Wide-Complex Tachycardia ======================== ώ Wide, Bizarre rhythm - ? Hyperkalemia - ? TCA or similar OD - ? Cocaine toxicity - ? Reperfusion arrhythmia - do NOT treat with lidocaine or amiodarone - causes asystole - treat empircally with calcium and bicarb (Amal Mattu, ACEP 2010) ώ Treatment of Ventricular Tachycardia Pulseless VT — defibrillate (unsynchronized) 200J, etc. Unstable VT with pulse — cardiovert (synchronized) 100J, etc. Stable VT — lidocaine was considered the treatment of choice Myth: Lidocaine is a very effective treatment for patients in stable VT. Reality: Lidocaine has a very poor success rate (~20-30%) for conversion of stable VT to NSR. Armengol, et al (Ann Emerg Med, 1989) — Conversion rates of lidocaine for stable VT • 17 consecutive patients with stable VT treated with up to three boluses of lidocaine • Overall success rate 5/17 (29%) Ho, et al (Lancet, 1994) — Sotalol vs. lidocaine for stable VT • 33 patients randomized (double blind) to receive either 100 mg sotalol or 100 mg lidocaine • 11/16 (69%) converted with sotalol • 3/17 (18%) converted with lidocaine • Crossover trials for initial failures • Sotalol successful in 18/30 (60%) patients overall • Lidocaine successful in 4/22 (18%) patients overall Gorgels, et al (Am J Cardiol, 1996) — Procainamide vs. lidocaine for stable VT • 29 patients randomized to receive either procainamide 10 mg/kg at 100mg/min vs. lidocaine 1.5 mg/kg over 2 minutes • Procainamide successful in 12/15 patients (80%) • Lidocaine successful in 3/14 patients (21%) • Crossover trials for initial failures • Procainamide successful in 20/26 patients (77%) • Lidocaine successful in 4/15 patients (27%) • Marill, et al (Acad Emerg Med, 1997) — Conversion rates of lidocaine for stable VT • Single bolus successful in 6/35 patients • Second bolus successful in 4/22 patients • Overall success rate 10/35 (29%) • Electrical cardioversion successful in 16/18 cases (average dose 89J) Procainamide — excellent success rates for all types of WCT • Ventricular tachycardia • SVT or atrial fibrillation with BBB • SVT or atrial fibrillation with WPW Procainamide drawbacks • Hypotension • Prolongation of QRS and/or QT intervals • Avoid in TdP and TCA overdose • Slower onset of action than lidocaine and amiodarone • Side effects are all reversible • Cardiovert unstable patients • Currently listed as DOC for stable monomorphic VT with normal EF (??) Ventricular tachycardia — other drugs • Bretylium • Significant incidence of vomiting, prolonged hypotension • Production discontinued, removed from ACLS algorithms • Magnesium • May be effective in refractory stable VT (Allen, Am J Cardiol, 1989) • Bolus and continuous infusion • Amiodarone • Had become the DOC for stable VT, but on further review… • Marill, et al (Ann Emerg Med, 2006) — Conversion rates of amiodarone for stable VT only 29% • Cummins, et al (Ann Emerg Med, 2006) — most prior studies only indicated success rate 40-60% • Tomlinson, et al (Emerg Med J, 2008) — Conversion rates of amiodarone for stable VT only 29% • Only 15% success rate within 20 minutes • ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and Prevention of Sudden Cardiac Death — Executive Summary, Circulation, Sept. 5, 2006 • “Intravenous amiodarone is not ideal for early conversion of stable monomorphic VT. Intravenous procainamide is more appropriate when early slowing of the VT rate and termination of monomorphic VT are desired.” • “IV amiodarone is reasonable for patients with sustained monomorphic VT that is hemodynamically unstable, refractory to conversion with countershock, or recurrent despite procainamide or other agents.” • May cause hypotension (less often than procainamide), bradycardia, prolongation of QT interval • Overall summary of amiodarone • Dangerous in the setting of prolonged QT, pregnancy (Class D ? may cause fetal hypothyroidism), rapid atrial fibrillation + WPW, AIVR and other “slow VT” conditions • Not as effective as we had believed for stable VT • Ineffective for VF (see below) (Amal Mattu, ACEP 2010) ώ AIVR and other slow wide complex rhythms - do NOT give lidocaine or amiodarone, as may cause asystole and death (Amal Mattu ACEP 2010) ώ V Tach mimics ώ Diagnosing V Tach: - AV dissociation pathognomonic - all QRSs in the same direction across the precordium ώ Avoid lidocaine? - "A case report and review in this month's Annals of Emergency Medicine suggests this may not be the thing to do. McLean SA, et al.: Lidocaine-Induced Conduction Disturbance in Patients With Systemic Hyperkalemia. Ann Emerg Med 2000; 36(6):615-8. And Carins CB, Paradis NA: Empiric Lidocaine: Deja Vu (All Over Again?). Ann Emerg Med 2000; 36(6):626-7. Nice review of the state of Lidocaine therapy. Also suggests a role for Amiodarone. ώ Don't give calcium blockers! - if ventricular, won't help and may cause vsodilitation and vascular collapse and death (per case reports) - if rapid and supraventricular, high likelihood of bypass tract (e.g., WPW) that would not be inhibited by the calcium blocker, and retrograde conduction will not be inhibited either. (Procainamide or lidocaine good alternatives) (But for narrow-complex fast WPW calcium blockers may be effective; see .) ώ "Pacemaker Tachycardia" - occurs with dual-chamber pacemakers - ventricular paced impulse retrogradely transmitted to atria - this is interpreted as atrial impulse - if another ventricular impulse not sensed in what should be a "normal" PR interval, ventricular pacer fires again. ώ Algorithm: SVT vs. VT [Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991; 83:1649-1659.] Sensitivity claimed 0.987, and specificity 0.965 (but note that often can't tell if AV dissociation or not). RS complex absent in all precordial leads? Yes --> VT No --> next question R to S interval >100 ms in one precordial lead? Yes --> VT No --> next question A-V dissociation? Yes --> VT No --> next question VT morphology present in both V1-2 and V6 (see below)? Yes --> VT No --> SVT with aberration. Morphology criteria: RBBB-like QRS: V1: QR or RS V6: R/S ratio <1 LBBB-like QRS: V1-2: Q in V1 R > 30 ms >60 ms to nadir S, notched S V6: QR or QS Monophasic R ώ Adenosine for WCT? Adenosine Myth: Adenosine can reliably distinguish between VT and SVT-AC. Reality: 1. Adenosine will not convert all patients with SVT-AC. 2. Adenosine will convert some patients with VT! Adenosine-sensitive VT • Well-documented in the adult cardiology (EP) literature • Often are young patients with no known underlying cardiac disease • Hina, et al (Jpn Heart J, 1996) • Terminated VT in 5 out of 10 adult patients • Documented in pediatric patients as well • Lenk, et al (Acta Paediatr Jpn, 1997) • Terminated VT in 5 out of 8 pediatric patients (Amal Matu, ACEP 2010) Mel Herbert gave an outstanding lecture on this topic at the Boston Olive View "Advances in Emergency Medicine" conference this year -- a highly recommended biannual conference with many great discussions. Two references in particular made me sit up long enough to stop eating the free food. On use of adenosine in WCT: "adenosine's propensity to accelerate accessory pathway conduction could result in ventricular fibrillation (1) in effected individuals. A recent report describing two such cases confirms this as a potential risk (2). Accordingly in cases where the R-R interval is clearly irregular adenosine should not be used. Unfortunately at very rapid rates atrial fibrillation may appear regular." Since atrial fibrillation is the presenting rhythm for ~30% of WPW-type PSVTs (3), and since WPW presenting as a-fib is often too rapid (rate >250) to detect irregularity (4), a potentially fatal mistake would be to assume this was garden variety AV nodal reentry PSVT and push adenosine in such cases. In cases where a very rapid a-fib (>200) leads one to suspect WPW, or the patient has known WPW and presents in a-fib at any pulse rate, Dr. Herbert recommends cardioversion. His handout is explicit: "AF in WPW = cardioversion." In other presentations of potential WPW, he recommends procainamide first, stating that "people with WPW can have life threatening arrhythmias whose management differs from that of the usual ACLS protocols." Indeed, the ACLS protocol for "WCT of uncertain type" begins with lidocaine (5), which as Dr. Louzon has mentioned has itself precipitated v-fib in WPW patients. Rosen's text concurs: "procainamide is the drug of choice in all antidromic or irregular WPW-related tachycardias.... both decreased and enhanced conduction through the accessory pathway have been reported after lidocaine administration. For these reasons, lidocaine is not recommended for antidromic or irregular accessory pathway syndromes. (4)" References: 1) Huagui GL, Morillo CA, Zarini M, et al. Effect of adenosine and adenosine triphosphate on antidromic tachycardia. JACC 1994;24:728-731. 2) Exner DV, Muzyka T, Gillis AM. Proarrhythmia in patients with the Wolf-Parkinson-White syndrome after standard doses of intravenous adenosine. Ann Intern Med 1995;122:351-352. 3) Ferrer MI. Preexcitation. Am J Med 1977;62:715. 4) Rosen. Emergency Medicine, 3d ed 1992;1240. 5) AHA. 1996 Handbook of Emergency Cardiac Care 1996;22. --James Li, MD --------------------------- You express the concern that at rapid rates (over 250) atrial fibrillation may appear regular and that it might be confused with PSVT. First of all why are you diagnosing PSVT when the rate is over 250 in an adult? PSVT does not occur at this rate and, by definition, this implies that one is dealing with atrial fib/flutter (or possibly VT if wide). Are you aware of the fact that any side effects of adenosine are likely to be short-lived (including reports of accelerated conduction) because of the extremely short half-life (10 seconds) of this drug? It is a common error to point out a case report of a bad outcome in the literature and immediately generalize to all such instances as if an exception should be used to set a precedent for routine management. A simple example will clarify this. You mention the well known instances where adenosine has caused acceleration of the rate of atrial fibrillation in the setting of WPW. Are you aware of the fact that adenosine has also been implicated in accelerating the rate of PSVT in patients without WPW (1)? Are you aware that adenosine has resulted in prologed episodes of bradyasystole and seizure in patients without WPW (2)? Are you now going to recommend that adenosine should not be used even in cases of unequivacol PSVT? AN EPS study published in Circulation looked at the effects of adenosine on 30 patients with accessory pathways (3). They concluded that the decrease in antegrade refractoriness that was observed was related to reflex sympathetic stimulation. The acceleration of the ventrilcular response was abolished by the use of propranolol. They conclude that "Adenosine may cause acceleration of prexcited atrial arrhythmias, but these effects are transient and should not discourage the use of adenosine as a diagnostic agent in braoad complex regular tachycardias of uncertain origin." Is that a sufficiently clear recommendation? IN a study of adenosine in a broad range of patients with wide complex tachycardia including patients with VT and WPW with atrial fibrillation the authors found not a sinngle instance of hemodynamic deterioration and concluded that adenosine (actually ATP) was safe and effectivce in this setting (4). IN a comprehensive review of wide complex tachycardias the authors conclude that 'adenosine might have a diagnostic role in some patients with wice complex tachycardia..Adenosine also has a half-life of only ten seconds and does not appear to cause hypotension during wide complex tachycardia" (5). The emergency medicine literature concurs (6). For anybody interested I can provide them with dozens of other references both within and outside the EM literature on this topic. H. Louzon MD (1) Orebaugh et. al. Intravenous Adenosine Therapy Accelerating Rate of Paroxysmal Supraventricular Tachycardia. Am J Emer Med 1992;10:326-330. (2) Webster et.al. Prolonged Bradyasystole and Seizures Following Intravenous Adenosine for Supraventricular Tachycardia. AM J Emer Med 1993;11(2):192-194 (3) Garratt et. al. Effects of Intravenous Adenosine on Antegrade Refractoriness of Accessaory Atrioventricular Conduction. Circulation 1991;84:1962-1968 (4) Sharma et. al. Intravenous Adenosine Triphosphate during Wide QRS Complex Tachycaerdia: Safety, Therapeutic Efficacy, and DFiagnostic Utility. (5) Sager et. al. Wide Complex Tacycradias Differential Diagnosis and MAnagement. CArdiology Clinics 1991;9(4):595-618 (6) Wrenn Management Startegies in Wide QRS Complex Tacycardia. Am J Emer Med 1991;9(6):592-597 --------------------- >First of all why are you diagnosing PSVT when the rate is over 250 in an >adult? PSVT does not occur at this rate and, by definition, this implies >that one is dealing with atrial fib/flutter (or possibly VT if wide). I agree. However, I have seen many physicians make this mistake and use adenosine or, worse yet, a calcium channel blocker, as a first choice med in this instance. In a-fib this rapid, the use of a CCB may be fatal if the patient is actually presenting with accessory pathway conduction (a-fib with WPW). Verapamil is the oft-cited culprit, but diltiazem, which is commonly used for rate control in a-fib with rapid v-response is also potentially a fatal choice. I have also seen physicians use adenosine followed by beta-blockers in extreme sinus tachycardia misdiagnosed as PSVT in patients with sepsis (fever, hypotension, pyuria, bandemia, the works). This seemed like an obvious mistake to everyone, but was justified by the comment "Let's just try these meds and see if they work. Perhaps the patient has both sepsis *and* PSVT." A poor choice, and one subsequently presented as an M&M case by one of our former chiefs. So my main point is to be careful in the management of very rapid tachyarrhythmias, which may not be as simple as pouring on the CCBs, adenosine, or even lidocaine. Assuming that adenosine is absolutely safe is an error. You may remember a previous discussion we had along the same lines where adenosine precipitated prolonged bronchospasm in certain patients, ultimately requiring management by mechanical ventilation in one elderly man with COPD. >Are you aware of the fact that any side effects of adenosine are likely to >be short-lived (including reports of accelerated conduction) because of >the extremely short half-life (10 seconds) of this drug? Having said this, I do believe that adenosine is a fairly safe medication, having used it often. However, I've seen both accelerated conduction, prolonged asystole lasting longer than 10 seconds, and one case of severe bronchospasm resulting from its use (not requiring intubation, thank goodness). Some authors, including Dr. Herbert, have cited literature justifying use of adenosine as a diagnostic maneuver in WCT of uncertain origin. One reference which I'll post later when I'm back at my desk actually demonstrates several conversions from VT to sinus using adenosine. Other authors, including Dr. Kathy Hebert (no relation to Herbert), a cardiologist here, prefer using procaine first in stable patients. ACLS says neither, recommending lidocaine first, which as you state may precipitate v-fib in WPW patients presenting in a-fib. >It is a common error to point out a case report of a bad outcome in the >literature and immediately generalize to all such instances as if an >exception should be used to set a precedent for routine management. My intention is to draw the group's attention to the possibility of bad outcomes using adenosine, which prior to this year I was unaware could be possible, having been taught by many that its use was absolutely safe in every circumstance. This is certainly not the case. It is worth mentioning here also, that most WPW presents in a non-classical fashion, that is, without delta waves or a-fib or a wide QRS, looking for all intents like AV nodal reentry PSVT. In these instances, according to Rosen's, adenosine as well as calcium channel blockers are safe to use. In the case of a patient with known WPW presenting in what appearedto be stable regular narrow complex PSVT (orthodromic accessory conduction), I think I would still use procaine before verapamil, though I'd not be afraid to use adenosine also, both after vagal maneuvers. One question which I have yet to have answered is whether vagal maneuvers are dangerous in the classical (antidromic conduction) or a-fib presentation of WPW, since these selectively block the AV node much like calcium channel blockers. James Li, MD Resident, emergency medicine Charity Hospital, New Orleans ------------------ On Fri, 29 Nov 1996, James Li, MD wrote: > It is worth mentioning here also, that most WPW presents in a > non-classical fashion, that is, without delta waves or a-fib or a wide QRS, > looking for all intents like AV nodal reentry PSVT. In these instances, > according to Rosen's, adenosine as well as calcium channel blockers are safe > to use. In the case of a patient with known WPW presenting in what appearedto > be stable regular narrow complex PSVT (orthodromic accessory conduction), I > think I would still use procaine before verapamil, though I'd not be afraid > to use adenosine also, both after vagal maneuvers. One question which I have > yet to have answered is whether vagal maneuvers are dangerous in the > classical (antidromic conduction) or a-fib presentation of WPW, since these > selectively block the AV node much like calcium channel blockers. The bottom line with WCT is that the most prudent course is to assume that you are dealing with VT. At least 80% of WCT is actually VT and this number may be consierably higher when patients with ischemic heart disease present in this manner. In one study of 150 cases of WCT, 122 had VT, 21 SVT with abberency and only 7 had accessory pathway conduction (1). Statistics like this may help to put this problem into perspective from the standpoint of treatment objectives. As far as WPW is concerned two distinct problems emerge. One are arrythmias in which the AV node is essential to sustain the tachycardia (i.e., PSVT whether of the antidromic or orthodromic variety) and the other are arrythmias in which the AV node is not needed to sustain the arrhythmia (i.e., atrial fib/flutter or SVT utilizing 2 accessory pathways). In the former case if the AV node is blocked the arrhythmia is terminated. Period. It is irrelevant what happens to accessory pathway conduction. In this regard all the ususal drugs used to block AVN conduction should work i.e., CCBs, beta-blockers and adenosine. The problem arises in the latter instnace when the AVN is not essential to sustain the arrythmia. In that situation preventing AVN conduction causes preferential conduction down the accessory pathway (and in many cases will actually shorten the refractory period of the pathway) causing dangerous ventricular rates which may (and have) degenerated into v fib. An example of the latter situation is the use of digoxin in WPW with atrial fib. This drug is known to directly enhance accessory pathway (AP) conduction and is thus contraindicated in that circumstance. CCBs actually have very little direct effect on AP conduction but may indirectly enhance it by causing vasodilation and resultant sympathetic stimulation (2). Precipitation of cardiac arrest in patients with a fib and WPW have been well described (3). Acceleration of the ventricular rate in the same setting with the use of diltiazem has also been observed (4). Beta-blockers have little direct effect on AP conduction but, by blocking AVN conduction may cause preferential conduction at accelerated rates down the AP (as the latter does not exhibit the decremental conduction properties of the AVN) (5). To answer your question about CSM it has been observed that it may, rarely, be detremental in WPW by precipitating atrial fibrillation with rapid ventricular response (6). Finally, the adenosine responsive VT that you alluded to, is a rare form of right ventricular outflow tract tachycardia that I have mentioned on several pervious occasions in a similar context (7). For, that matter, *verapamil* sensitive VTs have also been described in the literature. H. Louzon MD (1) Akhtar et. al. Wide QRS Complex Tachycardia Reapprsisal of a Common Clinical Problem. Ann Int Med 1988;109:905-912 (2) Akhtar M, Tchou P, Jazayeri M Use of calcium channel entry blockers in the treatment of cardiac arrhythmias. Circulation 1989 Dec;80(6 Suppl):IV31-9 (3) McGovern et. al. Precipitation of Cardiac Arrest by Verapamil in Patients with Wolff-Parkinson-White Syndrome. Ann Int Med 1986;104:791-794 (4) Shenasa et. al. Efficacy and Safety of Intravenous and Oral Diltilzem for Wolff-Parkinson-White Syndrome. Am J Card 1987;59:301-306 (5) Morady F, DiCarlo LA Jr, Baerman JM, De Buitleir M Effect of propranolol on ventricular rate during atrial fibrillation in the Wolff-Parkinson-White syndrome. Pacing Clin Electrophysiol 1987 May;10(3 Pt 1):492-6 Atrial fibrillation was induced during an electrophysiology study in 10 patients with the Wolff-Parkinson-White (WPW) syndrome, after determination of baseline properties of the accessory atrioventricular (AV) connection; intravenous propranolol (0.2 mg/kg) was then administered. Atrial fibrillation terminated during the drug infusion in three patients, allowing determination of propranolol's effects on conduction and refractoriness during sinus rhythm, before atrial fibrillation was reinduced. In these three patients propranolol had no effect on refractoriness or conduction properties of the accessory AV connection during sinus rhythm. The mean ventricular rate during atrial fibrillation was slowed by 15-56 beats/min in six patients, had no effect on the mean rate in three patients, and markedly increased the ventricular rate (203 to 267 beats/min) in one patient. In this patient, 54% of QRS complexes during atrial fibrillation were narrow, compared to 0-25% in the other patients. Propranolol reduced the percentage of QRS complexes that were narrow from 13 +/- 16% to 1 +/- 2% (mean +/- standard deviation, p less than 0.05). We conclude that propranolol may slow the ventricular rate during atrial fibrillation in some patients with the WPW syndrome, probably by blocking the effects of adrenergic activation. However, propranolol should not be used in patients with the WPW syndrome who have atrial fibrillation, if most QRS complexes during atrial fibrillation are preexcited. When a large percentage of QRS complexes are narrow, propranolol may increase the ventricular rate, probably by eliminating concealed retrograde conduction in the accessory AV connection. (6) Paoloni P, Cardinali L, Pezzuoli F, Capone P [Atrial fibrillation induced by massage of the carotid sinus in patients with orthodromic reciprocal supraventricular tachycardia and Wolff-Parkinson-White syndrome] Minerva Cardioangiol 1995 Jan-Feb;43(1-2):55-9 A 46 years old man with WPW syndrome, due to a posteroseptal accessory pathway, was admitted because of orthodromic reciprocating tachycardia, 210/m'in frequency. At the end of the carotid sinus massage, for accomplish the conversion of tachycardia to sinus rhythm, the orthodromic reciprocating supraventricular tachycardia degenerated into atrial fibrillation associated with high ventricular rate and the presence of hemodynamic instability, reverted to sinus rhythm by intravenous propafenone. Vagal stimulation, induced by carotid sinus massage, probably caused dispersion of atrial refractorines and intraatrial reentry, converting the orthodromic tachycardia into atrial fibrillation. The transesophageal electrophysiologic study, executed in treatment with propafenone, not documented the accessory connection and atrial fibrillation or reciprocating tachycardia were not inducible. (7) Wilber et. al. Adenosine-Sensitive Ventricular Tachycardia Clinical Characteristics and Response to Catheter Ablation. Circulation 1993;87:126-134 ---------------------------- Date sent: Mon, 2 Dec 1996 13:54:43 +1100 Send reply to: Michael Hession From: Michael Hession Subject: Re: WCT... To: Multiple recipients of list EMED-L As regards the pharmacological management of atrial fibrillation in WPW, there are arguments against the use of adenosine and for the use of sotalol. On Fri, 29 Nov 1996 12:37:14 -0500, James Li quoted Harvey Louzon ><< wide complex tach (WCT) of uncertain type.... Failing vagal maneuvers and >adenosine, lidocaine and procaine are recommended for WCT that are KNOWN to >be SVT. Why is that? Because this covers the possibility of antidromic SVT >through an accessory pathway (WPW). My preference in this case would actually >be the opposite (i.e., procaine followed by lidocaine) because procaine >reliably slows accessory pathway conduction and lidocaine does so usually but >not always. Also, there have been rare reports of the precipitation of v-fib >in patients with WPW given lidocaine.>> Doesn't this define the ideal drug in atrial fibrillation with WPW? That is, a drug that depresses conduction in the accessory pathway which is the sole conduction pathway in atrial fibrillation. Adenosine does not depress conduction in the accessory pathway(1). Like procainamide, sotalol depresses accessory pathway transmission. Sotalol has a depressant effect in all parts of re-entrant circuit, including atria, ventricle, AV node and accessory bypass tracts (2). Sotalol has also been shown to prevent the induction of atrial fibrillation in patients with WPW in whom Vaughan and Williams Class 1c drugs had failed.(3) Sotalol has had some favour here since its demonstration of superiority over lignocaine in sustained ventricular tachycardia.(4) Nonetheless, there are the contraindications to sotalol use due to its beta antagonist effects and the risk of Torsades with prolonged QT. On Fri, 29 Nov 1996 12:56:54 -0600, Harvey Louzon wrote, >AN EPS study published in Circulation looked at the effects of adenosine >on 30 patients with accessory pathways (3). They concluded that the >decrease in antegrade refractoriness that was observed was related to >reflex sympathetic stimulation. The acceleration of the ventrilcular >response was abolished by the use of propranolol. They conclude that >"Adenosine may cause acceleration of prexcited atrial arrhythmias, but >these effects are transient and should not discourage the use of adenosine >as a diagnostic agent in braoad complex regular tachycardias of uncertain >origin." > >Is that a sufficiently clear recommendation? Why is it that reflex sympathetic stimulation enhancement of accessory pathway conduction is not of significance in the discussion of adenosine(Fri, 29 Nov 1996 12:56:54 -0600 H.Louzon) but it is significant for calcium channel blockers(Sat, 30 Nov 1996 04:22:42 -0600 H.Louzon)? Nonetheless,sotalol has been shown to reverse the accelerating effects of isoproterenol in atrial fibrillation with WPW (5) And as a general observation, we shouldn't expect reflex sympathetic stimulation in our patients? On Fri, 29 Nov 1996 12:56:54 -0600, Harvey Louzon wrote, >IN a study of adenosine in a broad range of patients with wide complex >tachycardia including patients with VT and WPW with atrial fibrillation >the authors found not a sinngle instance of hemodynamic deterioration and >concluded that adenosine (actually ATP) was safe and effectivce in this >setting (4). Was this a misprint? "In the setting of electrophysiology testing, adenosine triphosphate is a safe agent, even when administered inappropriately during arrhythmias for which it is relatively ineffective, such as ventricular tachycardia, and Wolff-Parkinson-White syndrome with atrial fibrillation." (6) Should the use of adenosine be advocated at all in wide complex tachycardias to diagnose WPW? The general approach to wide complex tachycardias as VT is noted(Sat, 30 Nov 1996 04:22:42 -0600 H.Louzon) (1) Garratt et. al. Effects of Intravenous Adenosine on Antegrade Refractoriness of Accessaory Atrioventricular Conduction. Circulation 1991;84:1962-1968 (2)Hohnloser,S Sotalol NEJM Vol 331 No1 P31-38 (3)Inama,G Sotalol in the Wolff-Parkinson-White Syndrome: an electrophysiological and clinical study. G-Ital-Cardiol.1992 Jun; 22(6): 701-713 (4)Ho,DS;Zecchin,RP et al Double-blind trial of lignocaine versus sotalol for acute termination of spontaneous sustained ventricular tachycardia. Lancet 1994;344(8914)(Nove 5,1994): 1300 (5)Madrid,AH Atrial fibrillation in Wolff-Parkinson-White syndrome: reversal of isoproterenol effects by sotalol. Pacing-Clin-Electrophysiol. 1992 Nov; 15(11 Pt 2):2111-5 (6)Sharma et. al. Intravenous Adenosine Triphosphate during Wide QRS Complex Tachycaerdia: Safety, Therapeutic Efficacy, and DFiagnostic Utility. Michael Hession M.B.,B.S.,MBIOMEDE Emergency Registrar Westmead Hospital, Sydney, Australia -------------------------------------- On Mon, 2 Dec 1996, Michael Hession wrote: > On Fri, 29 Nov 1996 12:37:14 -0500, James Li quoted Harvey Louzon > ><< wide complex tach (WCT) of uncertain type.... Failing vagal maneuvers and > >adenosine, lidocaine and procaine are recommended for WCT that are KNOWN to > >be SVT. Why is that? Because this covers the possibility of antidromic SVT > >through an accessory pathway (WPW). My preference in this case would actually > >be the opposite (i.e., procaine followed by lidocaine) because procaine > >reliably slows accessory pathway conduction and lidocaine does so usually but > >not always. Also, there have been rare reports of the precipitation of v-fib > >in patients with WPW given lidocaine.>> > > Doesn't this define the ideal drug in atrial fibrillation with WPW? That > is, a drug that depresses conduction in the accessory pathway which is the > sole conduction pathway in atrial fibrillation. > Adenosine does not depress conduction in the accessory pathway(1). > Either I'm extremely confused or you are extremely confused. Where in the world did you read into the recommendation that adenosine may, in general, be safely used in WCT for the purpose of converting atrial fib with WPW? That is not the purpose of a trial of adenosine in this situation. It is to attempt conversion of WCT that represents SVT with abberant conduction in someone without an accesaory pathway. The only point of mentioning adnosine in the context of WPW is to point out that it may convert antidromic SVT and that, although it may accelerate conduction down the AP, and thus the ventricular response, it is usually well tolerated. > > Why is it that reflex sympathetic stimulation enhancement of accessory > pathway conduction is not of significance in the discussion of > adenosine(Fri, 29 Nov 1996 12:56:54 -0600 H.Louzon) but it is significant > for calcium channel blockers(Sat, 30 Nov 1996 04:22:42 -0600 H.Louzon)? > Very simple. The half life of adenosine is considerably shorter than of any CCB. Any acceleration of ventricular rate is short-lived with the former which gives it a considerable margin of safety. The second answer are the studies that I quoted on the use of adenosine and diltiazem in WPW with atrial fib. IV diltiazem caused not only accelerated conduction but also hemodynamic deterioration in one patient (Shenasa1987). By comparison adenosine did not result in hemodynamic deterioration in the same population (Garrett1991, Sharma1990). The third answer lies in clinical experience. Many reports of verapamil resulting in v fib in the setting of WPW with a fib have been described (McGovern1986). Reports of similar events after the use of adenosine are rare. > > Was this a misprint? > "In the setting of electrophysiology testing, adenosine triphosphate is a > safe agent, even when administered inappropriately during arrhythmias for > which it is relatively ineffective, such as ventricular tachycardia, and > Wolff-Parkinson-White syndrome with atrial fibrillation." (6) > > Should the use of adenosine be advocated at all in wide complex > tachycardias to diagnose WPW? The general approach to wide complex > tachycardias as VT is noted(Sat, 30 Nov 1996 04:22:42 -0600 H.Louzon) > Once again the purpose of adenosine is not to diagnose WPW in this setting but to exclude the possiblity of aberrant conduction and secondarily to treat the rare case of WPW with antidromic conduction. In a previous citation (Akhatar1988) I indicated the relative likelihood of finding the various causes of WCT in an unselected population. Out of 150 cases of WCT, 122 had VT, 21 had SVT with abberant conduction and only 7 had accessary pathway conduction. This is critical information. The overwhelming etiology of WCT that an EM physician is likely to see is going to represent VT and should be treated as such. I would recommend the use of procainamide followed by lidocaine if WPW is likely (say a young person with a suspiciously rapid tachycardia) or the resverse if it is not (say an elderly man with known CAD). In selected cases the use of adenosine prior to these drugs appears to be generally safe and is an option. The literature has indicated that this is so. The comments on the use of sotalol are duly noted. I doubt that there is much experience with this drug in the ED setting in the USA at the present time, however. A person reading the recent threads on WCT and WPW might be mislead into thinking that these are everyday occurences in the ED. That patients with WPW and WCT are arriving in your local EDs in overwhelming numbers by boat, plane, air ambulance and private conveyance. Nothing could be further from the truth. I already cited the statistics on how likely (not very likely) that a WCT represents something other than VT. But more to the point, how many cases of previously *undiagnosed* WPW are you likely to see in your career in the ED. After all, the patient with WCT who tells you that he has WPW immediately alerts you to the possibiltity that the WCT you are seeing might be antidromic SVT or atrial fib. Well, personally, I can count on exactly 2 fingers the number of previously undiagnosed cases of WPW that I have seen in a decade and a half of ED work (and two other cases that were missed by the treating physician). I will hazard an estimate of how often this happens. My guess is that, unless you work in an arrhythmia referral center, you will be so thunderstruck by the novelty of seeing WPW with atrial fib that this will immediately generate a case report. Thus the yearly number of cases of WPW with WCT is equal to the number of case reports in the EM literature. Considering the low standards that many our journals have with regards to publishing original research it is quite unlikely that any of these reports would be rejected. This seems like an eminently safe assumption. H. Louzon MD ---------------------- On Tue, 3 Dec 1996, Garry Wilkes wrote: > >Where in the world did you read into the recommendation that adenosine > >may, in general, be safely used in WCT for the purpose of converting > >atrial fib with WPW? That is not the purpose of a trial of adenosine in > >this situation...... > > There seems to be some confusion here that adenosine is of use routinely for > AF. Adenosine is only of real value with REGULAR tachycardias. Trying it for > AF will be fairly harmless but also of no actual value therapeutically. >In the setting of WPW tachyarrhythmias there are two possibilities: AF or >SVT. In a regular rhythm ie SVT even in the presence of WPW, the usual drugs >are safe and have been used to effect. It is only in the setting of AF with >WPW that the real danger arises. I didn't want to to bring this up before out of fear of confounding the issue but although it true that the usual AVN blocking drugs are effective (and usually safe) in WPW with SVT there have been case reports of SVT degenerating into atrial fibrillation under these cirucumstances with acceleration of ventricular response. This has been well documented in the cases of digoxin and verapamil and now with adenosine as well (1). Sometimes the conversion to atrial fib occurs spontaneously, sometimes in proximity to administration of drugs for conversion of SVT. The only point here is that even in cases of regular narrow complex tachycardia one is not completely safe in administering drugs that block the AVN should WPW be present. Certainly in someome with known WPW who has a *history* of atrial fibrillation it might be prudent to avoid CCBs, beta-blockers, dig and to a lesser extent adenosine in the setting of PSVT. To place this in perspective, however, the majority of patients with WPW do not have atrial fibrillation. The breakdown is approximately 80% SVT, 15% atrial fib and 5% atrial flutter. Let me further point out that atrial fibrillation in the setting of WPW is usually described as a "grossly irregular" rhythym and is not often confused with SVT. It may, of course, be confused with VT but nobody in their right mind would elect to use CCBs or adenosine if the DDx has been reduced to VT versus WPW with atrial fib. I think that it is safe to say, as a general rule, that any ventricular rate above 200 in an adult should make one suspicious for the presence of an underlying accessory pathway and one should act accordingly. If one elects to use AVN blocking drugs anyway, just be prepared to cardiovert (or defibrillate) the patient as one should in any case. In cases of WCT it should be noted that procainamide is the only commonly used drug in the US that is both safe AND effective for converting all known causes of the underlying arrhythmia be it VT, SVT with abberancy, or antidromic SVT in the setting of WPW. H. Louzon MD (1) Tebbenjohanns J, Pfeiffer D, Schumacher B, Jung W, Manz M, Luderitz B Intravenous adenosine during atrioventricular reentrant tachycardia: induction of atrial fibrillation with rapid conduction over an accessory pathway. Pacing Clin Electrophysiol 1995 Apr;18(4 Pt 1):743-6 Adenosine is considered to be a safe agent for termination of orthodromic atrioventricular reentrant tachycardia in patients with accessory pathways. A case with initially successful accessory pathway ablation and without preexcitation during sinus rhythm is presented, in which intravenous adenosine (6 mg) during orthodromic tachycardia was followed by atrial fibrillation and sudden onset of preexcitation with subsequent rapid ventricular response with moderate hemodynamic compromise. --------------------