Case presentation

1
Case presentation

• Torsade de Pointes

2
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.

3
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

4
Special investigations

• FBC
• Plasmodium PCR
• Giemsa stained thick / thin smear
• CXR
• LP was deferred until platelet count returned
• Elected not to CT at this stage

5
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.

6
Patient deteriorated 2hours later

• Pulse rate 180/min with B/P 75/46.
• GCS 10/15
• And an ECG that looks like this.

7
ECG
8
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.

9
Polymorphic VT
10
Polymorphic VT

• Heart rate Variable
• Rhythm Irregular
• Mechanism
• Reentry
• Triggered activity
• Recognition
• Wide QRS with phasic variation
• Torsades de pointes

11
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

12
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

13
Triggered
Fogoros Electrophysiologic Testing. 3rd ed.
Blackwell Scientific 1999 158.
14
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 lt 30 seconds

15
Torsades de Pointes (TdP)

• Heart rate 200 - 250 bpm
• Rhythm Irregular
• Recognition
• Long QT interval
• Wide QRS
• Continuously changing QRS morphology

16
Causes

• 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,
  trimethoprim-sulfamethoxazole, clindamycin,
  pentamidine, amantadine, chloroquine,
  halofantrine
• Electrolyte abnormalities - Hypokalemia,
  hypomagnesemia, hypocalcemia

17
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.

18
Pathophysiology
19
Phases
20
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.

21
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.

22
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.

23
ECG Recognition
EGM used with permission of Texas Cardiac
Arrhythmia, P.A.
24
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.

25
ECG Long QT

• Marked QT prolongation in an asymptomatic patient
  on erythromycin. Patient also was found to be
  profoundly hypomagnesemic and hypokalemic.

26
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.

27
Mechanism

• Events leading to TdP are
• Hypokalemia
• Prolongation of the action potential duration
• Early afterdepolarizations
• Critically slow conduction that contributes to
  reentry

28
ECG Recognition

• QRS morphology continuously changes
• Complexes alternates from positive to negative

29
Treatment

• Pharmacologic therapy
• Potassium
• Magnesium
• Isoproterenol
• Possibly class Ib drugs (lidocaine) to decrease
  refractoriness/shorten length of action potential
• Overdrive ventricular pacing
• Cardioversion

30
Overdrive pacing
31
Treatment

• Discontinuation of the offending agent. Any
  offending agent should be withdrawn.
  Predisposing conditions such as hypokalemia,
  hypomagnesemia, and bradycardia should be
  identified and corrected.

32
Treatment

• Suppression of early after depolarizations.Magne
  sium 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.

33
Treatment

• 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 (adrenergic-dependent).

34
New ACLS Algorithm
35
END