Ventricular Tachyarrhythmias
Ventricular tachyarrhythmias include a number of different rhythms,
which arise in a number of different clinical situations. The
ventricular tachyarrhythmias are fast heart rhythms that arise entirely
within the lower chambers of the heart (the ventricles). They are faster
than 100 beats per minute by definition. Generally, the tachyarrhythmias
can be characterized as either monomorphic ventricular tachycardia or
polymorphic ventricular tachycardia. Monomorphic ventricular tachycardia
would appear on an ECG record with a regular rate and rhythm and fixed
shape or morphology of the ECG trace. Each beat of the tachycardia would
look the same, hence the designation monomorphic. Polymorphic
ventricular tachycardia typically is irregular in rate and rhythm and
has varying shapes or morphologies on the ECG. A problem that starts as
a monomorphic ventricular tachycardia may deteriorate into polymorphic
ventricular tachycardia. The most dangerous rhythm is a form of
polymorphic ventricular tachycardia called ventricular fibrillation. The
ECG is extremely disorganized and most often leads to death if not
corrected very quickly.
Ventricular tachycardia may give rise to symptoms such as
palpitations, shortness of breath, or lightheadedness, depending
upon the rate of the arrhythmia, its duration, and the underlying
heart disease. With faster heart rates and underlying heart disease
loss of consciousness (syncope) or sudden death may occur. Episodes
lasting only a few beats may produce no or minimal symptoms.
Tachycardia rates between 110 and 150 may be tolerated even if
sustained for minutes to hours. However, faster rates (>180 beats
per minute) may cause drops in arterial pressure and produce syncope.
Very fast rates (>220) are imminently dangerous because they rarely
terminate spontaneously and invariably cause drops in blood pressure
and low cardiac output. Most commonly, sufferers of ventricular
tachycardia have underlying cardiac disease. In developed countries,
the majority of the patients suffer from coronary artery disease.
Although most patients having ventricular tachycardia will have
underlying coronary disease or severely depressed heart function some
have no demonstrable disease of the heart muscle or coronary arteries.Medically it is helpful to considered ventricular
tachyarrhythmias as either being associated with structural heart
disease or not associated with any demonstrable structural problem
with the heart.
Structural Heart Disease
VT associated with coronary artery disease is by far the most common
form of VT. VT can be associated with acute myocardial infarction or
can also appear years after the infarct has healed. In the case of
acute myocardial infarction, electrical changes associated with cell
starvation and oxygen deprivation or death can result in either
ventricular tachycardia or ventricular fibrillation. In the case of
VT associated with prior myocardial infarction, scar tissue from the
myocardial infarction serves as insulating boundaries that set up
anatomic areas where viable tissue can form the reentrant pathway.
Reentry within circuits involving or in the vicinity of a healed
myocardial infarction arises in response to metabolically-induced
changes in impulse conduction or appropriately timed premature beats
in otherwise asymptomatic patients. Reentrant VT is typically
monomorphic.
VT circuits can also form when patients develop
heart disease that results in altered ventricular muscle due
scarring, atrophy (wasting away), or hypertrophy (thickening). The
likelihood of reentrant arrhythmia is proportional to the degree of
myocardial involvement in the underlying disease process, although
the correlation is far form perfect.
Right ventricular dysplasia is a rare condition with unclear etiology that produces VT. It is
most frequently found in young adult males, but is seen in both
sexes and at any age without overt heart disease. With this
condition a variable amount of ventricular myocardium is replaced by
fatty and fibrous tissue and contractions are abnormal. Symptoms
vary from palpitations to syncope. Some individuals who are
considered normal on physical examination experience malaise or
abrupt extreme weakness. This temporary incapacitation could lead to
create major risk for themselves and others. This VT, more common
than thought, is emerging as a cause of sudden death in young
otherwise healthy adults.
No Structural Heart Disease
Ventricular tachycardia most often occurs in the presence of
demonstrable structural heart disease. However, in young patients
with ventricular tachycardia it is common no structural heart
disease may be found. Two forms of ventricular tachycardia are
commonly found and they are right ventricular outflow tract and left
posterior septal fascicular ventricular tachycardia. Both of these
tachycardia are repetitive monomorphic ventricular tachycardias
likely due to an abnormal automatic focus amenable to rf ablation..
These distinctions are based on the location of the abnormal focus
causing these tachycardia and the resulting morphology on ECG. These
tachycardias are generally well tolerated and the patients complain
mainly of episodes of palpitations or fast pulse. These VT's have
well defined ECG patterns and are often triggered by exercise or
catecholamines. Unlike the VT associated with coronary artery
disease, these VT is not associated with an adverse prognosis. This
VT seldom degenerates into ventricular fibrillation, and it is often
responsive to drug therapy or RF ablation.
Treatment
Because VT tends to recur and may be fatal, therapy is geared to
managing episodes when they occur and if possible, to preventing
another episode. RF ablation has been used for repetitive
monomorphic VT and offers the only potential cure for VT; it has
proven to be effective in many cases. Most types of VT are not
readily amenable to ablation, however given the current technology
and understanding.
The implantable cardioverter-defibrillator (ICD) has
become the treatment of choice for patients with life-threatening
VT. The defibrillator is always present and monitors continuously
for VT. If an episode of VT commences, the ICD automatically detects
and terminates the VT without patient input. Some patients require
drug therapy in conjunction with the ICD in order to suppress
frequent VT episodes. In general, drug therapy alone is restricted
to patients who have well-tolerated arrhythmias or to those whose
life expectancy is poor despite aggressive therapy for their
arrhythmias.
Polymorphic Ventricular Tachycardia and Ventricular Fibrilation
Ventricular fibrillation results when multiple sites in the ventricles
fire impulses very rapidly in an uncoordinated fashion. Although this
general scheme appears correct, the exact mechanisms of ventricular
fibrillation remain unknown. The ventricles quiver and cease to pump
blood effectively, thereby stopping the circulation of blood. Death
follows within a few minutes, unless a normal rhythm is restored with
emergency treatment. . VF depicts the final common avenue for death in
most patients experiencing out of hospital cardiac arrest.Medically it is helpful to considered ventricular
tachyarrhythmias as either being due to structural heart disease,
caused by medicines or no associated with any demonstrable structural
problem with the hear of definable cause.
Structural Heart Disease
VF is most commonly associated with structural heart disease.
Specifically, coronary artery disease and myocardial infarction or
ischemia are the most common underlying heart disease. The next most
common group of causative structural heart diseases are the dilated
cardiomyopathies. Dilated cardiomyopathy is a condition where the
heart is very weakened and enlarged but there is no significant
coronary artery disease. Commonly these patients have had exposure to
a virus, other infections such as Chagas, or have suffered the
consequences of severe congenital heart or acquired valvular problems.
Another less common cause of ventricular fibrillation is hypertrophic
cardiomyopathy. This disease is when the muscle of the heart thickens
significant more than normal without any apparent mechanical reason.
This is most likely the cause of the rather well publicized deaths of
otherwise very healthy athletes that occurred during exercise.
After resuscitation and hospitalization it is
important to identify and correct any reversible arrhythmia prompting
factors such as an acute reduction in blood supply to heart muscle
(myocardial ischemia), abnormal blood chemistry or drug toxicity.
After initial emergency treatment, the cardiac electrophysiologist
most likely will perform an EP study to determine the mechanism of the
ventricular arrhythmias. An implanted cardioverter-defibrillator (ICD)
would be recommended unless there is a strong reason not to implant
such a device.
Torsade de pointes is a particular kind of polymorphic VT. It is
characterized by onset with an early complex that follows a long
pause. Torsades de pointes may be caused as a side effect of certain
drugs, including most of the antiarrhythmic drugs. These drugs include
commonly prescribed agents such as antiarrhythmias drugs, certain,
antibiotics such as erythromycin, psychotropic drugs such as Thorazine,
or antihistamines such as Seldane. The combination of Seldane and
erythromycin has especially been found undesirable. Episodes of this
rhythm are often self-terminating, but can be rapidly fatal if they
persist. The treatment is prompt cardioversion if the rhythm is
sustained, followed by intravenous magnesium, avoidance of agents that
prolong the QT interval, and correction of myocardial ischemia,
hypoxia, and electrolyte abnormalities. Torsade de Pointes can occur
with or without the presence of structural heart disease.
Long
QT syndrome (LQTS) has created great interest because of its unique
and dramatic manifestation. This familial disorder was recognized more
than 100 years ago. In 1856 a deaf girl was reported to have collapsed
and died while being publicly admonished at school. Previously two of
her brothers had died suddenly during under similar stressful
situations.In 1975 A. Jervell and F. Lange-Nielson provided the
first complete description of LQTS, a syndrome of deafness and sudden
cardiac death and associated with a characteristic ECG abnormality
(prolonged Q-T interval). The cardiac arrest in these victims, mostly
children and teenagers is due to ventricular tachyarrhythmia. Most
episodes of arrhythmias are usually self-terminating, even when they
provoke a transient loss of consciousness (syncope). However, when the
episodes are prolonged, circulatory failure due to arrhythmia may
result in sudden death.
LQTS was previously classified into a non-familial
sporadic form and two hereditary types, with deafness (Jervell and
Lange-Nielson syndrome, autosomal recessive) and without deafness
(Romano Ward syndrome, autosomal dominant). In 1991 M. T. Keating et
al. demonstrated linkage between LQTS and chromosome 11. Subsequent
genetic studies showed that different LQTS syndromes were due to
mutations of different genes (at least 5) localized on chromosomes
3,4,7 & 11. These genes are responsible for the synthesis
(encoding) of membrane channel proteins that play a pivotal role in
the cellular metabolism and regulation of the electric activity of
cardiac cells. LQTSs have thus been recognized as cardiac membrane
channel diseases ("channelopathies") that invite syncope and
SCD due to ventricular arrhythmias.
The two criteria for diagnosis of LQTS are unexplained
transient loss of consciousness and an abnormal ECG. Ventricular
arrhythmias and syncope are often provoked by increases in heart rate
in response to exercise or emotion. Because such responses involve
changes in the autonomic neural (non-voluntary) regulation of the
heart, it was believed that LQTS resulted from some imbalance in
sympathetic innervation of the heart. However nerve deafness and other
possible neural abnormalities associated with LQTSs remain to be
elucidated.
The incidence of fully expressed LQTS is probably
rare, although variations of the syndrome may remain unrecognized and
actually be frequent. Cases have been reported in every continent and
in every race. Four factors are associated with an increased risk of
SCD: deafness, history of syncope, males before puberty and episodes
of sustained females menarche, and sustained (>30sec) and/or very
irregular ("polymorphic", torsade de pointes) ventricular
tachycardia.
There may be channel gene mutations which by
themselves do not seriously affect cardiac cell electric activity, but
that may render the heart susceptible to drugs that prolong the QT
interval of the ECG. These drugs include commonly prescribed agents
such as antiarrhythmic drugs, certain antibiotics (antifungals),
psychotropic drugs, or diuretics causing wasting of potassium in the
urine.
Ideally, drug treatments should be guided by new
genetic and electrophysiologic insights into the different LQTS's.
Until recently, anti-adrenergic therapy (beta-blockers) has been the
major treatment for LQTS. However based on current information, new
targeted treatments may now be considered. The underlying mechanisms
of LQT3 are an increase in sodium current, whereas LQT1 and LQT2 arise
from deficient potassium currents. These changes in membrane currents
can be influenced with specific drugs that selectively block excess
sodium currents (sodium channel blockers) or activate potassium
currents (potassium channel openers).
In some patients with life-threatening arrhythmias, an
implanted cardioverter defibrillator (ICD) may be an appropriate
therapy.