Postgraduate Medicine

ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20

Supraventricular tachycardia Anthony C. Caruso MD To cite this article: Anthony C. Caruso MD (1991) Supraventricular tachycardia, Postgraduate Medicine, 90:2, 73-82, DOI: 10.1080/00325481.1991.11701008 To link to this article: http://dx.doi.org/10.1080/00325481.1991.11701008

Published online: 17 May 2016.

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Second of three articles on arrhythmias

Supraventricular tachycardia Changes in management

Preview Is it important to detennine whether patients with paroxysmal supraventricular tachycardia have a participating accessory pathway? Dr Caruso says yes, for a number of reasons, including the possibility that atrial fibrillation in such patients may easily deteriorate into ventricular fibrillation. Moreover, if an accessory pathway is present but not suspected, a patient may be given drugs that enhance this threat. Adenosine is currently preferred to treat both orthodromic atrioventricular reentrant tachycardia and atrioventricular nodal reentrant tachycardia.

Anthony C. Caruso, MD •:• "Supraventricular tachycardia" is a broad term fur a variety of rhytlun disorders that originate at or above the atrioventricular (AV) node. In the past, abrupt onset of a regular narrow QRS complex tachycardia was called paroxysmal atrial tachycardia. This term has been replaced with two terms that are descriptive of the most common mechanisms responsible for this type of arrhythmia, namely, AV nodal reentrant tachycardia and orthodromic AV reentrant tachycardia. AV nodal

reentrant tachycardia is due to reentry of electrical impulses within the AV node. Once initiated, this arrhythmia does not require participation of the atrium. Other types of paroxysmal supraventricular tachycardia include sinus nodal reentrant tachycardia and atrial ectopic tachycardia. These are much less common than AV nodal reentrant tachycardia and orthodromic tachycardia. Table 1 shows electrocardiographic clues that aid in the differentiation of various types of paroxysmal supraventricular tachycardia.

VOL 90/NO 2/AUGUST 1991/POSTGRADUATE MEDICINE • SUPRAftNTRICULAR TACHYCARDIA

Definitions AV nodal reentrant tachycardia is the most common form of paroxysmal supraventricular tachycardia in the older population. When atrial fibrillation and atrial flutter are excluded, this form of supraventricular tachycardia represents up to SO% of all cases. Arrhythmia is due to the presence of fi.mctional dual conducting pathways within or adjacent to the AV node. Dual conduction (figure 1) is a requisite for this type of tachycardia. AV nodal reentrant tachycardia is of two types: 1. The slow-fast sequence is more common, occurring in 90% of patients. Electrical impulses are conducted from the atrium to the ventricle via a slow pathway within the AV node and return to the atrium via a fast AV nodal pathway. 2. The . so-called fast-slow se. . quence IS uncommon, occurnng m about 10% of patients. Conduction from the atrium to the ventricle occurs via a fast AV nodal pathway, with reentry to the atrium by way of a slow pathway. Orthodromic AV reentrant tachycardia, which involves participation of an accessory pathway, is usually seen in younger patients (ie, under 35 years old). Impulses travel down the AV node, depolarizing the ventricle in the usual fashion; the result is a narrow QRS complex. The impulses rerum to the atrium via continued

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Ventricular fibrillation may follow the onset of atrial fibrillation in patients who have an accessory bypass tract.

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Table 1. Electrocardiographic (surface) clues to differentiation of paroxysmal supraventricular tachycardia Classification

QRS complex

Rate (beats/min)

Configuration of P wave in lead II

Comments

Sinus nodal reentrant tachycardia

Narrow

100-160

Precedes QRS; same morphology as in sinus rhythm

Differentiated from sinus tachycardia by abrupt onset and termination

Automatic atrial tachycardia

Narrow

100-180

Precedes QRS; upright or inverted; gradual increase in rate

Onset with premature atrial beat late in diastole

Intra-atrial tachycardia

Narrow

100-180

Precedes QRS; morphology may vary from beat to beat

CSM may induce AV block without termination of tachycardia

AV nodal reentrant tachycardia (common type)

Narrow

140-200

Inverted; usually not seen on EGG

May terminate with CSM

AV nodal reentrant tachycardia (uncommon type)

Narrow

100-150

Inverted; appears late with long R-P interval

May terminate with CSM

Orthodromic AV reciprocating tachycardia

Narrow

150-240

Inverted; appears after QRS complex, with short R-P interval

AV block excludes this diagnosis

AV, atrioventricular; CSM, carotid sinus massage; ECG, electrocardiogram; LBBB, left bundle-branch block.

an accessory bypass tract and then go on to the AV node, resulting in circus movement tachycardia (figure 2).

Need for differentiation How can the two forms of supraventricular tachycardia be differentiated? Does differentiation matter? To answer the second question first, yes, it does matter, for several reasons. In patients who have an accessory pathway, electrical impulses may be conducted in a direction opposite to that just described. Im-

74

pulses then may traverse the accessory pathway &om the atrium to the ventricle, resulting in a wide QRS complex. If atrial fibrillation occurs, the rate may exceed 200 beats a minute, because the accessory pathway does not have the unique electrical properties characteristic of the AV node to prevent such rapid impulses &om conducting to the ventricle. If atrial fibrillation develops, every atrial impulse may conduct to the ventricle. It is no wonder, then, that ventricular fibrillation may follow the onset of atrial fibrillation in pa-

tients who have an accessory bypass tract. Moreover, the presence of digitalis, verapamil hydrochloride (Calan, lsoptin, Verelan), or other medications that depress AV nodal conduction may facilitate rapid conduction &om the atrium to the ventricle via the accessory pathway and thereby enhance the possibility of ventricular fibrillation. Patients with accessory pathways at times have orthodromic tachycardia yielding narrow QRS complexes; at other times, antidromic tachycardia occurs, resulting in wide QRS

SUPRAVI!NTRICULAR TACHYCARDIA • VOL 90/NO 2/AUGUST 1991/POSTGRADUATE MEDICINE

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Irregular or notched T waves are uncommon in adults and should alert the physician to the presence of P waves.

complexes. If the presence of an accessory pathway is not suspected in a patient with regular narrow QRS complex tachycardia, digitalis and verapamil may be given to prevent further episodes. In this event, the next episode of tachycardia could be atrial fibrillation with a rapid ventricular response. What findings suggest the presence of an accessory pathway? If the patient is having an episode of irregular narrow QRS tachycardia, atrial activity immediately after the QRS complex may be seen as notching on the T waves. Irregular or notched T waves are uncommon in adults and should alen the physician to the presence of P waves. The finding of atrial activity should suggest panicipation of an accessory pathway. This can be explained as follows: An atrial impulse must traverse the AV node in the ventricle before reactivating the atrium (figure 2). The time required fur the electrical impulse to traverse the ventricle and return to the atrium is usually in excess of 100 milliseconds, or 0.10 second. Because the usual duration of the Q RS complex is less than 0.10 second, a P wave often is seen immediately after the QRS complex. In contrast, the regular narrow QRS tachycardia that is due to AV nodal reentry revolves entirely within (or closely adjacent to) the AV node. The time needed fur an electrical impulse to return to the atrium is less than 0.08 second; therefore, the

Figure 1. Two types of atrioventricular nodal reentrant tachycardia and their electrocardiographic manifestation. a. Slow-fast sequence is seen in 90% of patients. b. Fast-slow sequence occurs in about 10% of patients.

Slow

V\fW\1\

Fast

Adapted from Ewy GA. Caruso A, Marcus Fl. Supraventricular tachycardias: recognition and management. In: Ewy GA. Bressler R, eds. The heart: drug therapy of cardiovascular disease. New York: Raven Press (in press).

P wave is buried within the AV node (figure 1). A useful guideline, then, in differentiating regular tachycardia from AV nodal reentrant tachycardia is to suspect that an accessory bypass tract may be parr of the circuit if atrial activity occurs just after the QRS complex. There may be exceptions to this rule, but they are unusual. After tachycardia has resolved, delta waves should be carefully sought. They are recognized by slurring of the upslope of the QRS complex (figure 3). Slurring may appear

in a variety of leads, depending on the location of the accessory pathway. Even ifslurring is not seen at the beginning of the QRS complex, the possibility of an accessory pathway panicipating in the tachycardia is not excluded, because the pathway may conduct only from ventricle to atrium. In this case, the pathway is considered concealed.

Important developments in management Until recendy, the only reason to differentiate AV nodal reentrant tachy-

continued

VOL 90/NO 2/AUGUST 1991/POSTGRADUATE MEDICINE •IIUPRAWNTRICULAA TACHYCARDIA

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Vagal maneuvers such as carotid sinus massage are still valid to temporarily interrupt conduction through the AV node in patients who have AV nodal reentrant tachycardia or orthodromic tachycardia.

Figure 2. Schematic illustration of orthodromic (a) and antidromic (b) atrioventricular reciprocating tachycardia. Adapted from Ewy GA. Caruso A. Marcus Fl. Supraventricular tachycardias: recognition and management. In: Ewy GA, Bressler R, eds. The heart: drug therapy of cardiovascular disease. New York: Raven Press (in press).

cardia from orthodromic tachycardia was to avoid the use of digitalis and verapamil in patients with an acces- · sory pathway. However, two important developments--catheter ablation of the pathway and use of adenosine (Adenocard) to terminate certain arrh~rovide additional incentive for differential diagnosis. CATHETER ABlATION-It is now possible to substantiate the presence of an accessory pathway during electrophysiologic studies and to eliminate the pathway nonsurgically by burning it out with radiofrequency

76

energy (similar to microwave energy) through an electrode catheter. This procedure is both safe and effective and may obviate lifelong pharmacologic therapy or, in some patients, the possibility of sudden cardiac death from ventricular fibrillation. ADENOSINE VERSUS VERAB\MIL-

Generally, physicians have relied on vagal maneuvers such as carotid sinus massage or the Valsalva maneuver to temporarily interrupt conduction though the AV node in patients who have AV nodal reentrant tachycardia or orthodromic tachycardia.

These approaches are still valid. In the past, if these maneuvers failed, the next approach was to stimulate baroreflex receptors by raising blood pressure with phenylephrine (Neo-Synephrine). Treatment with veraparnil, a calcium channel blocker, is still useful; however, it has distinct disadvantages and hazards. The drug may cause marked sinus bradycardia or even prolonged sinus arrest, particularly in patients raking digitalis and/or beta blockers. Prolonged AV block may also occur. Verapamil also has negative inotropic effects and may exacerbate congestive heart failure in patients with poor left ventricular function. Hypotension also may occur because of the drug's negative inotropic effect and vasodilating properties. In addition, all of these adverse effects may be prolonged because the half-life of verapamil is 4 to 7 hours. Particularly hazardous is the administration of verapamil to patients with suspected acute supraventricular tachycardia who have a wide QRS complex. If the diagnosis is incorrect and the patient has ventricular tachycardia, the compensatory mechanisms of arteriolar and venous vasoconstriction may be reversed. These effects, in addition to the negative inotropy, may produce severe hypotension. Because ventricular tachycardia usually persists after administration of verapamil, further lowering of blood pressure may cause reflex sympathetic activity, continued

SUPRAWIITRICUUR TACHYCARDIA • VOL 90/NO 2/AUGUST 1991/POSTGRAOUATE MEDICINE

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Study shows that intravenous adenosine depresses both sinoatrial and AV nodal function without adverse effects.

which, in turn, may increase the rate of ventricular tachycardia with resulting cardiovascular collapse. 1 An important maxim, therefore, is never give verapamil to patients with wide QRS tachycardia, unless (1) they have supraventricular tachycardia with known bundle-branch block and (2) the QRS complex is identical to that which was present before the onset of supraventricular arrhythmia. Adenosine, a narurally occurring nucleoside with numerous cardiac effects, has long been known to slow or block sinoatrial and AV nodal depression.1 Honey and associat~ showed that intravenous administration of the drug depresses both sinoatrial and AV nodal function in humans without causing adverse effects. Although not clearly established, adenosine's mechanism of action involves extracellular receptors that cause depression of cyclic adenosine monophosphate. Adenosine is (1) potentiated by drugs such as dipyridamole (Persantine) that prevent intracellular transpon and (2) attenuated by theophylline and the methylxanthines, which block adenosine receptors. Adenosine is rapidly metabolized by blood elements and vascular endothelium, with rapid cellular uptake and subsequent conversion by adenosine dearninase to inosine, an inactive metabolite, or phosphorylation to adenosine diphosphate and subsequendy to adenosine triphos-

Figure 3. Narrow QRS complex supraventricular tachycardia converted to sinus rhythm with adenosine. Arrows show typical delta wave, which in this case appears in leads II and Ill during sinus rhythm and indicates presence of accessory pathway.

phate. Adenosine has a half-life of less than 1 second in whole blood and is totally cleared from the plasma within 30 seconds.4 DiMarco and associates5 assessed the electrophysiologic and hemodynamic effects of adenosine in both healthy subjects and patients with paroxysmal supraventricular tachycardia. In their study of 17 patients, 11 had normal sinus rhythm and 6 had either AV reciprocating tachycardia (onhodromic, accessory pathway-mediated Wolff-ParkinsonWhite syndrome), AV nodal reentrant tachycardia, or intra-atrial reentrant tachycardia. Adenosine was administered after baseline determinations of sinus and AV nodal function were obtained.

VOL 90/NO 2/AUGUST 1991/POSTGRADUATE MEDICINE • SUPRAVENTRICULAR TACHYCARDIA

Adenosine produced significant effects on sinus nodal function and a 50% increase in sinus cycle length within 10 to 20 seconds after intravenous administration. 1bis effect was transient, lasting less than 10 seconds, and a mild reflex tachycardia occurred after sinus cycle length slowed. In animal models, this has been found to be an indirect effect mediated by the vagus nerve; it may be prevented by vagal interruption and concurrent administration ofbeta blockers. In all17 patients in this study, adenosine significandy prolonged AV nodal conduction, leading to AV nodal block. Hemodynamic effects of adenosine in patients with normal sinus rhythm were essentially insigcontinued

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A recent study of patients with paroxysmal supraventricular tachycardia showed that injection of adenosine terminates the arrhythmia in an average of 30 seconds.

Anthony C. Caruso, MD Dr Caruso is assistant clinical professor of medicine and director, cardiac electrophysiology laboratory, section of cardiology, department of internal medicine, University of Arizona Health Sciences Center, Tucson.

nificant, and doses necessary for AV block had no measurable effect on blood pressure. In patients with AV reciprocating tachycardia or AV nodal reentrant tachycardia, doses required for termination of reentrant tachycardia produced no hypotension; however, systemic blood pressure increased afi:er termination of tachycardia. Flushing was a side effect in 5 of the 17 patients. My associates and 16 conducted a double-blind comparative study of adenosine and placebo fOr termination of spontaneous or induced paroxysmal supraventricular tachycardia. The efficacy and safety of

80

adenosine were evaluated in 37 patients undergoing baseline electrophysiologic studies. Of the 37 patients, 23 had orthodromic AV reciprocating tachycardia with an accessory pathway acting as the retrograde limb, 13 had AV nodal reentrant tachycardia, and 1 had a Mahaim connection. The response to adenosine was the same in patients with AV reciprocating tachycardia as in those with AV nodal reentrant tachycardia; that is, supraventricular tachycardia converted to sinus rhythm in all patients. The time to conversion to sinus rhythm in the adenosine group was 23.3 ± 8.9 seconds afi:er administration of an effective bolus. The dose of adenosine required for conversion to sinus rhythm was 6 mg or less in 28 patients. All of the patients tolerated the drug without hemodynamic compronuse. Should adenosine replace veraparnil as the treatment of choice for supraventricular tachycardia? Answers to this question may be found in a recent study of adenosine for paroxysmal supraventricular tachycardia. 7 In the first protocol of this study, 359 patients with supraventricular tachycardia were sequentially randomized to receive a maximum intravenous bolus of3, 6, 9, or 12 mg of adenosine with an equal volume of saline solution. The drug terminated acute episodes of tachycardia in 35.2%, 62.3%, 80.2%, and 91.4% of patients, respectively. In the second protocol, patients re-

ceived 6 or 12 mg of adenosine and 5 or 7.5 mg of veraparnil. Response rates to adenosine were 57.4% to 6 mg and 93.4% to 12 mg. Response rates to veraparnil were 81.3% to 5 mg and 89.4% to 7.5 mg. The average time afi:er injection of adenosine to termination of tachycardia was 30 seconds. Transient adverse ef-. fecrs occurred in 36% of patients. It was concluded from this trial that even though the overall efficacy of adenosine is similar to that of veraparnil, the onset of action of adenosine is more rapid. Although adverse effectS to adenosine are relatively common, they also are minor and transient. Clearly, then, an intravenous bolus of adenosine in a dose up to 12 mg is effective and safe for terminating supraventricular tachycardia when the AV node is part of the reentry circuit. While the efficacy of adenosine is not significantly different from that of veraparnil, the brief duration and relative mildness of adverse effectS make adenosine the preferred drug for patients with paroxysmal supraventricular tachycardia. An increased dose of adenosine may be necessary in patients receiving theophylline or other methylxanthines, because these drugs competitively bind the same receptor used by adenosine. Conversely, a reduced dose may be necessary in patients receiving dipyridamole. Also, it must be remembered that (1) the drug is rapidly inactivated by blood elements and the vascular endothecontinued

SUPRAnNTRICULAR TACHYCARDIA • VOL 90/NO 2/AUGUST 1991/POSTGRADUATE MEDICINE

AXID®

(nizatidine capsules)

Briel SUmmary. Caa111H the poclagellteratvre for complete inforlllllion. :J:'~':Or~~~i~f,;,:;k~cli., duodenal ulc8r-for up to aweeks of treatment Most 2. Maintenance the"''r -lor healed duodenal ulcer patients at areduced dosage of 150 mg h.s. The consequences of therapy with Axid for longer than 1year are not known. Cootrelndi011ion.: Known hypersensnoity to tfle drug. Because cross sensitivity in this class of compounds has been observed, H2-receptor antagonists, including Axid, should not be adminislered to patients with ahistory of hypersensit~ity to other H2-receptor antagonists. PreOiullolll: General-f. Symptomatic response to nizatidine therapy does not preclude thepresenceofgastricmalignancy. 2. Dosage should be reduced in patientswitflmoderatetosevererenal insufficiency. 3.1npatientswnhnormalrenallunctionanduncomplicatedhepalicdyslunction, the

dist't::~~~~g ~;;j~~n~;~~~~~jf~ \~;\~nf~~~~;:li~~~~with Mullistix" may occur during therapy. Dlll!l tntoractions - No interactions hatl! been observed with theophyllin~ chlordiazepoxid~ lorazepam, lidocaine. phenytoin, and wartarin. Ax1d does not inhibit the cytochrome P-450 enzyme system: therefore, drug interactiOns mediated by inhibitiOn of hepatic metabolism are not expected to occur. In patients given very high doses (3,900 mg) of aspirin dai~. increased serum salicylate levels were seen when nizatidine. 150 mg b.i.d .. wasadministeredconcurrenlly. Carcinogenesis. Mutagenesis. Impairment of Fertility- A2-year oral carcinogenicity study in rats wnh doses as high as 500 mglkgiday (about SO times the recommended

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mucosa. In a2-yearstudy tn mice, there was no evidence of acarcinogenic effect in male mice,allhoughhyperplasticnodulesoftheliverwereincreasedinthehigh·dosemalesas compared wnh placebo. Female m1ce given the high dose of Axid (2,000 mgikgiday, about330 t1mes the human dose) showed marginally statistically sigmficant increases in hepaticcarcinomaandhepaticnodularhyperplasiawllhnonumericalincreaseseenin

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adose larger than the maximum tolerated dose. as indicated by excessive (30%) weight decrement as compared with concurrent controls and ev1dence of mild liver injury (transaminase elevations). The occurrence o1 a marginal finding at high dose only in animals given an excessive and somewhat hepatotoxic dose, with no evidence of a carcino e~ic effect in rats, · ~~~~~,;~:-~c\1~-~~~n:~~ ~.3~:', ~ji;e{:~~ Axid was not mutagenic'" abattery of tests pertonned to evaluate its potential genetic toxicity, including bactenal mutation tests. unscheduled DNA synthesiS, sister chromatid exchange, mouse lymphoma assay, chromosome aberration tests, and amicronucleus test. lna2-generation,pennatalandpostnatalfertilitystudyinrats, dosesofnizatidineup to 650 mglkglday produced no adverse effects on the reproductive pertonmance of

pa~~;~;~;e~ir~;~r,~~~s-lffgnancyCaregory C-Oral reproduction studies in rats at doses up to 300 limes the human dose and in Dutch Belled rabbits at doses up to 55 times the human dose revealed no evidence of impaired fertility or teratogenic effect: but, at adose equivalent to 3110 times the human dose, treated rabbits had abortions. decreased number of live fetuses. and depressed fetal weights. On intravenous administration to pregnant New Zealand White rabbits. n11alidine at20 mgl