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NARROW COMPLEX TACHYCARDIAS (INAPPROPRIATE SINUS TACHYCARDIA (CLINICAL…
NARROW COMPLEX TACHYCARDIAS
INAPPROPRIATE SINUS TACHYCARDIA
peak incidence of 38 yrs old
AETIOLOGY
common causes:
drugs - adrenaline, salbutamol, anti-histamines, tricyclic antidepressants
pulmonary embolism
physiological - exercise, pain, anxiety, pregnancy
other causes
infection
substances - cocaine, amphetamines, cannabis, caffeine
metabolic -hyperthyroidism, anaemia
psychological - anxiety
cardiac - HF, IHD, cardiomyopathies
majority of pts (90%) are female
Sinus tachycardia is the most common ECG finding in pts with pulmonary embolism
normal sinus rhythm is observed
the second most common finding is right axis deviation with or without RBBB
an increase in HR to >100bpm in adults
It is important to note that S1,Q3,T3 (inversion) pattern rarely seen in clinical practice
PATHOPHYSIOLOGY
Increased automaticity as a result of sympathetic activation and/or parasympathetic inhibition
CLINICAL FEATURES
CHEST PAIN
BREATHLESS
PALPITATIONS
LIGHT-HEADED
ECG
Normal visible P waves often buried in preceding t wave (camel hump appearance)
100BPM
MANAGEMENT
pharmacological therapy: B-blockers or ivabridine used if symptomatic pts with chronic inappropriate sinus tachycardia
Surgical: radiofrequency ablation of SAN if pt is resistant to medical therapy. rarely used for sinus tachy
Treat underlying cause or remove offending agent
All narrow complex tachy are generally supraventricular in origin i.e. they either occur in SAN, atria, or AVN
MOST SUPRAVENTRICULAR TACHY ARE BENIGN AND RARELY LIFE-THREATENING
ATRIAL FIBRILLATION
atrial tachyarrhythmia characterised by an irregularly irregular heart rhythm and indiscernible P waves on the ECG
affects 10% of >70y/o, prevalence inc with age
male predominance
AETIOLOGY [ATRIALE PhIB]
Atrial myxoma
Lungs (pulmonary HTN, pneumonia)
IHD
Electrolyte disturbances
Rheumatic Fever and mitral valve pathologies
Pharmacological
Thyrotoxicosis
Iatrogenic (drugs, surgery)
Alcohol and caffeine
BP
Others: Infection
Thyroxine shortens the duration of action potential and inc automaticity of cardiac myocytes = predicposes form tachyarrhythmia
3 most common causes of AF
HTN
Mitral Valve Pathologies
IHD
PATHOPHYSIOLOGY
often initiated by an area of ectopic focal activity with increased automaticity
this area typically originates at or around the pulmonary veins
the rapid activation of these foci propogate ectopic beats that create micro-re-entrant circuits throughout the atrial muscle
no organisation of atrial elec activity = myocytes cant contract simultaneously
results in blood pooling in atria = predispose to thrombus
loss of atrial conduction also leads to inadequate ventricular filling and as a result poor CO
CLINICAL FEATURES
Palpitations, breathlessness on exertion and lightheadedness
irregularly irregular pulse with or without pulse deficit
pulse deficit refers to the difference in apical and peripheral pulse rate
in fast AF (rapid ventric rates ) there is inadequate diastolic filling
the subsequent SV will be reduced and this might not be sufficient to generate a palpable periph pulse
Asymptomatic (25% of pts)
RE-ENTRY MECHANISM of AF
(b) inc myocardial excitability e.g. adrenaline release during exercise, thyrotoxicosis = shortens refractory period = allow re-entry
(c) inc atrial vol e.g. atrial dilatation secondary to mitral regurg = lengthen circuit duration = re-entry can ocur
(a) an area of infarct slows conduction pathway = inc circuit time and as a result encourages re-entry
CLINICAL ASSESSMENT
(1)INITIAL IX
ECG - holter ambulatory monitoring may be used for patients with supsected paroxysmal AF episodes
BLOOD TEST - identify underlying cause; FBC (anaemia, infection), TFTs (hyperthyroidism), U&Es (electrolyte disturbances), glucose
ECHO (transthoracic) - consideration of cardioversion for rhythm control management; high suspicion of structural heart disease; if additional information is needed for anticoagulation risk stratification
(2) ASSESS DURATION OF SYMPTOMS AND EPISODES
PERSISTENT
non self-resolving episode of more than 7 days
PERMANENT
AF for more than 1 year resistant to treatment
PAROXYSMAL
Self-resolving episode of less than 7 days
(3) CONTROLLING HR AND RHYTHM
rate control indicated as a first line option unless:
AF is secondary to HF
new-onset AF
there is a reversible cause
NICE AF MANAGEMENT
Rate Control
Monotherapy B-blocker or CCB
Combination therapy Digoxin +/- B blocker +/- CCB
2 more items...
+/- Digoxin (if in HF)
+/- flecainide (contraindicated: structural HD)
Rhythm Control
Chronic
B blocker (Except sotalol)
no LV impairment/HF
dronedarone
1 more item...
LV impairment/HF
amiodarone
1 more item...
paroxysmal AF + no structural heart disease
'pill in pocket'
flecainide
1 more item...
Acute
symptomatic >48hrs
delayed cardioversion
TTE-guided elec cardioversion
1 more item...
INR >2.0 for at least 4 wks
symptomatic <48hrs
immediate cardioversion +/- IV heparin
No structural HD
1 more item...
structural HD
1 more item...
rapid AF is a medical emergency
GENERAL RULE OF THUMB
Asymptomatic or mildly symptomatic pt >65 - consider rate control
symptomatic pts <65 or concomitant HF consider rhythm control
(4) ASSESSMENT FOR ANTICOAGULATION
All pts with AF have stroke risk calculated: CHA2DS2VASC
Age (65-74 =1, >75 =2)
HTN (1)
Diabetes (1)
CHF Hx (1)
Stroke, VTE Hx (2)
Vasc disease (1)
Sex (F=1)
if score >/= in men, consider anticoag
if score >/=2, offer anticoag
decision to initiate anticoag weighed up with bleeding risk: HASBLED
bleeding hx/predisposition
labile INR (time in therapeutic range <60%)
Stroke hx
elderly (>65yrs old)
Abnormal renal/liver function
drugs (NSAIDs, antiplatelets) or alcohol
HTN (SBP >160mmHg)
score of </=2 offer anticoagulation
score >/=3 consider alternative anticoagulation
the choice of anticoag is based on the clinical picture and pt preference:
direct thrombin inhibitor - dabigatran
direct factor Xa inhibitors - apixaban, rivaroxaban
vitamin K antagonist - warfarin (target INR 2.0-3.0)
ECG
irregularly irregular rhythm
absent P waves
ATRIAL FLUTTER
atrial tachyarrhythmia which is characterised by a regular, rapid atrial rate
EPIDEMIOLOGY
the prevalence ratio in males to females is 5:2
incidence inc with age
less common than atrial fibrillation
AETIOLOGY
Common Causes
idiopathic - no underlying heart disease
normal variant - tall males
IHD
pts with a hx of endurance sport (causing atrial enlargement)
right atrial dilatation - pulmonary embolus, mitral and/or tricuspid pathologies, congestive HF
Other Causes
Iatrogenic - previous catheter ablation, cardiac surgery
metabolic disturbances -hyperthyroidism, alcohol
drugs - flecainide, propafenone (15% post-AF therapy)
PATHOPHYSIOLOGY
atrial flutter is characterised by a macro re-entrant circuit within the atrium, most commonly around the tricuspid annulus in an anti-clockwise fashion
this results in a rapid, regular atrial activity at a rate of around 300bpm
many of these fast impulses are unable to pass through the AVN secondary to the refractory period.
this results in a decreased rate of firing of the ventricles.
CLINICAL FEATURES
commonly presents with breathlessness and palpitations
syncope and severe dyspnoea (At very rapid rates)
vagal manoevures (Eg carotid sinus massage, adenosine) may be useful in diagnosing atrial flutter as it causes a transient AV block and reduces the ventricular rate. This might reveal the classic sawtooth flutter waves
ECG
regular sawtooth pattern of flutter waves
fixed conduction ratios (2:1, 3:1, etc)
narrow complex tachycardia with a classic atrial rate of 300bpm
MANAGEMENT
60% of pts with flutter present acutely and cardioversion is recommended in this group
radiofrequency ablation is highly recommended in pts with chronic atrial flutter as therapy can induce high rates of remission (90%)
management similar to AF, but should be noted that achieving rate control in flutter is more difficult
ATRIOVENTRICULAR NODAL RE-ENTRANT TACHYCARDIA
AETIOLOGY common causes
idiopathic (most commonly in structurally normal hearts)
PATHOPHYSIOLOGY
In AVN re-entrant tachycardia, a re-entrant circuit occurs within the AVN. These circuits tend to be functional (non-anatomical) in nature, most commonly involving dual pathways of different conduction velocities. AVNRT accounts for 60% of all regular SVTs
EPIDEMIOLOGY
female predominance
incidence 35 per 100 000
Most common cause of paroxysmal SVT (40-50%)
CLINICAL FEATURES
Sudden onset of rapid palpitations
dizziness
breathlessness
syncope occasionally occurs
a type of paroxysmal supraventricular tachycardia a(SVT) caused by an aberrant circuit within the AVN
ECG Appearance
regular narrow complex tachycardia
P waves may not be visible as they are buried in QRS complexes
MANAGEMENT
Some AVNRTs can be terminated with vagal manoevures (eg valsalva manoevures, carotid sinus massage)
IV adenosine or rate-limiting CCBs may be used if vagal manoevures fail
in emergencies, when pts present with haemodynamic compromise, DC cardioversion is advised
catheter ablation- indicated in pts with recurrent episodes; associated with a less than 1% risk of heart attack
ATRIOVENTRICULAR RE-ENTRANT TACHYCARDIA
Atrioventricular re-entrant tachycardia (AVRT) refers to a form of paroxysmal SVT caused by an anatomically defined re-entrant circuit involving one or more accessory pathways.
Wolff-Parkinson-White (WPW) syndrome, a pre-excitation syndrome which can often lead to AVRT, is characterised by a short PR interval and delta waves on ECG
EPIDEMIOLOGY
Prevalence: 0.1 to 30 per 1000
60-70% of pts with WPW have no evidence of heart disease
AETIOLOGY
Congenital
associated with hypertrophic cardiomyopathy and ebstein's anomaly
PATHOPHYSIOLOGY
as electrical impulses travel faster through the accessory pathway, the circuit tends to occur in an anti-clockwise direction
results in anatomical re-entrant circuit comprising the normal AV conduction system and the accessory pathway
Accessory pathways (eg bundle of kent in WPW) are fibres of abnormal myocytes extending across the atrioventricular groove forming an aberrant connection between the atria and ventricles
there are 2 forms of AVRT:
orthodromic
the most common type (95%) that involves anterograde conduction via AVN and retrograde conduction via the accessory pathway
antidromic
anterograde conduction occurs via the accessory pathway and retrograde conduction through the AVN
CLINICAL FEATURES
chest pain
syncope
palpitations
ECG
Broad QRS (>0.12s)
delta wave - slurring of the QRS upstroke
short PR interval (<0.2s)
therefore there is a premature activation of the ventricles, eliminating the delay through the AVN.
the QRS complex is widened and slurred because it represents a fusion of both excitation waves
conduction via the accessory pathway is faster than that of the native Purkinje system
MANAGEMENT
flecainide and amiodarone may also be useful in the acute setting
catheter ablation of the accessory pathway is the definitive therapy
in the acute setting, vagal manoevures, IV adenosine and procainamide, or rarely DC cardioversion may be used to terminate the tachyarrhythmia
PROGNOSIS - associated with a small risk of sudden death