Supraventricular Tachycardia
Identifieur interne : 001E31 ( Main/Corpus ); précédent : 001E30; suivant : 001E32Supraventricular Tachycardia
Auteurs : Vijay S. Chauhan ; Andrew D. Krahn ; George J. Klein ; Allan C. Skanes ; Raymond YeeSource :
- Medical Clinics of North America [ 0025-7125 ] ; 2001.
Abstract
Supraventricular tachycardias (SVTs) affect more than 1 of the population, making them a relatively common clinical problem.48 SVTs encompass a large group of arrhythmias that originate above the bifurcation of the bundle of His. An antiquated term, paroxysmal atrial tachycardia, previously was used to describe SVTs that began and ended abruptly. This term has become obsolete because many such arrhythmias arise from not only the atria, but also the atrioventricular (AV) node, bundle of His, and accessory pathway tissue. Most SVTs have normal narrow-complex morphology,31 but they also may have wide QRS complexes resulting from aberrant conduction or, less commonly, preexcitation. This article discusses SVTs with respect to their classification, mechanisms, electrocardiogram (ECG) manifestations, and medical management. Catheter ablation is available for patients who fail medical therapy or who do not wish to take medications. A detailed discussion of catheter ablation is found in the article by Calkins elsewhere in this issue.
Url:
DOI: 10.1016/S0025-7125(05)70313-8
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Supraventricular Tachycardia</title><author><name sortKey="Chauhan, Vijay S" sort="Chauhan, Vijay S" uniqKey="Chauhan V" first="Vijay S." last="Chauhan">Vijay S. Chauhan</name></author><author><name sortKey="Krahn, Andrew D" sort="Krahn, Andrew D" uniqKey="Krahn A" first="Andrew D." last="Krahn">Andrew D. Krahn</name></author><author><name sortKey="Klein, George J" sort="Klein, George J" uniqKey="Klein G" first="George J." last="Klein">George J. Klein</name></author><author><name sortKey="Skanes, Allan C" sort="Skanes, Allan C" uniqKey="Skanes A" first="Allan C." last="Skanes">Allan C. Skanes</name></author><author><name sortKey="Yee, Raymond" sort="Yee, Raymond" uniqKey="Yee R" first="Raymond" last="Yee">Raymond Yee</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:6543F8C3FEACA696A3301CDE1B36202D2DBE5432</idno><date when="2001" year="2001">2001</date><idno type="doi">10.1016/S0025-7125(05)70313-8</idno><idno type="url">https://api.istex.fr/document/6543F8C3FEACA696A3301CDE1B36202D2DBE5432/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001E31</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Supraventricular Tachycardia</title><author><name sortKey="Chauhan, Vijay S" sort="Chauhan, Vijay S" uniqKey="Chauhan V" first="Vijay S." last="Chauhan">Vijay S. Chauhan</name></author><author><name sortKey="Krahn, Andrew D" sort="Krahn, Andrew D" uniqKey="Krahn A" first="Andrew D." last="Krahn">Andrew D. Krahn</name></author><author><name sortKey="Klein, George J" sort="Klein, George J" uniqKey="Klein G" first="George J." last="Klein">George J. Klein</name></author><author><name sortKey="Skanes, Allan C" sort="Skanes, Allan C" uniqKey="Skanes A" first="Allan C." last="Skanes">Allan C. Skanes</name></author><author><name sortKey="Yee, Raymond" sort="Yee, Raymond" uniqKey="Yee R" first="Raymond" last="Yee">Raymond Yee</name></author></analytic><monogr></monogr><series><title level="j">Medical Clinics of North America</title><title level="j" type="abbrev">MDC</title><idno type="ISSN">0025-7125</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001">2001</date><biblScope unit="volume">85</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="193">193</biblScope><biblScope unit="page" to="223">223</biblScope></imprint><idno type="ISSN">0025-7125</idno></series><idno type="istex">6543F8C3FEACA696A3301CDE1B36202D2DBE5432</idno><idno type="DOI">10.1016/S0025-7125(05)70313-8</idno><idno type="PII">S0025-7125(05)70313-8</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0025-7125</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Supraventricular tachycardias (SVTs) affect more than 1 of the population, making them a relatively common clinical problem.48 SVTs encompass a large group of arrhythmias that originate above the bifurcation of the bundle of His. An antiquated term, paroxysmal atrial tachycardia, previously was used to describe SVTs that began and ended abruptly. This term has become obsolete because many such arrhythmias arise from not only the atria, but also the atrioventricular (AV) node, bundle of His, and accessory pathway tissue. Most SVTs have normal narrow-complex morphology,31 but they also may have wide QRS complexes resulting from aberrant conduction or, less commonly, preexcitation. This article discusses SVTs with respect to their classification, mechanisms, electrocardiogram (ECG) manifestations, and medical management. Catheter ablation is available for patients who fail medical therapy or who do not wish to take medications. A detailed discussion of catheter ablation is found in the article by Calkins elsewhere in this issue.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Vijay S. Chauhan MD, FRCPC</name></json:item><json:item><name>Andrew D. Krahn MD, FRCPC, FACC</name></json:item><json:item><name>George J. Klein MD, FRCPC, FACC</name></json:item><json:item><name>Allan C. Skanes MD, FRCPC</name></json:item><json:item><name>Raymond Yee MD, FRCPC, FACC</name></json:item></author><language><json:string>eng</json:string></language><abstract>Supraventricular tachycardias (SVTs) affect more than 1 of the population, making them a relatively common clinical problem.48 SVTs encompass a large group of arrhythmias that originate above the bifurcation of the bundle of His. An antiquated term, paroxysmal atrial tachycardia, previously was used to describe SVTs that began and ended abruptly. This term has become obsolete because many such arrhythmias arise from not only the atria, but also the atrioventricular (AV) node, bundle of His, and accessory pathway tissue. Most SVTs have normal narrow-complex morphology,31 but they also may have wide QRS complexes resulting from aberrant conduction or, less commonly, preexcitation. This article discusses SVTs with respect to their classification, mechanisms, electrocardiogram (ECG) manifestations, and medical management. Catheter ablation is available for patients who fail medical therapy or who do not wish to take medications. A detailed discussion of catheter ablation is found in the article by Calkins elsewhere in this issue.</abstract><qualityIndicators><score>6.824</score><pdfVersion>1.3</pdfVersion><pdfPageSize>396 x 647.759 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1041</abstractCharCount><pdfWordCount>7982</pdfWordCount><pdfCharCount>52579</pdfCharCount><pdfPageCount>31</pdfPageCount><abstractWordCount>152</abstractWordCount></qualityIndicators><title>Supraventricular Tachycardia</title><pii><json:string>S0025-7125(05)70313-8</json:string></pii><genre><json:string>research-article</json:string></genre><host><volume>85</volume><pii><json:string>S0025-7125(05)X7020-1</json:string></pii><pages><last>223</last><first>193</first></pages><issn><json:string>0025-7125</json:string></issn><issue>2</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><title>Medical Clinics of North America</title><publicationDate>2001</publicationDate></host><categories><wos><json:string>MEDICINE, GENERAL & INTERNAL</json:string></wos></categories><publicationDate>2001</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1016/S0025-7125(05)70313-8</json:string></doi><id>6543F8C3FEACA696A3301CDE1B36202D2DBE5432</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/6543F8C3FEACA696A3301CDE1B36202D2DBE5432/fulltext/pdf</uri></json:item><json:item><original>true</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6543F8C3FEACA696A3301CDE1B36202D2DBE5432/fulltext/txt</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/6543F8C3FEACA696A3301CDE1B36202D2DBE5432/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/6543F8C3FEACA696A3301CDE1B36202D2DBE5432/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Supraventricular Tachycardia</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>2001</date></publicationStmt><notesStmt><note>Address reprint requests to Andrew D. Krahn, MD, Division of Cardiology, University of Western Ontario, 339 Windermere Road, London, Ontario, N6A 5A5, Canada. e-mail: akrahn@julian.uwo.ca</note><note type="content">Figure 1: A, Mechanism of atrioventricular node reentrant tachycardia (AVNRT). AVNRT can be broadly classified as typical or atypical. In typical AVNRT, the reentrant circuit includes a slowly conducting anterograde limb and a rapidly conducting retrograde limb. The less common atypical AVNRT may have various forms. In this example, the atypical AVNRT is comprised of a fast anterograde limb and a slow retrograde limb. B, Mechanism of atrioventricular reentrant tachycardias (AVRT). AVRT can broadly be classified as orthodromic or antidromic. In this example of orthodromic AVRT, anterograde conduction proceeds via the AV node and retrograde conduction is via a left-sided accessory pathway. The reverse is the case with antidromic AVRT, which appears preexcited on the ECG.</note><note type="content">Figure 2: A, EKGs from a patient with typical AV node reentrant tachycardia. PseudoS waves are evident in the terminal portion of the QRS complexes of leads II, III, and aVF, which are not seen in sinus rhythm. PseudoS waves (arrow) represent atrial activation via the rapidly conducting retrograde limb of the reentrant circuit. B, Another patient with typical AVNRT exhibits pseudoR waves (arrow) in the terminal portion of the QRS complexes of lead V1, which are not evident in sinus rhythm.</note><note type="content">Figure 3: A 12-lead ECG in a patient with WolffParkinsonWhite (WPW) syndrome, involving a left lateral accessory pathway. Note the delta wave and short PR interval present in sinus rhythm (arrow).</note><note type="content">Figure 4: A 12-lead ECG of orthodromic atrioventricular reentrant tachycardia involving a left-sided accessory pathway. The tachycardia is narrow complex because of anterograde conduction down the AV node and HisPurkinje system. Retrograde atrial activation over the accessory pathway results in a P wave within the early ST segment.</note><note type="content">Figure 5: A 12-lead ECG of antidromic atrioventricular reentrant tachycardia involving a left paraseptal accessory pathway. The tachycardia is pre-excited because of anterograde conduction via the accessory pathway. Rapid retrograde atrial activation over the HisPurkinje conduction system and AV node results in a P wave within the early ST segment.</note><note type="content">Figure 6: A 12-lead ECG of the permanent form of junctional reciprocating tachycardia (PJRT). The tachycardia is narrow complex because of anterograde conduction down the AV node and HisPurkinje system. The retrograde limb of the reentrant circuit involves a slowly conducting, decremental posteroseptal accessory pathway. Atrial activation is therefore delayed producing negative P waves in leads II, III, and aVF with an RP interval longer than the PR interval.</note><note type="content">Figure 7: Orthodromic atrioventricular reentrant tachycardia (AVRT) involving a left-sided accessory pathway. Retrograde atrial activation is over a left-sided accessory pathway, which produces negative P waves in leads I and aVL.</note><note type="content">Figure 8: In this patient with orthodromic atrioventricular reentrant tachycardia (AVRT), QRS alternans is evident in all leads, particularly V4. QRS alternans is believed to result from the rapid rate of tachycardias and does not suggest a specific tachycardia mechanism.</note><note type="content">Figure 9: A 12-lead ECG of atrial tachycardia with 1:1 AV conduction arising from the anterior right atrium. P waves are evident in the middle of the T wave.</note><note type="content">Figure 10: A, The P waves in atrial tachycardia are often distinct (arrow) with an isoelectric baseline between them. B, In contrast, the P waves or flutter waves (F) in atrial flutter have a characteristic saw-tooth appearance without a discernible isoelectric baseline (arrow). These distinctions are most evident in leads II, III, and aVF.</note><note type="content">Figure 11: In multifocal atrial tachycardia (MAT), at least three atrial foci give rise to an irregular narrow complex rhythm with at least three different P wave morphologies and/or PR intervals. Note the irregularity of the atrial rate, accompanied by variable PR intervals and subtle changes in P wave morphology, with resumption of sinus rhythm in the last beat on the tracing. This patient has a history of severe obstructive pulmonary disease with resting hypoxia.</note><note type="content">Figure 12: A, A systematic approach to the diagnosis of supraventricular tachycardias (SVT) using the 12-lead ECG. The key initial step is to assess the regularity of the rhythm, followed by identification of P waves and the AV relationship. B, Usefulness of vagal maneuvers and adenosine in the diagnosis of SVT. Vagal maneuvers and adenosine can be both diagnostic and therapeutic. AVNRT = atrioventricular node reentrant tachycardia; AVRT = atrioventricular reentrant tachycardia; AT = atrial tachycardia; JT = junctional tachycardia; AF = atrial fibrillation; AFL = atrial flutter; MAT = multifocal atrial tachycardia; PJRT = permanent form of junctional reciprocating tachycardia; s/f = slow-fast variant of AVNRT; f/s = fast-slow variant of AVNRT.</note><note type="content">Figure 13: Adenosine (6 mg iv push) is administered to typical atrioventricular node reentrant tachycardia (AVNRT). After 6 beats, the tachycardia terminates with a P wave (pseudoR, arrow) implying block in the anterograde, slow pathway. Following AVNRT termination, there is gradual resumption of sinus rhythm. Note that the pseudoR waves during AVNRT are not present in the subsequent sinus beats.</note><note type="content">Figure 14: Latent preexcitation is unmasked after adenosine administration which blocks AV nodal conduction. In this patient, progressive preexcitation develops during sinus rhythm after adenosine.</note><note type="content">Figure 15: A 12-lead ECG of preexcited atrial fibrillation involving a posteroseptal accessory pathway. Note the irregular rhythm with varying degrees of preexcitation. The shortest RR interval of 240 ms (*) suggests that this patient is at high risk of sudden death.</note><note type="content">Table 1: CLASSIFICATION OF SUPRAVENTRICULAR TACHYCARDIAS</note><note type="content">Table 2: COMMONLY USED DRUGS IN ACUTE AND LONG-TERM MANAGEMENT OF SUPRAVENTRICULAR TACHYCARDIA</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Supraventricular Tachycardia</title><author><persName><forename type="first">Vijay S.</forename><surname>Chauhan</surname></persName><roleName type="degree">MD, FRCPC</roleName><note type="biography">Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</note><affiliation>Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</affiliation></author><author><persName><forename type="first">Andrew D.</forename><surname>Krahn</surname></persName><roleName type="degree">MD, FRCPC, FACC</roleName><note type="biography">Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</note><affiliation>Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</affiliation></author><author><persName><forename type="first">George J.</forename><surname>Klein</surname></persName><roleName type="degree">MD, FRCPC, FACC</roleName><note type="biography">Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</note><affiliation>Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</affiliation></author><author><persName><forename type="first">Allan C.</forename><surname>Skanes</surname></persName><roleName type="degree">MD, FRCPC</roleName><note type="biography">Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</note><affiliation>Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</affiliation></author><author><persName><forename type="first">Raymond</forename><surname>Yee</surname></persName><roleName type="degree">MD, FRCPC, FACC</roleName><note type="biography">Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</note><affiliation>Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</affiliation></author></analytic><monogr><title level="j">Medical Clinics of North America</title><title level="j" type="abbrev">MDC</title><idno type="pISSN">0025-7125</idno><idno type="PII">S0025-7125(05)X7020-1</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001"></date><biblScope unit="volume">85</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="193">193</biblScope><biblScope unit="page" to="223">223</biblScope></imprint></monogr><idno type="istex">6543F8C3FEACA696A3301CDE1B36202D2DBE5432</idno><idno type="DOI">10.1016/S0025-7125(05)70313-8</idno><idno type="PII">S0025-7125(05)70313-8</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Supraventricular tachycardias (SVTs) affect more than 1 of the population, making them a relatively common clinical problem.48 SVTs encompass a large group of arrhythmias that originate above the bifurcation of the bundle of His. An antiquated term, paroxysmal atrial tachycardia, previously was used to describe SVTs that began and ended abruptly. This term has become obsolete because many such arrhythmias arise from not only the atria, but also the atrioventricular (AV) node, bundle of His, and accessory pathway tissue. Most SVTs have normal narrow-complex morphology,31 but they also may have wide QRS complexes resulting from aberrant conduction or, less commonly, preexcitation. This article discusses SVTs with respect to their classification, mechanisms, electrocardiogram (ECG) manifestations, and medical management. Catheter ablation is available for patients who fail medical therapy or who do not wish to take medications. A detailed discussion of catheter ablation is found in the article by Calkins elsewhere in this issue.</p></abstract></profileDesc><revisionDesc><change when="2001">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier doc found" wicri:toSee="Elsevier, no converted or simple article"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 5.0.1//EN//XML" URI="art501.dtd" name="istex:docType"><istex:entity SYSTEM="f019301" NDATA="IMAGE" name="f019301"></istex:entity><istex:entity SYSTEM="f019302" NDATA="IMAGE" name="f019302"></istex:entity><istex:entity SYSTEM="f019303" NDATA="IMAGE" name="f019303"></istex:entity><istex:entity SYSTEM="f019304" NDATA="IMAGE" name="f019304"></istex:entity><istex:entity SYSTEM="f019305" NDATA="IMAGE" name="f019305"></istex:entity><istex:entity SYSTEM="f019306" NDATA="IMAGE" name="f019306"></istex:entity><istex:entity SYSTEM="f019307" NDATA="IMAGE" name="f019307"></istex:entity><istex:entity SYSTEM="f019308" NDATA="IMAGE" name="f019308"></istex:entity><istex:entity SYSTEM="f019309" NDATA="IMAGE" name="f019309"></istex:entity><istex:entity SYSTEM="f019310" NDATA="IMAGE" name="f019310"></istex:entity><istex:entity SYSTEM="f019311" NDATA="IMAGE" name="f019311"></istex:entity><istex:entity SYSTEM="f019312" NDATA="IMAGE" name="f019312"></istex:entity><istex:entity SYSTEM="f019313" NDATA="IMAGE" name="f019313"></istex:entity><istex:entity SYSTEM="f019314" NDATA="IMAGE" name="f019314"></istex:entity><istex:entity SYSTEM="f019315" NDATA="IMAGE" name="f019315"></istex:entity></istex:docType><istex:document><article docsubtype="fla"> <item-info> <jid>MDC</jid> <aid>70313</aid> <ce:pii>S0025-7125(05)70313-8</ce:pii><ce:doi>10.1016/S0025-7125(05)70313-8</ce:doi> <ce:copyright type="other" year="2001">W. B. Saunders Company</ce:copyright> </item-info> <ce:floats> <ce:figure id="f1"> <ce:label>Figure 1</ce:label> <ce:caption> <ce:simple-para><ce:italic>A,</ce:italic> Mechanism of atrioventricular node reentrant tachycardia (AVNRT). AVNRT can be broadly classified as typical or atypical. In typical AVNRT, the reentrant circuit includes a slowly conducting anterograde limb and a rapidly conducting retrograde limb. The less common atypical AVNRT may have various forms. In this example, the atypical AVNRT is comprised of a fast anterograde limb and a slow retrograde limb. <ce:italic>B,</ce:italic> Mechanism of atrioventricular reentrant tachycardias (AVRT). AVRT can broadly be classified as orthodromic or antidromic. In this example of orthodromic AVRT, anterograde conduction proceeds via the AV node and retrograde conduction is via a left-sided accessory pathway. The reverse is the case with antidromic AVRT, which appears preexcited on the ECG.</ce:simple-para> </ce:caption> <ce:link locator="f019301"></ce:link> </ce:figure> <ce:figure id="f2"> <ce:label>Figure 2</ce:label> <ce:caption> <ce:simple-para><ce:italic>A,</ce:italic> EKGs from a patient with typical AV node reentrant tachycardia. PseudoS waves are evident in the terminal portion of the QRS complexes of leads II, III, and aVF, which are not seen in sinus rhythm. PseudoS waves <ce:italic>(arrow)</ce:italic> represent atrial activation via the rapidly conducting retrograde limb of the reentrant circuit. <ce:italic>B,</ce:italic> Another patient with typical AVNRT exhibits pseudoR waves <ce:italic>(arrow)</ce:italic> in the terminal portion of the QRS complexes of lead V1, which are not evident in sinus rhythm.</ce:simple-para> </ce:caption> <ce:link locator="f019302"></ce:link> </ce:figure> <ce:figure id="f3"> <ce:label>Figure 3</ce:label> <ce:caption> <ce:simple-para>A 12-lead ECG in a patient with Wolff–Parkinson–White (WPW) syndrome, involving a left lateral accessory pathway. Note the delta wave and short PR interval present in sinus rhythm <ce:italic>(arrow).</ce:italic></ce:simple-para> </ce:caption> <ce:link locator="f019303"></ce:link> </ce:figure> <ce:figure id="f4"> <ce:label>Figure 4</ce:label> <ce:caption> <ce:simple-para>A 12-lead ECG of orthodromic atrioventricular reentrant tachycardia involving a left-sided accessory pathway. The tachycardia is narrow complex because of anterograde conduction down the AV node and His–Purkinje system. Retrograde atrial activation over the accessory pathway results in a P wave within the early ST segment.</ce:simple-para> </ce:caption> <ce:link locator="f019304"></ce:link> </ce:figure> <ce:figure id="f5"> <ce:label>Figure 5</ce:label> <ce:caption> <ce:simple-para>A 12-lead ECG of antidromic atrioventricular reentrant tachycardia involving a left paraseptal accessory pathway. The tachycardia is pre-excited because of anterograde conduction via the accessory pathway. Rapid retrograde atrial activation over the His–Purkinje conduction system and AV node results in a P wave within the early ST segment.</ce:simple-para> </ce:caption> <ce:link locator="f019305"></ce:link> </ce:figure> <ce:figure id="f6"> <ce:label>Figure 6</ce:label> <ce:caption> <ce:simple-para>A 12-lead ECG of the permanent form of junctional reciprocating tachycardia (PJRT). The tachycardia is narrow complex because of anterograde conduction down the AV node and His–Purkinje system. The retrograde limb of the reentrant circuit involves a slowly conducting, decremental posteroseptal accessory pathway. Atrial activation is therefore delayed producing negative P waves in leads II, III, and aVF with an RP interval longer than the PR interval.</ce:simple-para> </ce:caption> <ce:link locator="f019306"></ce:link> </ce:figure> <ce:figure id="f7"> <ce:label>Figure 7</ce:label> <ce:caption> <ce:simple-para>Orthodromic atrioventricular reentrant tachycardia (AVRT) involving a left-sided accessory pathway. Retrograde atrial activation is over a left-sided accessory pathway, which produces negative P waves in leads I and aVL.</ce:simple-para> </ce:caption> <ce:link locator="f019307"></ce:link> </ce:figure> <ce:figure id="f8"> <ce:label>Figure 8</ce:label> <ce:caption> <ce:simple-para>In this patient with orthodromic atrioventricular reentrant tachycardia (AVRT), QRS alternans is evident in all leads, particularly V4. QRS alternans is believed to result from the rapid rate of tachycardias and does not suggest a specific tachycardia mechanism.</ce:simple-para> </ce:caption> <ce:link locator="f019308"></ce:link> </ce:figure> <ce:figure id="f9"> <ce:label>Figure 9</ce:label> <ce:caption> <ce:simple-para>A 12-lead ECG of atrial tachycardia with 1:1 AV conduction arising from the anterior right atrium. P waves are evident in the middle of the T wave.</ce:simple-para> </ce:caption> <ce:link locator="f019309"></ce:link> </ce:figure> <ce:figure id="f10"> <ce:label>Figure 10</ce:label> <ce:caption> <ce:simple-para><ce:italic>A,</ce:italic> The P waves in atrial tachycardia are often distinct <ce:italic>(arrow)</ce:italic> with an isoelectric baseline between them. <ce:italic>B,</ce:italic> In contrast, the P waves or flutter waves (F) in atrial flutter have a characteristic saw-tooth appearance without a discernible isoelectric baseline <ce:italic>(arrow).</ce:italic> These distinctions are most evident in leads II, III, and aVF.</ce:simple-para> </ce:caption> <ce:link locator="f019310"></ce:link> </ce:figure> <ce:figure id="f11"> <ce:label>Figure 11</ce:label> <ce:caption> <ce:simple-para>In multifocal atrial tachycardia (MAT), at least three atrial foci give rise to an irregular narrow complex rhythm with at least three different P wave morphologies and/or PR intervals. Note the irregularity of the atrial rate, accompanied by variable PR intervals and subtle changes in P wave morphology, with resumption of sinus rhythm in the last beat on the tracing. This patient has a history of severe obstructive pulmonary disease with resting hypoxia.</ce:simple-para> </ce:caption> <ce:link locator="f019311"></ce:link> </ce:figure> <ce:figure id="f12"> <ce:label>Figure 12</ce:label> <ce:caption> <ce:simple-para><ce:italic>A,</ce:italic> A systematic approach to the diagnosis of supraventricular tachycardias (SVT) using the 12-lead ECG. The key initial step is to assess the regularity of the rhythm, followed by identification of P waves and the AV relationship. <ce:italic>B,</ce:italic> Usefulness of vagal maneuvers and adenosine in the diagnosis of SVT. Vagal maneuvers and adenosine can be both diagnostic and therapeutic. AVNRT = atrioventricular node reentrant tachycardia; AVRT = atrioventricular reentrant tachycardia; AT = atrial tachycardia; JT = junctional tachycardia; AF = atrial fibrillation; AFL = atrial flutter; MAT = multifocal atrial tachycardia; PJRT = permanent form of junctional reciprocating tachycardia; s/f = slow-fast variant of AVNRT; f/s = fast-slow variant of AVNRT.</ce:simple-para> </ce:caption> <ce:link locator="f019312"></ce:link> </ce:figure> <ce:figure id="f13"> <ce:label>Figure 13</ce:label> <ce:caption> <ce:simple-para>Adenosine (6 mg iv push) is administered to typical atrioventricular node reentrant tachycardia (AVNRT). After 6 beats, the tachycardia terminates with a P wave (pseudoR, <ce:italic>arrow</ce:italic>) implying block in the anterograde, slow pathway. Following AVNRT termination, there is gradual resumption of sinus rhythm. Note that the pseudoR waves during AVNRT are not present in the subsequent sinus beats.</ce:simple-para> </ce:caption> <ce:link locator="f019313"></ce:link> </ce:figure> <ce:figure id="f14"> <ce:label>Figure 14</ce:label> <ce:caption> <ce:simple-para>Latent preexcitation is unmasked after adenosine administration which blocks AV nodal conduction. In this patient, progressive preexcitation develops during sinus rhythm after adenosine.</ce:simple-para> </ce:caption> <ce:link locator="f019314"></ce:link> </ce:figure> <ce:figure id="f15"> <ce:label>Figure 15</ce:label> <ce:caption> <ce:simple-para>A 12-lead ECG of preexcited atrial fibrillation involving a posteroseptal accessory pathway. Note the irregular rhythm with varying degrees of preexcitation. The shortest RR interval of 240 ms (*) suggests that this patient is at high risk of sudden death.</ce:simple-para> </ce:caption> <ce:link locator="f019315"></ce:link> </ce:figure> <ce:table id="cetable1" frame="topbot" colsep="1" rowsep="0"> <ce:label>Table 1</ce:label> <ce:caption> <ce:simple-para>CLASSIFICATION OF SUPRAVENTRICULAR TACHYCARDIAS</ce:simple-para> </ce:caption> <tgroup cols="2"> <colspec colnum="1" colname="col1" colwidth="50*" align="left"></colspec> <colspec colnum="2" colname="col2" colwidth="50*" align="center"></colspec> <thead> <row rowsep="1"> <entry colname="col1"><ce:bold>AV Node Independent</ce:bold></entry> <entry colname="col2"><ce:bold>AV Node Dependent</ce:bold></entry> </row> </thead> <tbody> <row> <entry colname="col1">Sinus tachycardia</entry> <entry colname="col2">AV node reentry</entry> </row> <row> <entry colname="col1"> Appropriate</entry> <entry colname="col2">Slow-fast variant</entry> </row> <row> <entry colname="col1"> Inappropriate</entry> <entry colname="col2">Fast-slow variant</entry> </row> <row> <entry colname="col1"> Sinus node reentry</entry> <entry colname="col2"></entry> </row> <row> <entry colname="col1">Atrial tachycardia</entry> <entry colname="col2">AV reentrant</entry> </row> <row> <entry colname="col1"> Unifocal</entry> <entry colname="col2">Orthodromic (concealed AP)</entry> </row> <row> <entry colname="col1"> Multifocal</entry> <entry colname="col2">Antidromic (manifest AP)</entry> </row> <row> <entry colname="col1"></entry> <entry colname="col2">PJRT (concealed slowly conducting AP)</entry> </row> <row> <entry colname="col1">Atrial flutter</entry> <entry colname="col2">Junctional tachycardia</entry> </row> <row> <entry colname="col1">Atrial fibrillation</entry> <entry colname="col2"></entry> </row> <row> <entry namest="col1" nameend="col2">AV = Atrioventricular; AP = accessory pathway; PJRT = permanent form of junctional reciprocating tachycardia.</entry> </row> </tbody> </tgroup> </ce:table> <ce:table id="cetable2" frame="topbot" colsep="1" rowsep="0"> <ce:label>Table 2</ce:label> <ce:caption> <ce:simple-para>COMMONLY USED DRUGS IN ACUTE AND LONG-TERM MANAGEMENT OF SUPRAVENTRICULAR TACHYCARDIA</ce:simple-para> </ce:caption> <tgroup cols="5"> <colspec colnum="1" colname="col1" colwidth="20*" align="left"></colspec> <colspec colnum="2" colname="col2" colwidth="20*" align="center"></colspec> <colspec colnum="3" colname="col3" colwidth="20*" align="center"></colspec> <colspec colnum="4" colname="col4" colwidth="20*" align="center"></colspec> <colspec colnum="5" colname="col5" colwidth="20*" align="center"></colspec> <thead> <row rowsep="1"> <entry colname="col1"><ce:bold>Drug</ce:bold></entry> <entry colname="col2"><ce:bold>Mode of Action</ce:bold></entry> <entry colname="col3"><ce:bold>Dosage</ce:bold><ce:cross-ref refid="cetablefn1">†</ce:cross-ref></entry> <entry colname="col4"><ce:bold>Side Effects</ce:bold></entry> <entry colname="col5"><ce:bold>Proarrhythmia</ce:bold></entry> </row> </thead> <tbody> <row> <entry colname="col1">Adenosine</entry> <entry colname="col2">AV node blocker</entry> <entry colname="col3">6–12 mg IV bolus</entry> <entry colname="col4">Dyspnea, flushing, chest pain</entry> <entry colname="col5">Atrial fibrillation</entry> </row> <row> <entry colname="col1">Verapamil</entry> <entry colname="col2">AV node blocker</entry> <entry colname="col3">5–10 mg IV over 2 min</entry> <entry colname="col4">Hypotension, CHF, constipation</entry> <entry colname="col5">Bradycardia</entry> </row> <row> <entry colname="col1"></entry> <entry colname="col2"></entry> <entry colname="col3">80–120 mg orally tid</entry> <entry colname="col4"></entry> <entry colname="col5"></entry> </row> <row> <entry colname="col1">Diltiazem</entry> <entry colname="col2">AV node blocker</entry> <entry colname="col3">10–20 mg IV over 2 min</entry> <entry colname="col4">Hypotension, CHF</entry> <entry colname="col5">Bradycardia</entry> </row> <row> <entry colname="col1"></entry> <entry colname="col2"></entry> <entry colname="col3">60–120 mg orally tid</entry> <entry colname="col4"></entry> <entry colname="col5"></entry> </row> <row> <entry colname="col1">Metoprolol</entry> <entry colname="col2">AV node blocker</entry> <entry colname="col3">5–15 mg IV over 5–15 min</entry> <entry colname="col4">Hypotension, CHF, bronchospasm</entry> <entry colname="col5">Bradycardia</entry> </row> <row> <entry colname="col1"></entry> <entry colname="col2"></entry> <entry colname="col3">50–100 mg orally bid</entry> <entry colname="col4"></entry> <entry colname="col5"></entry> </row> <row> <entry colname="col1">Atenolol</entry> <entry colname="col2">AV node blocker</entry> <entry colname="col3">25–50 mg orally od</entry> <entry colname="col4">Hypotension, CHF, bronchospam</entry> <entry colname="col5">Bradycardia</entry> </row> <row> <entry colname="col1">Procainamide</entry> <entry colname="col2">Class IA antiarrhythmic</entry> <entry colname="col3">700–1000 mg IV over 1 h</entry> <entry colname="col4">Hypotension</entry> <entry colname="col5">TdP</entry> </row> <row> <entry colname="col1">Flecainide</entry> <entry colname="col2">Class IC antiarrhythmic</entry> <entry colname="col3">140 mg IV over 10 min<ce:cross-ref refid="cetablefn2">*</ce:cross-ref></entry> <entry colname="col4">Confusion, headache</entry> <entry colname="col5">2.3%<ce:cross-ref refid="bib27"><ce:sup>27</ce:sup></ce:cross-ref></entry> </row> <row> <entry colname="col1"></entry> <entry colname="col2"></entry> <entry colname="col3">50–200 mg orally bid</entry> <entry colname="col4"></entry> <entry colname="col5"></entry> </row> <row> <entry colname="col1">Propafenone</entry> <entry colname="col2">Class IC antiarrhythmic</entry> <entry colname="col3">140 mg IV over 2 min</entry> <entry colname="col4">Gastrointestinal upset</entry> <entry colname="col5">2.1%<ce:cross-ref refid="bib11"><ce:sup>11</ce:sup></ce:cross-ref></entry> </row> <row> <entry colname="col1"></entry> <entry colname="col2">AV node blocker</entry> <entry colname="col3">150–300 mg orally tid</entry> <entry colname="col4"></entry> <entry colname="col5"></entry> </row> <row> <entry colname="col1">Sotalol</entry> <entry colname="col2">Class III antiarrhythmic</entry> <entry colname="col3">100 mg IV over 10 min<ce:cross-ref refid="cetablefn2">*</ce:cross-ref></entry> <entry colname="col4">Hypotension, CHF, bronchospasm</entry> <entry colname="col5">Bradycardia, TdP (2.4%)<ce:cross-ref refid="bib44"><ce:sup>44</ce:sup></ce:cross-ref></entry> </row> <row> <entry colname="col1"></entry> <entry colname="col2">AV node blocker</entry> <entry colname="col3">80–240 mg orally bid</entry> <entry colname="col4"></entry> <entry colname="col5"></entry> </row> <row> <entry colname="col1">Ibutilide</entry> <entry colname="col2">Class III antiarrhythmic</entry> <entry colname="col3">2 mg IV over 10 min</entry> <entry colname="col4">Hypotension</entry> <entry colname="col5">Bradycardia, TdP (3.6%)<ce:cross-ref refid="bib18"><ce:sup>18</ce:sup></ce:cross-ref></entry> </row> <row> <entry colname="col1">Amiodarone</entry> <entry colname="col2">Class III antiarrhythmic</entry> <entry colname="col3">200–300 mg orally daily</entry> <entry colname="col4">Hypothyroidism, hyperthyroidism, lung toxicity, liver toxicity</entry> <entry colname="col5">TdP (1%)<ce:cross-ref refid="bib26"><ce:sup>26</ce:sup></ce:cross-ref></entry> </row> <row> <entry colname="col1"></entry> <entry colname="col2">AV node blocker</entry> <entry colname="col3"></entry> <entry colname="col4"></entry> <entry colname="col5"></entry> </row> <row> <entry namest="col1" nameend="col5">AV = Atrioventricular; CHF = congestive heart failure; TdP = torsades de pointes; IV = intravenously; tid = 3 times/d; bid = 2 times/d.</entry> </row> </tbody> </tgroup> <ce:table-footnote id="cetablefn1"> <ce:label>†</ce:label> <ce:note-para>Drug dose calculated for average 70 kg patient.</ce:note-para> </ce:table-footnote> <ce:table-footnote id="cetablefn2"> <ce:label>*</ce:label> <ce:note-para>Not available in North America.</ce:note-para> </ce:table-footnote> </ce:table> </ce:floats> <head> <ce:article-footnote> <ce:note-para><ce:italic>Address reprint requests to</ce:italic> Andrew D. Krahn, MD, Division of Cardiology, University of Western Ontario, 339 Windermere Road, London, Ontario, N6A 5A5, Canada. e-mail: <ce:inter-ref xlink:href="mailto:akrahn@julian.uwo.ca">akrahn@julian.uwo.ca</ce:inter-ref></ce:note-para> </ce:article-footnote> <ce:title>Supraventricular Tachycardia</ce:title> <ce:author-group> <ce:author> <ce:degrees>MD, FRCPC</ce:degrees> <ce:given-name>Vijay S.</ce:given-name> <ce:surname>Chauhan</ce:surname><ce:cross-ref refid="fn1"><ce:sup>*</ce:sup></ce:cross-ref> </ce:author> <ce:author> <ce:degrees>MD, FRCPC, FACC</ce:degrees> <ce:given-name>Andrew D.</ce:given-name> <ce:surname>Krahn</ce:surname><ce:cross-ref refid="fn1"><ce:sup>*</ce:sup></ce:cross-ref> </ce:author> <ce:author> <ce:degrees>MD, FRCPC, FACC</ce:degrees> <ce:given-name>George J.</ce:given-name> <ce:surname>Klein</ce:surname><ce:cross-ref refid="fn1"><ce:sup>*</ce:sup></ce:cross-ref> </ce:author> <ce:author> <ce:degrees>MD, FRCPC</ce:degrees> <ce:given-name>Allan C.</ce:given-name> <ce:surname>Skanes</ce:surname><ce:cross-ref refid="fn1"><ce:sup>*</ce:sup></ce:cross-ref> </ce:author> <ce:author> <ce:degrees>MD, FRCPC, FACC</ce:degrees> <ce:given-name>Raymond</ce:given-name> <ce:surname>Yee</ce:surname><ce:cross-ref refid="fn1"><ce:sup>*</ce:sup></ce:cross-ref> </ce:author> <ce:footnote id="fn1"> <ce:label>*</ce:label> <ce:note-para>Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</ce:note-para> </ce:footnote> </ce:author-group> <ce:abstract> <ce:abstract-sec> <ce:simple-para>Supraventricular tachycardias (SVTs) affect more than 1% of the population, making them a relatively common clinical problem.<ce:cross-ref refid="bib48"><ce:sup>48</ce:sup></ce:cross-ref> SVTs encompass a large group of arrhythmias that originate above the bifurcation of the bundle of His. An antiquated term, <ce:italic>paroxysmal atrial tachycardia,</ce:italic> previously was used to describe SVTs that began and ended abruptly. This term has become obsolete because many such arrhythmias arise from not only the atria, but also the atrioventricular (AV) node, bundle of His, and accessory pathway tissue. Most SVTs have <ce:italic>normal</ce:italic> narrow-complex morphology,<ce:cross-ref refid="bib31"><ce:sup>31</ce:sup></ce:cross-ref> but they also may have wide QRS complexes resulting from aberrant conduction or, less commonly, preexcitation. This article discusses SVTs with respect to their classification, mechanisms, electrocardiogram (ECG) manifestations, and medical management. Catheter ablation is available for patients who fail medical therapy or who do not wish to take medications. A detailed discussion of catheter ablation is found in the article by Calkins elsewhere in this issue.</ce:simple-para> </ce:abstract-sec> </ce:abstract> </head> <body> <ce:sections> <ce:section id="cesec1"> <ce:section-title>CLASSIFICATION</ce:section-title> <ce:para>The most common mechanism of SVT is reentry with a smaller proportion caused by abnormal automaticity or triggered activity.<ce:cross-ref refid="bib62"><ce:sup>62</ce:sup></ce:cross-ref> Classification by mechanism is not uniformly discernible, making this classification scheme clinically impractical. Instead, SVTs have been classified broadly based on their anatomic origin as either AV node dependent or AV node independent, which is helpful in formulating treatment strategies <ce:cross-ref refid="cetable1">(Table 1)</ce:cross-ref><ce:float-anchor refid="cetable1"></ce:float-anchor>.<ce:cross-ref refid="bib63"><ce:sup>63</ce:sup></ce:cross-ref> AV node–dependent SVTs involve a reentrant circuit or ectopic focus that must include the AV node. Block in the AV node terminates these tachycardias. AV node–dependent tachycardias include AV node reentry, AV reentry involving an accessory pathway, and junctional tachycardia. For AV node–independent tachycardias, the AV node is not necessary to sustain the tachycardia. These tachycardias include atrial tachycardia (unifocal and multifocal) and sinus node reentry. Atrial flutter and atrial fibrillation also are AV node–independent SVTs, but they are distinct in their electrophysiology and management and are not discussed in this article.</ce:para> </ce:section> <ce:section id="cesec2"> <ce:section-title>MECHANISMS OF SUPRAVENTRICULAR TACHYCARDIA</ce:section-title> <ce:section id="cesec3"> <ce:section-title>Atrioventricular Node Reentrant Tachycardia</ce:section-title> <ce:para>The most common form of paroxysmal SVT is AV node reentrant tachycardia (AVNRT), which accounts for greater than 60% of cases referred to an electrophysiology laboratory. Patients typically present in their 30s or 40s, with greater than 70% being women.<ce:cross-ref refid="bib1"><ce:sup>1</ce:sup></ce:cross-ref> Although the mechanism for AVNRT is reentry involving the AV node, the precise location of the reentrant circuit is uncertain but includes atrial tissue surrounding the AV node. The reentrant circuit consists of an anterograde limb and a retrograde limb <ce:cross-ref refid="f1">(Fig. 1)</ce:cross-ref><ce:float-anchor refid="f1"></ce:float-anchor>. AVNRT can be classified broadly as typical or atypical. Typical AVNRT is more common (90%) and includes the <ce:italic>slow-fast</ce:italic> variant, in which the anterograde limb is conducting slowly, while the retrograde limb is conducting rapidly. The less common, atypical AVNRTs (10%) may have various forms, including <ce:italic>fast-slow</ce:italic> (rapidly conducting anterograde limb and slowly conducting retrograde limb), <ce:italic>slow-slow,</ce:italic> and <ce:italic>fast-fast.</ce:italic></ce:para> <ce:para>Typical AVNRT usually is initiated with a premature atrial impulse, which blocks in the fast pathway and conducts over the slow pathway. Then the impulse returns up the fast pathway, which did not conduct anterogradely. Activation of the ventricle by way of the slow pathway occurs almost simultaneously with atrial activation by way of the fast pathway. This activity produces P waves on the surface ECG, which either are hidden within the QRS complex or are apparent in the initial or terminal portion of the QRS complex as a <ce:italic>pseudoR</ce:italic> wave (in lead V1) or a <ce:italic>pseudoS</ce:italic> wave (in leads II, III, aVF). If the P wave is distinguishable, it is negative in the inferior leads because of caudocranial atrial activation. Comparison with the QRS complex during sinus rhythm often is helpful in identifying pseudoR and pseudoS waves during AVNRT <ce:cross-ref refid="f2">(Fig. 2)</ce:cross-ref><ce:float-anchor refid="f2"></ce:float-anchor>. In atypical AVNRT (fast-slow), atrial activation is delayed relative to ventricular activation because the retrograde limb conducts slowly. Retrograde P waves are distinguishable more easily from the QRS complex, and the R-P interval usually is longer than the P-R interval. In AVNRT, the ventricle is not part of the reentrant circuit, and 1:1 AV activation is not necessary. Although clinically rare, conduction block may develop below the nodal reentrant circuit, producing 2:1 AV dissociation.</ce:para> </ce:section> <ce:section id="cesec4"> <ce:section-title>Atrioventricular Reentrant Tachycardia Mediated by Accessory Pathways</ce:section-title> <ce:para>The second most common form of paroxysmal SVT is AV reentrant tachycardia (AVRT) using an accessory pathway.<ce:cross-ref refid="bib20"><ce:sup>20</ce:sup></ce:cross-ref> Accessory pathways are discrete bundles of myocardial tissue bridging the atrium and ventricle along the tricuspid or mitral valve annulus. More than half of accessory pathways are situated in the left free wall, 20% to 30% occur in the posteroseptal location, 10% to 20% occur in the right free wall, and 5% to 10% occur in the anteroseptal location near the AV node. These pathways can conduct anterogradely from the atrium to the ventricle, retrogradely from the ventricle to the atrium, or, most commonly, bidirectionally. In patients with anterogradely conducting accessory pathways, ventricular activation is through the normal AV node–His bundle branches as well as the accessory pathway. Because the accessory pathway conducts more rapidly than the normal conduction system, the ventricle is <ce:italic>preexcited,</ce:italic> producing a short P-R interval and a delta wave on the surface ECG. The degree of preexcitation depends on the relative contribution of the normal conduction system and the accessory pathway to ventricular activation, which can be modified by autonomic tone and antiarrhythmic drugs. In contrast, about 25% of accessory pathways conduct only retrogradely and are not manifest on the ECG during sinus rhythm. Such accessory pathways are referred to as <ce:italic>concealed</ce:italic> pathways. Patients with anterograde or retrograde accessory pathway conduction and symptomatic tachycardia have Wolff-Parkinson-White (WPW) syndrome <ce:cross-ref refid="f3">(Fig. 3)</ce:cross-ref><ce:float-anchor refid="f3"></ce:float-anchor>.<ce:cross-ref refid="bib67"><ce:sup>67</ce:sup></ce:cross-ref></ce:para> <ce:para>AV reentrant circuits are relatively large involving an anterograde and retrograde limb between the atria and ventricles. Reentry typically is initiated with a premature atrial or ventricular impulse that blocks in one limb while conducting over the other. There are two types of AVRT involving accessory pathways—orthodromic AVRT and antidromic AVRT (see <ce:cross-ref refid="f1">Fig. 1</ce:cross-ref>). In the former, the anterograde pathway is the AV node, whereas the retrograde limb is the accessory pathway. Orthodromic AVRT commonly uses bidirectionally conducting accessory pathways. Only retrograde conduction is present during tachycardia, giving rise to a normal QRS complex <ce:cross-ref refid="f4">(Fig. 4)</ce:cross-ref><ce:float-anchor refid="f4"></ce:float-anchor>. In antidromic AVRT, the anterograde limb is the accessory pathway, resulting in preexcitation on the surface ECG <ce:cross-ref refid="f5">(Fig. 5)</ce:cross-ref><ce:float-anchor refid="f5"></ce:float-anchor>. The retrograde limb usually is the AV node but may be another accessory pathway capable of retrograde conduction. Antidromic AVRT may involve multiple accessory pathways and is far less common than orthodromic AVRT.<ce:cross-ref refid="bib3"><ce:sup>3</ce:sup></ce:cross-ref></ce:para> <ce:para>Most orthodromic AVRTs use a rapidly conducting accessory pathway, giving rise to a P wave shortly after the QRS complex in the ST segment (see <ce:cross-ref refid="f4">Fig. 4</ce:cross-ref>). In contrast, a few orthodromic AVRTs involve a slowly conducting retrograde accessory pathway, which delays atrial activation relative to the QRS complex; this is manifest on the ECG as an R-P interval longer than the P-R interval. These accessory pathways also display decremental conduction similar to the AV node, resulting in further conduction slowing as a function of more rapid rates. AVRTs involving decremental, slowly conducting pathways frequently are incessant, beginning spontaneously during sinus rhythm without a premature atrial or ventricular impulse. This arrhythmia was initially referred to as <ce:italic>permanent form of junctional reciprocating tachycardia</ce:italic> (PJRT) because AV nodal reentry originally was thought to be the mechanism of the tachycardia <ce:cross-ref refid="f6">(Fig. 6)</ce:cross-ref><ce:float-anchor refid="f6"></ce:float-anchor>.<ce:cross-ref refid="bib13"><ce:sup>13</ce:sup></ce:cross-ref> Left untreated, PJRT may lead to tachycardia-induced cardiomyopathy.<ce:cross-ref refid="bib14"><ce:sup>14</ce:sup></ce:cross-ref></ce:para> <ce:para>The retrograde P wave polarity during AVRT may indicate the accessory pathway's location. For example, a negative P wave in lead I suggests a left atrial insertion of an accessory pathway, and a positive P wave in the inferior leads during orthodromic tachycardia suggests a posteroseptal accessory pathway <ce:cross-ref refid="f7">(Fig. 7)</ce:cross-ref><ce:float-anchor refid="f7"></ce:float-anchor>.<ce:cross-ref refid="bib47"><ce:sup>47</ce:sup></ce:cross-ref> Because the atria and ventricles are part of the reentrant circuit, 1:1 AV association is obligatory. The finding of electric alternans of the QRS complex is seen most commonly in orthodromic AVRT <ce:cross-ref refid="f8">(Fig. 8)</ce:cross-ref><ce:float-anchor refid="f8"></ce:float-anchor>.<ce:cross-ref refid="bib21"><ce:sup>21</ce:sup></ce:cross-ref> QRS alternans is believed to be a rate-related phenomenon and is not suggestive of a specific tachycardia mechanism. AVNRT with rapid rates (uncommon because of slow anterograde AV nodal conduction) also may manifest QRS alternans.</ce:para> <ce:para>Atrial fibrillation and atrial flutter sometimes are seen with WPW syndrome.<ce:cross-ref refid="bib9"><ce:sup>9</ce:sup></ce:cross-ref> For reasons that are unclear, these arrhythmias often are induced by an episode of AVRT.<ce:cross-refs refid="bib35 bib59"><ce:sup>35,59</ce:sup></ce:cross-refs> In older patients, the prevalence of atrial fibrillation increases and may not relate to the observed accessory pathway. Atrial fibrillation in patients with accessory pathways having short refractory periods may cause ventricular fibrillation and sudden death resulting from rapid ventricular rates. Patients with WPW syndrome at highest risk of sudden death have accessory pathways capable of conducting faster than 240 beats/min during atrial fibrillation.<ce:cross-ref refid="bib35"><ce:sup>35</ce:sup></ce:cross-ref> In contrast, patients with intermittent preexcitation on the resting ECG (preexcitation in some QRS complexes) have a low clinical risk of sudden death because their accessory pathways have long refractory periods and cannot conduct at lethal rates.<ce:cross-ref refid="bib36"><ce:sup>36</ce:sup></ce:cross-ref></ce:para> </ce:section> <ce:section id="cesec5"> <ce:section-title>Atrial Tachycardia</ce:section-title> <ce:para>Atrial tachycardia is less common than AVNRT or AVRT, accounting for fewer than 15% of patients referred for electrophysiology study. It can occur in the pediatric population, especially in children with surgically corrected congenital heart disease. Atrial tachycardia usually arises from a single localized atrial focus. The tachycardia mechanism is variable and may depend on the presence of underlying atrial disease. Localized reentry is more likely with diseased, dilated atrial muscle, which creates the electric milieu of slowed conduction velocity and prolonged refractoriness necessary for a reentrant circuit.<ce:cross-refs refid="bib24 bib53"><ce:sup>24,53</ce:sup></ce:cross-refs> In children, reentrant forms of atrial tachycardia frequently are associated with prior surgery for congenital heart disease, such as correction of transposition of the great vessels or repair of atrial septal defects. These atrial tachycardias involve large reentrant circuits around atriotomies, baffles, and other scars related to repair of congenital lesions.<ce:cross-ref refid="bib4"><ce:sup>4</ce:sup></ce:cross-ref> Reentrant atrial tachycardias typically are initiated with a spontaneous atrial premature beat and tend to be paroxysmal. In healthy atrial muscle, enhanced automaticity or triggered activity may play a role.<ce:cross-refs refid="bib53 bib55"><ce:sup>53,55</ce:sup></ce:cross-refs> Automatic atrial tachycardia usually is not paroxysmal but tends to accelerate or <ce:italic>warm up</ce:italic> on initiation and decelerate or <ce:italic>cool down</ce:italic> during termination. These arrhythmias also may have slight beat-to-beat variability in rate. Some automatic atrial tachycardias also are incessant and have been associated with the development of tachycardia-induced cardiomyopathy.<ce:cross-ref refid="bib51"><ce:sup>51</ce:sup></ce:cross-ref></ce:para> <ce:para>Because the AV node or the ventricles are not necessary for the initiation or maintenance of atrial tachycardia, the AV relationship can be 1:1, or varying degrees of AV block may be present <ce:cross-ref refid="f9">(Fig. 9)</ce:cross-ref><ce:float-anchor refid="f9"></ce:float-anchor>. For example, digitalis toxicity can cause atrial tachycardia mediated by triggered activity, which usually is accompanied by variable AV block.<ce:cross-ref refid="bib57"><ce:sup>57</ce:sup></ce:cross-ref> The P wave morphology during atrial tachycardia depends on the location of the focus. Analysis of leads aVL and V1 provides a reasonable guide to the right-sided or left-sided origin of the atrial tachycardia. A positive P wave in V1 has a sensitivity of 93% and a specificity of 88% in predicting a left atrial focus. A positive or biphasic P wave in lead aVL has a sensitivity of 88% and specificity of 79% for predicting a right atrial focus.<ce:cross-ref refid="bib61"><ce:sup>61</ce:sup></ce:cross-ref> Examination of P wave polarity in the inferior leads is helpful in distinguishing a superior focus (positive P wave) from an inferior focus (negative P wave) in right and left atria. The P-R interval often is shorter than the R-P interval in atrial tachycardia (see <ce:cross-ref refid="f9">Fig. 9</ce:cross-ref>). Although the rate of atrial tachycardia generally is 140 to 200 beats/min, it may exceed 250 beats/min, which can be similar to the rate of atrial flutter. A key distinguishing feature is the absence of an isoelectric baseline between P waves and the characteristic saw-tooth P wave morphology of atrial flutter, which is not seen in atrial tachycardia <ce:cross-ref refid="f10">(Fig. 10)</ce:cross-ref><ce:float-anchor refid="f10"></ce:float-anchor>.</ce:para> </ce:section> <ce:section id="cesec6"> <ce:section-title>Multifocal Atrial Tachycardia</ce:section-title> <ce:para>Multifocal atrial tachycardia is a rare SVT. It involves more than one atrial focus and requires at least three distinct P wave morphologies to be diagnosed on the surface ECG <ce:cross-ref refid="f11">(Fig. 11)</ce:cross-ref><ce:float-anchor refid="f11"></ce:float-anchor>. Because the foci fire independently of one another, the atrial rate is irregular and typically averages 100 beats/min. The P-R interval also may vary depending on the location of the foci relative to the AV node. Isoelectric periods between adjacent P waves help distinguish multifocal atrial tachycardia from atrial fibrillation. The mechanism for multifocal atrial tachycardia has not been defined clearly but may be due to enhanced automaticity or triggered activity.<ce:cross-ref refid="bib32"><ce:sup>32</ce:sup></ce:cross-ref> Most patients with this arrhythmia have exacerbations of severe underlying pulmonary disease with hypoxia.</ce:para> </ce:section> <ce:section id="cesec7"> <ce:section-title>Junctional Tachycardia</ce:section-title> <ce:para>Junctional tachycardias arise from a discrete focus within the AV node or the His bundle. In the pediatric population, junctional tachycardia also is known as junctional ectopic tachycardia. Junctional ectopic tachycardia presenting before 6 months of age usually is associated with underlying heart disease that carries a high mortality. In contrast, adult junctional tachycardia has a more benign prognosis and typically develops after the acute phase of myocardial infarction, digitalis intoxication, and acute myocarditis. Junctional tachycardia also is seen immediately after cardiac surgery in children and adults and may be due to perinodal AV node trauma.<ce:cross-ref refid="bib34"><ce:sup>34</ce:sup></ce:cross-ref> Although the precise mechanism for junctional tachycardia has not been defined, it is likely due to enhanced impulse initiation in the region of the AV node by automaticity or triggered activity rather than reentry.<ce:cross-ref refid="bib52"><ce:sup>52</ce:sup></ce:cross-ref> Automatic junctional tachycardia tends to warm up and cool down. The junctional rate often is irregular, which can mimic atrial fibrillation if the P waves are not obvious. Retrograde atrial activation may follow each junctional impulse, giving 1:1 ventriculoatrial activation, with P waves often concealed within the QRS complex. More commonly, however, some junctional impulses fail to conduct retrogradely to the atrium, giving VA dissociation, which can be mistaken for ventricular tachycardia if bundle-branch block aberration also is present.</ce:para> </ce:section> <ce:section id="cesec8"> <ce:section-title>Tachycardias Arising From the Sinus Node Region</ce:section-title> <ce:para>Sinus node reentry and inappropriate sinus tachycardia are less common SVTs. Sinus node reentry tachycardia arises from a reentrant circuit involving the sinus node, producing P waves that are fairly similar if not identical to those during sinus rhythm.<ce:cross-ref refid="bib68"><ce:sup>68</ce:sup></ce:cross-ref> In contrast to sinus rhythm and inappropriate sinus tachycardia, sinus node reentry can be initiated and terminated abruptly by a premature atrial stimulus, which is consistent with its reentrant mechanism. It is usually nonsustained and associated with slower rates than inappropriate sinus tachycardia, making it clinically insignificant. Carotid sinus massage and other vagal maneuvers typically slow or terminate sinus node reentry.</ce:para> <ce:para>Inappropriate sinus tachycardia is a clinical syndrome characterized by sinus tachycardia without an identifiable physiologic stimulus. Secondary causes for resting sinus tachycardia must be ruled out, such as anemia, hyperthyroidism, pheochromocytoma, and diabetes mellitus with autonomic dysfunction. At least two clinical variants have been described: (1) resting heart rate of 100 beats/min or greater and (2) increased heart rate response to minimal exertion. These patients have preserved left ventricular function with no underlying heart disease. Sinus rates greater than 200 beats/min are not characteristic of inappropriate sinus tachycardia, and paroxysmal increases in heart rate are not seen. Because atrial depolarization is through the sinus node, P waves have typical sinus morphology.<ce:cross-ref refid="bib38"><ce:sup>38</ce:sup></ce:cross-ref> The mechanism of inappropriate sinus tachycardia is still speculative but is thought to be a primary abnormality of the sinus node complex characterized by a high intrinsic heart rate, β-adrenergic hypersensitivity, and accentuation by a depressed cardiovagal reflex.<ce:cross-ref refid="bib46"><ce:sup>46</ce:sup></ce:cross-ref></ce:para> </ce:section> </ce:section> <ce:section id="cesec9"> <ce:section-title>CLINICAL PRESENTATION</ce:section-title> <ce:para>SVTs can produce a wide spectrum of symptoms. Palpitations are the most common symptom, which can be of variable frequency, severity, and duration. It is useful to characterize the onset and regularity of the palpitations to help distinguish the mechanism of SVT. For example, sudden-onset, regular palpitations suggest a reentrant or triggered paroxysmal SVT, such as AVNRT, AVRT, atrial flutter, sinus node reentry tachycardia, or junctional tachycardia. In contrast, gradual-onset, regular palpitations may be due to an automatic SVT, such as an atrial or junctional tachycardia. Irregular palpitations of sudden onset most likely are due to atrial fibrillation. In many patients, the description of the palpitations may not reflect reliably the underlying SVT mechanism. For example, SVTs that have a paroxysmal termination may be perceived as gradual because sinus tachycardia usually follows SVT termination. The palpitations may be accompanied by other nonspecific symptoms, such as chest or neck discomfort, pressure in the head, dyspnea, lightheadedness, or frank syncope. Syncope usually is related more to impaired vasomotor adaptation to the tachycardia than to the rapid heart rate.<ce:cross-ref refid="bib41"><ce:sup>41</ce:sup></ce:cross-ref> In patients with coronary artery disease, impaired left ventricular function, or stenotic valvular heart disease, SVTs with rapid heart rates may precipitate myocardial ischemia or congestive heart failure. Most regular SVTs occur in patients without organic heart disease, however, and carry an excellent overall prognosis. SVTs usually have no identifiable triggers, but in some patients maneuvers that alter autonomic tone, such as bending down or neck pressure, may be a precipitant. The cardiovascular examination usually does not help in the diagnosis of SVT. Nonetheless, the most useful sign to look for is the presence of cannon A waves in the jugular venous pressure, which can be seen in AVNRT.</ce:para> </ce:section> <ce:section id="cesec10"> <ce:section-title>DIFFERENTIAL DIAGNOSIS</ce:section-title> <ce:para>Several features in the patient's history may be helpful. Although the nature of the palpitations is important, gender, age of SVT onset, and the presence of heart disease also should be considered. For instance, AVNRT and AVRT usually are associated with younger patients and structurally normal hearts. AVNRT is more common in women, whereas AVRTs have a male preponderence. In contrast, patients with heart disease or prior cardiac surgery are more likely to have atrial tachycardia, atrial flutter, atrial fibrillation, or junctional tachycardia.</ce:para> <ce:para>After reviewing the patient's clinical presentation, the 12-lead ECG provides further diagnostic information. A high-quality 12-lead ECG should be recorded during SVT before initiating empirical therapy, provided that the patient is hemodynamically stable. SVTs typically present as a narrow-complex tachycardia.<ce:cross-ref refid="bib31"><ce:sup>31</ce:sup></ce:cross-ref> In contrast, SVTs with a wide QRS complex are seen with (1) a preexisting or rate-related bundle-branch block; (2) preexcitation with a participating accessory pathway, such as antidromic AVRT; or (3) preexcitation with bystander accessory pathway, such as in atrial tachycardia.<ce:cross-ref refid="bib64"><ce:sup>64</ce:sup></ce:cross-ref> It is important to discriminate wide-complex SVTs from ventricular tachycardia. Once the clinical diagnosis of SVT is made, the tachycardia must be characterized further in a systematic fashion. <ce:cross-ref refid="f12">Figure 12</ce:cross-ref><ce:float-anchor refid="f12"></ce:float-anchor> illustrates one approach to ECG diagnosis of SVTs, beginning with an assessment of the regularity of the tachycardia. An irregular SVT is atrial fibrillation or sometimes junctional tachycardia if P waves are absent. In contrast, multifocal atrial tachycardia or atrial flutter should be considered if P waves are present. For regular SVTs, it is helpful to identify P waves by careful examination of all ECG leads. Depending on the SVT mechanism, P waves may not be apparent because they overlap with the QRS complex or T wave. Comparing ECGs during SVT and sinus rhythm may help to identify P waves. Suspicious <ce:italic>bumps</ce:italic> in the terminal QRS or the T wave should be considered P waves if they are not present during sinus rhythm (see <ce:cross-ref refid="f2">Fig. 2</ce:cross-ref>).</ce:para> <ce:para>If P waves can be identified reliably, the presence of AV dissociation should be determined, which is suggested by P waves outnumbering QRS complexes as a result of failure to conduct through the AV node or the His-Purkinje system. AV dissociation excludes AVRT, which requires the atrium and the ventricle in its macro-reentry circuit. If 1:1 AV association is present, the R-P and P-R intervals should be measured. SVTs with an R-P > P-R are most likely to be atrial tachycardias but less commonly can include atypical AVNRT (fast-slow variant) and PJRT. In contrast, SVTs with an R-P < P-R can be typical AVNRT (slow-fast variant) or AVRT.</ce:para> <ce:para>AV node–dependent tachycardias can be discriminated from AV node–independent tachycardias using vagal maneuvers, such as carotid sinus massage or Valsalva, which block AV nodal conduction. Alternatively, AV node–blocking drugs, such as intravenous adenosine or verapamil, are effective (see <ce:cross-ref refid="f12">Fig. 12</ce:cross-ref>). In most patients, intravenous adenosine, 6 to 12 mg, terminates AV node–dependent SVTs by blocking in the anterograde limb of the reentrant circuit (slow or fast AV nodal pathway).<ce:cross-ref refid="bib16"><ce:sup>16</ce:sup></ce:cross-ref> Adenosine-induced SVT termination with a P wave favors AVNRT or AVRT and effectively excludes an atrial tachycardia <ce:cross-ref refid="f13">(Fig. 13)</ce:cross-ref><ce:float-anchor refid="f13"></ce:float-anchor>. For an atrial tachycardia to end with a P wave, the atrial focus must terminate at the same time as AV block, an unlikely coincidence. SVTs that do not terminate with adenosine are AV node independent and most likely are atrial tachycardias. Most atrial tachycardias are adenosine insensitive, and their P waves are unmasked transiently when the AV node blocks with adenosine. For the less common adenosine-sensitive atrial tachycardias, adenosine often slows the atrial rate before termination with a QRS complex. This response is nonspecific, however, and may be seen with AVNRT or AVRT. Adenosine-induced SVT termination with a P wave and not a QRS complex is discriminatory.</ce:para> <ce:para>Adenosine may be helpful in differentiating sinus node reentry from inappropriate sinus tachycardia because sinus node reentry tachycardia, similar to AVNRT, is adenosine sensitive. Sinus node reentry should terminate with a QRS complex. Adenosine also may have a diagnostic role when administered during sinus rhythm to patients with a previously documented SVT. In these patients, adenosine may reveal latent preexcitation by slowing or blocking AV nodal conduction, exposing conduction through an accessory pathway <ce:cross-ref refid="f14">(Fig. 14)</ce:cross-ref><ce:float-anchor refid="f14"></ce:float-anchor>.<ce:cross-refs refid="bib5 bib36"><ce:sup>5,36</ce:sup></ce:cross-refs></ce:para> <ce:para>In addition to the surface ECG, a Holter monitor can be a useful diagnostic tool, particularly if the patient experiences symptoms suggestive of frequent episodic SVT. In these patients, the Holter monitor can characterize the SVT with respect to the (1) mean and peak heart rate, (2) mechanism of initiation and termination (e.g., premature atrial contraction, premature ventricular contraction, or sinus beat), (3) terminating electrogram (i.e., QRS or P wave), (4) acceleration on initiation or deceleration on termination, and (5) regularity.</ce:para> <ce:para>In many cases, AVNRT, AVRT, and atrial tachycardia cannot be discriminated from each other using noninvasive testing. The diagnosis may be particularly difficult if P waves are not visible on the surface ECG. Although an electrophysiology study can aid further in the diagnosis, it is not necessary for all patients, particularly if it will not influence therapy. A purely diagnostic electrophysiology study is indicated rarely unless catheter ablation therapy is contemplated as an alternative to medical therapy. In such patients, the electrophysiology study can assess suitability for ablation by defining precisely the mechanism of the SVT.</ce:para> </ce:section> <ce:section id="cesec11"> <ce:section-title>THERAPY</ce:section-title> <ce:section id="cesec12"> <ce:section-title>Acute Medical Therapy</ce:section-title> <ce:para>The rapid heart rates associated with SVTs typically are hemodynamically well tolerated, unless there is concomitant left ventricular dysfunction. Immediate electric cardioversion rarely is necessary. Nonetheless, a persistent SVT may produce unpleasant symptoms that require urgent conversion to normal sinus rhythm. Valsalva maneuvers or carotid sinus massage may be helpful in terminating AV node–dependent and sinoatrial node–dependent SVTs. After significant carotid stenosis has been ruled out, carotid sinus massage can be attempted for 5 to 10 seconds on the right and left side if necessary while the patient is supine. Alternative vagal maneuvers may include the gag reflex and facial immersion in cold water.<ce:cross-ref refid="bib45"><ce:sup>45</ce:sup></ce:cross-ref> Failing these maneuvers, adenosine is first-line therapy for the acute conversion of SVTs, most of which are AV node dependent <ce:cross-ref refid="cetable2">(Table 2)</ce:cross-ref><ce:float-anchor refid="cetable2"></ce:float-anchor>.<ce:cross-ref refid="bib16"><ce:sup>16</ce:sup></ce:cross-ref> A 6 mg bolus of adenosine is effective in terminating greater than 90% of AV node–dependent tachycardias. The patient should be warned about short-term side effects associated with adenosine, such as facial flushing, chest pain, and dyspnea. Certain drug interactions with adenosine should be considered before its administration. Dipyridamole potentiates the effect of adenosine,<ce:cross-ref refid="bib43"><ce:sup>43</ce:sup></ce:cross-ref> whereas methylxanthine derivatives, such as theophylline, antagonize its effects completely. Asthmatic patients may develop bronchospasm with adenosine, which is a relative contraindication to its use.<ce:cross-ref refid="bib40"><ce:sup>40</ce:sup></ce:cross-ref> Heart transplant recipients have denervation supersensitivity to adenosine.<ce:cross-ref refid="bib19"><ce:sup>19</ce:sup></ce:cross-ref> One of the disadvantages to adenosine is its extremely short half-life (5 seconds), with drug effects disappearing within 10 to 20 seconds. Patients are susceptible to SVT recurrence soon after termination, especially if they have frequent ectopy.<ce:cross-ref refid="bib42"><ce:sup>42</ce:sup></ce:cross-ref> Alternative drugs to adenosine with considerably longer half-lives are the intravenous calcium channel blockers, verapamil and diltiazem.<ce:cross-refs refid="bib17 bib60"><ce:sup>17,60</ce:sup></ce:cross-refs> Both drugs block AV nodal conduction and are equally effective for acute treatment of AV node–dependent tachycardias.<ce:cross-ref refid="bib54"><ce:sup>54</ce:sup></ce:cross-ref> When compared in a randomized, double-blinded study, intravenous verapamil was found to be as effective as adenosine in the acute termination of SVTs.<ce:cross-ref refid="bib15"><ce:sup>15</ce:sup></ce:cross-ref> Hypotension is the main side effect of intravenous calcium channel blockers and occurs in 10% to 15% of patients. Calcium channel blockers have peripheral vasodilating and negative inotropic effects that may be exaggerated in patients already taking a β-blocker. They generally should be avoided in patients with poor left ventricular function and heart failure.</ce:para> <ce:para>In the case of AV node–independent tachycardias, adenosine and verapamil provide diagnostic information and may be therapeutic. Ten percent of atrial tachycardias and most SNRTs terminate with adenosine.<ce:cross-refs refid="bib22 bib49"><ce:sup>22,49</ce:sup></ce:cross-refs> The remaining atrial tachycardias may convert with an antiarrhythmic drug that suppresses atrial electric activity. Traditionally, intravenous procainamide has been used, but class IC (intravenous flecainide, intravenous propafenone) or class III (intravenous sotalol,<ce:cross-ref refid="bib30"><ce:sup>30</ce:sup></ce:cross-ref> intravenous ibutilide) drugs should have similar therapeutic efficacy. Class IB agents, such as lidocaine, generally are not useful in terminating atrial tachycardias or other SVTs. During procainamide infusion, patients should be monitored closely because hypotension, QRS, and QT prolongation may develop. Failing adenosine and antiarrhythmics, the ventricular response to the atrial tachycardia should be slowed using an AV node blocker, such as intravenous diltiazem or verapamil, until more definitive therapy is determined (see later). Other AV node–suppressing drugs, such as β-blockers, work well in patients with high sympathetic tone. Digoxin has limited efficacy in acutely suppressing AV nodal conduction during SVT because it merely augments vagal tone in these sympathetically driven patients. Digoxin's delayed onset of action reduces its effectiveness as acute therapy.</ce:para> <ce:para>It is important to identify patients in whom certain drugs are contraindicated. In patients with atrial fibrillation and rapid ventricular response through an accessory pathway, digoxin should not be used because it can enhance anterograde accessory pathway conduction, leading to an increase in ventricular rate.<ce:cross-ref refid="bib56"><ce:sup>56</ce:sup></ce:cross-ref> High ventricular rates may induce ventricular fibrillation and sudden death. Calcium channel blockers also may increase anterograde accessory pathway conduction indirectly by sympathetic nervous system activation secondary to drug-induced hypotension.<ce:cross-ref refid="bib23"><ce:sup>23</ce:sup></ce:cross-ref> In contrast, adenosine and β-blockers have minimal effects on accessory pathway conduction and simply are ineffective. Instead, ventricular rates should be slowed with intravenous procainamide, which slows conduction and prolongs refractoriness of the accessory pathway. Other intravenous drugs, such as flecainide, propafenone, sotalol, or ibutilide, may be used with similar efficacy. Electric cardioversion of the atrial arrhythmia to sinus rhythm is an alternative to these drugs and should be performed if the patient is unstable. Hemodynamic collapse may result when a calcium channel blocker is used in patients whose ventricular tachycardia has been misdiagnosed as SVT with aberrant conduction.<ce:cross-ref refid="bib58"><ce:sup>58</ce:sup></ce:cross-ref> Other drugs that cause peripheral vasodilation, such as adenosine, also may be transiently harmful because cardiac output cannot augment during ventricular tachycardia to compensate for hypotension. Infrequently, adenosine may precipitate atrial fibrillation, which is of clinical significance if the patient has a concomitant rapidly conducting accessory pathway.</ce:para> </ce:section> <ce:section id="cesec13"> <ce:section-title>Long-Term Medical Therapy</ce:section-title> <ce:para>SVTs are associated with an excellent long-term prognosis in the setting of a structurally normal heart. Most patients can be reassured that their arrhythmia will not be life-threatening or cause permanent myocardial injury. Long-term management is not directed at improving survival but rather controlling symptoms. Therapy may not be indicated when attacks are uncommon and self-terminating. Long-term medical therapy or catheter ablation should be considered for patients with symptoms that are intolerably frequent, severe, or prolonged. With respect to medical therapy, patients must balance the potential benefit of drugs in suppressing their SVT against long-term side effects. There are some important principles in selecting a particular drug: (1) the SVT should be documented clearly and its mechanism defined using noninvasive testing, (2) the presence of associated heart disease should be defined, and (3) precipitating factors (such as electrolytes, hypoxia, ischemia, or other drugs) should be considered.</ce:para> <ce:para>In patients with AV node–dependent tachycardias, long-term medical therapy with an AV node blocker, such as a calcium channel blocker or a β-blocker, is first-line therapy. Verapamil and metoprolol or atenolol are the most commonly prescribed drugs for this purpose. No direct comparison of a calcium channel blocker with a β-blocker has been reported, although the combination of verapamil with digoxin was equally effective as propranolol.<ce:cross-ref refid="bib66"><ce:sup>66</ce:sup></ce:cross-ref> Digoxin alone is not preferred in the long-term treatment of AV node–dependent SVTs. Although digoxin slows AV nodal conduction by enhancing vagal tone, it usually does not control paroxysmal SVTs in which sympathetic tone is high and vagal tone is low. Second-line drug therapy for patients with AV node–dependent tachycardias who do not tolerate first-line drugs or who have recurrences while on therapy include class I antiarrhythmics. These drugs typically impair accessory pathways and retrograde fast AV nodal conduction. The class IA drugs, procainamide, quinidine, and disopyramide have been effective in some patients; however, side effects limit their long-term usefulness.<ce:cross-refs refid="bib6 bib69"><ce:sup>6,69</ce:sup></ce:cross-refs> Disopyramide can produce intolerable anticholinergic side effects. Procainamide can produce lupus-like syndrome, and quinidine often causes gastrointestinal symptoms. Procainamide and quinidine also prolong the QT interval, increasing the risk of torsades de pointes, particularly in patients with structural heart disease.<ce:cross-ref refid="bib12"><ce:sup>12</ce:sup></ce:cross-ref></ce:para> <ce:para>In comparison to class IA drugs, the class IC agents, flecainide and propafenone, are tolerated better. Randomized, placebo-controlled trials have shown that SVT recurrence is reduced by 33% with long-term flecainide therapy.<ce:cross-ref refid="bib25"><ce:sup>25</ce:sup></ce:cross-ref> When used to treat SVTs in patients without structural or ischemic heart disease, class IC agents do not increase the risk of death, as they do in patients with ventricular arrhythmias and recent myocardial infarction.<ce:cross-ref refid="bib50"><ce:sup>50</ce:sup></ce:cross-ref> The class III agents, sotalol and amiodarone, also are effective agents in preventing SVT recurrence and may offer better control of SVTs in some cases.<ce:cross-refs refid="bib39 bib65"><ce:sup>39,65</ce:sup></ce:cross-refs> No clinical trials are available currently to show the comparative efficacy of class IC with class III agents, however. There are important side effects of class III agents that make them less desirable in some patients. Sotalol is associated with early torsades de pointes. The proarrhythmic risk increases with age, female gender, renal dysfunction, and QT prolongation. Long-term amiodarone therapy may result in intolerable side effects, including thyroid, liver, and pulmonary toxicity that requires regular surveillance. It is appropriate to reserve amiodarone for drug-refractory SVTs that cannot be ablated successfully.</ce:para> <ce:para>For patients with atrial tachycardia, long-term drug therapy generally has limited effectiveness. Some atrial tachycardias are catecholamine sensitive, and β-blockers are appropriate therapy for them. Otherwise, a trial of class IC or III agents may offer better control. Class IA drugs are used less commonly because of frequent dosing, side-effect profile, and proarrhythmic risk. Clinical trials comparing class IA and IC drugs are not available to gauge their relative efficacy. Often an antiarrhythmic must be combined with an AV node–blocking drug to control the ventricular response better. Sotalol and amiodarone have additional β-blocking properties and can be used as single agents. Propafenone has weak β-blocking activity, which usually is not clinically adequate to affect AV node conduction.<ce:cross-ref refid="bib7"><ce:sup>7</ce:sup></ce:cross-ref> Nevertheless, propafenone must be used with caution in patients with contraindications to β-blockade.</ce:para> <ce:para>Long-term medical therapy of junctional tachycardia and multifocal atrial tachycardia is limited. Their management begins with improving the metabolic, cardiac, or pulmonary derangements that typically precipitate these arrhythmias.<ce:cross-ref refid="bib28"><ce:sup>28</ce:sup></ce:cross-ref> Metoprolol and verapamil may be effective in some cases of multifocal atrial tachycardia, provided that left ventricular function is preserved.<ce:cross-ref refid="bib2"><ce:sup>2</ce:sup></ce:cross-ref> For patients with sinus node–dependent tachycardias, β-blockers are appropriate therapy to suppress sinoatrial node activity.</ce:para> <ce:para>WPW syndrome is a special consideration. Anterogradely conducting accessory pathways can participate in the tachycardia (AVRT) or act as bystanders that are not essential to sustaining an AV node–independent tachycardia (atrial arrhythmias). In either case, accessory pathways with long anterograde effective refractory periods have a low risk of causing rapid, life-threatening ventricular rates and do not need to be suppressed with drugs. Reliable markers for poor anterograde conduction over an accessory pathway include intermittent preexcitation and abrupt disappearance of the delta wave on an exercise treadmill test. In contrast, when the effective refractory period is short, rapid ventricular rates and sudden death may develop during atrial fibrillation or flutter <ce:cross-ref refid="f15">(Fig. 15)</ce:cross-ref><ce:float-anchor refid="f15"></ce:float-anchor>. For these patients, medical therapy with class IC or III agents is required to lengthen the accessory pathway refractory period as well as to suppress the underlying atrial arrhythmia. These drugs may be used alone or in combination with an AV nodal blocker, such as a β-blocker. Long-term therapy with digoxin or a calcium channel blocker should be avoided, however, because both can potentiate accessory pathway conduction as mentioned earlier.<ce:cross-refs refid="bib23 bib56"><ce:sup>23,56</ce:sup></ce:cross-refs> WPW syndrome patients at highest risk for sudden death develop ventricular rates greater than 240 beats/min during atrial fibrillation.<ce:cross-ref refid="bib35"><ce:sup>35</ce:sup></ce:cross-ref> These patients should be offered catheter ablation instead of medical therapy as a more definitive means of preventing potentially lethal arrhythmia.</ce:para> </ce:section> <ce:section id="cesec14"> <ce:section-title>Catheter Ablation</ce:section-title> <ce:para>Major advances have been made in radiofrequency catheter ablation of SVTs in the 1990s. The role of long-term drug therapy has been challenged in the present era of safe, effective catheter ablation. Despite the high rate of success with ablation, there is still a small but finite risk of serious complications (1% to 2%), including stroke, myocardial infarction, cardiac or aortic perforation, aortic valve injury, femoral vein or artery injury, and AV node conduction block. Although catheter ablation is curative in most patients, it is still an elective, invasive procedure with some risks. Currently, catheter ablation should be offered as first-line therapy instead of medical therapy for symptomatic patients with accessory pathway conduction. The success and ease of catheter ablation is determined by pathway location, but overall success rates are greater than 95%.<ce:cross-ref refid="bib8"><ce:sup>8</ce:sup></ce:cross-ref> After an apparently successful ablation, 5% of patients experience a late recurrence of conduction over the pathway, which may be due to resolution of edema from the initial ablation lesion.<ce:cross-ref refid="bib10"><ce:sup>10</ce:sup></ce:cross-ref> For AVNRT, the reentrant circuit can be interrupted by ablating the fast or the slow pathway. Although both fast and slow pathway ablation are effective, slow pathway ablation is preferred because it minimizes the risk of AV node injury.<ce:cross-ref refid="bib29"><ce:sup>29</ce:sup></ce:cross-ref> Catheter ablation cures AVNRT in greater than 95% of cases. The major risk is heart block requiring implantation of a permanent pacemaker, which occurs in approximately 1% of patients. In the case of atrial tachycardia, catheter ablation is relatively less effective, primarily because the precise focus is more difficult to localize.<ce:cross-ref refid="bib33"><ce:sup>33</ce:sup></ce:cross-ref> Patients with other SVTs, such as junctional tachycardia or tachycardias involving the sinoatrial node, represent challenging ablations best handled by electrophysiology centers with considerable experience.</ce:para> </ce:section> <ce:section id="cesec15"> <ce:section-title>Recommendation for Management</ce:section-title> <ce:para>Patients with minimally symptomatic SVTs often can be managed conservatively without medical or ablation therapy. The decision to treat should take into account the patient's preference, age, myocardial function, and timely access to medical facilities. More symptomatic AVNRT should be treated initially with long-term β-blockers or calcium channel blockers. Failing this therapy, catheter ablation should be recommended before instituting class I or III antiarrhythmic therapy. The risks of ablation, including complete AV block requiring a pacemaker, probably are preferable to the cumulative risks of long-term antiarrhythmic use. Symptomatic patients with WPW syndrome most commonly are treated today with catheter ablation. Medical therapy may be preferred by some patients, however, particularly patients with minimal symptoms who are not willing to accept the low complication rate of ablation. In asymptomatic patients with preexcitation, no specific therapy is necessary. Such patients have a low risk of sudden death (approximately 1/1000 patient-years), and over time many develop anterograde accessory pathway conduction block.<ce:cross-ref refid="bib37"><ce:sup>37</ce:sup></ce:cross-ref> Exceptions include individuals engaged in high-risk occupations, such as airline pilots, police officers, and firefighters, who may be prohibited from pursuing their chosen occupation because of the finding of preexcitation, and for young people who want to participate in highly competitive athletic activities. In such patients, catheter ablation is recommended if the accessory pathway is accessible without risking injury to the AV node. In patients with symptomatic atrial tachycardia, single-drug therapy often is ineffective, and it is necessary to combine an AV node blocker with an antiarrhythmic. Catheter ablation should be considered for individuals who cannot tolerate or fail to respond to drug therapy. 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type="alternative" contentType="CDATA"><title>Supraventricular Tachycardia</title></titleInfo><name type="personal"><namePart type="given">Vijay S.</namePart><namePart type="family">Chauhan</namePart><namePart type="termsOfAddress">MD, FRCPC</namePart><description>Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew D.</namePart><namePart type="family">Krahn</namePart><namePart type="termsOfAddress">MD, FRCPC, FACC</namePart><description>Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">George J.</namePart><namePart type="family">Klein</namePart><namePart type="termsOfAddress">MD, FRCPC, FACC</namePart><description>Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Allan C.</namePart><namePart type="family">Skanes</namePart><namePart type="termsOfAddress">MD, FRCPC</namePart><description>Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Raymond</namePart><namePart type="family">Yee</namePart><namePart type="termsOfAddress">MD, FRCPC, FACC</namePart><description>Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Supraventricular tachycardias (SVTs) affect more than 1 of the population, making them a relatively common clinical problem.48 SVTs encompass a large group of arrhythmias that originate above the bifurcation of the bundle of His. An antiquated term, paroxysmal atrial tachycardia, previously was used to describe SVTs that began and ended abruptly. This term has become obsolete because many such arrhythmias arise from not only the atria, but also the atrioventricular (AV) node, bundle of His, and accessory pathway tissue. Most SVTs have normal narrow-complex morphology,31 but they also may have wide QRS complexes resulting from aberrant conduction or, less commonly, preexcitation. This article discusses SVTs with respect to their classification, mechanisms, electrocardiogram (ECG) manifestations, and medical management. Catheter ablation is available for patients who fail medical therapy or who do not wish to take medications. A detailed discussion of catheter ablation is found in the article by Calkins elsewhere in this issue.</abstract><note>Address reprint requests to Andrew D. Krahn, MD, Division of Cardiology, University of Western Ontario, 339 Windermere Road, London, Ontario, N6A 5A5, Canada. e-mail: akrahn@julian.uwo.ca</note><note type="content">Figure 1: A, Mechanism of atrioventricular node reentrant tachycardia (AVNRT). AVNRT can be broadly classified as typical or atypical. In typical AVNRT, the reentrant circuit includes a slowly conducting anterograde limb and a rapidly conducting retrograde limb. The less common atypical AVNRT may have various forms. In this example, the atypical AVNRT is comprised of a fast anterograde limb and a slow retrograde limb. B, Mechanism of atrioventricular reentrant tachycardias (AVRT). AVRT can broadly be classified as orthodromic or antidromic. In this example of orthodromic AVRT, anterograde conduction proceeds via the AV node and retrograde conduction is via a left-sided accessory pathway. The reverse is the case with antidromic AVRT, which appears preexcited on the ECG.</note><note type="content">Figure 2: A, EKGs from a patient with typical AV node reentrant tachycardia. PseudoS waves are evident in the terminal portion of the QRS complexes of leads II, III, and aVF, which are not seen in sinus rhythm. PseudoS waves (arrow) represent atrial activation via the rapidly conducting retrograde limb of the reentrant circuit. B, Another patient with typical AVNRT exhibits pseudoR waves (arrow) in the terminal portion of the QRS complexes of lead V1, which are not evident in sinus rhythm.</note><note type="content">Figure 3: A 12-lead ECG in a patient with WolffParkinsonWhite (WPW) syndrome, involving a left lateral accessory pathway. Note the delta wave and short PR interval present in sinus rhythm (arrow).</note><note type="content">Figure 4: A 12-lead ECG of orthodromic atrioventricular reentrant tachycardia involving a left-sided accessory pathway. The tachycardia is narrow complex because of anterograde conduction down the AV node and HisPurkinje system. Retrograde atrial activation over the accessory pathway results in a P wave within the early ST segment.</note><note type="content">Figure 5: A 12-lead ECG of antidromic atrioventricular reentrant tachycardia involving a left paraseptal accessory pathway. The tachycardia is pre-excited because of anterograde conduction via the accessory pathway. Rapid retrograde atrial activation over the HisPurkinje conduction system and AV node results in a P wave within the early ST segment.</note><note type="content">Figure 6: A 12-lead ECG of the permanent form of junctional reciprocating tachycardia (PJRT). The tachycardia is narrow complex because of anterograde conduction down the AV node and HisPurkinje system. The retrograde limb of the reentrant circuit involves a slowly conducting, decremental posteroseptal accessory pathway. Atrial activation is therefore delayed producing negative P waves in leads II, III, and aVF with an RP interval longer than the PR interval.</note><note type="content">Figure 7: Orthodromic atrioventricular reentrant tachycardia (AVRT) involving a left-sided accessory pathway. Retrograde atrial activation is over a left-sided accessory pathway, which produces negative P waves in leads I and aVL.</note><note type="content">Figure 8: In this patient with orthodromic atrioventricular reentrant tachycardia (AVRT), QRS alternans is evident in all leads, particularly V4. QRS alternans is believed to result from the rapid rate of tachycardias and does not suggest a specific tachycardia mechanism.</note><note type="content">Figure 9: A 12-lead ECG of atrial tachycardia with 1:1 AV conduction arising from the anterior right atrium. P waves are evident in the middle of the T wave.</note><note type="content">Figure 10: A, The P waves in atrial tachycardia are often distinct (arrow) with an isoelectric baseline between them. B, In contrast, the P waves or flutter waves (F) in atrial flutter have a characteristic saw-tooth appearance without a discernible isoelectric baseline (arrow). These distinctions are most evident in leads II, III, and aVF.</note><note type="content">Figure 11: In multifocal atrial tachycardia (MAT), at least three atrial foci give rise to an irregular narrow complex rhythm with at least three different P wave morphologies and/or PR intervals. Note the irregularity of the atrial rate, accompanied by variable PR intervals and subtle changes in P wave morphology, with resumption of sinus rhythm in the last beat on the tracing. This patient has a history of severe obstructive pulmonary disease with resting hypoxia.</note><note type="content">Figure 12: A, A systematic approach to the diagnosis of supraventricular tachycardias (SVT) using the 12-lead ECG. The key initial step is to assess the regularity of the rhythm, followed by identification of P waves and the AV relationship. B, Usefulness of vagal maneuvers and adenosine in the diagnosis of SVT. Vagal maneuvers and adenosine can be both diagnostic and therapeutic. AVNRT = atrioventricular node reentrant tachycardia; AVRT = atrioventricular reentrant tachycardia; AT = atrial tachycardia; JT = junctional tachycardia; AF = atrial fibrillation; AFL = atrial flutter; MAT = multifocal atrial tachycardia; PJRT = permanent form of junctional reciprocating tachycardia; s/f = slow-fast variant of AVNRT; f/s = fast-slow variant of AVNRT.</note><note type="content">Figure 13: Adenosine (6 mg iv push) is administered to typical atrioventricular node reentrant tachycardia (AVNRT). After 6 beats, the tachycardia terminates with a P wave (pseudoR, arrow) implying block in the anterograde, slow pathway. Following AVNRT termination, there is gradual resumption of sinus rhythm. Note that the pseudoR waves during AVNRT are not present in the subsequent sinus beats.</note><note type="content">Figure 14: Latent preexcitation is unmasked after adenosine administration which blocks AV nodal conduction. In this patient, progressive preexcitation develops during sinus rhythm after adenosine.</note><note type="content">Figure 15: A 12-lead ECG of preexcited atrial fibrillation involving a posteroseptal accessory pathway. Note the irregular rhythm with varying degrees of preexcitation. The shortest RR interval of 240 ms (*) suggests that this patient is at high risk of sudden death.</note><note type="content">Table 1: CLASSIFICATION OF SUPRAVENTRICULAR TACHYCARDIAS</note><note type="content">Table 2: COMMONLY USED DRUGS IN ACUTE AND LONG-TERM MANAGEMENT OF SUPRAVENTRICULAR TACHYCARDIA</note><relatedItem type="host"><titleInfo><title>Medical Clinics of North America</title></titleInfo><titleInfo type="abbreviated"><title>MDC</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">20010301</dateIssued></originInfo><identifier type="ISSN">0025-7125</identifier><identifier type="PII">S0025-7125(05)X7020-1</identifier><part><date>20010301</date><detail type="volume"><number>85</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>193</start><end>550</end></extent><extent unit="pages"><start>193</start><end>223</end></extent></part></relatedItem><identifier type="istex">6543F8C3FEACA696A3301CDE1B36202D2DBE5432</identifier><identifier type="DOI">10.1016/S0025-7125(05)70313-8</identifier><identifier type="PII">S0025-7125(05)70313-8</identifier><accessCondition type="use and reproduction" contentType="">© 2001W. 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