NEW THERAPEUTIC OPTIONS LIFE THREATENING ARRYTHMIAS

Malignant Arrhythmias in Critically Ill
V. arrhythmias
Ischemic HD
Cardiomyopathy
Heart Failure

The long QT Syndrome,
RV Dysplasia,
Brugada Syndrome.
Ventricular Arrhythmias in:

Preexcited A. Fibrillation
A. Flutter with 1:1 conduction
Incessant forms of SVT Automatic AT
Uncommon type of AVNRT

Adverse Effects of Dysrhythmias are
related to:
Underlying Heart Disease.
Potential for Progression (Degeneration).
Refractoriness to Therapy.

Electrolyte & Acid Base derangements
Hypokalemia, Hypomagnesemia,
Alkalosis
Hypoxia “Resp. failure, Pulm-Embolism”
Sympathodrenal activation “endogenously secreted
or exogenously administered”

Empiric Pharmcologic Therapy.
DC External Cardioversion & Defibrillation
Surgical Resection
Classic Approach:

EP Guided Pharmocologic Therapy,
DC Internal Cardioversion,
Anti Tachycardia Pacing.
Modified Approach:

Radiofrequency Catheter Ablation,
Implantable Cardioverter Defibrillators,
Cardiac Transplantation and
Hopefully Gene Therapy
Modern Approach:

ECG Monitoring: Diagnostic limitations
HRV and QT Dispersion: Risk stratification
Signal Averaged ECG: High negative and
Low positive predictive valve

Torsade de points: Starts with long short
coupling intervals,
Polymorphic VT: R an T ventricular ectopics.
Supraventricular tachycardia: Abrupt onset &
abrupt termination.
Routine monitoring:
Record the initiation & termination of arrhythmias:
Arrhythmias in Critically Ill

Lewis Lead
Intra atrial lead
Esophageal ECG
Special techniques:

May not detect the full PR, QRS, or QT interval,
The waveforms generated may be so small that they
do not consistently trigger the detection device.
Artifacts may lead to over counting of electrical
events generated by the heart.

Positional changes may lead to severe axis
shifts, which may be misleading if only one lead
is being monitored.
Loose electrodes may create artifacts resembling
ventricular fibrillation or asystole
Other mechanical activity such as gastric
suction, teeth brushing, may be responsible for
creation of artifacts.

Programmed Electric Stimulation
Inducibility
Optimal drug selection
Candidates for ICD implantation.

Arrhythmogenic Substrate,
Autonomic Modulation, and
Triggering Arrhythmias.
Targetted Against:

 Improving Myocardial Ischemia
 Correcting Hypoxia, Alkalosis, Hypokalemia
 Reducing Mechanical Overload
Arrhythmogenic Substrate:
Nitrates
PTCA
CABG
ACEI
Ang II Blockers
β-Blockers

 Adrenergically mediated: B-Blockers, Alpha, Beta
Blockers
 Vagally-mediated:
Vagolytic drugs,
Pacing,
Potassium-Channel- Blockers “Amiodarone”.
Autonomic Modulation:
α

Xylocaine.
Amiodarone.
Procainamide Hcl
Pharmacologic Therapy:
Triggering Arrhythmias:

Identify & correct abnormal homeostesis,
Suppress Triggering Arrhythmias,
Correct Overactive Autonomic System,
Terminate arrhythmia.
Treatment Algorithm:

Emergency Termination (ADENOSINE)
A short-acting drug (seconds) that is effective in
terminating AV nodal reentry tachyarrhythmias.
Also used for diagnostic purposes.
Causes transient complete AV block.
Administered rapidly to maximize its negative
dromotropic effect.

 Aminophylline is a competitive antagonist and
prevents the action of adenosine.
 If an initial bolus of adenosine does not cause AV
block, the dose should be doubled until block
occurs.
Emergency Termination (ADENOSINE)

Ventricular Tachycardia
Supraventricular Tachycardia with:
Aberrant conduction,
Preexisting BBB,
Antidromic conduction over an A-V bypass
tract.

ECG Differentiation:
 Fusion beats
 Capture beats
 V. ectopics having the same tachycardia
configuration recorded before the episode.
Definite
markers{

Left axis deviation
wide CRS > 14 sec
Monophasic QS in V1-V6
Suggestive markers
A-V dissociation with V. faster than A.
Mainly EPS characterization
ECG Differentiation:

Atrial flutter-fibrillation with frequent multrifocal VPCs
and ventricular group beats (indicated by arrows)

Sinus rhythm with frequent VPCs and ventricular
group beats (2 in a row)

A and B were obtained from the same patient with acute diaphragmatic MI. A. The
rhythm is sinus with first degree AV block, APCs (X), and frequent VPCs (V) with
group beats and a short run of VT. Leads II-a, II-b, II-c, and II-d are continuous. B.
Soon after the tracing A was taken, the patient developed VT as a result of frequent
VPCs with the R-on-T phenomenon. Leads II-a, II-b, and II-c are continuous

Sinus rhythm with intermittent nonparoxysmal VT
(rate: 96 beats/min). None ventricular fusion beats
(FB). Leads II-a and II-b are continuous

1. Antiarrhythmic drugs
Quinidine, procainamide, disopyramide, ajmaline,
amiodarone, and lidocaine
2. Other drugs
Prenylamine, phenothiazines, tricyclic antidepressant
drugs
A. Drug induced

Sinus rhythm with first degree AV block and frequent VPCs (V)
with R-on-T phenomenon leading to multiform VT (torsade de
pointes) and VF. The ECG abnormalities are fundamentally
caused by quinidine-induced prolonged Q-T interval with broad
T wave. Leads II-a, Leads II-a, II-b, II-c, and II-e are continuous.

1. Congenital Q-T prolongation syndrome
a. Jervell-Lange-Nielson syndrome
b. Romano-Ward syndrome
2. Electrolyte disturbances
a. Hypokalemia b. Hypomagnesemia
B. Nondrug induced

3. Intrinsic cardiac diseases
a. Myocardial ischemia and infarction b. Myocarditis
c. Bradyarrhythmias
1) Marked sinus bradycardia (e.g., sick sinus syndrome)
2) Advanced or complete AV block
d. Mitral valve prolapse syndrome (MVPS)
4. Liquid protein diets
5. Central nervous system disorders (e.g., subarachnoid
hemorrhage)
6. Hypothermia

Ventricular flutter with a rate of 214 beats/min

Atrial fibrillation with anomalous AV conduction because of
WPW syndrome, Ventricular tachycardia is closely simulated

In (C) a 12-lead ECG is depicted during sinus rhythm and
orthodromiccircus movement tachycrdia in a right free-wall and (D)
anteroseptally located AP. ECG indicates electrocardiogram; and AP,
accessory pathway.

In the left panel, AV conduction of 2:1 is present, changing into 1:1 AV
conduction. The origin of the arrhythmia is low in the intra-atrial
septum. AT indicates atrial tachycardial; and AV, atrioventricular

Shown here is AF in a patient with the WPW syndrome (A). Note AV conduction
over the AP on the left and right side of the panel, with AV conduction over the
AV node in the middle. As shown, the ventricular rate can become very high
during AV conduction over the AP. In (B), a posteroseptal location of the AP is
shown during sinus rhythm. AAAF indicates atrial fibrillation; WPW, Wolff-
Parkinson-White; AV, atrioventricualr; and AP, accessory pathway

Shown here is VT with a
relatively slow rate,
allowing the occurrence
of capture and fusion
beats. The tracing was
recorded in a patient with
recent anterior wall MI.
Note the QR pattern is
several leads during VT,
VT indicates ventricular
tachycardia; and MI,
myocardial infarction.

Here, a VT shows a negative concordant pattern in the precordial
leads. This is diagnostic of VT. The QRS following termination of
VT shows an old antero-apical MI. VT indicates ventricular
tachycardia; and MI, myocardial infarction.

Twelve-lead electrocardiogram in a patient with ventricular
preexcitation during AF with a rapid preecited ventricular response

Typical characteristics of Torsade des Pointes. The initiation of the first
ventricular ectopic beat of hte tachycardia tends to occur following a pause.
The QRS of this first beat initiates on the T wave making it difficult to
appreciate where the T wave ends. There is a beat-to-beat change in the QRS
axis in a sinusoidal pattern. The rate of hte tachycardia tends to be slower than
the polymorphic VT seen ischemia

Arr. Underling PathologyAdverse effect
Sinus tachy. Acute MI. Worseing ishcemia
AF WPW Pseudo V. Tachy.
HOCM Hypotenion
Valvular HD P. Edema
AF. Flutter
PACs Hypokalemia Forerunners of AF
PVCs Hyopkalemia Frequency, Salvos
Hypomognesion Salvos
AVNRT Fast slow pathway Incessant form

Arr. Underling Pathology Adverse effect
Automatic AT Atrial Disease Incessant form
Slow V. Tachycardia Reperfusion Arr. ?
V. Tachycardia Acute MI rerperfusion VF
Poly morphic VT Long QT Torsade de points

The presence of frequent PVCs appears to
be associated with an increased risk of SCD in
patients with substantial LVdysfunction (e.g.
LV (LVEF < 0.4) but not in those without heart
disease.

Lown and Wolf classified PVCs into simple and
complex forms, with examples of the latter being pairs,
and early-cycle PVCs or the R-on-T phenomenon.
Complex PVCs were considered warning arrhythmias,
i.e. arrhythmias that presaged the appearance of VF or
VT.

Subsequent studies showed the
shortcomings of warning arrhythmias. For
example, 155 (59%) of 262 patients with an
acute MI had warning arrhythmias, yet only
12 (7%) had primary VF, and 8 (40%) of 20
with primary VF had no warning arrhythmias.

Furthermore, most recorded episodes of VT
result from midcycle rather than R-on-T PVCs,
and R-on-T PVCs initiated VT in only 14 (15%)
of 94 episodes in 1 study. Event in 47 patients
with a history of VT, introduction of PVCs onto
the T wave at EP testing, did not initiate sustained
VT or VF.

It is the combination of Nonsustained VT or
frequent PVCs in patients with substantial
LVdysfunction (LVEF < 0.4) that identifies a
high risk group for subsequent SCD, not the
morphological aspects of the PVC itself.

The problem of sudden cardiac death (SCD)
resulted in the development of a device by
Mirowski and Colleagues in the late 1960s,
with initial reports in the 1970s and the first
human implantation in 1980s.
History

The limitations of Antiarrhythmic Drug
Therapy, recently amplified by data from the
Cardiac Arrhythmia Suppression Trial
(CAST) study, provided further support to
the need for a Non Pharmacologic approach.

Arrhythmia Surgery is restricted to those
who have discrete aneurysms and is usually
not performed in those with diffuse
aneursymal ventricles.

 Cardiac Arrest due to VF or VT and not due to a
transient or reversible cause
 Syncope of Undetermined Origin with clinically
relevant hemodynamically significant sustained VT or
VF induced at EPS testing, when prior drug therapy is
ineffective, not tolerated, or not preferred .
ACC/NASPE Guidelines, 1998

 Spontaneous Sustained VT.
 Nonsustained VT with CAD, prior LV
dysfunction, inducible VF, or sustained VT at
EPS testing that is not suppressible by a class-1
antiarrhythmic drug.
ACC/NASPE Guidelines, 1998

 Pre-Event Trials
 Post-Event Trials

I) The AVID (Antiarrhythmics Versus Implantable
Defibrillator) Trial: is a multicenter trial intended
to compare the results of best medical therapy
(Amiodarone or Sotalol) to a Transvenous ICD.
The patient group targeted was the most seriously ill
ventricular arrhythmia patient.
Post-Event Trials:

Not surprisingly, the ICD showed a survival
advantage for the patient population as a whole.
Over a mean follow-up of 18.2 months the accrued
death rates were 15.8+3.2% in the ICD group and
24+3.7% in the drug group.
ICD: Clinical Trials

The Multicenter Automatic Defibrillator
Implantation Trial (1996). A multicenter trial that
studied a very carefully selected group of post MI
patients who were at high risk for a future event.
I) MADIT

Three weeks removed from myocardial infarction,
Had Nonsustained VT on Holter (3-30 beats),
An EF of less than or equal to 35%,
NSVT was inducible into Sustained Monomorphic
VT or VF and
Not suppressed with procainamide.
Coronary artery disease patients

196 patients enrolled and randomized to either an ICD
or conventional therapy.
At a mean follow up of 27 months the trial was
terminated prematurely at a time at which the ICD
showed marked survival benefit over conventional
therapy (39 deaths in the conventional therapy arm and
15 deaths in the ICD arm).

The Kaplan-Meier survival curve for the Mutlicenter Automatic Defibrillator implantation
Trial population shows the clear-cut advantage of the Implantable cardivoerter defibrillator
over conventional therapy. Total mortality rate was reduced by 46% in the ICD group.
Defibrillator
Conventional
Therapy
0 1 2 3 4 5
0.0
0.2
0.4
0.6
0.8
1.0ProbabilityofSurvival
Patients, n
Defibrillator 95 80 53 31 17 3
Conventional therapy 101 67 48 29 17 0
Year

Patients in whom VT or VF is related to:
 Acute myocardial infarction,
 Transient electrolyte abnormalities, or
 Drug toxicity
CONTRAINDICATIONS
Implantable Cardioverter Defibrillators

Those with psychological conditions who
would not be able to adapt to this type of
therapy,
Those with a short life expectancy due to
terminal illness.
Who Should not be offered an ICD?
1.
2.

Those with incessant VT due to their poor
prognosis and continuous triggering of the ICD
if sinus rhythm is restored intermitently.
Patients with frequent long runs of nonsustained
VT would also trigger frequent ICD discharges.
Who Should not be offered an ICD?
3.
4.

Ventricular Tachycardia can be modified not
only by Drugs but also by pacing or
Cardioversion. This phenomonenon is familiar to
every electrophysiologist who has attempted
overdrive pacing of induced VT.
ICD Related Prblems
Exacerbation of the Arrhythmia:

Occasionally the tachycardia acclerates or
degenerates into VF. For this reason,
Antitachycardia Pacemakers without backup
Defibrillator Capability were abandoned.
Even during electrical cardivoersion, there is
a similar risk of exacerbating the arrhythmia.
Exacerbation of the arrhythmia:

Initially, when the ICD was investigational, the
patients viewed this device with some skepticism.
Most of the patients had few other options,
therapy with antiarrhythmic drugs having failed
while symptomatic arrhythmias continued.
Psychosocial Aspects of The ICDs

Once the ICD was implanted, however, their
outlook on life changed dramatically, becoming
hopeful once again.
They dervied a tremendous sense of security
from the ICD, knowing that if the arrhythmia
recurred, they would be rescued.

What does the patient sense when the ICD
discharges?
If the patient has a hemodynamically
compromising arrhythmia, collapses, and
immediately loses consciousness, there is no
sensation of the discharge.

Some patients note very little discomfort and
are barely aware that the device fired.
Some patients report a very noticeable and
sometimes painful shock. Most patients describe a
somewhat uncomfortable or unpleasant internal
twitch or shock.

Psychologically, Patients are disappoointed that
they had recurrence of the arrhythmia but also glad
to be alive.
Patients with frequent discharges find them not
only annoying but disconcerting. This situation
requires revision of the antiarrhythmic regimen.

Kim et al., (1991) observed a total mortality
ratet of 17% at 1 year, and 29% at 3 years.
Winkle et al., (1989) reported a total
mortality rate of 8%, 16% and 26% after 1, 2,
and 5 years of follow-up respectively.
Effect on Prognosis

Some investigators have questioned the
therapeutic value of ICD therapy as a whole.
ICD merely changes the mode of death,
converting a “Sudden Death” into a
“Nonsudden” Death, resulting in little or no
prolongation of life. (Conversion Hypothesis).
Effect on Prognosis

The defibrillator is superior to antiarrhythmic-
drug therapy in prolonging survival among patiens
resuscitated after symtpomatic, sustained
ventricualr tachycardia or ventricular fibrillation
causing hemodynamic compromise. It should be
offered as first-line therapy to such patients.

It would be unethical to withhold any therapy
with potential benefit from patients at very high
risk. Thus, physicians continued recommending
implantable cardioverter-defibrillator therapy for
high risk patients but were uncertain about the
magnitude of benefit.
ICD: Clinical Bi-Impact

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