Download Tachy-dysrhythmia Handout Mark Bromley Definitions Acute A

Tachy-dysrhythmia Handout
Mark Bromley
Definitions
 Acute A
 Paroxysmal AF
 Persistent AF
 Permanent AF
 Secondary
 Lone
ED Issues
Rate vs Rhythm
BB vs CCB
ED Cardioversion
 Patient selection
 Method of cardioversion
 Safety
Evaluation for underlying cause
Admission Requirements
AFIB anticoagulation clinic – 944-3339
Start by making your scheme for AFIB – work alone then compare
Case 1
47 year old M presents with palpitations
Triage 120 122/79 17 94% ORA
ECG: AFIB
He doesn’t like the feeling. How would you like to manage this patient?
Goal: identify stable patients in whom ED cardioversion is indicated.
Q: What is the etiology of atrial fibrillation? …list
 History
o Common contributors
 Alcohol – increased sympathetic tone
 Excessive cigarette smoking
 Diuresis-induced electrolyte disturbances
 Sleep apnea
 Caffeine
 Sleep deprivation
 Emotional stress
 Thyroid
o Dyspnea – heart disease
o Anginal – CAD
o Syncope – ventricular arrhythmia
 Exam
o Murmer  valvular heart disease
Q: What investigations would you like? …why?
 ECG
o Confirm AFIB
o Rate  Ashman, WPW
 Labs
o Thyroid
 In one series of 726 patients with recent onset AF, 39 (5.4
percent) had low serum TSH values. ½ were subclinical.
o Lytes
o CBC
 CXR
o CHF
o Pulmonary pathology (vascular)  RA dilatation
 Echo
Q: What are the indications for emergent cardioversion?
 Significant ischemia
 Hypotension – end organ perfusion
 CHF
 Pre-excitation syndrome
Q: Rate vs Rhythm
Wyse et al. AFFIRM: A comparison of rate control and rhythm control in patients
with atrial fibrillation. N Engl J Med (2002) vol. 347 (23) pp. 1825-33
 Randomized multicenter comparison
 Population: patients with atrial fibrillation and a high risk of stroke or death.
o >65 yrs or have risk factors for stroke or death
o 36% had no prior AFIB
o All were initially anticoagulated  rhythm could be withdrawn
 Primary end point: mortality
o More patients were in NSR in the rhythm control group at 5yr
 60% rhythm
 30% rate
o Mortality at five years, 23.8 percent and 21.3 percent, respectively;
hazard ratio, 1.15 [95 percent confidence interval, 0.99 to 1.34];
P=0.08
o Hospitalization:  rhythm
o Global function / Quality of life – no difference
 Rate was better in CHF and Age >65
Corley et al. AFFIRM FU: Relationships between sinus rhythm, treatment, and
survival in the Atrial Fibrillation Follow-Up Investigation of Rhythm Management
(AFFIRM) Study. Circulation (2004)
 Warfarin was beneficial and linked to survival
 NSR was linked to mortality
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# AFFIRM trial
# RACE trial
# PIAF trial
# STAF trial
# HOT CAFE trial
o All elderly patients
o Many chronic afibbers
o Antiarrhythmic meds were associated with non-cardiac mortality
o Sinus rhythm associated with reduced mortality
Q: How do we decide rate vs rhythm?
 Q: What are the chances they will stay in NSR?
o Duration – first episode  give them a chance
o Structural heart disease – LA size > 4.5cm
o Reversible disease – thyroid, pericarditis, PE, cardiac surgery
o No hypertension
o No heart failure
 Q: Do they need their atrial kick?
o CHF
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Q: Is rate control working?
o Inability to maintain adequate rate
Q: Is the patient unable to take warfarin?
o Very elderly – fall risk
o Sinus is much safer long term
Patient preference - symptoms
Q: What is the major risk to cardioversion?
o Stroke
Q: Is it safe to cardiovert patients with AFIB < 48h?
 TEE performed on 143 patients with AF of less than 48 hours duration found
left atrial clot in 20 patients (14%) – mostly valvular disease.
Q: What if these patients have a negative TEE?
 There is thromboembolic risk associated with cardioversion preceded by a
negative TEE: a 6% risk of thromboembolism following cardioversion
preceded by a negative TEE was demonstrated.
 This finding indicates either that TEE is an imperfect screen for left atrial clot
or that clot may develop post-cardioversion.
Q: Is it safe to cardiovert this patient? How can you make this decision?
Arnold et al. Role of prophylactic anticoagulation for direct current cardioversion in
patients with atrial fibrillation or atrial flutter. J Am Coll Cardiol (1992) vol. 19 (4)
pp. 851-5
o Retrospective review 545 AFIB patients > 48h duration
o 6 embolic events  earliest was at 72h
Stiell et al. Emergency department use of intravenous procainamide for patients
with acute atrial fibrillation or flutter. Academic Emergency Medicine (2007)
o 341 patients  no embolic events
Domanovits et al. Termination of recent-onset atrial fibrillation/flutter in the
emergency department: a sequential approach with intravenous ibutilide and
external electrical cardioversion. Resuscitation (2000).
o LMWH – single dose
o 51 cardioversions  no embolic events
Q: List 1 contraindication to cadioversion of unstable AFIB
 Slow afib – dig toxicity
Q: How many Joules?
 Conversion does not cause myocardial damage
o (Heart 1998, 80:3 and Resuscitation 1998;36:193)
 Shocks of > 200 J are associated with fewer tachyarrhythmic complications,
and do not increase the risk of other serious complications.
o (International Journal of Cardiology 123 (2008) 307 – 312)
Q: List 5 things that can be done to improve the chances of cardioversion.
 AP placement of the pads
 Expiration
 Direct pressure
 Biphasic conversion (86% v 51%)
Case 2 – Rate control
AFIB > 72h duration
Q: What patients with AFIB > 72h may warrant cardioversion?
o HF
o Syncope
o Other symptoms directly attributable to the dysrhythmia
Q: What is the ideal agent for rate control in AFIB?
o ESC recommendations
o Emerg
o Emerg Med J 2005;22:411–414. doi: 10.1136/emj.2003.012047
o Prospective RCT
o Diltiazem vs Metoprolol
o N=40 HR>120 BP>95
o Success rate higher for diltiazem at each time interval
o Success rate 90% vs 80% (HR<100)
o No hypotension
Q: List 3 circumstances when BBs are the preferred agents for rate control in AFIB
 AFIB due to MI
 Hyperthyroidism
 Catecholamine access
Q: What is your second line agent for rate control in AFIB?
o IV magnesium sulfate
o It slows conduction through the atrioventricular node and has been shown to
have rate control success rates equivalent to those of amiodarone and
digoxin in varying doses.
o 2x more likely to achieve HR<100 compared with placebo.
Case 3 – Anticoagulation
Goal: Examination of the role of anticoagulation in ED patients with AF
What are the Risk Factors for stroke in AFIB?
Is there a difference in the stroke risk in paroxysmal/persistent/permanent AFIB?
AFIB with…
 Prior stroke, TIA, systemic embolism
 Mitral stenosis
 Prosthetic valve
 2 or more RF
o Warfarin  INR: 2.5


1 RF
o Warfarin  INR: 2.5 or ASA 75 – 325 mg/day
Age < 75 and no RF
o ASA 75 – 325 mg/day
What are the issues with the data we use to anticoagulate?
o CHADS2
o Derived from trial cohort data  many potential RF not included
AHA Guidelines
Undergoing cardioversion
  48h or unknown duration
o Immediate anticoagulation – heparin or LMWH or Coumadin x 5d
o TEE  no thrombus  cardiovert
 Post cardioversion  coumadin x 4 weeks
o TEE  thrombus  postpone cardioversion and anticoagulate
 Repeat TEE before attempting later cardioversion
 < 48h
o Cardioversion
o Heparin or LMWH at presentation
o Post-cardioversion anticoagulation is based on whether the patient
has experienced more than one episode of AF and on his or her risk
factor status
 Emergency cardioversion
o Heparin or LMWH at presentation
o Coumadin x 4 weeks
ESC Guidelines
o CHA2DS2 – VASc
o High Risk
 CHADS2
 Framingaham – 10.2%
 CHADS2 VASc - 75.7%
o Intermediate
 CHADS2 – 61.9%
 FRAMINGHAM
 CHADS2 VASc – 15.1%
o Low Risk
 CHADS – (TE events – 1.4%)
 FRAMINGHAM – 48.3%
 CHADS2 VASc – 9.2%
o Low event rates in ‘low risk’ subjects and the classification of only a
o Small proportion of subjects into the ‘intermediate risk’ category.
Case 4
67F with known AFIB presents with altered mental status.
Q: What information would you like? Why?
o 162 85/50 22 37.9’C
o Urine
o Volume status - dehydrated
o Chronic but rapid atrial fibrillation is best managed by treating any trigger
(notably volume deficits, infection, or decompensated heart failure) and
rate control if needed.
Case 3
An otherwise healthy 17-year-old male presents following a syncopal episode
sustained while playing volleyball. He complains of intermittent palpitations, but is
currently asymptomatic. His blood pressure is 124/76.
Q: What is the pathophysiology behind a delta wave?
o Pathologic accessory pathway connecting the atrial and ventricular cells
o Pathways do not share the normal conduction delay of the AV node
o Allow rapid ventricular response   CO
Q: When do you see a delta wave?
 When not in circus rhythm
 Antidromic WPW
Q: Cardioversion or rate control in the ED?
Q: If rate control, what agent is the best choice for rate control in this patient?
 Not Rate Control
 AV nodal blockers may enhance conduction through the accessory path
o No Dig
o No BB
o No CCB
Q: What is the drug of choice for treating WPW and AFIB?
 Procainamide
o The actions of a class IA drug involve moderate depression of phase 0
upstroke, a slowing of repolarization, and a prolongation of
conduction time in the fast response cells of atrial muscle, ventricular
muscle, His-Purkinje cells, and APs.
o When these cellular events are translated to the intact heart, the main
results are increased duration of the QRS and prolongation of the QT
interval in the surface ECG (Fig. 29-52).
o These agents have minimal direct action on slow-response cells in the
SA and AV nodes but may indirectly increase the sinus rate and
enhance AV node conduction through anticholinergic side effects.
o
SVT
Q: What is SVT? …paroxysmal narrow-complex regular tachycardia
 Depends what you read
 Narrow complex tachycardia
 Usually re-entry tachycardias – AVRT, AVNRT, SRT
 Could also be unifocal atrial tach, NPJT, MFAT, Aflutter
Q: What is the first step in treating SVT?
 Vagal maneuvers
Q: What are the downsides to adenosine?
 11% - Cochrane review of 8 trials
o Flushing

o CP
o Sense of Doom
Case reports
o Brady arrhythmias
o Ventricular tachyarrhythmias
Q: How should adenosine be given?
 6mg IV push through a large antecubital vein
 Followed by a saline flush 10-20 ml (60% convert)
 No effect  12mg (90% convert)
 No effect  12mg
Q: How does the dose change with central access?
 ½ the dose
Q: List 2 conditions that may require more adenosine?
 Caffeine
 Theophyline
Q: List 2 conditions that may require less adenosine?
 Heart transplant (1-3 mg)
 Carbemazapine
Q: What are the 4 unique outcomes that may occur with adenosine and narrow
complex tachycardia?
1) Termination of the tachycardia
 AVRT
 AVNRT
 SNRT
2) Gradual slowing then re-acceleration of the tachycardia
 Sinus tach
 NPJT
 UAT
3) Demonstration of an atrial tachycardia with high grade AV block
 AFLUTTER
 AFIB
4) Unmasking of a concealed accessory pathway

5) No effect
 Inadequate dose
 Narrow complex VT
Q: What if the patient refuses adenosine – or we’re all out?
 Cardioversion
Q: Pill in the pocket?
 What Pill?
o RCT N=30 diltiazem/propranolol superior to flecainide and placebo
o 94% vs 61% vs 52%
 Who is not a candidate?
o Pre-excitation
o Sinus brady
o Heart failure
Q: What is the final step?
 Catheter ablation
Q: Who needs to come in to hospital?
 Wide complex
 Pre-excitation
Torsades
Definition: Torsade is defined as a polymorphous ventricular tachycardia in which
the morphology of the QRS complexes varies from beat to beat
o Regular variation of the QRS axis from negative to positive and back
o Twisting of the point
o  QT > 600 ms usually
Q: Why does  QT happen?
 Delay in phase III of the action potential
 K+ channels
 Repolarization is not homogenous
Q: Most torsades rhythms are started by a long pause. Why?
 QT interval is dependant on the preceeding R-R interval
 Long R-R (pause)  long QT
Q: Management for torsades?
 Withdraw all QT prolonging drugs
 Electrolytes
o MgSO4 2-4g IV slow push
 Adverse effects: hypotension, depression of NM function
o K+  if hypokalemic
 Isoproterenol (B1, B2)
 Overdrive pacing
o  rate until you get capture
o Reported up to 140 bpm
 Last ditch
o Lidocaine
o Cardioversion
References
Assessment
Page RL; Wilkinson WE; Clair WK; McCarthy EA; Pritchett EL. Asymptomatic arrhythmias in patients
with symptomatic paroxysmal atrial fibrillation and paroxysmal supraventricular tachycardia. Circulation
1994 Jan;89(1):224-7.
Israel CW; Gronefeld G; Ehrlich JR; Li YG; Hohnloser SH. Long-term risk of recurrent atrial fibrillation as
documented by an implantable monitoring device: implications for optimal patient care. J Am Coll Cardiol
2004 Jan 7;43(1):47-52.
Krahn AD; Klein GJ; Kerr CR; Boone J; Sheldon R; Green M; Talajic M; Wang X; Connolly S. How
useful is thyroid function testing in patients with recent-onset atrial fibrillation? The Canadian Registry of
Atrial Fibrillation Investigators. Arch Intern Med 1996 Oct 28;156(19):2221-4.
 5% of patients with new onset AFIB are hyperthyroid (subclinical)
Stroke Risk
Wolf PA, Mitchell JB, Baker CS Kannel WB, D'Agostino RB. Impact of atrial fibrillation on mortality,
stroke, and medical costs. Arch Int Med 1998;158:229-34
  Age =  Stroke risk …in those > 80y, AF accounts for 25% of strokes
Frost et al. Incident stroke after discharge from the hospital with a diagnosis of atrial fibrillation. Am J Med
(2000) vol. 108 (1) pp. 36-40
 Danish study – ½ the population – AFIB dx – no stroke hx – followed prospectively
o 1.3 in those aged 50 to 59 years
o 2.2 in those aged 60 to 69 years
o 4.2 for those aged 70 to 79 years
o 5.1 for those aged 80 to 89 years
Management
Anticoagulation
Stoddard MF. Left atrial appendage thrombus is not uncommon in patients with acute atrial fibrillation and
a recent embolic event: A transesophageal echocardiographic study. J Am Coll Cardiol 1995;25:452-459.
 TEE in patients with <3d AFIB  14% had thrombus (lots had valve disease)
Fatkin D. Transesophageal echocardiography before and during direct current cardioversion of atrial
fibrillation: Evidence for “atrial stunning”as a mechanism of thromboembolic complications. J Am Coll
Cardiol1994;23: 307-316.
 TEE during conversion showed stunning of myocardium
Rate versus Rhythm
Wyse et al. AFFIRM: A comparison of rate control and rhythm control in patients with atrial fibrillation. N
Engl J Med (2002) vol. 347 (23) pp. 1825-33
 Rhythm-control strategy offered no survival advantage over the rate-control strategy
o No difference in 5 year mortality
o No difference in composite: death, stroke, anoxic encephalopathy, bleeding and arrest
 Rhythm control strategy was associated with  rate of hospitalizations and  adverse drug effects
Corley et al. AFFIRM FU: Relationships between sinus rhythm, treatment, and survival in the Atrial
Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) Study. Circulation (2004)
 Anticoagulation and sinus rhythm were potent predictors of survival
  Mortality associated with anti-arrhythmic drug use offset the survival advantage
Cardioversion
Rao et al. Direct current cardioversion does not cause cardiac damage: evidence from cardiac troponin T
estimation. Heart (1998) vol. 80 (3) pp. 229-30
 Cardioversion doesn’t cause an increase in TNT  case series of 51 patients ½ received 960J
Gallagher et al. Arrhythmic complications of electrical cardioversion: Relationship to shock energy.
International journal of Cardiology (2008)
 Shocks of > 200 J are associated with fewer tachyarrhythmic complications, and do not increase
the risk of other serious complications
Rate Control
Moran JL,Gallagher J,Peake SL,et al. Parenteral magnesium sulfate versus amiodarone in the therapy of
atrial tachyarrhythmias:A prospective,randomized study. Crit Care Med1995; 23:1816-1824.
 MgSO4 has rate rate control success rates equivalent to those of amiodarone and digoxin
Davey MJ,Tuebner D. A randomized controlled trial of magnesium sulfate, in addition to usual care,for
rate control in atrial fibrillation. Ann Emerg Med2005;45:347-353.
 MgSO4 group was 2x more likely to achieve rates < 100bpm than placebo
www.escardio.org
944-3349 -bev
Dr. WYSE
CHADS
0 – ASA
1 – ASA or warfarin
2> - warfarin
CHADS vasc – European society of cardiology using
2