Supraventricular Tachycardia and Artial Fibrillation

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Transcript Supraventricular Tachycardia and Artial Fibrillation

Supraventricular
Tachycardia
and Atrial Fibrillation
Courtney Bunevich, D.O.
August 15, 2007
SVT: Clinical Features
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Regular, rapid rhythm
Usually narrow complex rhythm
Arises from atria or atrioventricular nodal tissue above
the bundle of His that initiate and maintain the rhythm
Either a reentry or an ectopic pacemaker above the
bundle of His
SVT: Pathophysiology
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Reentry: SVT associated with reentry is PSVT
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AV nodal reentry (AVNR) occurs in 60% of cases
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Orthodromic AVNR is antrograde conduction via AV
node and retrograde conduction via accessory pathway
AV reentry via an accessory pathway in 30%
 Intra-atrial reentry s/p cardiac surgery after large
atrial incision with scar formation
 Sinus node reentry, inappropriate sinus tachycardia,
ectopic junctional tachycardia, and nonparoxysmal
junctional tachycardia are rare
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PSVT: Clinical Features
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Can occur in a structurally normal heart
Can be associated with rheumatic heart disease,
acute pericarditis, MI, MVP, and preexcitation
syndromes.
Exacerbated by caffeine, alcohol, illicit drugs,
hyperthyroidism, diet supplements, herbal
supplements (ginseng). Can be induced by
PACs and PVCs
PSVT: Signs and Symptoms
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Sudden onset and termination
Can occur in patients of all ages
Regular, tachycardia
Palpitations, anxiety, diaphoresis,
lightheadedness, chest pain, dyspnea, pounding
in chest and neck.
Syncope is uncommon
Polyuria if SVT prolonged secondary to release
of atrial natriuretic peptide
Differential Diagnosis
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Atrial fibrillation/ Atrial flutter/ MAT
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Onset usually in patients > 60 y/o
Patients usually heave heart disease
Irregularly Irregular rhythm
Ventricular Tachycardia
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Patients usually > 50 y/o
Patients usually have IHD
Present with syncope and SCD
Wide complex regular rhythm
Abrupt onset
Physical Exam
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Patient can be diaphoretic, anxious, hypotensive,
or even asymptomatic
Prominent jugular venous A wave from atrial
contraction against closed tricuspid valve “frog
sign”
Emergency Care
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Get immediate set of vital signs including pulse
oximetry, IV, O2, monitor.
EKG
CKMB and Trop I, TSH, FT4
BMP
Connect patient to continuous 12 lead EKG
Is patient stable? Do they need immediate
cardioversion?
EKG
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The EKG in PSVT is usually a narrow, regular
complex tachycardia.
Less than 10% of cases will have SVT with
aberrancy
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To be discussed later
Treatment
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Try a vagal maneuver to slow rhythm to see the
underlying rhythm.
Carotid sinus massage
 Do if no bruits auscultated and no known carotid
disease
 Massage for 5 seconds and release
 Can also place an ice pack on the forehead
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Treatment
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Adenosine
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Causes flushing, CP, dyspnea
Half life is 15 seconds
First line treatment is Adenosine 6 mg IVP
If unsuccessful, give Adenosine 12mg IVP x 2
Cause transient AV nodal block by hyperpolarization of the node
Complications include bronchospams and VF
Will not work if patient has heart transplant
C/I if wide complex tachyarrhythmia
Caution in patients with severe COPD
Adensione 6mg terminate in 60-80% patients
Adenosine 12mg will terminate in 90-95% of patients
Treatment
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Next line treatments:
Verapamil 0.075 -0.15 mg /kg IV can repeat in 30
min. Hypotension can occur but can prevent this by
giving CaCl2 10% 4mL. Not commonly used.
 Diltiazem 10-20 mg bolus then continuous infusion
in at 5-15 mg/hour
 Esmolol protocol
 Metoprolol 5mg IV q5 x 3
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Treatment
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Consider cardioversion or venous atrial or ventricular
temporary pacing if unable to slow rhythm down with
adenosine, CCB, and BB before giving antiarrhythmics.
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Can also give IV flecainide, IV procainamide, IV
propafenone, IV ibutilide
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These drugs can cause hypotension, bradycardia, and
are proarrhythmic.
Synchronized Cardioversion
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Should be used immediately in any unstable
patient with hypotension, pulmonary edema,
chest pain, or other unstable signs.
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Required dose is usually small: 50 Joules
Long term Treatment
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Risk of developing long term PSVT after single
episode not defined. One episode is not
indication for long term treatment.
Long term Treatment
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SVT with No Preexcitation
Verapamil, Beta blockers, and Diltiazem
 Decrease symptoms in 30-60%
 Randomized clinical trials show no superiority
 Failure on a single drug therapy can try a combo of
two or add one a class IC or class III antiarrhythmic
 Long term treatment with class IC not
recommended, and patents should be referred for
catheter ablation
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Catheter Ablation
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Radiofrequency and Cyrothermal
95% success rate initially
<5% recurrence rate in the 1st few months
Complications occur in 2-3%
Damage to arteries, bleeding, AVF, venous
thrombosis, PE, myocardial perforation, valvular
damage, systemic embolism, and death (rare)
 Blocking near the AV node can cause total block of
the AV node and patient will need a pacemaker
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Wolf Parkinson White
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Associated Ebstein’s anomaly
EKG will show a short PR interval, a delta wave,
and a QRS interval up to 0.12 msec
Accessory pathway is the Bundle of Kent
Wolf Parkinson White
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Has 2 mechanisms for PSVT
Orthodromic, narrow complex (95%)
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Antrograde conduction via AV node and retrograde
conduction via accessory pathway
Can treat like PSVT
Antidromic, wide complex (5%)
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Antrograde conduction via accessory pathway and retrograde
conduction via AV node
DO NOT give Digoxin, BB, Verapamil
Try procainamide and cardioversion
SVT with WPW
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Catheter ablation is the treatment of choice
once stable
Risk of sudden death is 0.15 – 0.45 % / year
Wolf Parkinson White
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Can degenerate into Atrial Fibrillation
If life threatening: do immediate cardioversion.
If not unstable, you can try procainamine,
amiodarone, or lidocaine
Caution verapamil, BB, and digoxin will cause
degeneration into ventricular fibrillation!!
SVT with aberrancy
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Occur in less than 10% of cases
Regular, wide complex tachycardia
Causes:
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SVT with a preexcitation syndrome
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Antidromic reentry seen in <5% cases of patients who
have WPW
Patient with a preexisting BBB
 Bundle branch fatigue in PSVT
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Atrial Fibrillation
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Uncoordinated atrial activation with
deterioration of atrial mechanical dysfunction
Ventricular response to atrial fibrillation depends
on the integrity and electrophysical properties
of the AV node
Most common arrhythmia encountered in
clinical practice
Atrial Fibrillation
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Most common sustained tachyarrhythmia patients seek
treatment for
Affects 0.4-1% of the general population and 8% of
patients greater than 80 years old
AF occurring in patient without structural heat disease
and less than 65 y/o is termed lone AF
Types:
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First episode
Paroxysmal (self-terminating)
Persistent (requiring electrical or pharmacological treatment)
Permanent
Atrial Fibrillation
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Irregularly, irregular rhythm
Can be associated with rapid ventricular conduction/response or
AF with RVR
No atrial kick in atrial fibrillation. The firing of the atria and
ventricles is not synchronized. In patients with systolic
dysfunction, the atria makes an important contribution
Biopsies have shown patchy fibrosis of fibers in atria
Foci can be found in atria, pulmonary arteries, coronary sinus
Atrial rate is 350-600 beats/min
Multiple small areas of the atria are firing and contracting
(quivering)
Ventricular conduction rate is variable 40-180 bpm
Causes for Atrial Fibrillation
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Rheumatic heart disease
Nonrheumatic mitral valve disease disease
Hypertension
Chronic lung disease
ASD
Thyrotoxicosis *
Lone AF
Ischemic heart disease
Acute MI *
Dilated cardiomyopathy
Holiday heart- Alcohol ingestion *
Theophylline toxicity
Pheochromocytoma
Causes for Atrial Fibrillation
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Pericarditis *
Electrocution *
Post cardiothoracic surgery *
Myocarditis *
Pulmonary embolism *
Obesity
Intracardiac tumors or thrombi
Amyloidosis
SAH or CVA
Familial AF
Signs and Symptoms
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Can be severe:
Pulmonary edema, palpitations, angina, and syncope
 Relatively asymptomatic
 Nonspecific symptoms such as fatigue
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Treatment of AF with RVR
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Get an immediate set of vitals, pulse oximetry. Place a
patient on a monitor and O2. Get IV access.
Get EKG. Check BMP.
Check CKMB and Trop I. Get CXR.
Check TSH and FT4.
How long has AF been present? <48hrs or >48hrs or
unknown
Is patient unstable? Do they need immediate
cardioversion?
Treatment of AF with RVR
Rate Control
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Medications: IF preserved EF > 40%
Diltiazem 10-20 mg IV bolus and run a drip in at 515 mg/hour. Can repeat the bolus if needed.
 Esmolol protocol
 Metoprolol 5mg IV q5 min x 3
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Treatment of AF with RVR
Rate Control
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Medications: If EF < 40%
Recommend:
 Diltiazem 10-20 mg IV bolus and run a drip in at 515 mg/hour. Can repeat the bolus if needed.
 Amiodarone 150mg IV over 1 minute then 1
mg/minute for 6 hours then 0.5 mg/min for 18
hours
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Caution if patient on digoxin
 Watch for hypotension
 Low efficacy for acute conversion
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Treatment of AF with RVR
Rhythm Control
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If duration is < 48 hours and EF > 40%
DC Cardioversion at 100 Joules (60%) , 200
Joules (80%)
ONLY ONE of the following: Amiodarone,
ibutilide, flecainide, propafenone, and
procainamide
Treatment of AF with RVR
Rhythm Control
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If duration < 48 hours and EF< 40%
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DC cardioversion or Amiodarone
Treatment of AF with RVR
Rhythm Control
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If duration > 48 hours or unknown
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Do rate control. Start anticoagulation for 4
weeks with therapeutic INR. Exclude clot. Do
cardioversion. Continue anticoagulation for 4
more weeks.
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Begin IV heparin. TEE exclude clot.
Cardioversion. Anticoagulation for 4 weeks.
TEE
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TEE will show thrombus in 5-15% in atrial
fibrillation preparing for cardioversion
Thromboembolic events have been reported
after “normal” TEE and cardioversion
Contrast enhanced MRI is evolving diagnostic
modality for evaluation intracardiac thrombi
Statins have been shown to decreases risk of
recurrent AF after cardioversion possible due to
anti-inflammatory affects
Atrial Fibrillation
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AFFIRM trial 2002 showed no mortality
differences between rate and rhythm control
groups. Rhythm control should be reserved for
patients who are symptomatic even when rate
controlled.
Patients need either rate or rhythm control and
anticoagulation
New Onset AF
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Minimal Evaluation:
H and P for symptoms, type of AF, date of onset
and duration, treatment given, co-morbid or
predisposing conditions
 ECG- evaluate rhythm, LVH, preexcitation
syndromes, BBB, and old MI
 TTE- evaluate LV function, clots (inferior), valvular
disease
 Labs: TSH, Renal and Hepatic function
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New Onset AF
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Additional Testing:
6 minute walk test to assess for adequate rate control
 Exercise stress test
 Holter monitor
 TEE
 Electrophysical studies
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Atrial Fibrillation
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AFFIRM trial showed that patients despite being in
sinus rhythm are still at high risk of stroke.
Patients with paroxsymal AF still must be
anticoagulated.
CHADS2: criteria recommended that scores 0-2 can
use aspirin safely and scores greater than 3 need
warfarin in those with nonvalvular AF
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CHF – 1 point
HTN – 1 point
Age > 75 years – 1 point
DM – 1 point
Prior Stroke or TIA – 2 points
CHADS2
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Score:
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0
1
2
3
4
5
6
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Stroke rate per year (%):
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1.9
2.8
4.0
5.9
8.5
12.5
18.2
Risk of Stroke
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Atrial fibrillation is associated with increased risk of
stroke, heart failure, and all cause mortality
5% per year risk of CVA in patients with nonvalvular
atrial fibrillation
Framingham study showed 17 times increased risk of
CVA in patients with valvular AF and 5 times increased
risk in those with nonvalvular AF
1.5% risk of CVA in patients age 50-59
23.5% risk of CVA in patients age 80-89
Risk of Stoke
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NYHA classification:
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Risk of stroke/year (%):
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I
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4%
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II-III
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12-26%
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IV
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27-50%
Risk of Stroke
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Risk Factors:
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CVA/TIA
DM
HTN
HF
Age per decade
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Relative Increased Risk:
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2.5
1.7
1.6
1.4
1.4
ASA Treatment
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Treat of AF with ASA is a Class I
recommendation by the 2006 ACC guidelines in
the following subsets of patients:
Age < 60 and no heart disease
 Age 60-74 with heart disease and no risk factors
 Age 60-74 and no heart disease
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Risk factors: Heart failure, EF<35%, HTN
Pharmacologic Cardioversion
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Ibutilide is the only drug FDA approved for
pharmacologic cardioversion
45% conversion rate for AF
60% conversion rate for Atrial Flutter
Class III agent with a 4-8% risk of TdP
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Higher if patient has CHF or cardiomyopathy
0.01mg/kg (max 1 mg) over 10 minutes
Have external defibrillator ready
Monitor of telemetry for at least 4 hours
Pharmacologic Cardioversion
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Digoxin and sotalol are NOT recommended for
pharmacologic cardioversion
These drugs gave Class I and IIa recommendations for
pharmacologic cardioversion:
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Dofetilde
Flecanide
Propafenone
Ibutilide
Amiodarone (IIa)
Electrical Cardioversion
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Recommended if symptoms are known to be
less than 48 hours
Unstable in patients without accessory pathway
Unstable or in tachycardic patients with an
accessory pathway
Patients unable to tolerate symptoms
Contraindicated in hypokalemia and digitalis
toxicity
Other Treatments
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Maze procedure
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Can do as an adjunct procedure during open heart
surgeries
Catheter ablation after EP studies to determine
irritable foci
AVN ablation can be useful in patients with
tachycardia-mediated cardiomyopathy
 Small study showed increase in EF from 26% to
34% after AVN and pacemaker implantation
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References
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Harrison’s Internal Medicine 16th Edition
2006 ACC Guideline for Atrial Fibrillation
New England Journal of Medicine
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American Journal of Emergency Medicine
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Supraventicular Tachycardia
9 March 2006 pp 1039 volume 354
Wide Complex Tachycardias: Beyond Traditional Differential Diagnosis
of Ventricular Tachycardia versus SVT with Aberrant Conduction
November 2005 pp 876 volume 23
New England Journal of Medicine
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AFFRIM Trial pp 1825 volume 347