Dysrhythmias

Supraventricular Tachycardia

from Steve Smith

Narrow except Antidromic, Wide with aberrancy

• Sinus
• Paroxysmal SVT (PSVT)
  • lntranodal re-entry (60%)
  • Orthodromic “reciprocating” (bypass tract) (30%)
  • PAT (10%)
• A fib
• A flutter
• MAT
• Atrial tachycardia

Evaluating the EKG

• Rate/Rhythm
• Axis
• Intervals
• Chamber enlargement
• Conduction abnormalities
• Ischemia/Infarction

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   Three methods for dysrhythmias:

• Altered automaticity
• Reentry
  • AV node has two pathways (AVNRT):
    • Alpha-slow conduction, short refractory
    • Beta-fast conduction, long refractory
  • AVRT from aberrant pathway
• Triggers

Pacs-no pause, PVCs-pause MAT>2 foci   if nodal pacemaker, PRI will be 0.12 sec or greater

Alternative Leads

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.  

• Change paper speed to 50 mm/sec to make sure rhythm is regular or irregular, such as questionable a-fib

Valsalva

Found by Resus.me Emerg Med Australas. 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. make them blow until the plunger moves for 10 seconds   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)

Antidysrhythmics

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

Procainamide

hypotension (50 mg/min up to 30 mg/kg) until ARS>50%, hypotension

Amiodarone

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 Ventricular Arrhythmias Infusion < 1 week Infusion 1-3 Weeks Infusion < 1 week Infusion 1-3 weeks400 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.     Amio sides effects when given long term therapy only: pneumonitis/fibrosis, liver enzyme rise, bluish skin discoloration, hypo or hyperthyroidism, increases coumadin effects

Metoprolol

Metoprolol 50 mg po bid = 10 mg IV q6hr

Adenosine

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.   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,

Narrow Complex Tachycardias

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)   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.  

A-Fib/A-Flutter

 

Multifocal Atrial Tachycardia

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

AVNR Tachycardia

from life in the fast lane

What is AVNRT?

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.

Clinical Features of AVNRT

• AVNRT is typically paroxysmal and may occur spontaneously in patients or upon provocation with exertion, coffee, tea or alcohol. It is more common in women than men (~75% of cases occurring in women) and may occur in young and healthy patients as well as those suffering chronic heart disease.
• Patients will typically complain of the sudden onset of rapid, regular palpitations. The patient may experience a brief fall in blood pressure causing presyncope or occasionally syncope.
• If the patient has underlying coronary artery disease the patient may experience chest pain similar to angina (tight band around the chest radiating to left arm or left jaw).
• The patient may complain of shortness of breath, anxiety and occasionally polyuria due to elevated atrial pressure releasing atrial natriuretic peptide.
• The tachycardia typically ranges between 140-280 bpm and is regular in nature. It may cease spontaneously (and abruptly) or continue indefinitely until medical treatment is sought.
• The condition is generally well tolerated and is rarely life threatening in patients with pre-existing heart disease.

Pathophysiology and types of AVNRT

• AVNRT is caused by a reentry circuit in or around the AV node.
• The circuit is formed by the creation of two pathways forming the re-entrant circuit, namely the slow and fast pathways.
• The fast pathway is usually anteriorly situated along septal portion of tricuspid annulus with the slow pathway situated posteriorly, close to the coronary sinus ostium.
• Sustained reentry occurs over a circuit comprising the AV node, His Bundle, ventricle, accessory pathway and atrium.
• The various forms of AVNRT can be described in terms of ECG appearance such as R-P intervals or Slow/Fast pathway dominance.

The ‘descriptive’ terminology regarding AVNRT classification can be confusing…and I am still confused! Slow-Fast AVNRT (Common AVNRT)

• Accounts for 80-90% of AVNRT
• Associated with Slow AV nodal pathway for anterograde conduction and Fast AV nodal pathway for retrograde conduction.
• The retrograde P wave is obscured in the corresponding QRS or occurs at the end of the QRS complex as pseudo r’ or S waves
• ECG:
  • P waves are often hidden – being embedded in the QRS complexes.
  • Pseudo r’ wave may be seen in V1
  • Pseudo S waves may be seen in leads II, III or aVF.
• In most cases this results in a ‘typical’ SVT appearance with absent P waves and tachycardia

AVNRT Slow-Fast

• Cardiac rhythm strips demonstrating (top) sinus rhythm and (bottom) paroxysmal supraventricular tachycardia. The P wave is seen as a pseudo-R wave (circled in bottom strip) in lead V1during tachycardia. By contrast, the pseudo-R wave is not seen during sinus rhythm (it is absent from circled area in top strip). This very short ventriculoatrial time is frequently seen in typical Slow-Fast Atrioventricular Nodal Reentrant Tachycardia.

Fast-Slow AVNRT (Uncommon AVNRT)

• Accounts for 10% of AVNRT
• Associated with Fast AV nodal pathway for anterograde conduction and Slow AV nodal pathway for retrograde conduction.
• The retrograde P wave appears after the corresponding QRS
• ECG
  • QRS -P-T complexes
  • P waves are visible between the QRS and T wave

Slow-Slow AVNRT (AtypicalAVNRT)

• 1-5% AVNRT
• Associated with Slow AV nodal pathway for anterograde conduction and Slow left atrial fibres approaching the AV node as the pathway for retrograde conduction.
• ECG: Tachaycardia with a P-wave seen in mid-diastole… effectively appearing ‘before the QRS complex’…
• Confusing as a P wave appearing before the QRS complex in the face of a tachycardia might honestly be read as a sinus tachycardia..

Schematic of typical atrioventricular nodal reentry.

• Left Panel: Anterograde conduction from the atrium (ATR) to the ventricle (VTR) over both slow and fast pathways. The ventricle is activated initially in sinus rhythm by the fast pathway.
• Centre Panel: The effect of a premature atrial complex (PAC). Although the fast pathway conducts rapidly, it repolarizes slowly. In this hypothetical scenario, the fast pathway is refractory to the PAC, allowing the PAC to proceed via the slow pathway, which has a shorter refractory period.
• Right Panel: Anterograde conduction of the PAC occurs via the slow pathway, with subsequent recovery of the fast pathway. These conditions allow retrograde conduction into the atrium via the fast pathway, thereby creating the first beat of typical slow-fast atrioventricular nodal reentrant tachycardia.

InvestigationsThe ECG will typically show a tachycardia of 140-280 bpm with normal and regular QRS complexes. There will be either

• No visible P-waves (hidden within the QRS complex) or
• P-waves immediately before the QRS or
• P-waves immediately after the QRS complex

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). ManagementPatients 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:

• Adenosine, beta-blockers or calcium channel blockers can suppress an AVNRT event by blocking or slowing the AV node. Other second-line therapies may include amiodarone or flecainide.
• Cardioversion is rarely used on patients with AVNRT, usually when the tachycardia is refractory to other medical therapies or the tachycardia is causing haemodynamic instability (falling blood pressure, development of heart failure etc.)
• Radiofrequency catheter ablation can be offered to patients with frequent attacks for whom medical therapy isn’t appropriate in the long term, and can be curative.

Useful reading

 

Hypokalemia

(From Dr. Smith Ekg Blog) Here is the same ECG with some arrows: 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 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.

Torsades des Pointes

Hypokalemia/magnesemia. Genetic, cva, surgery. Overdrive and magnesium Irregular atrial rhythm>250 bpm, think WPW   list of drugs that can cause TdP http://www.torsades.org/medical-pros/drug-lists/drug-lists.htm

Fasicular Tachycardia

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). 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, 6 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). This again points to the ventricular origin of the tachycardia. 7-9 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 Rarely, this type of VT may respond to adenosine. 10

Brugada Syndrome:

best review (JACC 2008;51(12):1176)   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   can treat with quinidine po or isuprel iv while awaiting defib placement   The Brugada Syndrome is a malignant primary electrical disease of the heart resulting in abnormal electrophysiologic activity in the right ventricle and characterized by:

1. ST segment elevation in the pre-cordial leads V1-V3 accompanied by a morphology of the QRS complex resembling a right bundle branch block;
2. A heart that is grossly structurally normal;
3. A propensity for life-threatening ventricular tachyarrhythmias.

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)   The disease is genetically determined with an autosomal dominant pattern of transmission.   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.   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.   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.   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 “loss of function,” meaning that the channel is perpetually closed. Interestingly, long QT syndrome type 3, a completely different disease, occurs when the sodium channel experiences a “gain of function” 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–V3 (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 ≥ 2 mm followed by a trough displaying ≥ 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.     — 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   Worrisome Thoughts About the Diagnosis and Treatment of Patients With Brugada Waves and the Brugada Syndrome (Circulation. 2004;109:1463-1467.) 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.)

Explanation
1. Draw a horizontal line from top of r’ wave (black line 1)
2. Draw a horizontal line 5 mm below this (green line 2)
3. Extend the downsloping r’-ST segment (black line 3) until it intersects the green line
4. Measure the base.
If greater than 3.5 mm, then meets criteria (this is equivalent to a 35 degree beta angle)

from steve smith blog

Bradycardia

AMI Induced

Aminophylline can be used as a bridge to pacing. 100 mg/min to a max of 0.5 mg/kg. (Annals Int Med 1995; 7: 509, Emer Med Clin NA 2001; 19, Eur Heart J 1995; 16:862-865)

Regular Wide Complex Tachycardias

It is safe to use adenosine as a dx measure (CCM 2009;37(9):2512)

Brugada Criteria

1. absence of an RS complex in all precordial leads
2. an RS interval >100ms in any one precordial lead
3. AV dissociation
4. Suggestive QRS morphologies in leads V1-2 and V6. (For RBBB QRS: Monophasic R, QR, or RS in V1 and R/S<1, QS,QR or monophasic R in V6/For LBBB QRS: R>30 msec, S nadir >60 msec, or notched S in V1 and or V2 and QR or QS in V6)

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

1. A/V Disassociation
2. Ventriculoatrial Block
3. Positive QRS Concordance
4. QRS axis between -90 and +180
5. Combination of LBBB and rightward axis>90
6. Combination of RBBB and QRS>0.14 sec
7. Combination of LBBB and QRS>0.16 sec
8. QRS morphology during tachycardia different than baseline preexisting BBB

(Ann Int Med 1988, Dec 1;109:11)

Griffith Criteria for Aberrant SVT

Right Bundle QRS: rSR in V1 and RS in V6 with R/S>1 Left Bundle QRS 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)   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.)   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.

Rate Related BBB

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]

Slow V-Tach

In order to be V-tach, rate must be greater than 120-130 if it is not, probably a mimic. Ia anti-dysrhytmic toxicity, hyperkalemia, accelerated idioventricular rhythms, reperfusion dysrhythmia   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 • Hyperkalemia • Type IA medication toxicity TCA toxicity Cocaine toxicity • Reperfusion arrhythmia (accelerated idioventricular rhythm, AIVR) (From Mattu ACEP Lecture)

Electrical Alternans

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.

AVRT and Wolf Parkinson White

review of ekg findings   If afib with rate is > 200 consider References 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], the caveat is that ventricular rates of 160 to 190 beats/min can also occur in WPW-related AF [2], 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]. 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] but also of AF patients with broad QRS configuration attributable to WPW syndrome [4]. In either of those instances, misclassification of AF as supraventricular tachycardia can lead to inappropriate administration of adenosine [3] or verapamil [4], with attendant morbidity [3] and [4]. Also worth bearing in mind is that differential diagnosis of the occurrence of AF in a patient with “multiple episodes of sudden syncope in the absence of known cardiovascular disease” encompasses not only WPW syndrome [1] 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]. References [1] D.G. Mark, W.J. Brady and J.M. Pines, Preexcitation syndromes consideration in the ED, Am J Emerg Med 27 (2009), pp. 878–888. Article | PDF (3245 K) | View Record in Scopus | Cited By in Scopus (0)   Pretreatment with procainamide allows the use of AV blocking agents in WPW.   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 “filtering” (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 portions of the ECG may exceed 250-300 beats per minute. 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)   Heart rates above 200–220 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.   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   Can treat with ibutilide if antidromic a-fib (Circulation. 2001 Oct 16;104(16) & Pacing Clin Electrophysiol. 1999 Aug;22(8))   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)   Whereas the goal of treatment of non–WPW 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.     Summary of points (Steve Smith) 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!), 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.   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 (RBBB, LBBB, IVCD) 3) Antidromic reciprocating tachycardia (ART) –Since it is not irregular, it cannot be atrial fibrillation. Use of adenosine –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. —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, 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:

Cardiac Memory Post-Pacemaker

Deep t wave inversions identical to pattern present when pt was being paced can remain for a long period of time post pacing (JEM, 23:2)

A-V Disassociation

2nd Degree Type I (Wenckebach)

The PR interval is often normal in the first beat of the series. Progressive PR interval lengthening with subsequent beats is observed until an impulse is unable to reach the ventricles, resulting in a non-conducted P wave. After the dropped beat, the PR interval returns to normal and the cycle repeats itself. A pattern to the RR interval is also seen. As the PR lengthens with subsequent beats, the RR interval becomes shorter. After the dropped beat, the RR interval in the subsequent beats tends to shorten. In fact, the RR interval containing the dropped beat is less than two of the shorter cycles. One will also notice on the rhythm strip a grouping of beats that is especially noticeable with a tachycardia. Such a finding is referred to as grouped beating of Wenckebach. Evidence on the EKG for Mobitz type I AVB includes the following: 1) progressive lengthening of the PR interval, then dropped beat; 2) progressive shortening of the RR interval; 3) the RR length of the dropped beat is less than twice the shortest cycle; and 4) grouped beating.

2nd Degree Type II

The QRS complex, in most cases, is wide (i.e., greater than 0.12 s). This finding is explained by its association with bundle branch block [20 and 21]. His bundle recordings indicate that the block is never localized to the His bundle; instead, 20% of cases occur in the common bundle and 80% in the bundle branches [5]. Consistent with the general rule that blocks distal to the His bundle presume a more serious prognosis, type II blocks often progress to complete heart block (CHB) and produce Stokes-Adams syncope [3 and 4]. This progression to CHB is a common finding in particular with patients suffering from extensive anterior infarctions.

Sudden Death in Athletes

Hypertrophic Cardiomyopathy

Anomalous Origins of Coronary Arteries Predisposes to dysrhythmia and death

• Adult congenital heart disease (e.g. Tetralogy of Fallot)
• Long QT syndrome
• Brugada syndrome
• Viral myocarditis
• Hypertrophic Obstructive Cardiomyopathy (HOCM)
• Commotio Cordis

(from lithfl blog)

Aortic Stenosis

 

Aortic Dissection in Athletes with Marfan’s

Commotio Cordis

Sudden death from arrhythmia induced by direct blow to chest. Survival is rare. 70% less than 16 y/o

Dysrhythmia

WPW, QT prolongation and Brugada

CAD in Athletes>30

 

Tall R in V1

(A J EM 19, Number 6 October 2001 p. 504 Tall lead V1 (tall RV1), defined as an R/S ratio equal to or greater than 1, is not an infrequent occurrence in emergency department patients. This electrocardiographic finding exists as a normal variant in only 1% of patients. Physicians should therefore be familiar with the differential diagnosis for this important QRS configuration. The electrocardiographic entities which can present with this finding include right bundle branch block, left ventricular ectopy, right ventricular hypertrophy, acute right ventricular dilation (acute right heart strain), type a Wolff-Parkinson- White syndrome, posterior myocardial infarction, hypertrophic cardiomyopathy, progressive muscular dystrophy, dextrocardia, misplaced precordial leads, and normal variant. Various cases are presented to highlight the different causes of the tall RV1. (Am J Emerg Med 2001;19: 504-513. Copyright © 2001 by W.B. Saunders Company) In the normal heart, the general direction of ventricular depolarization is in a right-to-left, downward direction because of the larger mass of the left ventricle compared with the right ventricle. This results in a characteristic appearance of the QRS complex in lead V1 of the electrocardiogram (ECG), the rS configuration. The initial small R wave (symbolized as “r” to denote its small size) occurs because of septal depolarization from left to right. The subsequent larger S wave (symbolized as “S” to denote its larger size) occurs because of the dominant effect of the left ventricle.1 Tall R waves in lead V1 (tall RV1), defined as an R/S ratio equal to or greater than 1, is not an infrequent occurrence in emergency department (ED) patients. However, this ECG finding exists as a normal variant in only 1% of patients.2 Physicians should therefore be familiar with the differential diagnosis for this important QRS configuration   Right bundle branch block Left ventricular ectopy Right ventricular hypertrophy Acute right ventricular dilation (acute right heart strain) Type A Wolff-Parkinson-White syndrome Posterior myocardial infarction Hypertrophic cardiomyopathy Progressive muscular dystrophy Dextrocardia

Misplaced precordial leads Normal variant (1% of time)

avL

Major exceptions — downsloping ST-segment and inverted T-wave in aVL is normal finding in patients with LVH and LBBB

Polymorphic VT

Although magnesium is commonly used to treat torsades de pointes VT (polymorphic VT associated with long QT interval), it is supported by only 2 observational studies (LOE 5)42,43 showing effectiveness in patients with prolonged QT interval. One adult case series (LOE 5)44 showed that isoproterenol or ventricular pacing can be effective in terminating torsades de pointes associated with bradycardia and drug induced QT prolongation. Magnesium is unlikely to be effective in terminating polymorphic VT in patients with a normal QT interval (LOE 5),43 but amiodarone may be effective (LOE 4).45

Ventricular Tachycardia

So what should the Emergency Physician conclude and how to proceed? These observations only add support for clinicians’ widely held impression that pharmacologic treatment of sustained VT terminates far too few tachycardias. Synchronized DC cardioversion is the safest and most effective currently available treatment for the termination of sustained ventricular tachycardia (2). Clinicians should strongly consider the counsel of Dr. Richard Cummins, chief editor of the ACLS guidelines: “the prudent, multitasking emergency physician will best serve the patient in ventricular tachycardia by dismissing lidocaine, pining for sotalol, considering procainamide, and then ordering a properly dosed infusion of amiodarone. The physician performs these drug-oriented tasks, however, while authorizing the patient for procedural sedation, synchronizing the monitor display, and charging up the defibrillator capacitors (1).”

See this post on Right Ventricular Outflow Tachycardia RVOT VT

Fasicular VT

An Important Ventricular Tachycardia (Treated With Verapamil!) Fascicular VT (also known as idiopathic left VT) is a distinct subgroup of idiopathic VT that may be confused with either typical ventricular tachycardia or SVT. It is an entity well recognized by cardiologists but not as frequently by Emergency Physicians (3). This tachycardia is thought to arise from a reentrant mechanism in the posterior fascicle of the left bundle branch. Whereas the administration of calcium-channel blockers to a patient with ventricular tachycardia could result in hemodynamic instability, intravenous verapamil is the appropriate drug of choice for the treatment of fascicular VT. Fascicular VT occurs in hemodynamically stable young patients without any underlying ischemic heart disease. The ECG shows a right bundle-branch block pattern and left-axis deviation with a relatively narrow QRS complex (100-140 ms). Click here for an example of fascicular VT. Vagal maneuvers and adenosine are ineffective in converting this arrhythmia; amiodarone and sotalol have been reported to be effective (1,2).References:(1) Chew HC, et al. Verapamil for ventricular tachycardia Am J Emerg Med 2007; 25: 572-575. (2) Eynon CA, et al. Fascicular tachycardia: uncommon or just unrecognised? Emerg Med J 2002;19: 477-478. (3) Elswick BD, Niemann JT. Fascicular ventricular tachycardia: an uncommon but distinct ventricular tachycardia Ann Emerg Med 1998;31:406–409.

EKG Book by Amal Mattu

flutter requires atrial rates>250 In patients less than 40 y/o if they make LVH by voltage, the better term is high left ventricular voltage (HLVV) second degree heart block will have constant p-p interval hypokalemia will present with T-U fusion, which can present as abnormally wide and/or humped t waves Poor R wave progression V3 < 3mm increased ICP on ekg will show prolonged AT with wide inverted t waves Redfearn DP, Ratib K, Marshall HJ, et al. Supraventricular tachycardia promotes release of troponin I in patients with normal coronary arteries. International Journal of Cardiology. Jul 2005;102(3):521-522. (Retrospective case series; 7 patients) Zellweger MF, Schaer BA, Cron TA, et al. Elevated troponin levels in the absence of coronary artery disease after supraventricular tachycardia. Swiss Medical Weekly. Aug 2003;133(31-32):439-441. (Case series; 4 patients)   Prolonged QT Syndrome worry if >500   Short QT Syndrome <300   Regular, wide, rate > 120, always treat as Vtach, Always adenosine might convert these guys, so don’t consider it diagnostic of SVT Bizarre=give Ca and BIcarb

Procainamide

Stiell’s protocol Acad Emerg Med 2007;14:1158 1000 mg over 1 hour, if no conversion, D/C cardioversion do not use in prolonged QT 100 mg/min, 50 mg/min or 35 mg/min 35 is usually best, get effects at about 250-400 mg

QT Prolongation

Drugs that are known to prolong the QT interval     The diagnosis of LQTS is based on the association of a prolonged QTc interval with some clinical characteristics. Some secondary causes of QT prolongation should be ruled out (hypocalcemia, hypothyroidism, drugs). A complete list of drugs that cause QT prolongation can be found at www.torsades.org. Schwartz et al[9] have developed diagnostic criteria for LQTS in the form of a score that group the patients as at low probability of LQTS (score ≤ 1), intermediate (score 2 or 3), and high probability or definite LQTS (score ≥ 4) (Table 2). Table 2. Diagnostic criteria for LQTS Criteria Points ECG finding A. QTc ≥480 ms 3 460-479 ms 2 450 ms (males) 2 B. Torsades de pointes 2 C. T-wave alternans 1 D. Notched T waves in 3 leads 1 E. Low heart rate for age 0.5 Clinical history A. Syncope With stress 2 Without stress 1 B. Congenital deafness 0.5 Family history A. Family members with definite LQTS 1 B. Unexplained SCD <30 among immediate family members 0.5 can be associated with epilepsy or pseudo-seizure. check ekg in all seizure patients (Ann Emerg Med 2009;54(1):26)

 

Comment from Steve Smith from the EKG Blog: computer and manual QT measurement

Computer algorithms for measure the QT interval are good for normal QT intervals but not for long QT intervals, and are particularly inaccurate for very long QT intervals.

The QT is the interval from the beginning of the QRS to the end of the T-wave.  It should be the longest QT interval of all 12 leads, and this is the way most computer algorithms measure it.  However, taking the longest of leads II, V2, V5, and V6 will usually do.

One does not actually measure the end of the T-wave: instead, the technique involves drawing a line along the maximum downslope of the T-wave and measuring from where it intersects with the isoelectric line.  Here is a graphic of this from Life in the Fast Lane (same as the graphic in this link).

Once you measure the QT, then the most commonly used heart rate correction is the Bazett formula, which is the QT divided by the square root of the preceding R-R interval (example: if the preceding R-R interval is 810 ms = 0.81 sec, then the square root of 0.81 is 0.9, so a QT interval of 450 ms would result in a QTc of 500 ms (450 divided by 0.9 = 500).

Let’s measure the QT on the above tracing:

Lead V5 is the most convenient and appears to be as long as any other lead.  The first vertical line is the start of the QRS.  The angled line is on the steepest part of the T-wave slope.  The horizontal line is the isoelectric line.  The intersection of the angled line and the isoelectric is where the second vertical line is.  Then the measurement is between the two vertical lines.  There are 3 large 5 mm boxes (each 200 ms) + 2.25 mm to the left and 1.25 mm to the right.  That is 18.5 mm x 40 ms per mm = 740 ms.  QTc = 740 divided by the square root of the R-R interval of 1.08 seconds = 740 divided by 1.04 = 711 ms. QTc = 711 ms

Life in the Fast Lane has an excellent overview of QT prolongation.

Acquired long QT, and how it causes torsade: It is usually due to drugs.  The list is long.  And also due to electrolyte abnormalities, especially hypoK and hypoMg.   Corrected QT interval (Bazett correction = QT divided by the square root of the preceding R-R interval in milliseconds) is usually great than 600 ms.  Torsades in acquired long QT is much more likely in bradycardia because the QT interval following a long pause is longer still.  Thus, torsades in acquired long QT is called “pause dependent”: if there is a sinus beat after a long pause (which creates a longer QT interval), then an early PVC (“early afterdepolarization,” EAD) is much more likely to occur during repolarization and to initiate torsades.  The usual sequence is: sinus beat, then early PVC, then a long pause because the PVC was early, which then results in a particularly long QT, then another PVC with “R on T” that initiates torsades.

 

 

Standing Test

(From ER Ireland)This paper addresses this concept and while it’s in now waty perfect (ie it examined it in people known to have LQTS which undermines its use as a diagnostic test in undiagnosed QT problems) it suggests that in healthy people an increase in QTc on standing of about 10-15ms is allowed but in LTQS is likely to be in the range of 90-100 ms.

Viskin, Sami, Pieter G Postema, Zahurul A Bhuiyan, Raphael Rosso, Jonathan M Kalman, Jitendra K Vohra, Milton E Guevara-Valdivia, et al. “The Response of the QT Interval to the Brief Tachycardia Provoked by Standing: a Bedside Test for Diagnosing Long QT Syndrome..” Journal of the American College of Cardiology 55, no. 18: 1955–1961. doi:10.1016/j.jacc.2009.12.015. PMID 20116193

How to Diagnose IVCDs

(AJEM 2009;27:492)

ACLS Dysrhythmia Stuff

Narrow–QRS-complex (SVT) tachycardias (QRS <0.12 second), in order of frequency • Sinus tachycardia • Atrial fibrillation • Atrial flutter • AV nodal reentry • Accessory pathway–mediated tachycardia • Atrial tachycardia (including automatic and reentry forms) • Multifocal atrial tachycardia (MAT) • Junctional tachycardia (rare in adults) Wide–QRS-complex tachycardias (QRS 0.12 second)• Ventricular tachycardia (VT) and ventricular fibrillation (VF) • SVT with aberrancy • Pre-excited tachycardias (Wolff-Parkinson-White [WPW] syndrome) • Ventricular paced rhythms Irregular narrow-complex tachycardias are likely atrial fibrillation or MAT; occasionally atrial flutter is irregular. Initial Evaluation and Treatment of Tachyarrhythmias Many experts suggest that when a heart rate is <150 beats per minute, it is unlikely that symptoms of instability are caused primarily by the tachycardia unless there is impaired ventricular function.Supraventricular Tachycardia (Reentry SVT) Most SVTs are regular tachycardias that are caused by reentry, an abnormal rhythm circuit that allows a wave of depolarization to repeatedly travel in a circle in cardiac tissue. The rhythm is considered to be of supraventricular origin if the QRS complex is narrow (<120 milliseconds or <0.12 second) or if the QRS complex is wide (broad) and preexisting bundle branch block or rate-dependent aberrancy is known to be present. Reentry circuits resulting in SVT can occur in atrial myocardium (resulting in atrial fibrillation, atrial flutter, and some forms of atrial tachycardia). The reentry circuit may also reside in whole or in part in the AV node itself. This results in AV nodal reentry tachycardia (AVNRT) if both limbs of the reentry circuit involve AV nodal tissue. Alternatively, it may result in AV reentry tachycardia (AVRT) if one limb of the reentry circuit involves an accessory pathway and the other involves the AV node. The characteristic abrupt onset and termination of each of the latter groups of reentrant tachyarrhythmias (AVNRT and AVRT) led to the original name, paroxysmal supraventricular tachycardia (PSVT). This subgroup of reentry arrhythmias, due to either AVNRT or AVRT, is characterized by abrupt onset and termination and a regular rate that exceeds the typical upper limits of sinus tachycardia at rest (usually >150 beats per minute) and, in the case of an AVNRT, often presents without readily identifiable P waves on the ECG. Distinguishing the forms of reentrant SVTs that are based in atrial myocardium (such as atrial fibrillation) versus those with a reentry circuit partly or wholly based in the AV node itself (PSVT) is important because each will respond differently to therapies aimed at impeding conduction through the AV node. The ventricular rate of reentry arrhythmias based in atrial myocardium will be slowed but not terminated by drugs that slow conduction through the AV node. Conversely, reentry arrhythmias for which at least one limb of the circuit resides in the AV node (PSVT attributable to AVNRT or AVRT) can be terminated by such drugs. Yet another group of SVTs is referred to as automatic tachycardias. These arrhythmias are not due to a circulating circuit but to an excited automatic focus. Unlike the abrupt pattern of reentry, the characteristic onset and termination of these tachyarrhythmias are more gradual and analogous to how the sinus node behaves in gradually accelerating and slowing heart rate. These automatic arrhythmias include ectopic atrial tachycardia, MAT, and junctional tachycardia. These arrhythmias can be difficult to treat, are not responsive to cardioversion, and are usually controlled acutely with drugs that slow conduction through the AV node and thereby slow ventricular rate.

Electrical Storm

Best Review Article (Texas Heart J 2011; 38(2):111)