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Cardiovascular > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

what is an arrhythmia?

A

disturbances of heart rate, or rhythm

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2
Q

what may cause arrhythmias?

A

changes in impulse formation or impulse conduction

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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)

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4
Q

what is a bradycardia?

A

HR < 60 bpm during the day

HR < 50 bpm at night

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5
Q

what is a tachycardia?

A

HR > 100 bpm

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6
Q

what do alterations in impulse formation involve?

A

changes in automaticity

triggered activity

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7
Q

what do abnormalities in impulse conduction arise from?

A

re-entry
conduction block
accessory tracts

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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

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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

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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

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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

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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

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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

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14
Q

what can result in an ectopic rhythm?

A

ischaemia
hypokalaemia
increased sympathetic activity
fibre stretch

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15
Q

what is ischaemia?

A

a restriction in blood supply to tissues, causing a shortage of oxygen that is needed for cellular metabolism

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16
Q

what are afterdepolarisations (ADs)?

A

when a normal action potential triggers abnormal oscillations in membrane potential that occurs during or after depolarisation

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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

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18
Q

what are the two types of after depolarisations?

A

early and delayed

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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)

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20
Q

when are EADs most likely to occur in terms of HR?

A

when it is slow

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21
Q

where do EADs occur?

A

in purkinje fibres

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22
Q

what are EADs associated with?

A

prolongation of the action potential and drugs prolonging the QT interval

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23
Q

when can EADs be life threatening?

A

when sustained as they can cause torsades de pointes

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24
Q

when do DADs occur?

A

after complete repolarisation

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25
Q

what causes DADs?

A

large increases in Ca2+

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26
Q

when are DADs most likely to occur in terms of HR?

A

when it is fast

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27
Q

when are DADs increased and decreased in incidence?

A

by prolongation and shortening of the duration of the AP by drugs

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28
Q

what may trigger DADs?

A

drugs that increase Ca2+ influx eg catecholamines or release from the SR eg digoxin

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29
Q

what is re-entry?

A

when a self sustaining electrical circuit stimulates an area of myocardium repeatedly/rapidly

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30
Q

what does the re-entrant circuit require?

A

unidirectional blood

slowed retrograde conduction velocity

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31
Q

what causes unidirectional block?

A

anterograde conduction prohibited

retrograde conduction allowed

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32
Q

where is conduction block through?

A

the AV node

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33
Q

what happens during partial block?

A

either slowed conduction or intermittent block

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34
Q

what happens during slowed conduction?

A

tissue conducts all impulses but more slowly than usual eg first degree AV block

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35
Q

what happens during intermittent block?

A

tissue conducts some impulses but not other eg second degree AV block

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36
Q

what are the two types of second degree block?

A

Mobitz type I

Mobitz type II

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37
Q

describe Mobitz type I

A

PR interval gradually increases from cycle to cycle until AV node fails completely and a ventricular beat is missed

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38
Q

describe Mobitz type II

A

PR interval is constant but every nth, ventricular depolarisation is missing

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39
Q

what happens during complete block?

A

no impulses are conducted through the affected area eg 3rd degree AV block

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40
Q

what happens during 1st degree block?

A

there is a long PR interval

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41
Q

what happens during 3rd degree block?

A

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

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42
Q

what are accessory tract pathways?

A

electrical pathways in parallel to the AV node

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43
Q

describe the bundle of Kent

A

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

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44
Q

what do anti arrhythmic drugs usually do?

A

inhibit specific ion channels (or activate/block specific receptors) with the intention of suppressing abnormal electrical activity

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45
Q

what is the Vaughn Williams classification?

A 
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
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46
Q

what is the target of class I drugs?

A

voltage activated Na+ channels

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47
Q

what is the target of class II drugs?

A

B-adrenoreceptor (as antagonists)

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48
Q

what is the target of class III drugs?

A

voltage activated K+ channels

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49
Q

what is the target of class IV drugs?

A

voltage activated Ca2+ channels

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50
Q

describe the use dependant manner of class I agents

A

they bind preferentially to areas of the myocardium in which firing frequency is highest without preventing the heart from beating at normal frequencies

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51
Q

what happens to class I agents when the Na+ channel is in resting state?

A

they dissociate from it

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52
Q

what happens during ischaemia myocardium?

A

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

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53
Q

what does the ischamia tissue allow class I agents to do?

A

act preferentially on ischaemic tissue and block an arrhythmogenic focus at its source

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54
Q

what is a supraventricular arrhythmia?

A

origin is above the ventricle, ie SAN, atrial muscle, AV node or HIS origin

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55
Q

what is a ventricular arrhythmia?

A

origin is in ventricular muscle (common) or fascicles of the conducting system (uncommon)

56
Q

describe supraventricular tachycardia

A

atrial fibrillation
atrial flutter
ectopic atrial tachycardia

57
Q

describe bradycardia

A

sinus bradycardia

sinus pauses

58
Q

what are examples of ventricular arrhythmias?

A

ventricular ectopics or premature ventricular complexes
ventricular tachycardia
ventricular fibrillation
asystole

59
Q

what are atrio-ventricular node arrythmias?

A 
AVN re entry tachycardia
AV reciprocating or AV reentrant tachycardia
AV block (1st, 2nd or 3rd degree)
60
Q

what are the causes of arrythmias?

A 
abnormal anatomy
ANS
metabolic
inflammation
drugs
genetic
61
Q

what are the abnormal anatomy causes of arrhythmias?

A

LV hypertrophy
accessory pathways
congenital HD

62
Q

what are ANS causes of arrhythmias?

A

sympathetic stimulation eg stree, exercise, hyperthyroidism

increased vagal tone causing bradycardia

63
Q

what are metabolic causes of arrhythmias?

A

hypoxia: COPD, pulmonary embolus
ischaemic myocardium: acute MI, angina
electrolyte imbalances

64
Q

what is an inflammatory cause of arrhythmias?

A

viral myocarditis

65
Q

which drugs can cause arrhythmias?

A

direct electophysiologic effects or via ANS

66
Q

which mutations can cause arrhythmias?

A

those of genes encoding cardiac ion channels eg the congenital long QT syndrome

67
Q

what are ectopic beats?

A

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

68
Q

what causes ectopic beats?

A

altered automaticity eg ischaemia, catecholamines

triggered activity eg digoxin, long QT syndrome

69
Q

what causes re-entry?

A

requires more than one conduction pathway, with different speed of conduction (depolarisation) and recovery of excitability (refractoriness)

70
Q

what can cause re-entry?

A

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
Q

what is the mechanism of tachycardia?

A

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
Q

what happens if there is an increase in the phase 4 slope?

A

there is an increase in heart rate, ectopics

73
Q

what can cause an increase in phase 4?

A 
hyperthermia
hypoxia
hypercapnia
cardiac dilation
hypokalaemia
74
Q

what does a decrease in the phase 4 slope cause?

A

slowed conduction, bradycardia, heart block

75
Q

what can cause a decrease in phase 4?

A

hypothermia

hyperkalaemia

76
Q

what is triggered activity?

A

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
Q

what does triggered activity cause?

A

digoxin toxicity
torsades de pointes in the long QT syndrome
hypokalaemia

78
Q

what are the symptoms?

A 
palpitaions
SoB
dizziness
loss of consciousness; syncope
faintness; presyncope
sudden cardiac death 
angina, HF
79
Q

what are the investigations?

A 
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
Q

what is an ECG used for?

A

to assess rhythm

to look for signs of a previous MI (Q waves) or pre-excitation (Wolf Parkinson White syndrome)

81
Q

what is an exercise ECG used for?

A

to assess ischaemia

exercised induced angina

82
Q

what is a 24hr holtor ECG used for?

A

to assess for paroxysmal arrhythmia

to link symptoms to underlying heart rhythm

83
Q

what is echocardiography used for?

A

to assess for structural heart disease eg enlarged atria in AF, LV dilatation, previous MI scar, aneurysm

84
Q

what is an electrophysiological study used for?

A

to trigger the clinical arrhythmia and study its mechanisms/pathways
opportunity to treat the arrhythmia by delivering radiofrequency ablation to extra pathway

85
Q

what are normal sinus arrhythmias?

A

variation in HR, due to reflex changes in vagal tone during the respiratory cycle
inspiration reduces vagal tone and increases HR

86
Q

what is sinus bradycardia?

A

<60 bpm

can be physiological, due to drugs (B blockers) or due to ischaemia

87
Q

what is the treatment of bradycardia?

A

atropine (if acute eg acute MI)

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

88
Q

what is sinus tachycardia?

A

HR> 100 bpm
can be physiological (anxiety, fever, hypotension, anaemia)
inappropriate (drugs etc)

89
Q

what is the treatment of sinus tachycardia?

A

treat underlying cause

B-adrenergic blockers

90
Q

what are the symptoms of atrial ectopic beats?

A

asymptomatic

palpitations

91
Q

what is the treatment of atrial ectopic beats?

A 
generally none
B blockers may help 
avoid stimulants (caffeine, cigarettes)
92
Q

what is the acute management of supraventricular tachycardias?

A

increase vagal tone: valsalva, carotid massage
slow conduction in the AVN
- IV adenosine
- IV verapamil

93
Q

what is radiofrequency catheter ablation?

A

selective cautery of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit

94
Q

what are the causes of AVN conduction disease (hear block)?

A 
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
Q

discuss first degree heart block

A

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
Q

what is second degree heart block?

A

Intermittent block at the AVN (dropped beats)
2 types;
Mobitz I
Mobitz II

97
Q

what is Mobitz 1?

A

progressive lengthening of the PR interval, eventually resulting in a dropped beat.
Usually vagal in origin

98
Q

what is Mobitz 2?

A

Pathological, may progress to complete heart block (3rd degree HB)
Usually 2:1, or 3:1, but may be variable
Permanent pacemaker indicated

99
Q

what are single chamber pacemakers?

A

paces the right atria or right ventricle only

100
Q

what are dual chamber pacemakers?

A

paces the RA and RV
maintains AV synchrony
used for AVN disease

101
Q

what are the causes of ventricular ectopics?

A

structural causes: LVH, heart failure, myocarditis
metabolic: ischaemic heart disease, electrolytes
may be marker for inherited cardiac conditions

102
Q

when does a ventricular ectopic need to be investigated?

A

if worse on exercise

103
Q

what causes ventricular tachycardia?

A

CAD
previous MI
cardiomyopathy
inherited/ familial arrhythmia syndromes- long QT, brugada syndrome

104
Q

what is a ventricular tachycardia with haemodynamic compromise?

A

large sustained reduction of arterial pressure

105
Q

what is ventricular fibrillation?

A

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

106
Q

what is the treatment of an acute VT?

A

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
Q

what is long term treatment for VT?

A

correct ischaemia if possible
optimis CHF therapies
implantable cardiovertor defibs if life threatening
VT cath ablation

108
Q

discuss VT/ VF pearls

A

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
Q

what is atrial fibrillation?

A

Chaotic and disorganized atrial activity
Irregular heartbeat
Can be paroxysmal, persistent or 
permanent (chronic)
Can be symptomatic or asymptomatic

110
Q

what is the mechanism of AF?

A

ectopic foci in muscle sleeves in the ostia of the pulmonary veins

111
Q

how can AF be terminated?

A

pharmacologic cardioversion with anti-arrhythmic drugs
electrical cardioversion
spontaneous reversion to sinus rhythm

112
Q

what is paroxysmal AF?

A

lasting less then 48 hours

often recurrent

113
Q

what is persistent AF?

A

an episode of AF lasting greater than 48 hours which can still be cardioverted to NSR
unlikely to spontaneously revert to NSR

114
Q

what is permanent AF?

A

inability of pharmacologic or non-pharmacologic methods to restore NSR

115
Q

what are diseases associated with AF?

A 
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
Q

what is lone (idiopathic) AF?

A

absence of any heart disease and no evidence of ventricular dysfunction
a diagnosis of exclusion
could be genetic
significant stroke rate

117
Q

describe the ECG of someone with AF

A 
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
Q

what are the consequences of AF?

A

Lost ‘atrial kick’ and decreased filling times (reduced diastole)&raquo_space; reduced cardiac output
Can result in congestive heart failure, especially in the presence of diastolic dysfunction

119
Q

what is the management of AF?

A

rhythm control: maintain SR
or
rate control: accept AF but control ventricular rate

anticoagulants for both approaches if high risk for thromboembolism

120
Q

what are the drug options for rate control?

A

digoxin
betablockers
verapamil, diltiazem

121
Q

what is used for rhythm control?

A 
pharmacologic cardioversion 
direct current cardioversion
anti-arrhytmic drugs
catheter ablation of atrial focus/ pulmonary veins 
surgery (Maze procedure)
122
Q

what are class I anti-arrhythmic drugs?

A

reduce Na channel current

lignocaine, quinidine, flecainide, propafenone

123
Q

what are class II anti-arrhythmic drugs?

A

B- adrenergic antagonists

propranolol

124
Q

what are class III anti-arrhythmic drugs?

A

action potential prolongation
amiodarone, sotalol
dronedarone

125
Q

what are class IV anti-arrhythmic drugs?

A

Ca channel antagonists

verapamil

126
Q

what are the indications for anti-coagulation in AF?

A 
Valvular AF
mitral valve disease: MS and MR
Non valvular AF if:
Age >75
Hypertension
Heart failure
Previous stroke/ thromboembolism
CAD / DM
Diabetes
127
Q

what is radiofrequency ablation used for in AF?

A

to maintain SR by ablating AF focus and for rate control by ablation of the AVN to stop fast conduction to the ventricles

128
Q

what is left atrial catheter ablation for AF?

A

isolates triggers in the pulmonary veins by pulmonary in LA vein isolation

129
Q

what is an atrial flutter?

A

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
Q

what are the treatment options for atrial flutter?

A 
RF ablation
Pharmacologic therapy
-Slow the ventricular rate
-Restore sinus rhythm
-Maintain sinus rhythm once converted
Cardioversion
Warfarin for prevention of thromboembolism
131
Q

what are the indications for anti-coagulation in AF?

A 
Valvular AF
mitral valve disease: MS and MR
Non valvular AF if:
Age >75
Hypertension
Heart failure
Previous stroke/ thromboembolism
CAD / DM
Diabetes
132
Q

what is radiofrequency ablation used for in AF?

A

to maintain SR by ablating AF focus and for rate control by ablation of the AVN to stop fast conduction to the ventricles

133
Q

what is left atrial catheter ablation for AF?

A

isolates triggers in the pulmonary veins by pulmonary in LA vein isolation

134
Q

what is an atrial flutter?

A

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
Q

what are the treatment options for atrial flutter?

A 
RF ablation
Pharmacologic therapy
-Slow the ventricular rate
-Restore sinus rhythm
-Maintain sinus rhythm once converted
Cardioversion
Warfarin for prevention of thromboembolism

Cardiovascular (31 decks)

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