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