Cardiac Arrhythmias Flashcards
what ‘insulates’ the electrical regions of the heart
the fibrous ring between the atria and ventricles
where is the origin of a supraventricular arrhythmia
above the ventricle; sino atrial node, atrial muscle, AV node or HIS origin
where is the origin of a ventricular arrhythmia
ventricular muscle or the fascicles of the conducting system (conducting tissue)
what are the two types of supraventricular arrhythmias
supraventricular tachycardia and bradycardia
give three examples of supraventricular tachycardia
atrial fibrillation, atrial flutter, ectopic atrial tachycardia
give two examples of bradycardia
sinus bradycardia, sinus pauses
what are four examples of ventricular arrhythmias
ventricular ectopics/ premature ventricular complexes (PVC)
ventricular tachycardia
ventricular fibrillation
a-systole- not contracting
what is a focus
somewhere in the ventricles that can fire signals independently
give three examples of atrio-ventricular node arrhythmias
AVN re-entry tachycardia
AV reciprocating/ AV re-entrant tachycardia
AV block (1st, 2nd and 3rd degree)
what are the clinical causes of arrhythmias
abnormal anatomy, autonomic nervous system (ANS), metabolic, inflammation, drugs, genetics
what causes the abnormal anatomies associated with arrhythmias
left ventricular hypertrophy,
accessory pathways,
what can cause autonomic nervous system disruptions which cause arrhythmias
sympathetic stimulation (stress, exercise, hyperthyroidism, stimulants)
increased vagal tone (bradycardia)
what can cause the metabolic disruptions which cause arrhythmias
hypoxia (chronic pulmonary disease, pulmonary embolus)
ischaemic myocardium (acute MI, angina)
electrolyte imbalances (K+, Ca2+, Mg2+)
what can cause the inflammation which can cause arrhythmias
viral myocarditis, influenza
what genetic issues cause arrhythmias
mutations of genes encoding cardiac ion channels (abnormal proteins= abnormal currents)
what is an ectopic beat
beats or rhythms that originate in places other than the SA node
what two things can cause ectopic beats
altered automaticity (e.g. ischaemia, catecholamines)
triggered activity (e.g. digoxin, long QT syndrome)
what allows re-entry arrhythmias
requires more than one conduction pathway with different speed of conduction (depolarisation) and recovery of excitability (refractoriness)
what can cause re-entry arrhythmias
accessory pathway tachycardia, previous myocardial infarction, congenital heart disease or conditions that depress conduction velocity or shorten refractory period (as they promote functional block)
what is a sustained arrhythmia
series of ectopic beats
what are the two electrophysiological mechanisms causing arrhythmias
ectopic beats, re-entry
how can the ectopic focus cause tachycardia
focus can cause single beats or a sustained run of beats that if faster than sinus rhythm can take over intrinsic rhythm
how can re-entry arrhythmias cause tachycardia
triggered by an ectopic beat, resulting in a self perpetuating circuit
is tachycardia dangerous
maybe, depending on how they effect the cardiac output
what is the clinically presentation of tachycardia
variable
what is altered automaticity
change in slope, threshold, rate of action potential changing heart rate
what happens when the slope of phase 4 of an action potential is increased
increase in heart rate
what causes an increase in phase 4 slope in an action potential
hyperthermia, hypoxia, hypercapnia, cardiac dilation, hypokalaemia (prolongs repolarisation)
what does a decrease in the slope of phase 4 of an action potential cause
slowed conduction- bradycardia, heart block
what can cause a decrease in slope 4 of the action potential
hypothermia, hyperkalaemia
what is an after-depolarisation
a small depolarisation that occurs in the terminal phase of the AP (phase 3)
what happens when and after depolarisation reaches depolarisation threshold
lead to a sustained train of depolarisations= triggered activity
what is triggered activity the mechanism behind
digoxin toxicity, torsades de Pointes in the long QT syndrome and hypokalaemia
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
what causes a alternative conduction pathway to slow down
if pathway becomes ischaemic
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.
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
what are the symptoms of an arrhythmia
palpitations ‘pounding heart’, SOB, dizziness (CO impaired), loss of consciousness (syncope), sudden cardiac death, angina, heart failure
why do arrhythmias cause angina
as heart going fast and ischaemia present (re-entrant)
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
why is an ECG done in arrhythmias
to assess rhythm, signs of previous MI, and pre-excitation
what is a true accessory pathway
connection between atria and ventricles
how is pre-excitation seen in an ECG
delta wave
what does an exercise ECG look for in ECG in arrhythmias
to assess for ischaemia and exercise induce arrhythmia
what does a 24hr holter ECG look for in arrhythmias
assess for paroxysmal (sudden attacks) arrhythmia,
link symptoms to underlying heart
what does an echocardiography asses for in arrhythmias
structural heart disease (enlarged atria in AF, LV dilatation, previous MI scar, aneurysm)
what does an electrophysiological study look for and how
triggers the clinical arrhythmia and study its mechanism/pathway
what does electophysiological study allow
opportunity to treat the arrhythmia by delivering radio-frequency ablation to extra pathway
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’
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)
what can cause sinus bradycardia
physiological (athlete), drugs (B-blocker), ischaemia
how is sinus bradycardia treated
atropine (anti vagal, speeds up HR)
pacing if haemodynamic compromise: hypotension, CHF, angina, collapse
what can cause sinus tachycardia
physiological (anxiety, fever, hypotension, anaemia), drugs/stimulants etc
how is sinus tachycardia treated
treat underlying cause, Beta blockers
what are the symptoms of atrial ectopic beats
asymptomatic, palpitations
how are atrial ectopic beats treated
generally no treatment, beta blockers must help, avoid stimulants
what does an ECG showing a narrow complex tachycardia suggest
superventricular tachycardia
what does a sinus rhythm ECG have
a P wave before the QRS complex
what can cause regular supraventricular tachycardia
AV nodal re-entrant tachycardia,
AV reciprocating tachycardia/ AV re-entrant tachycardia (via accessory pathway),
ectopic atrial tachycardia
how are regular supraventricular tachycardia
vagal manoeuvres, adenosine
what is AVNRT
AV nodal re-entrant tachycardia
what is AVRT
AV re-entrant tachycardia
what is mechanism between a AV node re-entrant tachycardia
circuit with the AV node (micro-re entry)
what is the mechanism behind AV re-entrant tachycardia
circuit using the AV node and accessory pathway (macro-re entry)
how is AVNRT treated
ablation- getting ride of slow pathway (creates scar tissue)
what causes atrial tachycardia
focus in heart firing regardless of AV node, if faster than AV will take over.
what does the QRS complex look like in atrial tachycardia
normal as using correct conduction pathway
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)
what is the chronic management of supra-ventricular tachycardia
avoidance of stimulants
electrophysiologic study and radiofrequency ablation
beta blockers
anti-arrhythmic drugs
how to ECG catheters reach the heart
via femoral veins
how are the location and mechanism of the tachycardia identified
intracardiac ECG recorded during sinus rhythm, tachycardia and pacing manoeuvres
how does radio-frequency ablation specifically target problem areas
catheter placed over focus/ pathway and tip heated to 55-65c
what is heart block
AV node conduction disease
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
what is amyloid
starch like protein which is deposited in tissues
describe 1st degree AV block
conduction following each P wave takes longer, resulting in a prolonged P-R interval (>0.2 sec)
what is the treatment for 1st degree heart block
nothing
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
what are the two types of 2nd degree AV bock
mobitz I and II
describe mobitz type I
progressive lengthening of the PR interval, eventually resulting in a dropped beat
what usually causes mobitz type I
usually of vagal origin
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
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
describe 2nd degree heart block (3:1)
three p waves per QRS complex
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
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
what is the treatment for mobitz II block and 3rd degree AV block
ventrciular pacing
what does a broad QRS complex suggest
activity coming from myocytes not purkinje system
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)
what is the basic mechanism of action of a pacemaker
if doesn’t sense electrical activity sends signal to SA node
what are the two types of pacemakers
single chamber (paces right atria or right ventricle only)
dual chamber (paces both PA and PV)
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
what is a premature ventricular complex
A premature beat arising from an ectopic focus within the ventricles (ectopic beat)
what can cause ventricular ectopics
structural causes: LVH, heart failure, myocarditis
metabolic: ischaemic heart disease, electrolytes
inherited cardiac conditions
how are ventricular ectopics treated
beta blockers, ablation of focus
what is the severity of ventricular tachycardia
life threatening but may be haemodynamically stable
what does most patients with VT also have
heart disease; coronary artery disease, previous MI (or more rarely cardiomyopathy/ inherited arrhythmia syndromes)
give examples of inherited arrhythmia syndromes
long QT syndrome, brugada syndromes
when does VT cause haemodynamic compromise
when rhythm causes large, sustained reduction of arterial pressure- due to extreme HRs and lack of coordinated contraction
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
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
in what type of tachycardia do capture and fusion beats occur
ventricular, not supraventricular
how is polymorphic VT different from monomorphic VT
rhyth, constantly changing
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
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.
what is ventricular fibrillation
chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump
what is the immediate treatment for VF
defibrillation, cardiopulomnary resuscitation
what is the long term treatment for VF
correct ischaemia if possible (revascularisation)
CHF therapies
implantable cardiovertor defibrillators
VT catheter ablation
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)
what are pro-arrhythmic medications and give an example
drugs that prolong the QT interval e.g. sotalol
what is an ICD
implantable cardioverter defibrillator
what are the therapies provided by an ICD
termination of VT/VF
- anti-tachycardia pacing
- cardioversion
- defibrillation
pacing for brady cardia
wide QRS tachycardia with history of CAD/ HF = ?
VT until proven otherwise
do anti arrhythmic drugs help in survival of VT/VF
no but helpful after with ICD to reduce symptoms
what causes irregularly irregular rhythms
atrial fibrillation,atrial or ventricular ectopic beats, multi focal atrial tachycardia,
what can cause regularly irregular rhythms
sinus arrhythmia, second degree heart block
what are the characteristics of artial fibrillation on an ECG
absence of P waves, irregularly irregular rhythm, chaotic and disorganised
how is LVH seen on an ECG
very tall R waves and ST depression in more than 3 waves
in what diseases can LVH been seen in an ECG
hypertension and hypertensive heart disease
what are three types of onset of AF
paroxysmal, persistent or permanent (chronic)
what causes the irregular heartbeat in AF
disorganised electrical activity of the atria
what is sustained AF facilitated by
increased parasympathetic tone-atrial refractory periods are decreased, shortening wave length
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
how is AF terminated
electrical cardioversion with anti arrhythmic drugs (flecainide, sotalol and amiodarone), pharmacological cardioversion, spontaneous reversion to sinus rhythm
describe paroxysmal AF
paroxysmal (sudden), lasting less than 48 hours, often recurrent
describe persistent AF
lasts longer than 48 hours, can still be converted to normal sinus rhythm, unlikely to do so spontaneously
describe permanent AF
inability of pharmacological or on pharmacological methods to restore NSR
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)
what is sick sinus syndrome
tachy brady syndrome
what is lone/ idiopathic AF
absence of any heart disease and no evidence of ventricular dysfunction
could be genetic
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
why should anticoagulants be considered in patients over 75 with AF
as significant stroke rate
what are the symptoms of AF
palpitations, pre-syncope (dizziness), syncope, chest pain, dyspnea, sweatiness, fatigue– can be asymptomatic
what is the atrial rate in AF
more than 300 BPM
what are the characteristics of AF on an ECG
irregularly irregular, ventricle rate variable, absence of P and T waves, presence of ‘F’ waves
what is the ventricual rate in AF dependant on
AV node conduction propertiesm sympathetic and parasympathetic tone, drugs
what facilitates and inhibits AV node conduction
facillitated by symp stim
inhibited by para stim
what can be used to control ventricular rate in AF
drugs that decrease conduction in AV (beta blockers and calcium channel blockers)
what are F waves
flutter waves
what is the QRS complex like in AF
normal
why are P and T waves not recognisable in AF
as atria quiver instead of contract, replaced by wave deflections
why is the rhythm irregular in AF
as delay in AV node
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
what is pseudo-regularisation
fake tachycardia as ventricles have fast response to AF
how does AF reduce cardiac output
as loss of atrial kick- active filling of the ventricles, reduced diastole as reduces filling times
what does a ventricle rate lower than 60 in AF suggest
AV conduction disease
can AF cause CHF
yes
what permanent treatment may patients with AF require
permanent pacing
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
what is diastolic dysfunction
failure to relax, leads to pulmonary oedema as of increased pressures in pulmonary system
what can cause diastolic dysnfunction
LVH, hypertension, ischaemia and AF
what events occur during diastole
coronary perfusion, ventricular filling, atria active relaxation
how is AF managed
rhythm control (maintain sinus rhythm) OR rate control (control VR)
Anti-coagulation for both approaches if high risk for thromboembolism
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)
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
in rhythm control of AF how is normal sinus rhythm restored
pharmacological cardioconversion (anti-arrhythmic drugs e.g. amiodarone)
DCCV
in rhythm control of AF how is normal sinus rhythm maintained
anti-arrhythmic drugs, catheter ablation of atrial focus/ pulmonary veins, surgery (maze procedure)
what is the major complication of AF
embolism and stroke
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
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
how do anti arrhythmic drugs work
block ionic currents across cell membranes that create action potentials
what do class 1 anti arrhythmic drugs act on and give 4 examples
reduce Na channel current
lignocaine, quinidine, flecainide, propafenone
what do class 2 anti arrhythmic drugs act on and give an example
B-adrenergic antagonists
propranalol
what do class 3 anti arrhythmic drugs act on and give 3 examples
action potential elongation
amiodarone, sotalol, DRONEDARONE
what do class 4 anti arrhythmic drugs act on and give an example
Ca channel antagonists
verapamil
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
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)
five two examples of anticoagulants patient should be on when high risk of thromboembolism in AF
warfarin, rivaroxaban
where do AF focus usually come from
pulmonary veins
what part of heart is ablated to maintain SR
AF focus (usually in pulmonary veins)
what part of the heart is ablated for rate control in AF
AVN to stop fast conduction to the ventricles
what is atrial flutter
rapid and regular form of atrial tachycardia
describe the onset of atrial flutter and its mechanism of action
usually paroxysmal, sustained by macro-reentry circuit located in the right atrial myocardium
how long can flutter episodes last
from seconds to years
what does chronic atrial flutter eventually convert into
chronic atrial fibrillation
where is atrial flutter present in the heart
confined to right atrium
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
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
how does pharmacological treatment help atrial flutter
slows ventricular rate, restores sinus rhythm, maintains sinus rhythm
what could also be given in A flutter
warfarin for prevention of thromboembolism
