Transcript Ablation

Case presentation
Torsade de Pointes
C15 Case
• Mr X presented to ED from Bosbokrandt (Nelspruit area)
visiting in CPT.
• He is previously well 28yr old who looks acutely ill.
• History from family
• General malaise for 7days, Pyrexia (Rigors),
Deteriorating mental state for past 2 days (Confused).
• No history of trauma, drug abuse or current medical
problems. He is RVD negative.
• Noted to be Penicillin allergic. Visited GP 2days ago
received an antibiotic.
Examination
• Vitals
• B/P 105/65, H/R 130, Temp 39, R/R 16,
GCS 14/15 (Not orientated), Sats 98% RA
• Dipstix +1 Blood
• Glucose 4.5 Hb 9.5
• Examination
• Splenomegaly of 2cm noted
Special investigations
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FBC
Plasmodium PCR
Giemsa stained thick / thin smear
CXR
LP was deferred until platelet count
returned
• Elected not to CT at this stage
Treatment commenced
• Anti-Malaria treatment was started on
clinical suspicion and a preliminary
positive smear from the Lab.
• Quinine sulphate IV was started as a
loading dose of 20mg/kg in 5% Dextrose
over 4hours.
• ………
Patient deteriorated 2hours later
• Pulse rate 180/min with B/P 75/46.
• GCS 10/15
• And an ECG that looks like this….
ECG
Treatment
• Patient was given Midazolam 5mg IV and
was cardioverted at 200J Biphasic with
return of sinus tachycardia.
• Quinine infusion was stopped and urgent
gas was done and CEU + Magnesium was
sent to lab.
• Later restarted in ICU.
Polymorphic VT
Polymorphic VT
• Heart rate: Variable
• Rhythm: Irregular
• Mechanism:
– Reentry
– Triggered activity
• Recognition:
– Wide QRS with phasic variation
– Torsades de pointes
Reentrant
• Reentrant ventricular arrhythmias
– Premature ventricular complexes
– Idiopathic left ventricular tachycardia
– Bundle branch reentry
– Ventricular tachycardia and fibrillation when
associated with chronic heart disease:
• Previous myocardial infarction
• Cardiomyopathy
Triggered
• Triggered activity ventricular arrhythmias
– Pause-dependent triggered activity
• Early afterdepolarization (phase 3)
• Polymorphic ventricular tachycardia
– Catechol-dependent triggered activity
• Late afterdepolarizations (phase 4)
• Idiopathic right ventricular tachycardia
Triggered
Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 158.
Sustained vs. Nonsustained
• Sustained VT
– Episodes last at least 30 seconds
– Commonly seen in adults with prior:
• Myocardial infarction
• Chronic coronary artery disease
• Dilated cardiomyopathy
• Non-sustained VT
– Episodes last at least 6 beats but < 30
seconds
Torsades de Pointes (TdP)
• Heart rate: 200 - 250 bpm
• Rhythm: Irregular
• Recognition:
– Long QT interval
– Wide QRS
– Continuously changing QRS morphology
Causes
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Congenital long QT syndromes (adrenergic-dependent)
Jervell and Lange-Nielsen syndrome
Acquired long QT syndromes
Antiarrhythmic drugs
– Class 1A - Quinidine, disopyramide, procainamide
– Class III - Sotalol, amiodarone (rare), ibutilide, dofetilide,
almokalant
Histamine1-receptor antagonists - Terfenadine, astemizole
Cholinergic antagonists - Cisapride, organophosphates (pesticides)
Antibiotics - Erythromycin, clarithromycin, trimethoprimsulfamethoxazole, clindamycin, pentamidine, amantadine,
chloroquine, halofantrine
Electrolyte abnormalities - Hypokalemia, hypomagnesemia,
hypocalcemia
Pathophysiology
• The association between torsade and a
prolonged QT interval has long been
known, but the mechanisms involved at
the cellular and ionic levels have been
made clearer in approximately the last
decade.
Pathophysiology
Phases
Phase 1
• Phase 1: During initial upstroke of action
potential in a normal cardiac cell, a rapid
net influx of positive ions (Na+ and Ca++)
occurs, which results in the depolarization
of the cell membrane. This is followed by a
rapid transient outward potassium current
(Ito), while the influx rate of positive ions
(Na+, Ca++) declines. This represents the
initial part of the repolarization, or phase 1.
Phase 2
• Phase 2 is characterized by the plateau,
the distinctive feature of which is the
cardiac repolarization. The positive
currents flowing inward and outward
become almost equal during this stage.
Phase 3
• Phase 3 of the repolarization is mediated by
activation of the delayed rectifier potassium
current (IK) moving outward while the inward
positive current decays. If a slow inactivation of
the Ca++ and Na+ currents occurs, this inward
"window" current can cause single or repetitive
depolarization during phases 2 and 3 (ie, EADs).
These EADs appear as pathologic U waves on a
surface ECG, and, when they reach a threshold,
they may trigger ventricular tachyarrhythmias.
ECG Recognition
EGM used with permission of Texas Cardiac Arrhythmia, P.A.
ECG changes
• Patients have paroxysms of 5-20 beats, with a heart rate
faster than 200 bpm; sustained episodes occasionally
can be seen.
• Progressive change in polarity of QRS about the
isoelectric line occurs.
• Complete 180° twist of QRS complexes in 10-12 beats is
present.
• Usually, a prolonged QT interval and pathological U
waves are present, reflecting abnormal ventricular
repolarization. The most consistent indicator of QT
prolongation is a QT of 0.60 s or longer or a QTc
(corrected for heart rate) of 0.45 s or longer.
• A short-long-short sequence between the R-R interval
occurs before the trigger response.
ECG – Long QT
• Marked QT prolongation in an asymptomatic
patient on erythromycin. Patient also was found to
be profoundly hypomagnesemic and hypokalemic.
ECG
• This shows an example of recurrent nonsustained torsade
de pointes that occurred several hours after the ECG was
performed. With discontinuation of the erythromycin and
aggressive repletion of the magnesium and potassium, no
further torsade de pointes occurred and the patient's QT
interval returned to normal.
Mechanism
• Events leading to TdP are:
– Hypokalemia
– Prolongation of the action potential duration
– Early afterdepolarizations
– Critically slow conduction that contributes to
reentry
ECG Recognition
• QRS morphology continuously changes
• Complexes alternates from positive to
negative
Treatment
• Pharmacologic therapy:
– Potassium
– Magnesium
– Isoproterenol
– Possibly class Ib drugs (lidocaine) to
decrease refractoriness/shorten length of
action potential
• Overdrive ventricular pacing
• Cardioversion
Overdrive pacing
Treatment
1. Discontinuation of the offending agent.
Any offending agent should be
withdrawn.
Predisposing conditions such as
hypokalemia, hypomagnesemia, and
bradycardia should be identified and
corrected.
Treatment
2.
Suppression of early after depolarizations.
Magnesium is the drug of choice for suppressing EADs
and terminating the arrhythmia.
This is achieved by decreasing the influx of calcium,
thus lowering the amplitude of EADs.
Magnesium can be given at 1-2 g IV initially in 30-60
seconds, which then can be repeated in 5-15 minutes.
Alternatively, a continuous infusion can be started at a
rate of 3-10 mg/min. Magnesium is effective even in
patients with normal magnesium levels.
Treatment
3.
Isoproterenol
This drug can be used in bradycardia-dependent
torsade that usually is associated with acquired long
QT syndrome (pause-dependent).
It should be administered as a continuous IV infusion
to keep the heart rate faster than 90 bpm.
Isoproterenol accelerates AV conduction and
decreases the QT interval by increasing the heart rate
and reducing temporal dispersion of repolarization.
Beta-adrenergic agonists are contraindicated in the
congenital form of long QT syndrome (adrenergicdependent).
New ACLS Algorithm
END