{"id":5099,"date":"2011-07-14T20:23:25","date_gmt":"2011-07-14T20:23:25","guid":{"rendered":"http:\/\/crashtext.org\/misc\/dysrhythmias.htm\/"},"modified":"2018-11-29T20:14:54","modified_gmt":"2018-11-30T01:14:54","slug":"dysrhythmias","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/medical-surgical\/dysrhythmias.htm\/","title":{"rendered":"Dysrhythmias"},"content":{"rendered":"
from Steve Smith<\/p>\n
Narrow except Antidromic, Wide with aberrancy<\/p>\n
<\/a> Tall R in V1=WPW, Dextrocardia, RVH, RBBB, Posterior Wall MI, PE RVH-right axis deviation and right atrial enlargement RBBB-AVR has an R wave \u00a0 Three methods for dysrhythmias:<\/p>\n Pacs-no pause, PVCs-pause MAT>2 foci \u00a0 if nodal pacemaker, PRI will be 0.12 sec or greater<\/p>\n Lewis Lead: Place your monitor selector switch on Lead I and move your right arm electrode to the manubrium. Next, place your left arm electrode on the 5th intercostal space right parasternal line. The left leg electrode is placed over the right rib margin. The negative electrode goes on top of the manubrium and the positive electrode goes over the 5th intercostal space parasternal line. \u00a0 <\/a><\/p>\n <\/a><\/p>\n Found by Resus.me Emerg Med Australas.<\/a> 2009 Dec;21(6):449-54. The 10 mL syringe is useful in generating the recommended standard of 40 mmHg intrathoracic pressure for the Valsalva manoeuvre.<\/strong> make them blow until the plunger moves for 10 seconds \u00a0 the modifiedValsalva manoeuvre, that is, while lying supine on thebed in a Trendelenberg position, they forcefully expireinto a section of suction tubing and pressure gauge for atleast 15 s and at a pressure of at least 40 mm Hg. (Emerg Med J 2010 27: 287-291)<\/p>\n Vaughan-Williams Classification I. Sodium Channel Blockers a. Prolong repolarization leading to long QRS\/QT (Disopyramide, Quinidine, Procainamide) b. Shorten Action Potential Normal QRS\/QT (Lidocaine, Phenytoin, Tocainide, Mexiletine) c. Most effect on QRS prolongation (Flecainide, Propafenone, Encainide, Cocaine) II. Beta Blockers III. Block Potassium Channels, but most have effects of the other 3 categories as well (Amiodarone, Bretylium, Ibutilide, Sotalol) IV. Calcium Channel Blockers<\/p>\n hypotension (50 mg\/min up to 30 mg\/kg) until ARS>50%, hypotension<\/p>\n Thyroid, Pulmonary Fibrosis Prolonged QT 150 mg over 10 min then 1 mg\/min for 6 hours then 0.5 mg\/min for 18 hours then keep on this rate or switch to oral. May give additional boluses of 150 mg, maintenance infusion rate may also be raised. Half life is ~53 days. PO Conversion: Atrial Arrhythmias<\/strong> Ventricular Arrhythmias<\/strong> Infusion < 1 week<\/strong> Infusion 1-3 Weeks<\/strong> Infusion < 1 week<\/strong> Infusion 1-3 weeks<\/strong>400 mg TID x 5 days then 200 mg QD 400 mg BID x 5 days then 200 mg QD 400 mg TID x 5 days then 400 mg QD 400 mg BID x 5 days then 400 mg QD decrease dose in hepatic failure 2.2 g IV max per 24 hours. \u00a0 \u00a0 Amio sides effects when given long term therapy only: pneumonitis\/fibrosis, liver enzyme rise, bluish skin discoloration, hypo or hyperthyroidism, increases coumadin effects<\/p>\n Metoprolol 50 mg po bid = 10 mg IV q6hr<\/p>\n Dose should be reduced through central lines (JEM 22:2, 195) If the patient has more than 4 seconds of asystole, have them cough . Use a smaller initial dose in patients taking Disopyramide (Norpace, rythmodan) or dipyridamole (aggrenox and persantine) as profound, prolonged bradycardia can result. \u00a0 Adenosine is safe and effective in pregnancy.23 Adenosine, however, does have several important drug interactions. Larger doses may be required for patients with a significant blood level of theophylline, caffeine, or theobromine. The initial dose should be reduced to 3 mg in patients taking dipyridamole or carbamazepine,<\/p>\n Atrial Tachycardias are A\/V node independent. Localization can be guessed at by Left Atrial focus if positive p in V1 (sens 93%, spec 88%) or Right Atrial focus if positive p in aVL (sens 88%, spec 79%) (J Am Coll Cardio 1995; 26:1315-24) \u00a0 The effect of adenosine is potentiated in the face of: Tegretol and Dipyridamole and especially in patients with heart transplants! In these patients start at a lower dose (eg 1mg and double with each dose). In patients taking methylxanthines adenosine may not be effective and verapamil is the preferred agent. \u00a0 <\/a><\/p>\n <\/p>\n At least 3 different p wave morphologies seen mostly in the setting of cardiopulmonary disease, e.g. COPD or CHF Possible to see this rhythm with PE as well. (Chest 113:1, p. 203; 1998) no medications or defib are effective<\/p>\n from life in the fast lane<\/p>\n Atrioventricular Nodal Reentrant Tachycardia is a type of supraventricular tachycardia (ie it originates above the level of the Bundle of His) and is the commonest cause of palpitations in patients with hearts exhibiting no structurally abnormality.<\/p>\n The \u0091descriptive\u0092 terminology regarding AVNRT classification can be confusing\u0085and I am still confused! Slow-Fast AVNRT (Common AVNRT)<\/strong><\/p>\n <\/a> AVNRT Slow-Fast<\/p>\n Fast-Slow AVNRT (Uncommon AVNRT)<\/strong><\/p>\n <\/a> Slow-Slow AVNRT (AtypicalAVNRT)<\/strong><\/p>\n <\/a> Schematic of typical atrioventricular nodal reentry.<\/p>\n Investigations<\/strong>The ECG will typically show a tachycardia of 140-280 bpm with normal and regular QRS complexes. There will be either<\/p>\n For recurrent episodes of palpitations, a Holter monitor and EPS may be useful in identifying rhythms typical of AVNRT. An echocardiogram may be useful in evaluating for structural heart disease and electrophysiological studies may be necessary if considering ablative therapy. Blood tests that may be appropriate in patients experiencing palpitations include cardiac markers (to investigate for myocardial infarction), urea and electrolytes (to identify imbalances in potassium, magnesium or calcium) or thyroid function tests (hyperthyroidism may trigger AVNRT or other arrhythmias). Management<\/strong>Patients may be instructed to undertake vagal manoeuvres upon the onset of symptoms which can be effective in stopping the AVNRT. This may involve carotid sinus massage or valsalva manoeuvres, which will both stimulate the vagus nerve. Alternative strategies include:<\/p>\n <\/p>\n (From Dr. Smith Ekg Blog) Here is the same ECG with some arrows: <\/a> The QTc is 387 ms, very short for ischemia. There are also prominent U-waves (arrows). Any patient in atrial fibrillation might be on Digoxin. Etiologies of ST depression with a normal QRS (“primary” ST depression, in contrast to “secondary” ST depression that is due to abnormal QRS such as in LVH, LBBB, RBBB, WPW, hyperkalemia, Brugada, RVH, or paced rhythm) include hypokalemia, digoxin, and ischemia, as well as baseline ST depression of unknown etiology. Digoxin results in ST depression with a short QT and often with prominent U-waves such as in this case. Hypokalemia results in a long<\/strong> QT with prominent U-waves. Ischemia results in ST depression with a relatively long QT, and is likely to be accompanied by ischemic symptoms. Syncope is not an ischemic symptom; it is a relatively rare sole manifestation of ischemia. It is important to keep in mind that ST depression due to digoxin happens at therapeutic concentrations, and is not a sign of Dig toxicity.<\/p>\n Hypokalemia\/magnesemia. Genetic, cva, surgery. Overdrive and magnesium Irregular atrial rhythm>250 bpm, think WPW \u00a0 list of drugs that can cause TdP http:\/\/www.torsades.org\/medical-pros\/drug-lists\/drug-lists.htm<\/p>\n This case emphasizes certain important aspects of tachyarrhythmia recognition. Single-lead monitoring is insufficient to make an accurate diagnosis of the presenting arrhythmia as QRS duration may vary from lead to lead. There may not be significant QRS prolongation on the surface ECG even if the tachycardia is ventricular in origin. As demonstrated in this case, the QRS duration in lead III is 80 milliseconds compared with 150 milliseconds in lead I (Fig. 2<\/a>). In children, during tachycardia, there may not be a dissociation between the QRS complex and the P waves on the surface ECG, making it difficult to distinguish SVT from VT. The failure of adenosine to have any effect on the atrial or ventricular rate of the tachycardia should alert the physician to the possibility of an arrhythmia of ventricular origin. Wide or narrow complex tachycardia of right bundle branch block morphology with left axis deviation is almost always consistent with fascicular VT. 5<\/a>, 6<\/a> Although our patient has not undergone an electrophysiologic study with intracardiac mapping to confirm the origin of the tachycardia, the aforementioned factors are consistent with the diagnosis of fascicular VT. Verapamil is often used to acutely terminate SVT. Its blocking action is predominantly at the atrioventricular node and therefore ECG recording of tachycardia termination would show interruption after an inscribed P wave. In this case, tachycardia terminated with IV verapamil and the interruption of the arrhythmia was after an inscribed QRS complex (Fig. 3<\/a>). This again points to the ventricular origin of the tachycardia. 7-9<\/a> The unique pharmacological response of fascicular VT to calcium channel blockers rather than conventional sodium channel blockers, such as lidocaine, is hypothesized to be due to a slow calcium channel-dependent mechanism operating at the level of left intraventricular conduction system. 5<\/a> Rarely, this type of VT may respond to adenosine. 10<\/a> <\/a><\/a><\/p>\n best review (JACC 2008;51(12):1176) \u00a0 Move V1 from 3rd to 2nd ICS to bring out type 1 pattern large meals will bring out ekg changes can bring out pattern with flecainide or procainamide \u00a0 can treat with quinidine po or isuprel iv while awaiting defib placement \u00a0 The Brugada Syndrome is a malignant primary electrical disease of the heart resulting in abnormal electrophysiologic activity in the right ventricle and characterized by:<\/p>\n First described as a distinct entity in 1992, there is a predilection for southeast Asian and Japanese males, but it is possible in females and African Americans (Am J Emerg Med 21(2):146, March 2003) \u00a0 The disease is genetically determined with an autosomal dominant pattern of transmission. \u00a0 The mean age of affected individuals is in the mid to late 30s. All clinical manifestations of the Brugada Syndrome are attributed exclusively to the life-threatening ventricular tachyarrhythmias. Sudden death is the first and only clinical event in some patients. In sudden death survivors, arrhythmias are recurrent with life-threatening episodes in as many as 40 percent of cases over a 2- to 3-year follow-up. The prevalence of VF associated with the Brugada Syndrome has been estimated to be as high as 40 to 60 percent of all cases of idiopathic VF. \u00a0 There are no specific pharmacologic treatments for the prevention of sudden death in these patients. Diagnosis and prevention of life-threatening ventricular tachyarrhythmias is the main objective of therapy. Implantation of an ICD is the only effective intervention for preventing sudden death. Of special interest are individuals displaying the ECG features of the Brugada Syndrome but without arrhythmic complications, whose prognosis is also poor without treatment. Their potential risk of sudden death should be evaluated during electrophysiologic study; inducibility of VT\/VF should be considered an indication for an ICD. \u00a0 <\/a><\/a><\/a><\/a><\/a>BS can be suspected from a standard EKG, but if one shifts the right precordial leads to the second and third intercostal space, type 1 Brugada EKG findings may be unmasked. The rather unusual syndrome of arrhythmogenic right ventricular cardiomyopathy (a new diagnosis for me) displays a characteristic BS pattern, and produces similar morbidity and mortality. The vast majority of patients with BS, however, possess a structurally normal heart, suggesting that BS is primarily an electrical malfunction. \u00a0 Brugada syndrome is an autosomally dominant genetic disease whereby the cardiac sodium channel (SCN5A) responsible for cardiac depolarization is mutated (4, 5). With each heartbeat, the heart must repolarize or electrically reset. This cardiac repolarization occurs due to the regular opening and closing of various ion channels in the heart, particularly of cardiac potassium channels (IKr and IKs or rapid and slow delayed-rectifier potassium channels). The cardiac sodium channel opens and closes rapidly at the onset of the action potentials. In Brugada syndrome, there is a \u0093loss of function,\u0094 meaning that the channel is perpetually closed. Interestingly, long QT syndrome type 3, a completely different disease, occurs when the sodium channel experiences a \u0093gain of function\u0094 or is perpetually open. Brugada syndrome was first described in 1992 (6). It is believed to be far more common in Asia, particularly in Japan and southeast Asia. Brugada syndrome is classically diagnosed by characteristic ECG findings. Three ECG repolarization patterns in the right precordial leads have been described. Type 1, the most common subtype, is characterized by coved STsegment elevation 2 mm, especially in leads V1\u0096V3 (6). The ECG findings can also be unmasked in affected patients by pharmacologic challenge with a drug that blocks the sodium channel such as flecainide, ajmaline, or procainamide (7). Genetic testing for Brugada syndrome is largely a research tool, since only 20% of genepositive patients will have their mutation identified with the current technology. Brugada syndrome is an autosomal dominant disease, meaning that the child of an affected patient has a 50% chance of inheriting the mutation. For unclear reasons, most symptomatic patients are middle- aged males; females with Brugada syndrome face less than a 20% risk of developing symptoms. Symptoms include syncope, cardiac arrest, or sudden death. Such events may occur during sleep or at any time, although there are reports of episodes occurring during times of a fever (8). Treatment options for symptomatic patients with Brugada syndrome are limited. The Second Consensus Conference on Brugada syndrome recommended that such patients receive an implantable cardioverter- defibrillator (9). Drug therapy in symptomatic patients has been tried with sotalol and quinidine, although no data are available on large numbers of affected patients (10, 11). Therapy for asymptomatic patients, as in the current report, is unclear. Most groups advocate defibrillator placement in those asymptomatic patients with Brugada syndrome who are at high-risk for cardiac events, namely those with a history of syncope. Patients with an ECG consistent with Brugada syndrome at baseline are likely at higher risk for an untoward clinical event than those whose ECG findings are only provoked by drug therapy or occur intermittently. There is controversy in the literature regarding the usefulness of electrophysiology study in risk stratification for Brugada syndrome. The large international registry spearheaded by the Brugada brothers has advocated electrophysiology testing, with consideration of implantable cardioverter-defibrillator placement in those patients who are inducible for (Crit Care Med 2005 Vol. 33, No. 7) — Up to 3 ECG variants of Brugada syndrome have been described, but the main one, type 1, is associated with ST segment elevation in right precordial leads. It usually is a J point elevation with a downsloping ST segment, and the ST elevation usually tapers off going toward leads V4 to V6. Additional features that can help to differentiate it from other causes of ST elevation are: associated T wave inversion, absence of reciprocal ST depression, pseudo RBBB pattern, and normal QTc. Type 2 has a saddleback appearance with a high take-off ST-segment elevation of \u2265 2 mm followed by a trough displaying \u2265 1 mm ST elevation followed by either a positive or a biphasic T-wave. Type 3 has either a saddleback or a coved appearance with an ST-segment elevation of < 1 mm and a positive T wave. The type 2 and type 3 Brugada patterns are not specific enough to be considered diagnostic.[3] The Brugada pattern is a dynamic ECG finding and it may not always appear on 12-lead ECG. Because the disorder is a sodium channelopathy, it usually is reproduced by sodium channel blockers. A procainamide challenge test is used to establish the diagnosis[5]; however this test is not required if the type 1 Brugada pattern exists on the 12-lead ECG. \u00a0 \u00a0 — arrhythmia consultation to get the EP service fever brings out brugada cocaine can induce as well, so can tcas some have family history of sudden cardiac death \u00a0 Worrisome Thoughts About the Diagnosis and Treatment of Patients With Brugada Waves and the Brugada Syndrome (Circulation<\/em>. 2004;109:1463-1467.) <\/strong> Criteria for Diagnosis There are 3 types of Brugada waves.5 Type I was described in 1991 by the Brugadas. The ST-segment elevation in leads V1 through V3 is triangular; there may or may not be right ventricular conduction system block or right ventricular conduction system delay; and the T waves may be inverted in leads V1 through V3. There are 2 types of saddleback ST-segment abnormalites.5 In type 2, the downward displacement of the ST segment lies between 2 elevations of the segment in leads V1 through V3 but does not reach the baseline, whereas in type 3, the middle part of the ST segment touches the baseline.5 The T waves in types 2 and 3 may not be inverted, and there may or may not be right ventricular conduction system block or delay. When the ECG abnormalities are precipitated by or unmasked by drugs such as flecainide, procainamide, ajmaline, disopyramide, propafenone, or pilsicainide, elevated body temperature, vagotonia, -adrenergic blockers, -adrenergic agonists, dimenhydrinate, cocaine, and tricyclic antidepressants (see Figure 4),6 the ST-segment abnormalities are referred to as secondary Brugada waves. Such patients are commonly middle-aged or elderly adults. Arrhythmogenic right ventricular dysplasia\/cardiomyopathy (ARVD\/C) should be considered a possible cause of Brugada waves in some patients. It is now known that Brugada waves are linked to mutations in the SCN5A gene and that ARVD\/C is linked to several chromosomes and 3 putative genes.4,5 The ECG abnormalities that suggest the diagnosis of ARVD\/C are epsilon waves (or Fontain waves) in leads V1 through V3.7 Corrado et al8 described a subset of patients with ARVD\/C who had the Brugada syndrome. Therefore, it is necessary to consider the possibility of ARVD\/C in patients with the Brugada syndrome or Brugada waves. Knowing this, can a clinician state with certainty that there is no structural heart disease in every patient with Brugada waves? The Brugadas reported that 8% of asymptomatic patients with Brugada waves had subsequent cardiac events.10 This figure may need to be altered as more cases are observed. Assuming that 8% is correct, does the information justify the use of an internal cardiac defibrillator? The answer to this question would vary from physician to physician. Accordingly, a definite answer to this question must be found. Only Type I pattern or patients with syncope or aborted sudden cardiac death probably need admission, the others probably can get f\/u (Fingers trial (Circulation. 2010;121:635-643.)<\/p>\n <\/a><\/p>\n Explanation<\/b> from steve smith blog<\/p>\n Aminophylline can be used as a bridge to pacing. 100 mg\/min to a max of 0.5 mg\/kg. (Annals Int Med<\/em> 1995; 7: 509, Emer Med Clin NA <\/em>2001; 19, Eur Heart J<\/em> 1995; 16:862-865)<\/p>\n It is safe to use adenosine as a dx measure (CCM 2009;37(9):2512)<\/p>\n The presence of any one of the four criteria was considered diagnostic of VT. The absence of all four might suggest SVT c AC. (Circ 1991, 83:5, 1649) Akhtar Criteria Criteria Suggestive of V. Tach<\/p>\n (Ann Int Med 1988, Dec 1;109:11)<\/p>\n Right Bundle QRS: <\/strong>rSR in V1 and RS in V6 with R\/S>1 Left Bundle QRS <\/strong>rS or QS in V1 and V2 and delay to S wave nadir < 70 msec, R wave and no Q wave in V6 Absence of one of these criteria=V. Tach (Lancet, 1994, 343:8894, p. 386) \u00a0 There is Adenosine Sensitive V-Tach, so conversion is not indicative of SVT-AC (Effects of adenosine triphosphate on wide QRS tachycardia. Analysis in 18 patients. Jpn Heart J 1996;37:463-70, Role of adenosine in the diagnosis and treatment of tachyarrhythmias in pediatric patients. Acta Paediatr Jpn 1997;39:570-7, Ventricular arrhythmias in normal hearts. Cardiology Clinics 2000;18:265-291.) \u00a0 Lidocaine converts V-Tach only 20-30% of the time (Magnesium sulfate therapy for sustained monomorphic ventricular tachycardia. Am J Cardiol 1989;64:1202-4, Lack of effectiveness of lidocaine for sustained, wide QRS complex tachycardia. Ann Emerg Med 1989;18:254-7, Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Am J Cardiol 1996;78:43-6, Double-blind trial of lidocaine versus sotalol for acute termination of spontaneous sustained ventricular tachycardia. Lancet 1994;344:18-23, Analysis of the treatment of spontaneous sustained stable ventricular tachycardia. Acad Emerg Med 1997;4:1122-8) So use amiodarone, procainamide, or sotalol.<\/p>\n Rate-dependent BBB is an uncommon condition in the differential diagnosis of WCT. A patient with this conduction abnormality has a normal QRS complex until a certain critical heart rate, most often a tachyarrhythmia, is reached.[2 and 3] The electrophysiology of this condition is complex and not fully understood, but is related to an increase in the refractoriness of the affected bundle. [2, 3, 4 and 5] Most patients have underlying coronary artery disease [2, 3, 6 and 7] and eventually develop permanent BBB. [3 and 7] Like in this case, the transition from normal to wide QRS is usually abrupt, [3 and 7] and there is a prevalence for left BBB. [6] The transition can occur at relatively slow rates, as low as 80 beats\/min. [6 and 7] Vagal maneuvers can slow the heart and correct the BBB. [4 and 7] Procainamide has been shown to worsen the conduction abnormality and should be avoided. [4 and 5]<\/p>\n In order to be V-tach, rate must be greater than 120-130<\/strong> if it is not, probably a mimic. Ia anti-dysrhytmic toxicity, hyperkalemia, accelerated idioventricular rhythms, reperfusion dysrhythmia \u00a0 Ventricular tachycardia: ventricular rhythm with rate > 120 BPM Beware the diagnosis of VT in the patient with heart rate < 120 BPM!! If HR < 120, consider \u0095 Hyperkalemia \u0095 Type IA medication toxicity TCA toxicity Cocaine toxicity \u0095 Reperfusion arrhythmia (accelerated idioventricular rhythm, AIVR) (From Mattu ACEP Lecture)<\/p>\n The pattern of electrical alternans, in which the height of the QRS alternates with each complex, is generally associated with the presence of a large pericardial effusion. However, this pattern may also be seen with supraventricular tachycardia, as demonstrated in this patient. Although this pattern is usually seen with ventricular rates in the range of 200, when it is seen at slower rates.<\/p>\n review of ekg findings<\/a> \u00a0 If afib with rate is > 200 consider References<\/a> Although ventricular rates of the order of 190 beats\/min or more are highly specific for atrial fibrillation (AF) attributable to Wolff-Parkinson-White (WPW) syndrome[1]<\/a>, the caveat is that ventricular rates of 160 to 190 beats\/min can also occur in WPW-related AF [2]<\/a>, and at the lower end of this range, WPW-related AF has to be distinguished from AF occurring in patients with preexisting bundle branch block, given the fact that AF, in its own right, can generate ventricular rates of the order of 159 beats\/min (SD, 16), sometimes blurring the distinction between irregularity and regularity of the ventricular rate [3]<\/a>. The consequence of the latter phenomenon may be a misclassification of AF as reentrant supraventricular tachycardia, and this is true not only of AF patients with narrow-complex QRS configuration during rapid AF [3]<\/a> but also of AF patients with broad QRS configuration attributable to WPW syndrome [4]<\/a>. In either of those instances, misclassification of AF as supraventricular tachycardia can lead to inappropriate administration of adenosine [3]<\/a> or verapamil [4]<\/a>, with attendant morbidity [3]<\/a> and [4]<\/a>. Also worth bearing in mind is that differential diagnosis of the occurrence of AF in a patient with \u0093multiple episodes of sudden syncope in the absence of known cardiovascular disease\u0094 encompasses not only WPW syndrome [1]<\/a> but also the syndrome of short QT interval, identifiable from scrutiny of the electrocardiogram during sinus rhythm and from a family history of syncope and sudden death [5]<\/a>. References [1]<\/a> D.G. Mark, W.J. Brady and J.M. Pines, Preexcitation syndromes consideration in the ED, Am J Emerg Med 27 (2009), pp. 878\u0096888. Article | PDF (3245 K) | View Record in Scopus | Cited By in Scopus (0) \u00a0 Pretreatment with procainamide allows the use of AV blocking agents in WPW. \u00a0 Wolff-Parkinson-White Syndrome (WPW) is the most common form of ventricular preexcitation, involving an accessory conduction pathway known as the bundle of Kent. This pathway creates a direct electrical connection between the atria and ventricles, bypassing the AV node. As a result, electrical impulses utilizing the accessory pathway are conducted very rapidly directly to the ventricles without the usual slowing or \u0093filtering\u0094 (blocking) effect of the AV node. In the presence of AF, WPW patients can achieve ventricular rates in excess of 300 beats per minute. Patients with AF and WPW (AF-WPW) will display three electrocardiographic characteristics that will distinguish them from patients with VT, AF with bundle branch block, and other types of wide complex tachycardias: the rhythm will be irregularly irregular; the QRS morphologies will change in size and shape reflecting some conduction through the accessory pathway, some conduction through the normal pathway, and some fusion beats; ventricular rates in some<\/em> portions of the ECG may exceed 250-300 beats per minute. <\/a> Confused c A-FIB c BBB, but that rhythm will not have ventricular rates >200 or varying QRS morphologies. Avoid confusing c SVT-AC, as A. Fib with aberrant conduction is IRREGULAR (must use calipers) \u00a0 Heart rates above 200\u0096220 suggest that the AV node is not controlling the rate, implying either an accessory pathway or ventricular ectopy The presence of an accessory pathway can be confirmed by either a baseline or post-cardioversion EKG showing pre-excitation. The criteria for pre-excitation are the following: first, an initial slurring of the upstroke of the QRS, called the delta wave; second, the PR interval will be accordingly shortened, less than 0.12 s. Third, the QRS will be prolonged, at least 0.10 s, although some authors think 0.12 s are necessary for the diagnosis (JEM April 2003) Sedation\/Cardioversion is first line treatment for stable and unstable patients, but a trial of procainamide can be attempted. \u00a0 Procainamide slows conduction through accessory pathways. It can increase conduction through the AV node. One regimen is to load with procaine then add an AV node blocker ? Procainamide load at 100mg IV q10min or: ? Run infusion at up to 20mg\/min ? To a total of no more than 17mg\/kg or: ? 1) QRS widens > 50% ? 2) Dysrhythmia suppressed ? 3) Hypotension \u00a0 Can treat with ibutilide if antidromic a-fib (Circulation. 2001 Oct 16;104(16) & Pacing Clin Electrophysiol. 1999 Aug;22(8)) \u00a0 One article questions the use of amio in WPW citing no evidence of benefit and numerous reports of induced ventricular dysrhythmias (Can J Emerg Med 2005;7(4):262) \u00a0 Whereas the goal of treatment of non\u00c2\u0096WPW AFib is to slow the refractory period of the AV node, the treatment principle in WPW AFib is to prolong the anterograde refractory period of the accessory pathway relative to the AV node. This slows the rate of impulse transmission through the accessory pathway and, thus, the ventricular rate. Drugs that prolong the refractory period of the AV node (e.g., calcium channel blockers) increase the rate of transmission through the accessory pathway, with a corresponding increase in ventricular rate. This can possibly cause the arrhythmia to deteriorate into ventricular fibrillation. Procainamide, which slows down conduction via the accessory pathway, forms the cornerstone of treatment in hemodynamically stable rapid wide complex atrial fibrillation of unknown origin. Amiodarone may be used in this situation, and is a second-line choice (1). (Emedhome) References: (1) Chew CH, et al. Broad complex atrial fibrillation Am J Emerg Med 2007;25: 459-463. (2) Manurung D, et al. Wolf-parkinson-white Syndrome Presented with Broad QRS Complex Tachycardia Acta Med Indones 2007;39: 33-5. (3) Rosner MH, et al. Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues Am J Emerg Med 1999;17: 705-14. \u00a0 <\/a><\/a><\/a> \u00a0 Summary of points (Steve Smith)<\/strong> 1) Any fast rhythm which worries you may be treated with electrical cardioversion. If confused, use electricity. If the patient is unstable, use electricity. 2) AV nodal blockers are only contraindicated when there is atrial fib with WPW 3) In regular tachycardias due to WPW(even wide ones!)<\/strong>, AV nodal blockers are safe and effective. They block the limb of the re-entrant rhythm which goes through the AV node, thus interrupting the circuit. 4) Atrial fib with WPW is very recognizable: there are bizarre QRS with multiple morphologies, and very fast rhythms with short R-R intervals. If you can find any R-R interval shorter than 240 ms, then AV nodal blockers are definitely dangerous. \u00a0 Regular wide complex tachycardia. It could be: 1) Ventricular tachycardia (VT) 2) PSVT [AV nodal re-entry tachycardia (AVNRT, 60% of PSVT), orthodromic WPW (30% of PSVT)] with aberrancy<\/strong> (RBBB, LBBB, IVCD) 3) Antidromic reciprocating tachycardia (ART) –Since it is not irregular, it cannot be atrial fibrillation. Use of adenosine<\/strong> –PSVT would usually terminate. The QRS does not look like any recognizable aberrancy (discussion beyond our scope right now). It looks more like VT, but could be ART, except that this is relatively rare –Ventricular tachycardia would not terminate, but adenosine would not be dangerous. –ART is a reentrant rhythm that goes down a bypass tract (causing a wide complex) and up the AV node; therefore AV nodal blockade (adenosine) will terminate it. Thus, adenosine is safe in a patient with this ECG (whether VT or ART) and usually will terminate the rhythm. <\/strong> —<\/strong>Of course, one can also use electricity, but that requires sedation and is not required unless adenosine fails (and one should try 6mg, then 12mg, then probably also 18 mg before it is true failure). If the patient were unstable<\/strong>, which he is not, then one would immediately use electrical cardioversion. Re-entrant tachycardia in WPW, whether orthodromic (ORT) or antidromic (ART), usually starts with a premature atrial beat (PAC) that is able to go down one of the tracts while the other is still refractory. In this case, cocaine may have contributed by leading to a PAC. The patient was electrically cardioverted, and this was his ECG after:<\/p>\n from Steve Smith is estimated to have a prevalence of 1 in 5000 adults and is responsible for approximately 11% of sudden death in young adults and 22% in a study of athletes in northern Italy. The diagnosis is not easy (see below).<\/p>\n\n
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\n
<\/span>Alternative Leads<\/span><\/h3>\n
\n
<\/span>Valsalva<\/span><\/h2>\n
<\/span>Antidysrhythmics<\/span><\/h2>\n
Procainamide<\/h4>\n
Amiodarone<\/h4>\n
Metoprolol<\/h4>\n
Adenosine<\/strong><\/h4>\n
<\/span>Narrow Complex Tachycardias<\/span><\/h2>\n
<\/span>A-Fib\/A-Flutter<\/a><\/span><\/h2>\n
<\/span>Multifocal Atrial Tachycardia<\/span><\/h2>\n
<\/span>AVNR Tachycardia<\/span><\/h2>\n
What is AVNRT?<\/h4>\n
Clinical Features of AVNRT<\/h4>\n
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Pathophysiology and types of AVNRT<\/h4>\n
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Useful reading<\/h4>\n
<\/span>Hypokalemia<\/span><\/h2>\n
<\/span>Torsades des Pointes<\/span><\/h2>\n
<\/span>Fasicular Tachycardia<\/span><\/h2>\n
<\/span>Brugada Syndrome:<\/span><\/h2>\n
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\n1. Draw a horizontal line from top of r’ wave (black line 1)
\n2. Draw a horizontal line 5 mm below this (green line 2)
\n3. Extend the downsloping r’-ST segment (black line 3) until it intersects the green line
\n4. Measure the base.
\nIf greater than 3.5 mm, then meets criteria (this is equivalent to a 35 degree\u00a0beta<\/u>\u00a0angle)<\/b><\/p>\n<\/span>Bradycardia<\/span><\/h2>\n
<\/span>AMI Induced<\/span><\/h3>\n
<\/span>Regular Wide Complex Tachycardias<\/span><\/h2>\n
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Brugada Criteria<\/h4>\n
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Griffith Criteria for Aberrant SVT<\/h4>\n
<\/span>Rate Related BBB<\/span><\/h3>\n
<\/span>Slow V-Tach<\/span><\/h2>\n
<\/span>Electrical Alternans<\/span><\/h2>\n
<\/span>AVRT and Wolf Parkinson White<\/span><\/h2>\n
<\/span>ARVD, also known as arrhythmogenic RV cardiomyopathy<\/span><\/h2>\n
<\/p>\n