c_electricstorm
Table of Contents
electric storm
see also:
Introduction
- generally defined by 3 or more sustained episodes of ventricular tachycardia (VT), torsade de pointes VT, ventricular fibrillation (VF), or appropriate shocks from an implantable cardioverter-defibrillator within 24 hours and typically have a poor outcome
- occurs in 10% to 20% of ICD recipients (4% in those having ICD for primary prevention and 20% if for secondary prevention)
- acute myocardial infarction (AMI/STEMI/NSTEMI) patients and those who have an inherited arrhythmic syndrome are also susceptible
- 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
- thus maximise heart failure Rx
- revascularisation if indicated
- prevent further arrhythmias
c_electricstorm.txt · Last modified: 2023/09/09 07:44 by gary1