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:

NitratesPTCACABG

ACEIAng II Blockersβ-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 diseasesa. 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 Pathology Adverse 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

ConventionalTherapy

0 1 2 3 4 5

0.0

0.2

0.4

0.6

0.8

1.0P

rob

abili

ty o

f S

urv

ival

Patients, nDefibrillator 95 80 53 31 17 3Conventional 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

new therapeutic options life threatening arrythmias

Health & Medicine

ventricular arrhythmias

andtriggering arrhythmias

illmalignant arrhythmias

blockers amiodarone

qt dispersion

modified approach

illthe long qt syndrome

autonomic modulation