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Cardiovascular > Cardiac Arrhythmias > Flashcards

Cardiac Arrhythmias Flashcards

1
Q

what ‘insulates’ the electrical regions of the heart

A

the fibrous ring between the atria and ventricles

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2
Q

where is the origin of a supraventricular arrhythmia

A

above the ventricle; sino atrial node, atrial muscle, AV node or HIS origin

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3
Q

where is the origin of a ventricular arrhythmia

A

ventricular muscle or the fascicles of the conducting system (conducting tissue)

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4
Q

what are the two types of supraventricular arrhythmias

A

supraventricular tachycardia and bradycardia

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5
Q

give three examples of supraventricular tachycardia

A

atrial fibrillation, atrial flutter, ectopic atrial tachycardia

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6
Q

give two examples of bradycardia

A

sinus bradycardia, sinus pauses

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7
Q

what are four examples of ventricular arrhythmias

A

ventricular ectopics/ premature ventricular complexes (PVC)

ventricular tachycardia

ventricular fibrillation

a-systole- not contracting

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8
Q

what is a focus

A

somewhere in the ventricles that can fire signals independently

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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)

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10
Q

what are the clinical causes of arrhythmias

A

abnormal anatomy, autonomic nervous system (ANS), metabolic, inflammation, drugs, genetics

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11
Q

what causes the abnormal anatomies associated with arrhythmias

A

left ventricular hypertrophy,

accessory pathways,

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12
Q

what can cause autonomic nervous system disruptions which cause arrhythmias

A

sympathetic stimulation (stress, exercise, hyperthyroidism, stimulants)

increased vagal tone (bradycardia)

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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+)

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14
Q

what can cause the inflammation which can cause arrhythmias

A

viral myocarditis, influenza

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15
Q

what genetic issues cause arrhythmias

A

mutations of genes encoding cardiac ion channels (abnormal proteins= abnormal currents)

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16
Q

what is an ectopic beat

A

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

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17
Q

what two things can cause ectopic beats

A

altered automaticity (e.g. ischaemia, catecholamines)

triggered activity (e.g. digoxin, long QT syndrome)

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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)

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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)
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20
Q

what is a sustained arrhythmia

A

series of ectopic beats

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21
Q

what are the two electrophysiological mechanisms causing arrhythmias

A

ectopic beats, re-entry

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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

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23
Q

how can re-entry arrhythmias cause tachycardia

A

triggered by an ectopic beat, resulting in a self perpetuating circuit

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24
Q

is tachycardia dangerous

A

maybe, depending on how they effect the cardiac output

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25
Q

what is the clinically presentation of tachycardia

A

variable

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26
Q

what is altered automaticity

A

change in slope, threshold, rate of action potential changing heart rate

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27
Q

what happens when the slope of phase 4 of an action potential is increased

A

increase in heart rate

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28
Q

what causes an increase in phase 4 slope in an action potential

A

hyperthermia, hypoxia, hypercapnia, cardiac dilation, hypokalaemia (prolongs repolarisation)

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29
Q

what does a decrease in the slope of phase 4 of an action potential cause

A

slowed conduction- bradycardia, heart block

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30
Q

what can cause a decrease in slope 4 of the action potential

A

hypothermia, hyperkalaemia

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31
Q

what is an after-depolarisation

A

a small depolarisation that occurs in the terminal phase of the AP (phase 3)

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32
Q

what happens when and after depolarisation reaches depolarisation threshold

A

lead to a sustained train of depolarisations= triggered activity

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33
Q

what is triggered activity the mechanism behind

A

digoxin toxicity, torsades de Pointes in the long QT syndrome and hypokalaemia

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34
Q

what causes an after-depolarisation in triggered activity

A

when there is an excess of digoxin/ calcium, cells try to have early depolarisation to get rid of it

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35
Q

what causes a alternative conduction pathway to slow down

A

if pathway becomes ischaemic

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36
Q

what happens when an alternative conduction pathway is slowed down

A

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.

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37
Q

why is it called a re-entrant current

A

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

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38
Q

what are the symptoms of an arrhythmia

A

palpitations ‘pounding heart’, SOB, dizziness (CO impaired), loss of consciousness (syncope), sudden cardiac death, angina, heart failure

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39
Q

why do arrhythmias cause angina

A

as heart going fast and ischaemia present (re-entrant)

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40
Q

what investigations are done when an arrhythmia is suspected

A 
12 lead ECG, 
CXR, echocardiogram, stress ECG (look for myocardial ischaemia,
exercise related arrhythmias),
24 hour ECG holter monitoring,
event recorder,
electrophysiological study
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41
Q

why is an ECG done in arrhythmias

A

to assess rhythm, signs of previous MI, and pre-excitation

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42
Q

what is a true accessory pathway

A

connection between atria and ventricles

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43
Q

how is pre-excitation seen in an ECG

A

delta wave

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44
Q

what does an exercise ECG look for in ECG in arrhythmias

A

to assess for ischaemia and exercise induce arrhythmia

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45
Q

what does a 24hr holter ECG look for in arrhythmias

A

assess for paroxysmal (sudden attacks) arrhythmia,

link symptoms to underlying heart

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46
Q

what does an echocardiography asses for in arrhythmias

A

structural heart disease (enlarged atria in AF, LV dilatation, previous MI scar, aneurysm)

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47
Q

what does an electrophysiological study look for and how

A

triggers the clinical arrhythmia and study its mechanism/pathway

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48
Q

what does electophysiological study allow

A

opportunity to treat the arrhythmia by delivering radio-frequency ablation to extra pathway

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49
Q

what is radio-frequency ablation

A

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’

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50
Q

what causes variation in normal sinus rhythm

A

reflex changes in vagal tone during the respiratory cycle (inspiration causes reduced vagal tone and increase heart rate)

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51
Q

what can cause sinus bradycardia

A

physiological (athlete), drugs (B-blocker), ischaemia

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52
Q

how is sinus bradycardia treated

A

atropine (anti vagal, speeds up HR)

pacing if haemodynamic compromise: hypotension, CHF, angina, collapse

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53
Q

what can cause sinus tachycardia

A

physiological (anxiety, fever, hypotension, anaemia), drugs/stimulants etc

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54
Q

how is sinus tachycardia treated

A

treat underlying cause, Beta blockers

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55
Q

what are the symptoms of atrial ectopic beats

A

asymptomatic, palpitations

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56
Q

how are atrial ectopic beats treated

A

generally no treatment, beta blockers must help, avoid stimulants

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57
Q

what does an ECG showing a narrow complex tachycardia suggest

A

superventricular tachycardia

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58
Q

what does a sinus rhythm ECG have

A

a P wave before the QRS complex

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59
Q

what can cause regular supraventricular tachycardia

A

AV nodal re-entrant tachycardia,
AV reciprocating tachycardia/ AV re-entrant tachycardia (via accessory pathway),
ectopic atrial tachycardia

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60
Q

how are regular supraventricular tachycardia

A

vagal manoeuvres, adenosine

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61
Q

what is AVNRT

A

AV nodal re-entrant tachycardia

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62
Q

what is AVRT

A

AV re-entrant tachycardia

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63
Q

what is mechanism between a AV node re-entrant tachycardia

A

circuit with the AV node (micro-re entry)

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64
Q

what is the mechanism behind AV re-entrant tachycardia

A

circuit using the AV node and accessory pathway (macro-re entry)

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65
Q

how is AVNRT treated

A

ablation- getting ride of slow pathway (creates scar tissue)

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66
Q

what causes atrial tachycardia

A

focus in heart firing regardless of AV node, if faster than AV will take over.

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67
Q

what does the QRS complex look like in atrial tachycardia

A

normal as using correct conduction pathway

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68
Q

what is the acute management of supra ventricular management

A

increase vagal tone (valsalva, carotid massage)

slow conduction in the AV node (IV adenosine-vasodilator and anti arrhythmic or verapamil-calcium channel blocker)

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69
Q

what is the chronic management of supra-ventricular tachycardia

A

avoidance of stimulants

electrophysiologic study and radiofrequency ablation

beta blockers

anti-arrhythmic drugs

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70
Q

how to ECG catheters reach the heart

A

via femoral veins

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71
Q

how are the location and mechanism of the tachycardia identified

A

intracardiac ECG recorded during sinus rhythm, tachycardia and pacing manoeuvres

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72
Q

how does radio-frequency ablation specifically target problem areas

A

catheter placed over focus/ pathway and tip heated to 55-65c

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73
Q

what is heart block

A

AV node conduction disease

74
Q

what are the cause of heart block

A 
ageing, 
acute MI, 
myocarditis, 
infiltrative disease (amyloid), 
drugs (beta blockers, calcium channel blockers), 
calcific aortic valve disease, 
post-aortic valve disease, 
genetics
75
Q

what is amyloid

A

starch like protein which is deposited in tissues

76
Q

describe 1st degree AV block

A

conduction following each P wave takes longer, resulting in a prolonged P-R interval (>0.2 sec)

77
Q

what is the treatment for 1st degree heart block

A

nothing

78
Q

describe 2nd degree AV block

A

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
Q

what are the two types of 2nd degree AV bock

A

mobitz I and II

80
Q

describe mobitz type I

A

progressive lengthening of the PR interval, eventually resulting in a dropped beat

81
Q

what usually causes mobitz type I

A

usually of vagal origin

82
Q

describe mobitz type II

A

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
Q

describe 2nd degree heart block (2:1)

A

two p waves per QRS complex. normal and constant PR interval in the conducted beat. one QRS complex dropped

84
Q

describe 2nd degree heart block (3:1)

A

three p waves per QRS complex

85
Q

describe third degree heart block

A

complete heart block. when atrial conduction is normal but no beats are conducted to the ventricles. ventricles are stimulated by slow escape mechanism

86
Q

describe third degree heart block on an ECG

A

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
Q

what is the treatment for mobitz II block and 3rd degree AV block

A

ventrciular pacing

88
Q

what does a broad QRS complex suggest

A

activity coming from myocytes not purkinje system

89
Q

how does the heart respond to a dropped beat

A

can either stop or make escape rhythm (comes from automatic drift of the action potential towards trigger potential)

90
Q

what is the basic mechanism of action of a pacemaker

A

if doesn’t sense electrical activity sends signal to SA node

91
Q

what are the two types of pacemakers

A

single chamber (paces right atria or right ventricle only)

dual chamber (paces both PA and PV)

92
Q

what is the advantage of dual chamber pacemakers and what disease type are they used in

A

able to maintain Atria-ventricle synchrony

used for AVN disease

93
Q

what is a premature ventricular complex

A

A premature beat arising from an ectopic focus within the ventricles (ectopic beat)

94
Q

what can cause ventricular ectopics

A

structural causes: LVH, heart failure, myocarditis

metabolic: ischaemic heart disease, electrolytes

inherited cardiac conditions

95
Q

how are ventricular ectopics treated

A

beta blockers, ablation of focus

96
Q

what is the severity of ventricular tachycardia

A

life threatening but may be haemodynamically stable

97
Q

what does most patients with VT also have

A

heart disease; coronary artery disease, previous MI (or more rarely cardiomyopathy/ inherited arrhythmia syndromes)

98
Q

give examples of inherited arrhythmia syndromes

A

long QT syndrome, brugada syndromes

99
Q

when does VT cause haemodynamic compromise

A

when rhythm causes large, sustained reduction of arterial pressure- due to extreme HRs and lack of coordinated contraction

100
Q

what are the ECG characteristics of monomorphic VT

A

Regular rhythm.
Originates from a single focus within the ventricles.
Produces uniform QRS complexes within each lead — each QRS is identical

101
Q

what are the ECG characteristics of VT

A

p waves not usually visible

PR interval not measurable

QRS complexes rapid and wide

Large T waves with defliections opposite the QRS complexes

102
Q

in what type of tachycardia do capture and fusion beats occur

A

ventricular, not supraventricular

103
Q

how is polymorphic VT different from monomorphic VT

A

rhyth, constantly changing

104
Q

what is a capture beat

A

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
Q

what is a fusion beat

A

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
Q

what is ventricular fibrillation

A

chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump

107
Q

what is the immediate treatment for VF

A

defibrillation, cardiopulomnary resuscitation

108
Q

what is the long term treatment for VF

A

correct ischaemia if possible (revascularisation)

CHF therapies

implantable cardiovertor defibrillators

VT catheter ablation

109
Q

what is the acute treatment for ventricular tachycardia

A

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
Q

what are pro-arrhythmic medications and give an example

A

drugs that prolong the QT interval e.g. sotalol

111
Q

what is an ICD

A

implantable cardioverter defibrillator

112
Q

what are the therapies provided by an ICD

A

termination of VT/VF

  • anti-tachycardia pacing
  • cardioversion
  • defibrillation

pacing for brady cardia

113
Q

wide QRS tachycardia with history of CAD/ HF = ?

A

VT until proven otherwise

114
Q

do anti arrhythmic drugs help in survival of VT/VF

A

no but helpful after with ICD to reduce symptoms

115
Q

what causes irregularly irregular rhythms

A

atrial fibrillation,atrial or ventricular ectopic beats, multi focal atrial tachycardia,

116
Q

what can cause regularly irregular rhythms

A

sinus arrhythmia, second degree heart block

117
Q

what are the characteristics of artial fibrillation on an ECG

A

absence of P waves, irregularly irregular rhythm, chaotic and disorganised

118
Q

how is LVH seen on an ECG

A

very tall R waves and ST depression in more than 3 waves

119
Q

in what diseases can LVH been seen in an ECG

A

hypertension and hypertensive heart disease

120
Q

what are three types of onset of AF

A

paroxysmal, persistent or permanent (chronic)

121
Q

what causes the irregular heartbeat in AF

A

disorganised electrical activity of the atria

122
Q

what is sustained AF facilitated by

A

increased parasympathetic tone-atrial refractory periods are decreased, shortening wave length

123
Q

what is the mechanism behind AF

A

multiple waveltes of re-entry=

ectopic foci in muscle sleeves in the ostia of the pulmonary veins- atria firing randomly

124
Q

how is AF terminated

A

electrical cardioversion with anti arrhythmic drugs (flecainide, sotalol and amiodarone), pharmacological cardioversion, spontaneous reversion to sinus rhythm

125
Q

describe paroxysmal AF

A

paroxysmal (sudden), lasting less than 48 hours, often recurrent

126
Q

describe persistent AF

A

lasts longer than 48 hours, can still be converted to normal sinus rhythm, unlikely to do so spontaneously

127
Q

describe permanent AF

A

inability of pharmacological or on pharmacological methods to restore NSR

128
Q

name some disease/ causes associated with AF

A

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
Q

what is sick sinus syndrome

A

tachy brady syndrome

130
Q

what is lone/ idiopathic AF

A

absence of any heart disease and no evidence of ventricular dysfunction

could be genetic

131
Q

when determining the cause of AF why is it to differentiate between non and valvular heart disease

A

treated very differently, valvular has very high risk of stroke

132
Q

why should anticoagulants be considered in patients over 75 with AF

A

as significant stroke rate

133
Q

what are the symptoms of AF

A

palpitations, pre-syncope (dizziness), syncope, chest pain, dyspnea, sweatiness, fatigue– can be asymptomatic

134
Q

what is the atrial rate in AF

A

more than 300 BPM

135
Q

what are the characteristics of AF on an ECG

A

irregularly irregular, ventricle rate variable, absence of P and T waves, presence of ‘F’ waves

136
Q

what is the ventricual rate in AF dependant on

A

AV node conduction propertiesm sympathetic and parasympathetic tone, drugs

137
Q

what facilitates and inhibits AV node conduction

A

facillitated by symp stim

inhibited by para stim

138
Q

what can be used to control ventricular rate in AF

A

drugs that decrease conduction in AV (beta blockers and calcium channel blockers)

139
Q

what are F waves

A

flutter waves

140
Q

what is the QRS complex like in AF

A

normal

141
Q

why are P and T waves not recognisable in AF

A

as atria quiver instead of contract, replaced by wave deflections

142
Q

why is the rhythm irregular in AF

A

as delay in AV node

143
Q

what cause AF with slow ventricular rate and how is it treated

A

AV block, no escape rhythm

pacemaker as cant give drugs to slow HR

144
Q

what is pseudo-regularisation

A

fake tachycardia as ventricles have fast response to AF

145
Q

how does AF reduce cardiac output

A

as loss of atrial kick- active filling of the ventricles, reduced diastole as reduces filling times

146
Q

what does a ventricle rate lower than 60 in AF suggest

A

AV conduction disease

147
Q

can AF cause CHF

A

yes

148
Q

what permanent treatment may patients with AF require

A

permanent pacing

149
Q

when can AF cause VF and sudden cardiac death

A

when there is AF with pre-excitation

pre-excitation of the ventricles broadens the QRS via an accessory pathway

150
Q

what is diastolic dysfunction

A

failure to relax, leads to pulmonary oedema as of increased pressures in pulmonary system

151
Q

what can cause diastolic dysnfunction

A

LVH, hypertension, ischaemia and AF

152
Q

what events occur during diastole

A

coronary perfusion, ventricular filling, atria active relaxation

153
Q

how is AF managed

A

rhythm control (maintain sinus rhythm) OR rate control (control VR)

Anti-coagulation for both approaches if high risk for thromboembolism

154
Q

how is the rate control approach in AF carried out

A

pharmacological therapy to slow down AVN conduction

  • digoxin
  • beta blockers
  • calcium channel blockers: verapamil, diltiazem
  • adenosine

(alone or in combo)

155
Q

when is rate control carried out in patients with AF

A

where the restoration of sinus rhythm is not possible- aims to control ventricular rate and prevent thromboembolism

156
Q

in rhythm control of AF how is normal sinus rhythm restored

A

pharmacological cardioconversion (anti-arrhythmic drugs e.g. amiodarone)

DCCV

157
Q

in rhythm control of AF how is normal sinus rhythm maintained

A

anti-arrhythmic drugs, catheter ablation of atrial focus/ pulmonary veins, surgery (maze procedure)

158
Q

what is the major complication of AF

A

embolism and stroke

159
Q

if pharmacological methods don’t, how else can rate be controlled in AF

A

by completely ablating the AV node and controlling the HR by a pacing system

160
Q

how does electric cardioversion work

A

delivers a dose of electrical current to the heart at a specific moment in the cycle to terminate the arrhythmia

161
Q

how do anti arrhythmic drugs work

A

block ionic currents across cell membranes that create action potentials

162
Q

what do class 1 anti arrhythmic drugs act on and give 4 examples

A

reduce Na channel current

lignocaine, quinidine, flecainide, propafenone

163
Q

what do class 2 anti arrhythmic drugs act on and give an example

A

B-adrenergic antagonists

propranalol

164
Q

what do class 3 anti arrhythmic drugs act on and give 3 examples

A

action potential elongation

amiodarone, sotalol, DRONEDARONE

165
Q

what do class 4 anti arrhythmic drugs act on and give an example

A

Ca channel antagonists

verapamil

166
Q

what is Torsades de Pointes and how is it identified

A

deadly and rapid VT (200-250 bpm)

irregular rhythm
wide QRS
long QT interval
continuously chanigng QRS morphology

167
Q

what puts patients at a high risk of thromboembolism

A

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
Q

five two examples of anticoagulants patient should be on when high risk of thromboembolism in AF

A

warfarin, rivaroxaban

169
Q

where do AF focus usually come from

A

pulmonary veins

170
Q

what part of heart is ablated to maintain SR

A

AF focus (usually in pulmonary veins)

171
Q

what part of the heart is ablated for rate control in AF

A

AVN to stop fast conduction to the ventricles

172
Q

what is atrial flutter

A

rapid and regular form of atrial tachycardia

173
Q

describe the onset of atrial flutter and its mechanism of action

A

usually paroxysmal, sustained by macro-reentry circuit located in the right atrial myocardium

174
Q

how long can flutter episodes last

A

from seconds to years

175
Q

what does chronic atrial flutter eventually convert into

A

chronic atrial fibrillation

176
Q

where is atrial flutter present in the heart

A

confined to right atrium

177
Q

what does atrial flutter look like on an ECG

A

atrial 300 (average) bpm, ventricle 150 bpm

p wave turns into saw tooth F wave

QRS normal

rhythm regular but may be variable

178
Q

how is a counterclockwise flutter terminated

A

rapid atrial pacing, cardioversion, drugs: Ia (moderate class 1), Ic (strong class 1), class 3 antiarrhythmic drugs

may also convert spontaneously

179
Q

how does pharmacological treatment help atrial flutter

A

slows ventricular rate, restores sinus rhythm, maintains sinus rhythm

180
Q

what could also be given in A flutter

A

warfarin for prevention of thromboembolism

Cardiovascular (34 decks)

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