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BROAD COMPLEX TACHYCARDIAS (VENTRICULAR TACHYCARDIA (CLINICAL FEATURES…
BROAD COMPLEX TACHYCARDIAS
WIDE QRS >0.12s (3 small squares)
often ventricular in origin, may also be supraventricular with an aberrant conduction (usually BBB)
They may be regular (monomorphic ventricular tachycardia) or irregular (torsades de pointes, polymorphic ventricular tachycardia) in nature
VENTRICULAR TACHYCARDIA
refers to a tachyarrhythmia that originates from the ventricles producing three or more successive broad QRS complexes at a rate of more than 100bpm
EPIDEMIOLOGY
peak incidence in middle-aged patients
VT and ventricular fibrillation (VF) account for the most common causes of sudden cardiac death
AETIOLOGY
common causes
Structural heart disease - cardiomyopathies, valvular heart disease
Electrolyte disturbances - hyper/hypokalaemia, hyper/hypomagnesaemia
IHD - scarring post MI
other causes
channelopathies - long QT syndromes, brugada syndrome
idiopathic
drugs and substances - digoxin toxicity, cocaine
CLASSIFICATION
Morphology
monomorphic - uniform QRS complexes in most leads (most common form)
monomorphic VT occurs as a result of a single distinct anatomical re-entrant circuit usually centred around an old MI.
polymorphic - QRS of varying amplitudes, axis and duration across the leads
caused by functional re-entry with varying circuits
Duration
sustained - occurs for more than 30 seconds
non-sustained - self terminating episodes (<30s)
PATHOPHYSIOLOGY
The mechanisms underlying VTs include:
triggered acivity - as seen in long QT syndromes
increased automaticity
re-entrant circuit (most common) - usually due to myocardial scarring post MI
CLINICAL FEATURES
HAEMODYNAMICALLY STABLE PTS PRESENT WITH
dizziness/light-headedness
syncope (inadequate cerebral perfusion)
palpitations
HAEMODYNAMICALLY UNSTABLE PTS (SEVERELY HYPOTENSIVE AND TACHYCARDIC)
low CO symptoms - severe dyspnoea, dizziness (Altered consciousness), syncope
eventually leading to cardiogenic shock and cardiac arrest
EXAMINATION FINDINGS
JVP may be elevated; intermittent cannon A waves may be seen
occur as a result of retrograde blood flow into jugular vein => right atrial contraction against tricuspid valve - due to AV dissociation
ECG
broad QRS complexes (>0.12s)
RULE OF THUMB - all rboad complex tachycardias should be suspected VT until proven otherwise
the other important differential is an SVT with aberrant conduction (eg atrial tachyarrhythmia with a co-existing LBBB or WPW)
MANAGEMENT
if the pt is haemodynamically stable, the management depends on the underlying cause:
IV amiodarone (non idiopathic VT)
elective synchronised DC cardioversion may be indicated if resistant to medical therapy
ongoing recurrent VT:
non-idiopathic VT - consider ICD or catheter ablation (pts with structural heart disease)
idiopathic VT - pharmacological therapy (B blockers, rate-limiting CCBs) may be considered
If the pt is haemodynamically unstable:
immediate resuscitation
emergency DC cardioversion - synchronised shock is recommended
ICD implantation
RULE OF THUMB - all broad complex tachycardia should be suspected VT until proven otherwise - other important DDX is an SVT with aberrant conduction (eg tachyarrhythmias with a co-existing LBBB or WPW)
Pts should not drive for up to 6mths after an unstavle VT/VF
TORSADES DE POINTES
a form of polymorphic VT associated with a prolonged QT interval. French for twisting of the points
female predominance (females have longer baseline QT intervals)
AETIOLOGY
congenital long QT syndrome - monogenic disorders inherited in an autosomal dominant fashion
acquired long QT syndrome
electrolyte imbalance
hypomagnesaemia
hypokalaemia
hypocalcaemia
drugs
PATHOPHYSIOLOGY
Derangement of cardiac ions, particularly sodium, potassium and calcium, increases the duration of action potential, resulting in early after-depolarisations (triggered activity)
in congenital forms of this condition, early after-depolarisations may be triggered by sympathetic stimulation (eg exercise, sudden loud noises)
CLINICAL FEATURES
usually symptomatic, commonly presents with self-limiting episodes of palpitations, light headedness or syncope
ECG
tachycardia with ventricle rates of 160-250bpm
prolonged qtc (male >0.43s female >0.45s)
irregular RR intervals
peaks of the QRS twist around the isoelectric
MANAGEMENT
Treat underlying cause - stop precipitating drug or correct electrolyte abnormalities
IV MgSO4 (given as a slow infusion)
if resistant to medical therapy, consider temporary pacing
consider IV isoproterenol as a bridge to pacing but pacing is preferable
if pt haemodynamically unstable, non synchronised elec cardioversion may be indicated
PROGNOSIS
May degenerate into VF if HR exceeds 220bpm
BRUGADA SYNDROME
Autosomal sodium channelopathy assoc with sudden cardiac deaths
it is most prevalent in Asia and has a high male predominance (8:1)
defective Na channels impair influx of Na ions resulting in shorter action potentials
classically presents with syncope and sudden cardiac arrest in an otherwise normal pt
ICD implantation is the only definitive treatment
ECG - downsloping coved ST elevation followed by an inverted T wave - only present in V1 and V2
VENTRICULAR FIBRILLATION
a rapid, uncoordinated and life-threatening ventricular arrhythmia resulting in poor myocardial contraction, eventually leading to cardiac death
EPIDEMIOLOGY
INCIDENCE 6 PER 1000
has a bimodal distribution peaking at under 6mths and 45 to 75yrs
1-8% occur out of hospital and are usually fatal
AETIOLOGY
common causes
electrolyte abnormalities (particularly hyperkalaemia)
idiopathic
IHD - relatively common following an acute MI
other causes
structural heart disease - cardiomyopathies, valvular heart disease
systemic - pulmonary embolus, sepsis
long QT syndromes
usually a progression from ventricular tachycardia
PATHOPHYSIOLOGY
very rapid (up to 500bpm) irregular electrical activity results in unsynchronised ventricular contractions
CO will be significantly reduced and ultimately the patient will go into cardiogenic shock
multiple wavelets - continuous micro re-entrant circuits are formed within the ventricles
ECG
unidentifiable P-waves, QRS complexes or T waves
chaotic waveforms with varying amplitudes
MANAGEMENT
Immediate
1) advanced cardiac life support - most important shockable rhythm
2) IV amiodarone (1st line) or procainamide (2nd line) can be used as a last resort if all other measures have failed
Long term
ICD insertion
Amiodarone may be used when ICDs are contraindicated
PROGNOSIS
the community survival rate is 4-33% depending on factors such as prompt bystander CPR and duration of CPR to defibrillation time
20% recurrence rate per year