG recorded during sinus rhythm, tachycardia and during pacing manoeuvres to find the location and mechanism of the tachycardia
- Catheter placed over focus/pathway and tip heated to 55-65C
- Cease antiarrhythmic drugs 3-5 days beforehand
69
Causes of heart block
Ageing process, acute MI, myocarditis, infiltrative disease, drugs, calcific aortic valve disease, port-aorta valve surgery, genetics
70
Drugs that can cause heart block
Beta-blockers, calcium channel blockers
71
Which types of heart block indicate pacemaker requirement?
Mobitz type II and complete heart block
72
Types of pacemakers
Single chamber (only paces right atria or right ventricle), dual chamber (paces both RA and RV)
73
Ventricular ectopics:
- Causes
- Treatment
- Structural causes (LVH, myocarditis, heart failure), metabolic causes (ischaemic heart disease, electrolytes)
- Treatment is beta blockers or ablation of focus
74
Ventricular tachycardia causes
Most patients will have significant heart disease (CAD, previous MI), other causes include cardiomyopathy, inherited/familial arrhythmia syndromes
75
ECG characteristics that help define VTs
- QRS complexes are wide and distorted
- T waves are large with deflections opposite QRS complexes
- Ventricular rhythm is usually regular
- P waves are not usually visible
- PR interval not measurable
76
Monomorphic VT vs polymorphic VT
Monomorphic VT = QRS complex same all the time
| Polymorphic VT = QRS complex changes all the time
77
Ventricular fibrillation
Chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump
78
Treatment for ventricular fibrillation
Defibrillation, CPR
79
Acute treatment for ventricular tachycardia
Direct current cardioversion if unstable, pharmacologic cardioversion with anti-arrhythmic drugs if stable, correct triggers
80
Long term treatment for ventricular tachycardia
Correct ischaemia if possible, optimise CHF therapies, implantable cardioverter defibrillators if life threatening, VT catheter ablation
81
What is the most common arrhythmia?
Atrial fibrillation
82
Forms of atrial fibrillation?
Paroxysmal, persistent, permanent
83
Paroxysmal atrial fibrillation
Paroxysmal and lasting <48 hours, often recurrent
84
Persistent atrial fibrillation
Episode lasting >48 hours which can still be cardioverted to sinus rhythm, however unlikely to spontaneously revert to normal sinus rhythm
85
Permanent atrial fibrillation
Inability of pharmacologic or non-pharmacologic methods to restore to normal sinus rhythm
86
Associated diseases/causes of atrial fibrillation
Hypertension, congestive heart failure, sick sinus syndrome, coronary heart disease, obesity, thyroid disease, familial, cardiac valve disease, alcohol abuse, congenital heart disease, cardiac surgery, COPD, pneumonia, septicaemia, pericarditis, tumours, vagal cause – high endurance athletes
87
Symptoms of atrial fibrillation
Palpitations, Pre-syncope, Syncope, Chest pain, Dyspnoea, Sweatiness, Fatigue
88
ECG changes in atrial fibrillation:
- Atrial rate
- Rhythm
- Recognition
- >300bpm
- Irregularly irregular
- Absence of P waves and presence of 'f' waves
89
Rate control in the treatment of AF
Digoxin, beta blockers, verapamil, diltiazem
90
Rhythm control in the treatment of AF:
- Restoration of normal sinus rhythm
- Maintenance of normal sinus rhythm
Restoration - pharmacologic cardioversion - anti-arrhythmic drugs, direct current cardioverson
Maintenance - anti-arrhythmic drugs, catheter ablation surgery
91
Indications for anticoagulation in AF
Thyrotoxicosis, hypertrophic cardiomyopathy, valvular AF (warfarin only), non-valvular AF with 2 or more risk factors (age >75, hypertension, heart failure, previous stroke, diabetes, CAD
92
Atrial flutter:
- What is it?
- What is it sustained by?
- How long does it last?
- What may it result in?
- Rapid and regular form of atrial tachycardia, which is usually paroxysmal
- Sustained by a macro-re-entrant circuit confined to the rate atrium
- Episodes last seconds to years
- Can result in thrombo-embolism
93
Treatment for atrial flutter
Radiofrequency ablation, pharmacologic therapy, cardioversion, warfarin for prevention of thromboembolism
