Cardiac Arrhythmias Flashcards
1
Q
what ‘insulates’ the electrical regions of the heart
A
the fibrous ring between the atria and ventricles
2
Q
where is the origin of a supraventricular arrhythmia
A
above the ventricle; sino atrial node, atrial muscle, AV node or HIS origin
3
Q
where is the origin of a ventricular arrhythmia
A
ventricular muscle or the fascicles of the conducting system (conducting tissue)
4
Q
what are the two types of supraventricular arrhythmias
A
supraventricular tachycardia and bradycardia
5
Q
give three examples of supraventricular tachycardia
A
atrial fibrillation, atrial flutter, ectopic atrial tachycardia
6
Q
give two examples of bradycardia
A
sinus bradycardia, sinus pauses
7
Q
what are four examples of ventricular arrhythmias
A
ventricular ectopics/ premature ventricular complexes (PVC)
ventricular tachycardia
ventricular fibrillation
a-systole- not contracting
8
Q
what is a focus
A
somewhere in the ventricles that can fire signals independently
9
Q
give three examples of atrio-ventricular node arrhythmias
A
AVN re-entry tachycardia
AV reciprocating/ AV re-entrant tachycardia
AV block (1st, 2nd and 3rd degree)
10
Q
what are the clinical causes of arrhythmias
A
abnormal anatomy, autonomic nervous system (ANS), metabolic, inflammation, drugs, genetics
11
Q
what causes the abnormal anatomies associated with arrhythmias
A
left ventricular hypertrophy,
accessory pathways,
12
Q
what can cause autonomic nervous system disruptions which cause arrhythmias
A
sympathetic stimulation (stress, exercise, hyperthyroidism, stimulants)
increased vagal tone (bradycardia)
13
Q
what can cause the metabolic disruptions which cause arrhythmias
A
hypoxia (chronic pulmonary disease, pulmonary embolus)
ischaemic myocardium (acute MI, angina)
electrolyte imbalances (K+, Ca2+, Mg2+)
14
Q
what can cause the inflammation which can cause arrhythmias
A
viral myocarditis, influenza
15
Q
what genetic issues cause arrhythmias
A
mutations of genes encoding cardiac ion channels (abnormal proteins= abnormal currents)
16
Q
what is an ectopic beat
A
beats or rhythms that originate in places other than the SA node
17
Q
what two things can cause ectopic beats
A
altered automaticity (e.g. ischaemia, catecholamines)
triggered activity (e.g. digoxin, long QT syndrome)
18
Q
what allows re-entry arrhythmias
A
requires more than one conduction pathway with different speed of conduction (depolarisation) and recovery of excitability (refractoriness)
19
Q
what can cause re-entry arrhythmias
A
accessory pathway tachycardia, previous myocardial infarction, congenital heart disease or conditions that depress conduction velocity or shorten refractory period (as they promote functional block)
20
Q
what is a sustained arrhythmia
A
series of ectopic beats
21
Q
what are the two electrophysiological mechanisms causing arrhythmias
A
ectopic beats, re-entry
22
Q
how can the ectopic focus cause tachycardia
A
focus can cause single beats or a sustained run of beats that if faster than sinus rhythm can take over intrinsic rhythm
23
Q
how can re-entry arrhythmias cause tachycardia
A
triggered by an ectopic beat, resulting in a self perpetuating circuit
24
Q
is tachycardia dangerous
A
maybe, depending on how they effect the cardiac output
25
what is the clinically presentation of tachycardia
variable
26
what is altered automaticity
change in slope, threshold, rate of action potential changing heart rate
27
what happens when the slope of phase 4 of an action potential is increased
increase in heart rate
28
what causes an increase in phase 4 slope in an action potential
hyperthermia, hypoxia, hypercapnia, cardiac dilation, hypokalaemia (prolongs repolarisation)
29
what does a decrease in the slope of phase 4 of an action potential cause
slowed conduction- bradycardia, heart block
30
what can cause a decrease in slope 4 of the action potential
hypothermia, hyperkalaemia
31
what is an after-depolarisation
a small depolarisation that occurs in the terminal phase of the AP (phase 3)
32
what happens when and after depolarisation reaches depolarisation threshold
lead to a sustained train of depolarisations= triggered activity
33
what is triggered activity the mechanism behind
digoxin toxicity, torsades de Pointes in the long QT syndrome and hypokalaemia
34
what causes an after-depolarisation in triggered activity
when there is an excess of digoxin/ calcium, cells try to have early depolarisation to get rid of it
35
what causes a alternative conduction pathway to slow down
if pathway becomes ischaemic
36
what happens when an alternative conduction pathway is slowed down
conduction times are now different: slowed pathway reaches ventricular muscle at stage three of the action potential of the other conduction pathway. muscle has recovered and is excitable in phase three so current causes an extra beat.
37
why is it called a re-entrant current
after current that passes down slowed pathway has caused an extra beat, it travels back up the other, un-slowed pathway where sinus beat coming down
38
what are the symptoms of an arrhythmia
palpitations 'pounding heart', SOB, dizziness (CO impaired), loss of consciousness (syncope), sudden cardiac death, angina, heart failure
39
why do arrhythmias cause angina
as heart going fast and ischaemia present (re-entrant)
40
what investigations are done when an arrhythmia is suspected
```
12 lead ECG,
CXR, echocardiogram, stress ECG (look for myocardial ischaemia,
exercise related arrhythmias),
24 hour ECG holter monitoring,
event recorder,
electrophysiological study
```
41
why is an ECG done in arrhythmias
to assess rhythm, signs of previous MI, and pre-excitation
42
what is a true accessory pathway
connection between atria and ventricles
43
how is pre-excitation seen in an ECG
delta wave
44
what does an exercise ECG look for in ECG in arrhythmias
to assess for ischaemia and exercise induce arrhythmia
45
what does a 24hr holter ECG look for in arrhythmias
assess for paroxysmal (sudden attacks) arrhythmia,
| link symptoms to underlying heart
46
what does an echocardiography asses for in arrhythmias
structural heart disease (enlarged atria in AF, LV dilatation, previous MI scar, aneurysm)
47
what does an electrophysiological study look for and how
triggers the clinical arrhythmia and study its mechanism/pathway
48
what does electophysiological study allow
opportunity to treat the arrhythmia by delivering radio-frequency ablation to extra pathway
49
what is radio-frequency ablation
putting catheters into the heart via the venous system to treat abnormal heart rhythm
'Selective cautery of cardiac tissue to prevent
tachycardia, targeting either an automatic focus or
part of a re-entry circuit'
50
what causes variation in normal sinus rhythm
reflex changes in vagal tone during the respiratory cycle (inspiration causes reduced vagal tone and increase heart rate)
51
what can cause sinus bradycardia
physiological (athlete), drugs (B-blocker), ischaemia
52
how is sinus bradycardia treated
atropine (anti vagal, speeds up HR)
pacing if haemodynamic compromise: hypotension, CHF, angina, collapse
53
what can cause sinus tachycardia
physiological (anxiety, fever, hypotension, anaemia), drugs/stimulants etc
54
how is sinus tachycardia treated
treat underlying cause, Beta blockers
55
what are the symptoms of atrial ectopic beats
asymptomatic, palpitations
56
how are atrial ectopic beats treated
generally no treatment, beta blockers must help, avoid stimulants
57
what does an ECG showing a narrow complex tachycardia suggest
superventricular tachycardia
58
what does a sinus rhythm ECG have
a P wave before the QRS complex
59
what can cause regular supraventricular tachycardia
AV nodal re-entrant tachycardia,
AV reciprocating tachycardia/ AV re-entrant tachycardia (via accessory pathway),
ectopic atrial tachycardia
60
how are regular supraventricular tachycardia
vagal manoeuvres, adenosine
61
what is AVNRT
AV nodal re-entrant tachycardia
62
what is AVRT
AV re-entrant tachycardia
63
what is mechanism between a AV node re-entrant tachycardia
circuit with the AV node (micro-re entry)
64
what is the mechanism behind AV re-entrant tachycardia
circuit using the AV node and accessory pathway (macro-re entry)
65
how is AVNRT treated
ablation- getting ride of slow pathway (creates scar tissue)
66
what causes atrial tachycardia
focus in heart firing regardless of AV node, if faster than AV will take over.
67
what does the QRS complex look like in atrial tachycardia
normal as using correct conduction pathway
68
what is the acute management of supra ventricular management
increase vagal tone (valsalva, carotid massage)
slow conduction in the AV node (IV adenosine-vasodilator and anti arrhythmic or verapamil-calcium channel blocker)
69
what is the chronic management of supra-ventricular tachycardia
avoidance of stimulants
electrophysiologic study and radiofrequency ablation
beta blockers
anti-arrhythmic drugs
70
how to ECG catheters reach the heart
via femoral veins
71
how are the location and mechanism of the tachycardia identified
intracardiac ECG recorded during sinus rhythm, tachycardia and pacing manoeuvres
72
how does radio-frequency ablation specifically target problem areas
catheter placed over focus/ pathway and tip heated to 55-65c
73
what is heart block
AV node conduction disease
74
what are the cause of heart block
```
ageing,
acute MI,
myocarditis,
infiltrative disease (amyloid),
drugs (beta blockers, calcium channel blockers),
calcific aortic valve disease,
post-aortic valve disease,
genetics
```
75
what is amyloid
starch like protein which is deposited in tissues
76
describe 1st degree AV block
conduction following each P wave takes longer, resulting in a prolonged P-R interval (>0.2 sec)
77
what is the treatment for 1st degree heart block
nothing
78
describe 2nd degree AV block
when excitation completely fails to pass
| through the AV node or the bundle of His= intermittent block at the AV node resulting in dropped beats
79
what are the two types of 2nd degree AV bock
mobitz I and II
80
describe mobitz type I
progressive lengthening of the PR interval, eventually resulting in a dropped beat
81
what usually causes mobitz type I
usually of vagal origin
82
describe mobitz type II
pathological, may progress to complete heart block. when most beats are conducted with a constant PR interval but occasionally there is atrial depolarisation without subsequent ventricular depolarisation
83
describe 2nd degree heart block (2:1)
two p waves per QRS complex. normal and constant PR interval in the conducted beat. one QRS complex dropped
84
describe 2nd degree heart block (3:1)
three p waves per QRS complex
85
describe third degree heart block
complete heart block. when atrial conduction is normal but no beats are conducted to the ventricles. ventricles are stimulated by slow escape mechanism
86
describe third degree heart block on an ECG
sinus rhythm. no relationship between P waves and QRS complexes. abnormal shaped QRS complexes (broad) because of abnormal spread of depolarisation from a ventricular focus. right axis deviation. right bundle branch block pattern
87
what is the treatment for mobitz II block and 3rd degree AV block
ventrciular pacing
88
what does a broad QRS complex suggest
activity coming from myocytes not purkinje system
89
how does the heart respond to a dropped beat
can either stop or make escape rhythm (comes from automatic drift of the action potential towards trigger potential)
90
what is the basic mechanism of action of a pacemaker
if doesn't sense electrical activity sends signal to SA node
91
what are the two types of pacemakers
single chamber (paces right atria or right ventricle only)
dual chamber (paces both PA and PV)
92
what is the advantage of dual chamber pacemakers and what disease type are they used in
able to maintain Atria-ventricle synchrony
used for AVN disease
93
what is a premature ventricular complex
A premature beat arising from an ectopic focus within the ventricles (ectopic beat)
94
what can cause ventricular ectopics
structural causes: LVH, heart failure, myocarditis
metabolic: ischaemic heart disease, electrolytes
inherited cardiac conditions
95
how are ventricular ectopics treated
beta blockers, ablation of focus
96
what is the severity of ventricular tachycardia
life threatening but may be haemodynamically stable
97
what does most patients with VT also have
heart disease; coronary artery disease, previous MI (or more rarely cardiomyopathy/ inherited arrhythmia syndromes)
98
give examples of inherited arrhythmia syndromes
long QT syndrome, brugada syndromes
99
when does VT cause haemodynamic compromise
when rhythm causes large, sustained reduction of arterial pressure- due to extreme HRs and lack of coordinated contraction
100
what are the ECG characteristics of monomorphic VT
Regular rhythm.
Originates from a single focus within the ventricles.
Produces uniform QRS complexes within each lead — each QRS is identical
101
what are the ECG characteristics of VT
p waves not usually visible
PR interval not measurable
QRS complexes rapid and wide
Large T waves with defliections opposite the QRS complexes
102
in what type of tachycardia do capture and fusion beats occur
ventricular, not supraventricular
103
how is polymorphic VT different from monomorphic VT
rhyth, constantly changing
104
what is a capture beat
A sinus impulse reaches the atrioventricular node and the ventricle in a nonrefractory phase between the wide QRS complexes, and produces a beat with a normal QRS duration. - the sinus node “captures” the ventricles producing a narrow-complex beat
105
what is a fusion beat
A fusion beat occurs when electrical impulses from different sources act upon the same region of the heart at the same time, makes QRS gain height and lose depth.
106
what is ventricular fibrillation
chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump
107
what is the immediate treatment for VF
defibrillation, cardiopulomnary resuscitation
108
what is the long term treatment for VF
correct ischaemia if possible (revascularisation)
CHF therapies
implantable cardiovertor defibrillators
VT catheter ablation
109
what is the acute treatment for ventricular tachycardia
direct current cardioversion- id unstable
pharmacological cardioversion (anti-arrhythmic drug therapy e.g Procainamide)- if stable whilst waiting for DCCV
correct triggers (electrolytes, ischaemia, hypoxia, pro-arrhythmic medications)
110
what are pro-arrhythmic medications and give an example
drugs that prolong the QT interval e.g. sotalol
111
what is an ICD
implantable cardioverter defibrillator
112
what are the therapies provided by an ICD
termination of VT/VF
- anti-tachycardia pacing
- cardioversion
- defibrillation
pacing for brady cardia
113
wide QRS tachycardia with history of CAD/ HF = ?
VT until proven otherwise
114
do anti arrhythmic drugs help in survival of VT/VF
no but helpful after with ICD to reduce symptoms
115
what causes irregularly irregular rhythms
atrial fibrillation,atrial or ventricular ectopic beats, multi focal atrial tachycardia,
116
what can cause regularly irregular rhythms
sinus arrhythmia, second degree heart block
117
what are the characteristics of artial fibrillation on an ECG
absence of P waves, irregularly irregular rhythm, chaotic and disorganised
118
how is LVH seen on an ECG
very tall R waves and ST depression in more than 3 waves
119
in what diseases can LVH been seen in an ECG
hypertension and hypertensive heart disease
120
what are three types of onset of AF
paroxysmal, persistent or permanent (chronic)
121
what causes the irregular heartbeat in AF
disorganised electrical activity of the atria
122
what is sustained AF facilitated by
increased parasympathetic tone-atrial refractory periods are decreased, shortening wave length
123
what is the mechanism behind AF
multiple waveltes of re-entry=
ectopic foci in muscle sleeves in the ostia of the pulmonary veins- atria firing randomly
124
how is AF terminated
electrical cardioversion with anti arrhythmic drugs (flecainide, sotalol and amiodarone), pharmacological cardioversion, spontaneous reversion to sinus rhythm
125
describe paroxysmal AF
paroxysmal (sudden), lasting less than 48 hours, often recurrent
126
describe persistent AF
lasts longer than 48 hours, can still be converted to normal sinus rhythm, unlikely to do so spontaneously
127
describe permanent AF
inability of pharmacological or on pharmacological methods to restore NSR
128
name some disease/ causes associated with AF
hypertension, CHF, CHD, obesity, thyroid disease, genentics, sick sinus syndrome, cardiac valve disease, alcohol, congenital heart disease, COPD, pneumonia, septicaemia, pericarditis, tumours, vagal cause (athletes)
129
what is sick sinus syndrome
tachy brady syndrome
130
what is lone/ idiopathic AF
absence of any heart disease and no evidence of ventricular dysfunction
could be genetic
131
when determining the cause of AF why is it to differentiate between non and valvular heart disease
treated very differently, valvular has very high risk of stroke
132
why should anticoagulants be considered in patients over 75 with AF
as significant stroke rate
133
what are the symptoms of AF
palpitations, pre-syncope (dizziness), syncope, chest pain, dyspnea, sweatiness, fatigue-- can be asymptomatic
134
what is the atrial rate in AF
more than 300 BPM
135
what are the characteristics of AF on an ECG
irregularly irregular, ventricle rate variable, absence of P and T waves, presence of 'F' waves
136
what is the ventricual rate in AF dependant on
AV node conduction propertiesm sympathetic and parasympathetic tone, drugs
137
what facilitates and inhibits AV node conduction
facillitated by symp stim
inhibited by para stim
138
what can be used to control ventricular rate in AF
drugs that decrease conduction in AV (beta blockers and calcium channel blockers)
139
what are F waves
flutter waves
140
what is the QRS complex like in AF
normal
141
why are P and T waves not recognisable in AF
as atria quiver instead of contract, replaced by wave deflections
142
why is the rhythm irregular in AF
as delay in AV node
143
what cause AF with slow ventricular rate and how is it treated
AV block, no escape rhythm
pacemaker as cant give drugs to slow HR
144
what is pseudo-regularisation
fake tachycardia as ventricles have fast response to AF
145
how does AF reduce cardiac output
as loss of atrial kick- active filling of the ventricles, reduced diastole as reduces filling times
146
what does a ventricle rate lower than 60 in AF suggest
AV conduction disease
147
can AF cause CHF
yes
148
what permanent treatment may patients with AF require
permanent pacing
149
when can AF cause VF and sudden cardiac death
when there is AF with pre-excitation
pre-excitation of the ventricles broadens the QRS via an accessory pathway
150
what is diastolic dysfunction
failure to relax, leads to pulmonary oedema as of increased pressures in pulmonary system
151
what can cause diastolic dysnfunction
LVH, hypertension, ischaemia and AF
152
what events occur during diastole
coronary perfusion, ventricular filling, atria active relaxation
153
how is AF managed
rhythm control (maintain sinus rhythm) OR rate control (control VR)
Anti-coagulation for both approaches if high risk for thromboembolism
154
how is the rate control approach in AF carried out
pharmacological therapy to slow down AVN conduction
- digoxin
- beta blockers
- calcium channel blockers: verapamil, diltiazem
- adenosine
(alone or in combo)
155
when is rate control carried out in patients with AF
where the restoration of sinus rhythm is not possible- aims to control ventricular rate and prevent thromboembolism
156
in rhythm control of AF how is normal sinus rhythm restored
pharmacological cardioconversion (anti-arrhythmic drugs e.g. amiodarone)
DCCV
157
in rhythm control of AF how is normal sinus rhythm maintained
anti-arrhythmic drugs, catheter ablation of atrial focus/ pulmonary veins, surgery (maze procedure)
158
what is the major complication of AF
embolism and stroke
159
if pharmacological methods don't, how else can rate be controlled in AF
by completely ablating the AV node and controlling the HR by a pacing system
160
how does electric cardioversion work
delivers a dose of electrical current to the heart at a specific moment in the cycle to terminate the arrhythmia
161
how do anti arrhythmic drugs work
block ionic currents across cell membranes that create action potentials
162
what do class 1 anti arrhythmic drugs act on and give 4 examples
reduce Na channel current
lignocaine, quinidine, flecainide, propafenone
163
what do class 2 anti arrhythmic drugs act on and give an example
B-adrenergic antagonists
propranalol
164
what do class 3 anti arrhythmic drugs act on and give 3 examples
action potential elongation
amiodarone, sotalol, DRONEDARONE
165
what do class 4 anti arrhythmic drugs act on and give an example
Ca channel antagonists
verapamil
166
what is Torsades de Pointes and how is it identified
deadly and rapid VT (200-250 bpm)
irregular rhythm
wide QRS
long QT interval
continuously chanigng QRS morphology
167
what puts patients at a high risk of thromboembolism
Valvular heart disease ( MS > MR)
Age >75 especially female
Hypertension
Heart failure (LVEF < 0.35)
Previous thromboembolism/ stroke
Coronary artery disease, or diabetes and > 60 years old
Thyrotoxicosis (excessive thyroid hormone)
168
five two examples of anticoagulants patient should be on when high risk of thromboembolism in AF
warfarin, rivaroxaban
169
where do AF focus usually come from
pulmonary veins
170
what part of heart is ablated to maintain SR
AF focus (usually in pulmonary veins)
171
what part of the heart is ablated for rate control in AF
AVN to stop fast conduction to the ventricles
172
what is atrial flutter
rapid and regular form of atrial tachycardia
173
describe the onset of atrial flutter and its mechanism of action
usually paroxysmal, sustained by macro-reentry circuit located in the right atrial myocardium
174
how long can flutter episodes last
from seconds to years
175
what does chronic atrial flutter eventually convert into
chronic atrial fibrillation
176
where is atrial flutter present in the heart
confined to right atrium
177
what does atrial flutter look like on an ECG
atrial 300 (average) bpm, ventricle 150 bpm
p wave turns into saw tooth F wave
QRS normal
rhythm regular but may be variable
178
how is a counterclockwise flutter terminated
rapid atrial pacing, cardioversion, drugs: Ia (moderate class 1), Ic (strong class 1), class 3 antiarrhythmic drugs
may also convert spontaneously
179
how does pharmacological treatment help atrial flutter
slows ventricular rate, restores sinus rhythm, maintains sinus rhythm
180
what could also be given in A flutter
warfarin for prevention of thromboembolism
