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    QRS Rong

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    DAT TRAN

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    21 Wide Complex Tachycardias Clinical Considerations, 730 Causes of Wide Complex Tachyeardias, 730 Clinial History, 730 Physical Examination, 752 Laboratory Testing, 732 Phasmacological Intervention, 792 ‘Hlectrocardiographic Features, 732 ‘Ventricular Tachycardia Versus Aberrantly Conducted Supraventricular Tachycardia, 732 Algorithme forthe Hlecrocardiographic Complex Tachycardia, 758 agnosis of Wide ‘Ventricular Tachycerdia Verous Preexcited Supraventricular Tachycardia, 722 imitations of Flectrocardiogeaphic Criteria for Diagnosis of Wide Complex Tachycardia, 712 Hlectrophysiological Testing, 742 Baseline Observations During Normal Sinus Rhythm, 742 Induction of Tachycardia, 713, ‘Tachycardia Featres, 743 Diagnostic Maneuvers During Tachycardia, 744 CLINICAL CONSIDERATIONS Causes of Wide Complex Tachycardi A narrow QRS complex (120 milliseconds or les) requires rapid, highly synchronous electrical activation of the right ventricle (RV) and left ventricle (LV), which can only be achieved through the specialized, ‘rapidly conducting His-Purkinje system (HPS). A wide QRS complex: samples less synchronous ventricular activation of longer duration, which can he due to intraventricular conduction disturbances (IVCDs), or ventricular activation not mediated by the His bundle (HB) but by a bypass tract (BT) (preexcitation) or from a ste within a ventricle (ventricular arrhythmias). [VCDs can be fixed and present ata heart, rates, and they can be intermittent and related to either tachycardia for bradycardia, TVCDs can be caused by structural abnormalities im the HPS of ventricular myocardium or by functional refactori= ress in a portion ofthe conduction system {i.e aberrant ventricular conduction). ‘Wide complex tachycardia (WC) is a rhythm with a rate of mote than 100 beats min and a QRS duration of more than 120 milliseconds (ig, 21.1), Several arrhythonias can manifest as WCTs (Table 21.1) the ‘most common is ventricular tachycardia (VT), which accounts for 80% ofall cases of WET. Supraventrcular tnchycardia (SVT) with aberrancy accounts for 15% (o 209% of WCTs, SVTs with bystander preexcitation and atrioventricular reentrant tachycardia (AVRT) account for 1% to 69% of WT. ‘in the stable patient who will undergo a more detailed assessment, the goal of evaluation should include determination ofthe cause of the WCT (particularly distinguishing between VT and SVT). Accurate Aiagnesis of the WCT requires information obtained from the history, physical eeamination response o certain maneuvers, and careful inspec- ‘on ofthe electrocardiogram (ECG) including rhythm strips and 12lead tracings. Comparison of the ECG during the tachycardia with that recorded uring sinus hythm, if avilable, can also provide valuable information, 730 WCT in a patent older than 35 years ie likely to be VE (positive prodic- tive value of up fo 85%), SVT is more likely in the younger patient (positive predictive value of 70%). ‘Symptoms Some patients with WCI present with few or no symaptome (e.., pale pitations, lightheadedness, digphoress), whereas others can have severe ‘manifestations, including chest pain, dyspnea, syncope, seizures, and cardiac arrest. The seventy of symptoms during a WCT is not wseful Jn determining the tachycardia mechanism because symptoms are pri- marily related to the fast heart rate, associated heart disease, and the presence and extent of LV dysfunction, rather than tothe mechanism of the tachycardia Itis important to recognize thal VT does not neces- sarily result in hemodynamic compromise or collapse; on the other hhand, rapid SVT can cause decompensation in susceptible patients. ‘Misdisgnosis of VI as SVT on the basis of hemodynamic stability isa ‘common ertor that an lead to inappropriate and potentially dangerous therapy, Duration of the Arrhythmia SSVI is mote key if the tachycardia hae recuteed over a period of more ‘than 3 years. The first occurrence of a WCT after myocardial infercion (MT strongly implies VE. Presence of Underlying Heart Disease ‘The presence of structural heart disease, especially coronary heart disease and a previous MA, strongly suggests VE asthe cause of WCTE In one report, more than 98% of patients with a previous MI had VT as the ‘cause of WCT, whereas only 796 of those with SVT had a MI. It should be realized, however, that VI can occur in patients with no apparent Inca disease, and SVT can occur in thore with structural heat disease CHAPTER 21. Wide Complex Tachycardias Fig. 21.1 Wide Complex Tachycardia. El -nocardiogram obtaned in a patent with prior inferior all fare ‘van. The underying mechanism is venvculr tachycarsia relatea to the lft venticler inferior wall sca. Cae ey eee Cause __Description, Examples __ w Mostoeeneant VF Focal Functional B38 Proexstant 988 Antonie AVRT AT or AVNAT with bystander BT Buarre ORS pattems in repaired cangental heart dzete, crac maosition, ‘usual hypermopy patterns ‘hace I and I agents yperalemia SVT with aeraney Proexsitd SVT SVT with preexisting oraberation ORS abramalty SVT with anianhythme drugs eto abromaltes Nentrulr pacing AT, Ail techycaraia; AVN, stiovertricular nodal reentrant tachyearala, AURT, atroventricule reentant tachycardia, S88, bundle branch olock; BT, bypess tract, SVT, supraventicuar tachycardia, Vi, venveubr txenyeard Pacemaker or Implantable Cardioverter-Defibrillator Implantation A bistory of pacemaker or implantable cardioverter defibrillator (ICD) ‘implantation should rage the possiblity ofa device-nesocatedtachy- cardia, Ventricular pacing can be associated with a small and almost imperceptible stimulus artifact on the ECG, The presence of an ICD is ako of importance because sch device should identify and teat a sustained tachyarrhythmia, depending on device programming, and because the presence of an ICD implies that the patient is known to hhave an increased ris of ventricular tachyarchythmiae Medications Many different medications have prossthythmic effects. The most common drug-induced tachyarrhythmia ie torsades de pointes. Fre- quently implicated agents include antarthythmie drugs (suchas stall, Aofetilde, and quinidine) and certain antimicrobial drugs (such as erythromycin). Diuretics are a common cause of hypokalemia and bypomagnssemia, which can predispose to ventricular tachyarsbythmias, particularly torsades de pointes in patients taking antiaeshytiic drugs Purchermore, clas antiarthythmic drugs, especially class IC agents, can decrease conduction velocity at ster heart rates (use dependency) Asa rsul these deugs can cause aberration and widening of the QRS complex dering any tachyatrhyshmia, Digoxin can cause almost any cardiac arrhythmia, specially with increasing plasma digoxin concentrations above 2.0 nglm (2.6 mmol). Digoxin-induced arrhythmias age more frequent at any given plasma concentration i hypokalemia is also presen. The most common digoxin Induced arhythmias include monomorphic VT (often with relatively narrow QRS complex), bidirectional VI (a regular alternation of two wide QRS morphologies, cach with a diferent axis), and nonparexysmal junctional tachycardia Physical Examination “Most ofthe elements ofthe physical examination, including te blood pressure and heart ate, are of importance primarily in determining the presence and severity of hemodynamic instability and, thus, how ‘urgently a therapeutic intervention is required In patients with signifi cant hemodynamic compromise, a thorough diegnostic evaluation should be postponed until acute management has been addresed. In this setting, emergency cardioversion isthe teeatment of choice ang docs not require knowledge ofthe mechanism ofthe aerhythmi idence of underlying cardiovascular disease should be sought including the sequelae of peripheral vascular disease o stroke, A healed sternal incision is obvious evidence of previous cardiothoracic surgery ‘A pacemaker or defibrillator if present, can typically be palpated in the rrr CHAPTER 21 Wide Complex Tachycardias left or less commonly, right pectoral area below the clavicle, although some older devices are found in the anterior abdominal wall orsubassl- lary region, ‘An important objective of the physical examination in the stable patient iso atempt to document the presence of AV dissociation, The presence of AV dissociation strongly suggests VI. although it absence ts lest helpful. AV dissociation, when presen, i typically diagnosed on ECG; however, it can produce a numberof characteristic findings on physical examination, Iermittent cannon A waves may be observed fon examination ofthe jugular pulsation in the neck, and they reflect intermittent simultaneous atrial and ventricular contraction. Cannon [waves must be distinguished from the continuous and regular peomi- rent A waves seen during come SVIs, Such prominent waves result Som simoltaneous atrial and ventricular contraction occurring with every beat In addition, highly inconsistent fluctuations in the blood pressure can occur because of the variability in the degree of LA con- Uribution to LY illing, stoke volume, and cardiac output, Moreover, ‘variability in the occurrence and intensity of heart sounds (especially 5) can alzo be observed and is heard more frequently when the rate ofthe tachycardia is slower. ‘The response to cazotd sinus massage can suggest the ease ofthe WCE The heart rate during sinus tachycardia and automatic AY will gradually slow with carotid sinus massage and then accelerate on release. ‘The ventriclar rate during AT and AFL can transiently slow with carotid sinus massage because of slowing and block of atrioventricular node (AVN) conduction. The arrhythmia itself, however, is unaffected. Atrio- ‘ventricular nodal eentrant tachycardia (AVNRT) and AVRT wil either terminate or remain unaltered with carotid sinus massage. VIs are generally unaffected by carotid sinus maseage, although (hit maneuver ‘an potentially slow the stil rate and, in some cases, expose AV dis- sociation, Some Vs, such a idiopathic VI trom the RV outlow tract, can infrequently terminate in response to carotid sinus massage Laboratory Testing ‘The plasma potassium and magnesium concentrations should be mes- sured as pat of the bboratery evaluation. Hypokalemia and byporagne~ emia can predzpote to the development of ventricular tachyarshythmias; however, correction of abnormalities of electrolytes is never sufficient for therapy. Hypetkalemia can cause a wide QRS complex rhythm, csually with a slow rte, with loss ofa detectable P wave (the putative sinoventricular chythm:eFig. 21.1) or abnormalities of AVN eonduc- tion, In patients taking digoxin, quinidine, or procainamide, plasma concentrations ofthese Grugs should be meseured toast in evaluating possible drug toxicity Pharmacological Intervention ‘The administration of certain drugs can be useful for diagnostic, as ‘opposed to therapeutic, purposes. Termination of the arrhythmia with lidocaine suggests, but doesnot prov, that VT is the mechanism. Infe~ quently an SVT. especially AVRT, can terminate with lidocaine. On the other hand, cermination of the tachycardia with procainamide or amio darone docs not distinguish between VI and SVT. Termination ofthe arrhythmia with digoxin, verapamil, diiazem, or adenosine strongly implies SVT However, VI can also occasionally terminate after the sdministration ofthese drugs Unless the cause for the WCT is definitely established, however, ‘verapamil and diltiazem should not be administered because chey have been reported to cause severe hemodynamic deterioration in patients with VP and can even provoke VF and cardiac arest, Adenosine is suggested in the 2010 Adult Advanced Cardiac Life Support (ACLS) guidlines if a WCF is monomorphic, regular, and hemodynamically tolerated, because adenosine may help convert the rhythm to sinus and may help in the diagnosis. When doubt exist it i safest to assume any WCT is VI, particularly i patients with known cardiovascular disease” Direct current cardioversion in unstable patients and IV procainamide ‘or amiodarone in hemodynamically stable patients ate the appropriate management approach, ELECTROCARDIOGRAPHIC FEATURES: Ventricular Tachycardia Versus Aberranily Conducted ‘Supraventricular Tachycardia Because the diagnosis of WCT cannot always be made with complete ‘certainty the unknown rhythm should be presumed to be VT in the absence of contrary evidence. The conclasion is appropriate both because VT accounts for up to 80% of cases of WCT and because making this assumption guards against inappropriate and potentially dangerous therapy. Ae noted the IV administration of drugs used forthe testment ‘of SVT (verapamil diltiazem, or beta-blockers) can cause severe hemo- ‘dynamic deterioration in patients with VT and can even provoke VE and cardiac ares. Therefore these drugs should not be used when the diagnosis is uncertain. Tn general, most WCTs can be clasitied as having one of two pat- terns: right Bundle branch block (RBBB)=Hike pattern (QRS polarity is predominantly positive in leads V, and V;), or left bundle branch block (LBBB)=Ltke pattern (QRS polarity i predominantly negative in leads Vand V,). The determination that the WCT has an RBBB-like pattern ‘or an LBBB-likepatern does not by itself assist in making a diagnosis; however, this assessment should be made intially because it has futher ‘implications for evaluating several other features on the ECG, including the QRS axis, the QRS duration, and the QRS morphology (Box 21.15 Fig. 212). Rate ‘The rte of the WCT i of limited value in distinguishing VT feom SVT because there is wide overlap in the distribution of heat rates for SVT and VI. When the rate is around 150 beatsmin, AFL with 2:1 AV ‘conduction and aberrancy should be considered. Regul: Regulasty ofthe WCT is not helpful in distinguishing VT from SVT because in general, both are regular. However, VT is often associated swith slight iregulaity ofthe RR intervals, QRS morphology and ST-T waves, Although marked iregulaitysteongly suggests AF VTs can be particularly irregular within the ist 30 seconds of onset and in patients treated with antiarrhythonic drugs. Atrioventricular Dissociation AV dissociation is characterized by atrial activity (P waves) that is com- pletely independent of ventricular activity (QRS complexes). The stial ‘ate is usually slower than the ventricular rate (Fig. 21.3). A regular ER interval in the presence of AF would mast likely be AV dissociated. AY dissociation i the hallmark of VE (specificity is almost 100%). However, although the presence of AV dissociation establishes VI as the cause its absence (because of retrograde atrial capture) isnot as Ihlpfl (sensitivity i 20% to 50%), AV dissociation canbe present but not obvious on the surface ECG because of rapid ventricular rates. In addition, AV dissociation is absent ina large subset of VTs (especially those at a slower rate; in fact, approximately 309% of VTS have 1:1 retrograde VA conduction (see Pig. 21.2) and an additional 15% to 20% have second-degree (2:1 or Wenckebach) VA block (Fig. 21.4). Furthermore, AV dissociation can be observed during subatrial SV, such as junctional ectopic tachycardia and nodofascicular reentrant tachycardia, CHAPTER 21. Wide Complex Tachycardias Feary WAAAY ‘Fig, 21.41 Wide QRS Complex Rhythm Caused by Hyperkalemia, CHAPTER 21 Wide Complex Tachycardias BOX 21.1 Electrocardiographic Criteria Favoring Ventricular Tachycar AV Relationship * DissoitedP waves + Fusin bate + Capture beats + Arata 40 dopreos between NSR and WET ‘+ Right superior fortwest ais -80 degrees to 180 degrees) + Lott ans devaan with ABB marphaogy “fight ai deviation with LBB marphaley Precordial QRS Concordance + Positive conardonce + Negatve concordance (ORS Morphology * Contralateral 888 in WCT and NS “+ Absonco of RS gators inal rocral leads ‘+ RS interval >160 ms in prosodal leads with an 8S mrphoosy + Lead NA wave peak tie 250 ms + Criteria in lad av * Presence a an intial R wave + Presence of an ita rr wave with width >40 ms ‘+ Noten onthe descending i of @ negative onset ofa predominantly negative ORS complex + Wst (ORS Morphology in RBBB-Like WCT Pattern + Lead Wp + MonophaseR ishasi Bo RY complex + Broad inital Rave 240 msec) ‘+ Rabbit er son Double peaked A ave with the lt peak tal than the rit peak + Lead Ve + 18,05, OR or complex * R/Sralio-70 see ‘+ fh wave during WC! tale than the B wave during NSB ‘+ Sow descent tothe nai of ho $ (natcing inthe downstoko ofthe S navel + Lead Ve ‘+ Ary Q wave o 0S complex Satter AY, Raverviculer, 888, bundle breneh block, LBBB, le bundle bronch block, NSR, normal sinus ‘hythes, PBBE, right bundle breneh block WT, wide complex tachyearsin Several ECG findings are helpful in establishing the presence of AV.

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