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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 pre-medication, 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 P-glycoprotein-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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2nd Virtual Congress of Cardiology

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