Arrhythmias Flashcards
(135 cards)
1
Q
what is an arrhythmia?
A
disturbances of heart rate, or rhythm
2
Q
what may cause arrhythmias?
A
changes in impulse formation or impulse conduction
3
Q
what is used to describe arrhythmias?
A
rate (bradycardia or tachycardia)
site of origin (supra ventricular eg atria and the AV node or ventricular)
4
Q
what is a bradycardia?
A
HR < 60 bpm during the day
HR < 50 bpm at night
5
Q
what is a tachycardia?
A
HR > 100 bpm
6
Q
what do alterations in impulse formation involve?
A
changes in automaticity
triggered activity
7
Q
what do abnormalities in impulse conduction arise from?
A
re-entry
conduction block
accessory tracts
8
Q
what is overdrive suppression?
A
SA node pacemaking is normally highest and is dominant over other ‘latent pacemakers’ such as the AV node and purkinje fibres
9
Q
what causes changes in automaticity?
A
in order for the SA node to exert its normal control of rate and rhythm it must discharge action potentials at a higher, regular, frequency than any other heart structure
10
Q
what may alter automaticity?
A
physiological eg normal autonomic function
pathophysiological when the function of the SA node as the normal pacemaker is taken over by another ‘latent pacemaker’ as the result of a loss of overdrive suppression
11
Q
what may cause loss of overdrive suppression?
A
if the SA node firing frequency is pathologically low or if conduction of the impulse from the SA node is impaired
if a latent pacemaker fires at an intrinsic rate faster than the SA node rate
response to tissue damage eg post MI
12
Q
describe what happens when SA node firing frequency is pathologically low or conduction of the impulse is impaired
A
a latent pacemaker may initiate an impulse that generates an escape beat
a run of such impulses may give rise to an escape rhythm, a series of escape beats
13
Q
describe what happens when a latent pacemakers fire at an intrinsic rate faster than the SA node rate
A
latent pacemaker initiates an ectopic beat or a series of such beats generating an ectopic rhythm
14
Q
what can result in an ectopic rhythm?
A
ischaemia
hypokalaemia
increased sympathetic activity
fibre stretch
15
Q
what is ischaemia?
A
a restriction in blood supply to tissues, causing a shortage of oxygen that is needed for cellular metabolism
16
Q
what are afterdepolarisations (ADs)?
A
when a normal action potential triggers abnormal oscillations in membrane potential that occurs during or after depolarisation
17
Q
how can ADs cause triggered activity?
A
if they are of amplitude significant to reach threshold they cause premature action potentials and beats
18
Q
what are the two types of after depolarisations?
A
early and delayed
19
Q
when do EADs occur?
A
during the inciting AP within the plateau phase (mediated by Ca2+ channels) or phase 3 (mediated by Na+ channels)
20
Q
when are EADs most likely to occur in terms of HR?
A
when it is slow
21
Q
where do EADs occur?
A
in purkinje fibres
22
Q
what are EADs associated with?
A
prolongation of the action potential and drugs prolonging the QT interval
23
Q
when can EADs be life threatening?
A
when sustained as they can cause torsades de pointes
24
Q
when do DADs occur?
A
after complete repolarisation
25
what causes DADs?
large increases in Ca2+
26
when are DADs most likely to occur in terms of HR?
when it is fast
27
when are DADs increased and decreased in incidence?
by prolongation and shortening of the duration of the AP by drugs
28
what may trigger DADs?
drugs that increase Ca2+ influx eg catecholamines or release from the SR eg digoxin
29
what is re-entry?
when a self sustaining electrical circuit stimulates an area of myocardium repeatedly/rapidly
30
what does the re-entrant circuit require?
unidirectional blood
| slowed retrograde conduction velocity
31
what causes unidirectional block?
anterograde conduction prohibited
| retrograde conduction allowed
32
where is conduction block through?
the AV node
33
what happens during partial block?
either slowed conduction or intermittent block
34
what happens during slowed conduction?
tissue conducts all impulses but more slowly than usual eg first degree AV block
35
what happens during intermittent block?
tissue conducts some impulses but not other eg second degree AV block
36
what are the two types of second degree block?
Mobitz type I
| Mobitz type II
37
describe Mobitz type I
PR interval gradually increases from cycle to cycle until AV node fails completely and a ventricular beat is missed
38
describe Mobitz type II
PR interval is constant but every nth, ventricular depolarisation is missing
39
what happens during complete block?
no impulses are conducted through the affected area eg 3rd degree AV block
40
what happens during 1st degree block?
there is a long PR interval
41
what happens during 3rd degree block?
atria and ventricles beat independently, governed by their own pacemakers
ventricular pacemaker is now the purkinje fibres so it manifests as bradycardia and low CO
42
what are accessory tract pathways?
electrical pathways in parallel to the AV node
43
describe the bundle of Kent
an accessory tract pathway
impulse through it is conducted more quickly than that through the AV node
ventricles receive impulses from both the normal and accessory pathways- can set up the condition for a re-entrant loop predisposing to tachyarrhythmias
44
what do anti arrhythmic drugs usually do?
inhibit specific ion channels (or activate/block specific receptors) with the intention of suppressing abnormal electrical activity
45
what is the Vaughn Williams classification?
```
it classifies drugs based upon their effects upon the cardiac action potential
it defines 4 classes with class I being subdivided into subclasses Ia, Ib and Ic
```
46
what is the target of class I drugs?
voltage activated Na+ channels
47
what is the target of class II drugs?
B-adrenoreceptor (as antagonists)
48
what is the target of class III drugs?
voltage activated K+ channels
49
what is the target of class IV drugs?
voltage activated Ca2+ channels
50
describe the use dependant manner of class I agents
they bind preferentially to areas of the myocardium in which firing frequency is highest without preventing the heart from beating at normal frequencies
51
what happens to class I agents when the Na+ channel is in resting state?
they dissociate from it
52
what happens during ischaemia myocardium?
myocytes are partially depolarised and the AP is of longer duration so the inactivated state of the Na+ channel is available to Na+ channel blockers for a greater period of time and the rate of channel recovery from block is decreased
53
what does the ischamia tissue allow class I agents to do?
act preferentially on ischaemic tissue and block an arrhythmogenic focus at its source
54
what is a supraventricular arrhythmia?
origin is above the ventricle, ie SAN, atrial muscle, AV node or HIS origin
55
what is a ventricular arrhythmia?
origin is in ventricular muscle (common) or fascicles of the conducting system (uncommon)
56
describe supraventricular tachycardia
atrial fibrillation
atrial flutter
ectopic atrial tachycardia
57
describe bradycardia
sinus bradycardia
| sinus pauses
58
what are examples of ventricular arrhythmias?
ventricular ectopics or premature ventricular complexes
ventricular tachycardia
ventricular fibrillation
asystole
59
what are atrio-ventricular node arrythmias?
```
AVN re entry tachycardia
AV reciprocating or AV reentrant tachycardia
AV block (1st, 2nd or 3rd degree)
```
60
what are the causes of arrythmias?
```
abnormal anatomy
ANS
metabolic
inflammation
drugs
genetic
```
61
what are the abnormal anatomy causes of arrhythmias?
LV hypertrophy
accessory pathways
congenital HD
62
what are ANS causes of arrhythmias?
sympathetic stimulation eg stree, exercise, hyperthyroidism
| increased vagal tone causing bradycardia
63
what are metabolic causes of arrhythmias?
hypoxia: COPD, pulmonary embolus
ischaemic myocardium: acute MI, angina
electrolyte imbalances
64
what is an inflammatory cause of arrhythmias?
viral myocarditis
65
which drugs can cause arrhythmias?
direct electophysiologic effects or via ANS
66
which mutations can cause arrhythmias?
those of genes encoding cardiac ion channels eg the congenital long QT syndrome
67
what are ectopic beats?
beats or rhythms that originate in places other than the SA node
68
what causes ectopic beats?
altered automaticity eg ischaemia, catecholamines
| triggered activity eg digoxin, long QT syndrome
69
what causes re-entry?
requires more than one conduction pathway, with different speed of conduction (depolarisation) and recovery of excitability (refractoriness)
70
what can cause re-entry?
accessory pathway tachycardia (wolf parkinson white syndrome)
previous MI
congenital heart disease
conditions that depress conduction velocity or shorten refractory period promote functional block eg ischaemia, drugs
71
what is the mechanism of tachycardia?
the ectopic focus may cause single beats or a sustained run of beats, that if faster than sinus rhythm, take over the intrinsic rhythm
re-entry is then triggered by an ectopic beat resulting in a self perpetuating circuit
72
what happens if there is an increase in the phase 4 slope?
there is an increase in heart rate, ectopics
73
what can cause an increase in phase 4?
```
hyperthermia
hypoxia
hypercapnia
cardiac dilation
hypokalaemia
```
74
what does a decrease in the phase 4 slope cause?
slowed conduction, bradycardia, heart block
75
what can cause a decrease in phase 4?
hypothermia
| hyperkalaemia
76
what is triggered activity?
in phase 3, an afterdepolarisation may occur and if of significant magnitude may reach depolarisation threshold and lead to a sustained train of depolarisations
77
what does triggered activity cause?
digoxin toxicity
torsades de pointes in the long QT syndrome
hypokalaemia
78
what are the symptoms?
```
palpitaions
SoB
dizziness
loss of consciousness; syncope
faintness; presyncope
sudden cardiac death
angina, HF
```
79
what are the investigations?
```
12 lead ECG (in tachycardia, during SR)
CXR
stress ECG- look for myocardial ischaemia, exercise related arrhythmias
24 hour ECG holtor monitoring
event recorder
electrophysiological study
```
80
what is an ECG used for?
to assess rhythm
| to look for signs of a previous MI (Q waves) or pre-excitation (Wolf Parkinson White syndrome)
81
what is an exercise ECG used for?
to assess ischaemia
| exercised induced angina
82
what is a 24hr holtor ECG used for?
to assess for paroxysmal arrhythmia
| to link symptoms to underlying heart rhythm
83
what is echocardiography used for?
to assess for structural heart disease eg enlarged atria in AF, LV dilatation, previous MI scar, aneurysm
84
what is an electrophysiological study used for?
to trigger the clinical arrhythmia and study its mechanisms/pathways
opportunity to treat the arrhythmia by delivering radiofrequency ablation to extra pathway
85
what are normal sinus arrhythmias?
variation in HR, due to reflex changes in vagal tone during the respiratory cycle
inspiration reduces vagal tone and increases HR
86
what is sinus bradycardia?
<60 bpm
| can be physiological, due to drugs (B blockers) or due to ischaemia
87
what is the treatment of bradycardia?
atropine (if acute eg acute MI)
| pacing if haemodynamic compromise: hypotension, CHF, angina, collapse
88
what is sinus tachycardia?
HR> 100 bpm
can be physiological (anxiety, fever, hypotension, anaemia)
inappropriate (drugs etc)
89
what is the treatment of sinus tachycardia?
treat underlying cause
| B-adrenergic blockers
90
what are the symptoms of atrial ectopic beats?
asymptomatic
| palpitations
91
what is the treatment of atrial ectopic beats?
```
generally none
B blockers may help
avoid stimulants (caffeine, cigarettes)
```
92
what is the acute management of supraventricular tachycardias?
increase vagal tone: valsalva, carotid massage
slow conduction in the AVN
- IV adenosine
- IV verapamil
93
what is radiofrequency catheter ablation?
selective cautery of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit
94
what are the causes of AVN conduction disease (hear block)?
```
ageing process
acute MI
myocarditis
infiltrative disease- amyloid
drugs- B blockers, Ca blockers
calcific aortic valve disease
post-aortic valve surgery
genetic- lenegre's disease, myotonic dystrophy
```
95
discuss first degree heart block
Not really “block”, conduction following each P wave but takes longer.
P-R interval longer than normal (> 0.2 sec)
Treatment: none
Rule out other pathology.
Long term follow up recommended, as more advanced block may develop over time
96
what is second degree heart block?
Intermittent block at the AVN (dropped beats)
2 types;
Mobitz I
Mobitz II
97
what is Mobitz 1?
progressive lengthening of the PR interval, eventually resulting in a dropped beat.
Usually vagal in origin
98
what is Mobitz 2?
Pathological, may progress to complete heart block (3rd degree HB)
Usually 2:1, or 3:1, but may be variable
Permanent pacemaker indicated
99
what are single chamber pacemakers?
paces the right atria or right ventricle only
100
what are dual chamber pacemakers?
paces the RA and RV
maintains AV synchrony
used for AVN disease
101
what are the causes of ventricular ectopics?
structural causes: LVH, heart failure, myocarditis
metabolic: ischaemic heart disease, electrolytes
may be marker for inherited cardiac conditions
102
when does a ventricular ectopic need to be investigated?
if worse on exercise
103
what causes ventricular tachycardia?
CAD
previous MI
cardiomyopathy
inherited/ familial arrhythmia syndromes- long QT, brugada syndrome
104
what is a ventricular tachycardia with haemodynamic compromise?
large sustained reduction of arterial pressure
105
what is ventricular fibrillation?
chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump
106
what is the treatment of an acute VT?
direct current cardioversion (DCCV) if unstable
if stable: consider pharmacologic cardioversion with AAD, in meantime prepare for DCCV
if unsure if VT or something else, consider adenosine to make a diagnosis
correct triggers
107
what is long term treatment for VT?
correct ischaemia if possible
optimis CHF therapies
implantable cardiovertor defibs if life threatening
VT cath ablation
108
discuss VT/ VF pearls
A wide QRS tachycardia with history of CAD/HF = VT until proven otherwise.
Most ventricular arrhythmias occur in the setting of structural heart disease (CHF, CAD).
Anti-arrhythmic drugs are ineffective on survival, but are often used together with ICDs to reduce symptoms.
Optimal management of the underlying condition e.g. CHF, CAD are important
Remember primary electrical disease
VT/VF in structurally normal hearts may be genetic
implications for family members
109
what is atrial fibrillation?
Chaotic and disorganized atrial activity
Irregular heartbeat
Can be paroxysmal, persistent or
permanent (chronic)
Can be symptomatic or asymptomatic
110
what is the mechanism of AF?
ectopic foci in muscle sleeves in the ostia of the pulmonary veins
111
how can AF be terminated?
pharmacologic cardioversion with anti-arrhythmic drugs
electrical cardioversion
spontaneous reversion to sinus rhythm
112
what is paroxysmal AF?
lasting less then 48 hours
| often recurrent
113
what is persistent AF?
an episode of AF lasting greater than 48 hours which can still be cardioverted to NSR
unlikely to spontaneously revert to NSR
114
what is permanent AF?
inability of pharmacologic or non-pharmacologic methods to restore NSR
115
what are diseases associated with AF?
```
Hypertension
Congestive heart failure
Sick sinus syndrome
‘tachy brady syndrome’
Coronary heart disease
Obesity
Thyroid disease
Familial
Cardiac Valve disease
Alcohol abuse
Congenital heart disease
Cardiac surgery
COPD, Pneumonia,
Septicaemia,
Pericarditis, tumors
Vagal cause – high endurance athletes
```
116
what is lone (idiopathic) AF?
absence of any heart disease and no evidence of ventricular dysfunction
a diagnosis of exclusion
could be genetic
significant stroke rate
117
describe the ECG of someone with AF
```
Atrial Rate: > 300 bpm
Irregularly irregular rhythm Variable ventricular rate
Dependent upon:
-AV node conduction properties
-Sympathetic and parasympathetic tone
-Presence of drugs with act on the AV node
Absence of P waves
Presence of ‘f’ waves
```
118
what are the consequences of AF?
Lost ‘atrial kick’ and decreased filling times (reduced diastole) >> reduced cardiac output
Can result in congestive heart failure, especially in the presence of diastolic dysfunction
119
what is the management of AF?
rhythm control: maintain SR
or
rate control: accept AF but control ventricular rate
anticoagulants for both approaches if high risk for thromboembolism
120
what are the drug options for rate control?
digoxin
betablockers
verapamil, diltiazem
121
what is used for rhythm control?
```
pharmacologic cardioversion
direct current cardioversion
anti-arrhytmic drugs
catheter ablation of atrial focus/ pulmonary veins
surgery (Maze procedure)
```
122
what are class I anti-arrhythmic drugs?
reduce Na channel current
| lignocaine, quinidine, flecainide, propafenone
123
what are class II anti-arrhythmic drugs?
B- adrenergic antagonists
| propranolol
124
what are class III anti-arrhythmic drugs?
action potential prolongation
amiodarone, sotalol
dronedarone
125
what are class IV anti-arrhythmic drugs?
Ca channel antagonists
| verapamil
126
what are the indications for anti-coagulation in AF?
```
Valvular AF
mitral valve disease: MS and MR
Non valvular AF if:
Age >75
Hypertension
Heart failure
Previous stroke/ thromboembolism
CAD / DM
Diabetes
```
127
what is radiofrequency ablation used for in AF?
to maintain SR by ablating AF focus and for rate control by ablation of the AVN to stop fast conduction to the ventricles
128
what is left atrial catheter ablation for AF?
isolates triggers in the pulmonary veins by pulmonary in LA vein isolation
129
what is an atrial flutter?
Rapid and regular form of atrial tachycardia
Usually paroxysmal
Sustained by a macro-reentrant circuit
Circuit is confined to the right atrium
Episodes can last from seconds to years
Chronic atrial flutter usually progresses to atrial fibrillation
May result in thrombo-embolism
130
what are the treatment options for atrial flutter?
```
RF ablation
Pharmacologic therapy
-Slow the ventricular rate
-Restore sinus rhythm
-Maintain sinus rhythm once converted
Cardioversion
Warfarin for prevention of thromboembolism
```
131
what are the indications for anti-coagulation in AF?
```
Valvular AF
mitral valve disease: MS and MR
Non valvular AF if:
Age >75
Hypertension
Heart failure
Previous stroke/ thromboembolism
CAD / DM
Diabetes
```
132
what is radiofrequency ablation used for in AF?
to maintain SR by ablating AF focus and for rate control by ablation of the AVN to stop fast conduction to the ventricles
133
what is left atrial catheter ablation for AF?
isolates triggers in the pulmonary veins by pulmonary in LA vein isolation
134
what is an atrial flutter?
Rapid and regular form of atrial tachycardia
Usually paroxysmal
Sustained by a macro-reentrant circuit
Circuit is confined to the right atrium
Episodes can last from seconds to years
Chronic atrial flutter usually progresses to atrial fibrillation
May result in thrombo-embolism
135
what are the treatment options for atrial flutter?
```
RF ablation
Pharmacologic therapy
-Slow the ventricular rate
-Restore sinus rhythm
-Maintain sinus rhythm once converted
Cardioversion
Warfarin for prevention of thromboembolism
```
