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Paroxistic Supraventricular
Tachycardia (PSVT):
Diltiazem Versus Adenosine
Flavio Tarasouchi, MD
Instituto do Coração da Faculdade de Medicina da Universidade de
São Paulo, São Paulo, Brasil
INITIALLY WE MUST BE ATTENTIVE TO THE PSVT DIAGNOSTIC
Atrial rate > 150 beats/min, generally regular, QRS complex width is < 0,12 seconds (it's worth to
remember that PSVT with wide -complex (like right bundle branch blocks) can simulate ventricular
tachycardia).
So, once the diagnostic is done, what is the treatment?
The treatment's objective is to interrupt an active cycle of impulses that activates the atriums and the
ventricles through a circuit at the AV node.
General treatment: the patient is taken to the emergency room, where an O2 catheter is installed at 2
liters/min., monitoring cardiac and arterial pressure, peripheral venous access and check pulse oximeter.
Specific treatment: depending on the patient's clinical state, we must observe if he/she is clinically
stable (normal conscience, without thoracic pain, normal breath) or unstable (hypotension or shock,
diminished level of consciousness, acute thoracic pain and intense dyspnea). In case the patient is
unstable, a synchronized electric cardioversion is needed (starting with 50J, 100J, etc...) after premedication, when possible with Diazepam or Midazolan.
If the patient keeps clinically stable, we keep the general treatment and initiate the vagal maneuver that
augments the symphatic tonus and slows conduction though the AV node. The most used maneuver is the
massage to the carotid sinus. It must be firm and last around 5 to 10 seconds. Never perform bilateral
massage. Special care (listen to the carotids) or even avoid in advanced aged patients.
DRUGS
Adenosine and Diltiazem - both are highly efficient agents in reversing stable PSVT.
This is usually best done at presentation in an acute setting. A 12-lead electrocardiogram should be a
routine aid in establishing the diagnosis. A continuous rhythm strip must be obtained during administration
of Adenosine and at the termination of tachycardia. Most recent treatment guidelines would include
Adenosine as first -line therapy. If Adenosine fails to restore normal sinus rhythm, Diltiazem or a Beta
Blocker should then be considered. If there is significant heart failure, Digoxin may be useful. In the
presence of wide complexes, agents that produce atrioventricular nodal block should be avoided.
Adenosine (class I) presents action mechanism by diminishing conduction at the AV node and blocks
reentry, does not cause as much hypotension as Diltiazem, it presents an average active life of less than
10 seconds and is the drug chosen by the AHA for the initial treatment of PSVT. Nevertheless it does not
replace of Diltiazem or Verapamil in the PSVT armamentarium, once that various studies have observed
higher arrhythmia recurrence with Adenosine.
Adenosine interacts with A1 receptors present on the extracellular surface of cardiac cells, activing K+
channels in a fashion similar to the produced by acetylcholine. The increase in K+ conductance shortens
atrial action potential duration, hyperpolarizes the membrane potential, and decreases atrial contractility.
Similar changes occur in the sinus and AV nodes.
Reflex - mediated sinus tachycardia can follow adenosine administration.
Adenosine slows the sinus rate in humans, which is followed by a reflex increase in sinus discharge.
Transient prolongation of the A-H interval result, often with transient first, second, or third degree AV
block. His - Purkinje conduction is generally not directly affected. Adenosine does not affect conduction in
normal accessory pathways.
Adenosine is removed from the extracellular space by washout, enzimatically by degradation to inosine,
by phosphorylation to AMP, or by re-uptake into cells via nucleoside transport system. The vascular
endothelium and former blood elements contain these elimination systems that result in very rapid
clearance of adenosine from the circulation.
Adenosine's success depends on an adequate administration, that is to say quick (3 to 6 seconds)
followed by an intravenous fluid bolus . The recommended initial dosage is of 6mg and can be repeated 12
mg after 1 to 2min. Maximum dosage is 30 mg. Immediately after receiving a Adenosine, often the patient
may present some seconds of assystolia until the reestablishment of the sinus rhythm. Side effects are:
flush, dyspnea by broncospasm, intense thoracic pain and vasodilatation. It can present medicinal drug
interactions with Teophylline that blocks the Adenosine receptor and diminishes the drug's effect.
Dipiridamol blocks Adenosine uptake and potentializes its effects. (Am J. Cardiol 1992,70(6), 587-92).
Adenosine may be useful to help differentiate wide QRS tachycardias, since it terminates many
supraventricular tachycardias with aberrance or reveals the underlying atrial mechanism, and it does not
block conduction over the accessory pathway nor terminates most ventricular tachycardias.
Wittwer and Murhr works, Prehospital Disaster Med. 12(3): 237-9, 1997 observed a reversion of PSVT
for sinus rhythm in 66 of 74 (89,2%) patients, reverted on 1st dose: 46 (69,7%), on 2nd dose: 15
(22,7%) and on 3rd dose 5 (7,6%) of the patients.
The use of Diltiazem is currently a good therapeutic option for PSVT bearers with normal ventricular
function. Verapamil and Diltiazem are effective in terminating paroxysmal supraventricular tachycardias
and slowing ventricular response during atrial fibrillation or flutter. Results from clinical trials for each
individual drug demonstrate comparative efficacy rates, and both drugs share the same contraindications
and relative precautions. Well-designed comparative clinical trials are needed to establish if either drug
has any clinical advantages in a particular patient population.
All currently available calcium antagonists cause vasodilation, lowering blood pressure. In vitro, all
classes of calcium-channel blockers depress sinus-node activity and slow atrioventricular conduction, yet
only Verapamil and Diltiazem delay atrioventricular conduction or cause sinus-node depression at doses
used clinically. Similarly, all classes cause concentration-dependent decreases in myocardial contractility in
vitro, but only Verapamil and Diltiazem do so in vivo. The disparities between the in vitro and in vivo
effects are probably explained by the sympathetic activation that occurs in response to the vasodilation
induced by dihydropyridines, which blunts their direct negative chronotropic and inotropic effects.
Verapamil and Diltiazem are approved for the treatment of patients with supraventricular arrhythmias specifically for the short- and long -term treatment of atrial fibrillation, atrial flutter, and atrioventricular
nodal reentry in patients without accessory bypass tracts. Verapamil and Diltiazem slow conduction
through the atrioventricular node and increase the atrioventricular nodal refractory period, which, in turn,
results in the slowing of the ventricular response rate in atrial fibrillation or flutter or in the conversion of
atrioventricular nodal reentry tachyarrhythmias to sinus rhythm by disruption of the timing of the reentry
circuit.
The ability of Verapamil and Diltiazem to block the actions of the atrioventricular node is more
pronounced at faster than slower heart rates, a property termed "use dependency" or "frequency
dependency." Verapamil and Diltiazem may also cause sinus-node depression. Long-term administration of
Diltiazem slows the ventricular response rate and increases exercise tolerance in patients with chronic
atrial fibrillation. However, neither drug prevents atrial fibrillation or flutter or completely suppresses
episodes of atrioventricular nodal reentry arrhythmia, whether given alone or in combination with digoxin
or a beta-blocker. Ongoing trials are evaluating the relative efficacy of controlling the ventricular rate as
compared with maintaining sinus rhythm in patients with chronic atrial fibrillation. The results should
further elucidate the role of treatment with Verapamil and Diltiazem.
In general, Verapamil and Diltiazem inhibit the clearance of other substrates of cytochrome P-450 CYP3A
(e.g., carbamazepine, cyclosporine, lovastatin, simvastatin, midazolam, triazolam, terfenadine, and
astemizole.
Diltiazem can also increase the absorption of drugs such as cyclosporine that are substrates for Pglycoprotein-mediated drug transport.
Its action mechanism further to diminishing conduction at the AV node, increases the node refraction.
Initial dosage: 0,25mg/kg IV and the 2nd dose 0,35 mg/kg EV.
Diltiazem side effects are: diminishing of myocardial contractility (smaller than with Verapamil), arterial
hypotension, should be avoided in enlarged QRS complex. Intravenous calcium injection will restore
arterial pressure
Luciardi and cols. Arch Inst Cardiol Mex. 66(6): 505-9,1996 observed with Diltiazem a reversion of SVPT
in sinus rhythm in 27 (90%) of 30 patients, being 77,8% on 1st dose and 22,2% on 2nd dose.
The safety and therapeutic efficacy (sinus rythm recovery) of intravenous Diltiazem vs Verapamil in
paroxysmal supraventricular tachycardias (PSVT), were compared. Sixty patients with PSVT were
randomized to have a bolus of 0.3 mg/Kg of Diltiazem or 75 micrograms/Kg of Verapamil. If after 15
minutes the PSVT persisted, a 6 hours i.v. infusion of Diltiazem was started (0.0028 mg/Kg/min) or a
second dose of Verapamil was repeated. Ninety per cent of the PSVT and 64% of de AF, recovered sinus
rhythm with Diltiazem. The same results were obtained with Verapamil in PSVT. In relation to the drug
safety, only 5 patients showed hypotension, without clinical relevance, in the Diltiazem group. With
Verapamil one patient had a transitory ischemic attack after recover sinus rhythm. There was a low
incidence of side effects with Diltiazem and Verapamil. Diltiazem is a first choice therapeutic agent in
reverting PSVT to sinus rhythm.
Grupta and cols. J Assoc Physicians India. 47(10): 969-72,1999 observed a reversion of all the 28
patients with SVPT in sinus rhythm, being that 55,6% reverted on 1st dose and 46,4% on 2nd dose.
Diltiazem (Can J Cardiol 1995 Jul-Aug;11(7): 538-40) is useful drug for sustained control of heart rate in
patients with rapid atrial fibrillation. The recommended intravenous dose is 0.25 mg/kg given over 2 mins
followed by a maintenance infusion of 5 to 15 mg/h. Clinical data on the electrophysiological effects of oral
Diltiazem are limited. The oral form may be used as an alternative agent for the prophylaxis of recurrent
supraventricular tachycardia.
Millaire A, et al (Cardiov Drugs Ther, 1996, 1, 11-6) studied the acute management of supraventricular
tachyarrhythmias in elderly patients. Diltiazem was given intravenously (loading dose of 0.25 mg/kg over
2 minutes followed by a 4 mg/kg/24 hr infusion) in 37 elderly patients (mean age 70 years, range 60 -91).
The 23 patients in atrial fibrillation, about half reverted to sinus rhythm after Diltiazem, and in most of the
others the ventricular rate decreased to less than 100 beats/min. Side effects occurred in 10 patients
(bradycardia in 6, cutaneous rash in 2, hypotension in 2). They rapidly reversed after cessation of
Diltiazem.
IN CONCLUSION
The diagnosis of supraventricular tachycardia the 12-lead electrocardiogram should be a routine aid in
making the diagnosis. A continuous rhythm strip must be obtained during administration of adenosine and
at the termination of tachycardia. Most recent treatment guidelines would include adenosine as first-line
therapy. Adenosine produces acute inhibition of sinus node and atrioventricular (AV) nodal function. This
profound but short lived electrophysiologic effect makes adenosine a suitable agent for treating
supraventricular tachycardias (SVT) that incorporate the sinus node or AV node as part of the arrhythmia
circuit, or for unmasking atrial tachyarrhythmias or ventricular pre-excitation.
If adenosine fails to restore normal sinus rhythm, diltiazem should then be considered. In the presence
of wide complexes, agents that produce atrioventricular nodal block should be avoided.
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