Dysrhythmias

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

o       AV node has two pathways (AVNRT):

§        Alpha-slow conduction, short refractory

§        Beta-fast conduction, long refractory

o       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

the modified
Valsalva manoeuvre, that is, while lying supine on the
bed in a Trendelenberg position, they forcefully expire
into a section of suction tubing and pressure gauge for at
least 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:

decrease dose in hepatic failure

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

ashman beats from variable repolarization of the bundles

Holiday heart=etoh generated a-fib, can also be from withdrawal.  Usually spontaneously resolves.

P-ulmonary Embolism

I-schemia

R-espiratory

A-trial myxoma, enlargement

T-hyroid

E-thanol

S-epsis

A. flutter less likely to have atrial clots, but in one study of hospitalized patients, 21% had a clot, most likely due to coexistence of A. Fib in these pts. (Am J Cardio 1995 76:3)

If there is any doubt about A. Fib on ekg, get a strip with 50 mm/sec speed and use calipers to determine regularity.

Cardioversion

·        Joglar et al, who showed an initial single shock success rate of 14% with 100J, 39% with 200J, and 95% with 360J in patients with AF for more than 48 hours

·        Use the steak sauce for best conduction

·        Lack of myocardial damage from DCC in AF at levels higher than 360. (Heart 1998, 80:3) and Resuscitation 1998;36:193-199. Latter article showed sig. increase in CK but CK-MB fraction and troponin not elevated

·        Start at 200J in stable patients, 360J in unstable patients.

·        Use Anterior-Posterior Shock, not Anterior-Lateral (Lancet 360:9342, 2002)

When acute AF was excluded incidence of embolism with inadequate anticoagulation was 1.7-4.7% (Mayo Clin Proc Sept 2002, Vol 77)

Medications

Conversion

• Ibutilide-1 mg over 10 minutes, may repeat in 10 minutes.  Causes prolonged QT in 5-10% and TdP in 1-5%, give MgSO4 prophylaxis . Facilitates electrical conversion if used as a premedication  (NEJM 340:24 June 1999 JB17)  Monitor for four hours after use.

• Dofetilide

• Amiodarone-150 mg over then 10 min, then 1 mg/min x 6 hours then .5 mg/min or  3-5 mg/kg over 10 minutes then 5 mg/kg q 8 hrs divided as infusion (One MA says it works (Ann Intern Med 2003, 163:777)

• Flecainide-300mg PO x 1 (In short cut review, more efficacious than Amiodarone Emerg Med J 2004; 21:199)

• Propafenone-600 mg PO

Rate Control

• Diltiazem  .25 mg/kg over 2 minutes, may repeat at .35 mg/kg if inadequate response, the drip at 5-15 mg/hr or 60 mg PO. (give 1-3 cc of CaCl or 5-10 cc CaGluc if hypotension develops or as pretreatment for pt’s with borderline BP
   

  Calcium Pretreatment

   

  Moser et al. the use of calcium salts in the prevention and management of verapamil induced hypotension. Ann Pharmoacother 2000;34:622-9

   

  Haft et al. treatment of atrial arrythmias. Effectiveness of verapamil when proceeded by calcium infusion, Arch Intern Med 1986;146:1085-9

   

  Barnett JC et al. Short term control of supraventricular tachycardia with verapamil infusion and calcium pretreatment. Chest 1990;97:1106-9

   

  Miyagawa K, et al. Administration of intravenous calcium before verapamil to prevent hypotension in elderly patients with paroxysmal supraventricular tachycardia. J Cardiovas Pharmacol 1993;22:273-9

   

  Weiss AT et a l. The use of calcium with verapamil in the management of SVT In J Cardiol 1983;4:275-84

   

  Salerno DM, et al. Intravenous verapamil for treatment of multifocal atrial tachycardia with and without calcium pretreatment. Ann Internal Med 1987;107:623-8

   

  Kuhn M et al. Low-dose calcium pretreatment to prevent verapamil-induced hypotension. AM Heart J 1992;124:231-2)

   

  Recent RCT of dilt c 3.33 cc cacl preinfusion showed no difference, but no side effect. Only 5 pts with hypotension, only one pt with sx hypotension. One pt had increased HR and LOC in placebo group, recovered with Ca

  
  Alternatively, use infusion of Diltiazem 2.5 mg/min to maximum of 50 mg (Resuscitation 52:167, 2002)
  If pt is unstable, give in 5 mg aliquots every few minutes.  Contraindicated in children < 1 y/o.

• Magnesium 2-4 g over 10 minutes.  Has effects of CCB and B-Blockers, but doesn't effect the sinus node.  (Clin Card 12:2, 1989 and J Am Coll Card 7:6, 1986)  Head to head with amiodarone (Crit Care Med 1995;23 equal for rate control and more effective conversion) or diltiazem ( Internat J Cardiol 2001;79 287-291 randomized, prospective 46 pts, 2.5 G MG over 15 min or 25 mg dilt over 15 min Mag was equal for rate control and more effective for conversion to sinus)

• another Blinded RCT (Ann Emerg Med 2005;45(4):347)
  Continue drip at  1-2 g/hr

Author Dose Response
Moran et al 1995 37mg/kg bolus followed by
infusion of 25mg/kg/hr
42 patients - 60% conversion in magnesium
group and 45% in amiodarone group.
Brodsky, et al, 1994 2 grams over 6 minutes - then 1
gram per hour
10/10 reduced HR to < 90 versus only 4 of
8 in placebo by 4 hours
Tachyarrhythmia’s Notes 10
Mel E. Herbert, MD, MBBS, BMedSci, FACEP, FAAEM
 

Hays et al 1994 2 grams bolus minutes - then 1
gram per hour
By 30 minutes, there was no significant
change in the ventricular rate in patients
receiving placebo while the rate decreased
an average of 16% within five minutes after
initiation of magnesium sulfate (p<0.02).
Gullestad, L., et al, 1993 1.2g given over five minutes, with
the dose repeated after five
minutes if there was no response,
followed by infusion of 0.6g per
hour
The rate of conversion to sinus rhythm
within four hours was 58% (15/26) in the
magnesium group and 23% (7/31) in the
verapamil group, and the frequency of a
heart rate reduction to less than 100/min
was 28% (6/26) and 48% (15/31),
respectively.
 

RCT (Annals of Emergency Medicine Volume 45, Issue 4 , April 2005, Pages 347-353)

Meta-analysis of magnesium therapy for the acute management of rapid atrial fibrillation. (Am J Cardiol. 2007 Jun 15;99(12):1726-32)
 

• Digoxin works only in sedentary folks, because when you add catecholamines to the mix, the vagal response is overcome.
  Load 0.5 mg then 0.125 mg QD

dilt was better than amio and dig but, dig and amio seemed the same for rate control (Crit Care Med 2009;37(7):2174)

Anticoagulation

Probably need to anticoagulate after cardioversion due to cardiac stunning, ie. atrial EMD.  (Am Heart J 2002 Jul;144(1):11-22, Eur Heart J 2001 Mar;22(6):520-1)

anticoagulation with intravenous heparin be initiated on
admission for all patients with atrial fibrillation, even if the
clinically estimated duration of atrial fibrillation is less than 48
hours, and the therapy with heparin be continued for at least
24 hours after conversion”
Weigner et al Ann Intern Med 1997;126:615-620

From Michelle Lin:

Atrial Fibrillation (AF) = 5x risk for CVA and increases with age
Stroke risk stratification for patients with AF:
• Prior CVA or TIA
• HTN
• Age ≥ 75
• CHF
• Poor LV function
• DM
CHADS2 stroke risk stratification scheme (Gage BF et al. JAMA 2001;285:2864–70.)
• C = Congestive heart failure (1 pt)
• H = Hypertension (1 pt)
• A = Age ≥ 75 (1 pt)
• D = DM (1 pt)
• S2 = prior Stroke or TIA (2 pts)
Deciding whether to anticoagulate with ASA or Warfarin:
(AHA/ ACC/ European Soc of Cardiology 2006 revised guidelines
for antithrombotic therapy based on stroke risk)
Weak Risk Factors Moderate Risk Factors High Risk Factors
Female gender Age > 75 Prior CVA, TIA, embolism
Age 65-74 HTN Mitral stenosis
CAD Heart failure Mechanical heart valve
Thyrotoxicosis LVEF ≤ 35%
DM
Treatment Treatment Treatment
ASA or Warfarin ASA or Warfarin (1 risk factor) Warfarin
Warfarin (≥ 2 risk factors)
* Anticoagulation goal with Warfarin is INR 2-3
* If age < 60 years and zero risk factors: No anticoagulation b/c low risk for CVA

LMWH is just as good as UFH in a-fib in a large RCT (Circulation 2004;109:997-1003)

Rate Control vs. Rhythm Control

rate control has more long term benefit than conversion and maintenance of sinus (NEJM 347:p. 1825, 2002 and NEJM 347:p. 1834, 2002)

One study showed safe to withhold anticoagulation if less than 48 hours (Ann Intern Med 1997;126:615)

Transient ST-depression with Rapid AF - Significance?

Transient ST-segment depression during rapid atrial fibrillation is a common finding in the ED. Frequently, patients without known CAD exhibit such ischemic ST-segment depression during an episode of rapid AF. Clinicians often consider this to be a "positive stress-test equivalent". However, a recent study indicates that in patients without a history of cardiovascular disease, there is no strong association between transient ischemic type ST-segment depression during paroxysms of AF and underlying occult CAD, i.e., they are not consistently associated with with positive stress testing or occlusions on cardiac catheterization (1).

Conversely, however, if the ST-segment depression persists after the rate is controlled, then there should be greater concern.


It should also be noted that new onset AF is rarely the sole manifestation of acute MI - in the absence of clinical predictors suggesting acute myocardial ischemia (e.g. chest pressure, dyspnea, diaphoresis, etc.), routine "rule-out ACS" admission is not supported by the literature.

References:
(1) Androoulakis A, et al. Transient ST-Segment Depression During Paroxysms of Atrial Fibrillation in Otherwise Normal Individuals J Am Coll Cardiol 2007;50:1909-1911.
(2) Friedman HZ, et al. Cardiac care unit admission criteria for suspected acute myocardial infarction in new-onset atrial fibrillation Am J Cardiol 1987;59:866-869.
(3) Mulcahy B, et al. New-onset atrial fibrillation: when is admission medically justified? Acad Emerg Med 1996;3: 114-19. (emedhome)

Ottowa Stuff (CJEM 2010;12(3):

1. Assessment: Assessment focuses on the stability of the patient, previous episodes and duration since onset. The decision of whether cardioversion is appropriate is made by the emergency physician involved and is usually based on the clarity of the history of arrhythmia onset. There is no upper age limit for the application of aggressive rhythm control. Every effort is made to ensure that the time from symptom onset is less than 48 hours and if this cannot be verified then rhythm control is not pursued unless the patient is on warfarin and has had a therapeutic international normalized ratio (INR) level for at least 3 weeks. If the time from symptom onset is longer than 48 hours or of uncertain duration, then transesophageal echocardiography can be pursued to determine the safety of cardioversion.19 Patients are not routinely screened for elevation of troponin unless there is chest pain or ST and T wave changes.

2. Rate control: Rate control is often omitted as there is no compelling evidence that its use facilitates cardioversion. Physicians who choose to control heart rate before attempting cardioversion typically use intravenous diltiazem or metoprolol.

3. Pharmacologic cardioversion: Typically, emergency physicians at our institution attempt pharmacologic cardioversion before electrical cardioversion. Intravenous procainamide is the drug of choice in Ottawa for rhythm control, and we have previously de - scribed its use in detail.20 Pharmacologic cardioversion is generally not attempted if the patient is deemed to be unstable (cardiac ischemia, severe congestive heart failure or hypotension) or if records indicate resistance to this approach on previous visits. The standard protocol is 1 g of procainamide in 250 mL of dextrose and water as a controlled infusion over 1 hour, under continuous cardiac and blood pressure monitoring. The infusion is interrupted if blood pressure falls below 100 mm Hg; if a bolus of 250 mL of normal saline corrects the hypotension, the infusion is resumed.

4. Electrical cardioversion: If chemical cardioversion fails, most patients then undergo electrical cardioversion in the ED, supervised by the emergency physician. Typically, procedural sedation and analgesia using fentanyl and propofol is administered and biphasic waveform energy levels of 150-200 J are delivered (during the study period most patients received monophasic waveform defibrillation as biphasic defibrillation was not yet widespread).

5. Anticoagulation: Patients with a time from symptom onset that is clearly less than 48 hours or with therapeutic INR levels typically do not receive anticoagulation in the ED. Although controversial, current recommendations advise warfarin be administered for patients with transesophageal echocardiogram- guided cardioversion or with a CHADS2 score of 1 or greater (Table 1).5,19,21,22 The role of heparin is unclear and is rarely used for any patients at our institution.

6. Disposition: Patients who undergo successful cardioversion are typically discharged home within an hour without medication (that is, no new oral anticoagulants, rate control agents or rhythm control agents are prescribed or given). For first-time episodes, outpatient echocardiography and cardiology follow-up is usually recommended. Monitoring of the INR and appropriate physician follow-up is arranged for the few patients started on warfarin.

7. Patients not treated with cardioversion: Patients who are not treated with cardioversion in the ED have their rate controlled and are then discharged on oral anticoagulants and rate control medication. Monitoring of the INR and physician follow-up is also arranged for this group. Heparin is rarely given to these patients in our ED.

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.

Investigations
The 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).

Management
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:

• 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

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.

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)

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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.

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Worrisome Thoughts About the Diagnosis and Treatment of Patients With Brugada Waves and the Brugada Syndrome (Circulation. 2004;109:1463-1467.)

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 V_1-2 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

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.

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

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

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 cliniciansÂ’ 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)."

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.

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

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