electrical storm is often the initial manifestation of ischaemia and in this scenario it is usually polymorphic VT / VF - often with normal QTc
in acute MI, polymorphic VT can be due to ischemia, altered membrane potential, triggered activity, necrosis, or scar formation MI
ischemia may result in dispersion of electrical refractory periods between the endocardium and epicardium, which is a requirement for multiple waves of reentry
ischemia increases Purkinje cell automaticity, and the spontaneous firing of these fibers triggers polymorphic VT or VF
in most cases other than in 1st 72hrs of an AMI, electrical storm presents as sustained monomorphic VT that is associated with structural heart disease
most monomorphic VT is due to electrical wavefront reentry around a fixed anatomic barrier, most commonly scar tissue after MI and the surface ECG morphology of the VT depends upon the location of the scar and the exit site into the ventricle
monomorphic VT due to wavefront reentry does not require active ischaemia as a trigger, and it is uncommon in patients who are having an acute MI
monomorphic VT is unusual during the first 72 hours of infarction unless the patient has previously infarcted myocardium that serves as a substrate for reentry
burden of ventricular arrhythmias is higher when inadequate reperfusion or large areas of infarction are present.
degree of hemodynamic compromise depends upon the ventricular rate, LV function, the presence of heart failure, any loss of atrioventricular synchrony, and the pattern of ventricular activation
ICD patients with electrical storm had a 7.4-fold higher risk of death than ICD patients without electrical storm
risk of death is highest within the first 3 months after a storm
these are generally driven by excessive sympathomimetic activity hence additional epinephrine Rx may be counter-productive
Rx options
monomorphic VT
beta blocker - propanolol may be better as also enters CNS
amiodarone which also acts via beta blockade can be useful
procainamide
lignocaine
sedation
general anaesthesia
IABP
VT radiofrequency ablation may be an option if still refractory
polymorphic VT / torsades VT
normal QTc:
ischaemia is the main trigger
the most effective treatment is to reverse the ischaemia with emergency coronary revascularization or with anti-ischaemic, antiplatelet, or thrombolytic agents.
amiodarone and β-blockers are the most effective antiarrhythmic agents.
IABP / revascularisation
LSGB
NB. magnesium therapy is unlikely to be effective in polymorphic VT that is associated with normal QT intervals!
prolonged QTc:
torsades de pointes is pause-dependent polymorphic VT with prolonged QTc, often in the presence of bradycardia and has a unique Rx
isoprenaline
magnesium
replace potassium
overdrive pacing
VF
ischaemia:
amiodarone
beta blockers
lignocaine
IABP / revascularisation
LSGB
PVC-initiated:
amiodarone
beta blockers
ablation
Brugada:
isoprenaline
quinidine
calcium channel blockers
Post-resolution Mx
recurrent VT or VF and ICD shocks may cause left ventricular (LV) systolic dysfunction and myocardial injury, which can lead to adrenergic neurohormonal activation and exacerbate heart failure