The diagnosis is
usually apparent at a first glance. Some doubts may
raise in case of high ventricular rate, when the
vagal maneuvers, by increasing nodal filter, may
consent the identification of an atrial activity,
thus allowing a correct diagnosis (fig. 9).
Figure
9. Diagnostic and therapeutic algorhythm in
narrow-QRS tachycardia
and
irregular ventricular rhythm.
Multifocal
atrial tachycardia is a rare arrhythmia, presenting P
waves of at least three different morphologies and
variable P-R and R-R intervals. It sometimes
alternates with atrial fibrillation.
The electrophysiologic mechanism underlying the
arrhythmia is an enhanced automatism triggered by
several pathological conditions (tab VI). The most
frequent are hypoxya, high catecholamins levels, or
drug toxicity. The arrhythmia carries a poor
prognosis due to severe lungs, heart or dysmethabolic
diseases (45-50% death rate). It is resistant to any
antiarrhythmic therapy and the treatment is directed
toward the underlying disease.
Table
VI. Pathologic conditions associated with multifocal
atrial tachycardia
Atrial
fibrillation
is the most frequent supraventricular arrhythmia.
At its onset, it
usually presents with an elevated ventricular rate
and with symptoms (palpitations, malaise, chest
dyscomfort, dyspnea, angina or, in the worst cases, a
clinical picture of cardiac failure or shock). The
rate of spontaneous reversion to sinus rhythm is in
the range of 60-75% at 24 hours. In case of
long-standing arrhythmia, the atrial standstill may
favor the formation of intracavitary thrombi that -
if mobilizing - can provoke embolic events. Since
this risk is particularly high following
sinusalization, when atrial mechanical function
resumes, chemical or electrical cardioversion can be
attempted only if the arrhythmia has been lasting no
more than 48 hours. These limit has to be tighten in
patients with low atrial flow (mitral stenosis, heart
failure) when thrombi may form in a shorter time. In
case of long-standing arrhythmia, or if the time of
onset of atrial fibrillation is not clear,
cardioversion should be deferred until 2-3 weeks of
full anticoagulation (INR = 2-3) have been elapsed.
Nevertheless, if a transoesophageal echocardiogram
rules out the presence of atrial thrombi, it will be
possible to cardiovert the patient under heparin
administration, to be started immediately and
maintained until oral anticoagulants do not provide
full protection. Anticoagulant therapy should be
continued for at least one month after cardioversion.
In recent onset atrial
fibrillation, the treatment depends on the clinical
setting. If the arrhythmia cause low cardiac output
or cardiac failure, DC cardioversion will be
mandatory. In the other cases the choice is between
slowing the ventricular rate, waiting for spontaneous
restoration of sinus rhythm - which occurs within 24
hours in more than 50% of the patients - or
attempting cardioversion by drugs. Heart rate can be
controlled by drugs acting on the atrio-ventricular
node (verapamil, diltiazem, beta blockers) (tab. IV).
Intravenous digitalis is slow-acting and less
efficient in reducing the ventricular rate, but it
remains the drug of choice in case of cardiac
insufficiency.
In our experience, a
conversion attempt is preferable in most cases, after
having excluded - and, if possible, treated - any
underlying cause of the arrhythmia (clinical
hyperthyroidism, alcoholic poisoning, acute
myocardial ischemia, hypertension, pericarditis,
myocarditis, cardiac or respiratory failure).
Intravenous IC
drugs (propafenone, flecainide) can rapidly interrupt
the arrhythmia in most of the patients. Provided
their contraindications are considered (tab. VII),
these drugs are safe.
We prefer Propafenone
because it is well tolerated and, by acting also on
the atrio-ventricular node, it slows ventricular rate
even in non-converted patients. Intravenous
amiodarone is not useful obtaining rapid conversion,
since its antiarrhythmic action requires several
hours of continuous infusion to occur. However, it
can be used in patients with bifascicular bundle
branch block or cardiac insufficiency, where class IC
drugs are contraindicated. The new pure class III
agents (ibutilide, dofetilide) do not depress
contractility nor conduction, so they can be used in
patients with heart failure or conduction
disturbances. However, their efficacy is inferior to
class IC agents and - during the infusion or shortly
after - they provoke torsade de pointes in about 5%
of the cases. In table VIII are reported the iv drugs
available for acute interruption of atrial
fibrillation and their principal characteristics.
The flow chart we use
for the management of recent-onset atrial
fibrillation is shown in figure 10 and the
therapeutic choices that we suggest in some frequent
clinical pictures are reported in table IX..
Table
VII. Contraindications to class IC drugs
