Transcript RTC ATRIAL FIBRILLATIONx

The Diagnosis and Management of
Cardiac Dysrhythmias - Atrial
tachycardia. Pharmacologic
treatment
8/19/09
Narrow–QRS-complex (SVT) tachycardias
(QRS 0.12second) in order of frequency
Sinus tachycardia
Atrial fibrillation
Atrial flutter
AV nodal reentry
Accessory pathway–mediated tachycardia
Atrial tachycardia (ectopic and reentrant)
Multifocal atrial tachycardia (MAT)
Junctional tachycardia
Initial Evaluation
Primary Survey
Is patient stable or unstable?
– stable: determine rhythm, treat accordingly
– unstable
• chest pain, dyspnea, decreased level of conciousness, low BP,
CHF, Acute MI
• If HR is cause of symptom (almost always HR>150): cardiovert
Secondary Survey
Specific Rhythms
– Atrial fib/flutter
– Narrow-Complex (Supraventricular) Tachycardia
– Wide-Complex Tachycardia, Unknown Type
Differential diagnosis
for narrow QRS tachycardia.
Questions to answer in order to identify an
unknown arrhythmia:
1. Is the rate fast (>100 bpm)?
Suggest increased/abnormal automaticity or reentry
2. Is the rhythm irregular?
Irregular  Suggests atrial fibrillation, 2nd degree AV block,
multifocal atrial tachycardia, or atrial flutter with variable AV
block
3. Is the QRS complex narrow or wide?
Narrow  Rhythm must originate from the AV node or above
Wide  Rhythm may originate from anywhere
Questions to answer in order to identify an
unknown arrhythmia:
4. Are there P waves?
Absent P waves  Suggests atrial fibrillation, ventricular
tachycardia, or rhythms originating from the AV node
5. What is the relationship between the P waves and QRS complexes?
More P waves than QRS complexes  Suggests 2nd or 3rd degree
AV block
More QRS complexes than P waves  Suggests an accelerated
junctional or ventricular rhythm
6. Is the onset/termination of the rhythm abrupt or gradual?
Abrupt  Suggests reentrant rhythm
Gradual  Suggests altered automaticity
Most Likely
Pulse
Most likely diagnosis
ECG to rule out
Regular and slow (~60 bpm)
Sinus rhythm Junctional rhythm
Complete heart block
Regular and fast (~150 bpm)
Atrial flutter with 2:1 AV block
Ventricular tachycardia
Regular and fast (>150 bpm)
AV node re-entrant tachycardia
Ventricular tachycardia
Irregular and fast
Atrial fibrillation with rapid
ventricular response
Ventricular tachycardia
Irregular and slow
Atrial fibrillation with controlled
ventricular response
Ventricular tachycardia
Four Major Classes of Supraventricular
Tachyarrhythmia
• Sinus tachycardia
• Paroxysmal supraventricular tachycardia
(PSVT)
• Atrial Fibrillation
• Atrial flutter
Class Antiarrhythmic Drugs
•
•
•
•
Class I Sodium Channel blocker
Class II Beta blockers
Class III Potassium channel blockers
Class IV Calcium channel blockers
Sinus Tachycardia
Sinus Tachycardia
Sinus Tachycardia
• Rate: Greater than or equal to 100.
• Rhythm: Regular. P waves: Upright, consistent, and normal in
morphology (if no atrial disease)
• P–R interval: Between 0.12–0.20 seconds and shortens with increasing
heart rate
• QRS complex: Less than 0.12 seconds, consistent, and normal in
morphology
Sinus tachycardia ACC/AHA/ESC criteria
1. The presence of a persistent sinus tachycardia (heart
rate more than 100 bpm) during the day with excessive
rate increase in response to activity and nocturnal
normalization of rate as confirmed by a 24-hour Holter
recording
2. The tachycardia (and symptoms) is nonparoxysmal
3. P-wave morphology and endocardial activation
identical to sinus rhythm
4. Exclusion of a secondary systemic cause (eg,
hyperthyroidism, pheochromocytoma, physical
deconditioning)
Recommendations for Treatment of
Inappropriate Sinus Tachycardia
The treatment of inappropriate sinus tachycardia is
predominantly symptom driven
ACC/AHA/ESC Guidelines
Paroxysmal Supraventricular Tachycardia
Paroxysmal supraventricular
tachycardia (PVST)
• PSVT suspected when a rhythm strip shows a
rapid and typically very regular nonsinus rate
at about 140 to 220 beats/min (range: 100 to
250 beats/min).
PVST
• The three major types of PSVT
• Atrial tachycardia (AT) Often MAT
• Atrioventricular nodal reentrant tachycardia
(AVNRT),
• AV reentrant tachycardia (AVRT) involving a
bypass tract of the type seen in the WolffParkinson-White (WPW) syndrome
PSVT
A Normal
B Atrial tachycardia
(MAT)
C atrioventricular
nodal reentrant
tachycardia (AVNRT)
D AV reentrant
tachycardia (AVRT)
involving a bypass
tract of the type seen
in the WolffParkinson-White
(WPW) syndrome
AV nodal reentrant tachycardia
(AVNRT)
• Distinct arrhythmia caused by a rapidly
circulating impulse in the AV node area.
The cardiac impulse literally spins around
and around and appears to “chase its
own tail.” Reentry can occur in virtually
any part of the heart.
• AVNRT produces a very rapid and regular
supraventricular rhythm with rates
typically between 140 and 250 beats/min
• This arrhythmia may occur with
otherwise normal hearts or with
underlying heart disease.
• Runs of AVNRT are generally initiated by
an APB
AV nodal reentrant tachycardia
Tachycardia due to a rapidly circulating impulse in the
atrioventricular (AV) node (junction) AV nodal reentrant
tachycardia
Marked regularity of rhythm rate of about 170 beats/min.
No P waves are visible
ECG pattern of typical atrioventricular nodal
reciprocating tachycardia (AVNRT)
Pseudo r in V1 (arrow) and accentuated S waves in 2, 3,
aVF (arrow) are pathognomonic for AVNRT.
Recommendations for Long-Term Treatment of Patients With Recurrent AVNRT
ATRIOVENTRICULAR REENTRANT (AVRT)
TACHYCARDIA
• Bypass tract (accessory pathway,
WPW syndrome ), an abnormal
tract of cardiac muscle that
connects the atria and ventricles,
circumventing the AV node.
• Tachycardia caused the impulse
travels down the normal conduction
system (AV node and His bundle)
into the ventricles, recycles rapidly
up into the atria via the bypass
tract, and then goes down the AV
node again.
• Repetition of this large reentrant
circuit leads to atrioventricular
reentrant (bypass tract) tachycardia
(AVRT), a type of PSVT
ATRIOVENTRICULAR REENTRANT (AVRT)
TACHYCARDIA
• Accessory Pathways
Causing PSVT. Accessory
pathways (WolffParkinson-White
syndrome) among other
bypass types.
• In Wolff-Parkinson-White
syndrome, a shortened PR
interval and a slurred
upstrike to the QRS
complex “delta wave” on
the resting ECG indicate
the presence of an
accessory pathway
Recommendations for Long-Term Therapy of Accessory Pathway–Mediated Arrhythmias
Atrial tachycardia (AT)
• Three or more consecutive Atrial Premature beats (APB)
• Most episodes involve an ectopic (nonsinus) pacemaker
located in either the left or right atrium that fires off
“automatically” in a rapid way.
• AT has been observed in patients without apparent
structural cardiac abnormality as well as in those with
virtually any type of heart disease.
• The atrial rate with AT may be as high as 200 beats per
minute or faster (usual range: 100 to 250 beats/min).
• A sustained episode that lasts 30 seconds or longer in
individuals with limited reserve, can induce angina or
congestive heart failure (CHF).
Atrial tachycardia (AT)
Atrial tachycardia terminating with resumption of sinus
rhythm.
The P waves of the tachycardia (rate: about 150
beats/min) are superimposed on the preceding T waves.
MULTIFOCAL ATRIAL TACHYCARDIA
• Tachyarrhythmia with multiple ectopic foci
stimulating the atria.
• Three or more (nonsinus) P waves with different
shapes at a rate of 100 or more per minute.
• The PR intervals often vary.
• MAT is usually seen in patients with chronic lung
disease.
• Ventricular rate is irregular and rapid, making this
arrhythmia likely to be mistaken for AF.
Rapidly occurring P waves showing variable shapes
and variable PR intervals
MAT
Increased Automaticity Causing PSVT
• Increased automaticity usually occurs when the
atrium is enlarged, as in patients with chronic lung
disease, congestive heart failure, or electrolyte and
acid-base disturbances.
• Usually, the stretched atria fire irregularly, producing
multiple premature beats that emanate from
different areas of the atria.
• Because the foci for the ectopic beats are in multiple
sites, the P waves vary in morphology
“multifocal atrial tachycardia.”
MAT
• Treatment is directed at correcting the
underlying cause.
• Antiarrhythmic drugs are usually not helpful.
Treatment Options for
Supraventricular Tachycardias
• Younger patients and individuals without
significant underlying cardiovascular disease may
tolerate heart rates up to 250 beats/min with
complaints of only palpitations or lightheadedness.
• In patients with limited cardiac reserve, however,
a heart rate above 160 beats/min (or even less)
may result hypotension, stroke myocardial
ischemia/ infarction may occur, CHF
Treatment Options for
Supraventricular Tachycardias
Electrical cardioversion should be performed
urgently if PSVT is sustained and there is
• Angina
• Shortness of breath
• Decreased level of consciousness
• Hypotension
• Congestive heart failure
Treatment Options for
Supraventricular Tachycardias
• If the symptoms are restricted to discomfort
(e.g., palpitations and anxiety), conservative
measures should be applied.
• Conservative management of PSVT can
include both nonpharmacologic and
pharmacologic measures
Treatment Options for
Supraventricular Tachycardias
Treatment Options for
Supraventricular Tachycardias
Treatment Options for
Supraventricular Tachycardias
The goal of pharmacologic management is to
slow or block atrioventricular nodal
conduction.
Agents used for this purpose include
• Adenosine
• Calcium channel blockers
• Beta blockers.
Adenosine
• Adenosine works by reducing conductance along the slow
antegrade pathway
• Ultra–short-acting agent that is cleared quickly (half-life of
1 to 6 seconds).
• Initial dose of 6 mg, followed by or two 12-mg boluses.
• Side effects include flushing, dyspnea, chest pain and
sense of doom. Warn first.
• Can also decrease the sinus rate transiently and produce a
“rebound” sinus tachycardia and should not be used in
patients with heart transplants, because such may be
highly suseptible
Calcium Channel Blockers
• Disrupt a reentrant pathway.
• Verapamil can be given in a 5- to 10-mg bolus over 2
minutes, followed by 10 mg in 15 to 30 minutes if
the initial dose does not convert the arrhythmia.
• Diltiazem is also effective. Initial treatment consists
of a bolus of 0.25 mg per kg administered over two
minutes. A repeat bolus of 0.35 mg per kg given
over two minutes can be administered 15 minutes
later.
• Calcium channel blockers should not be used in
patients with an undiagnosed wide-complex
tachycardia, because of the risk of fatal hypotension
or ventricular fibrillation if the arrhythmia is actually
ventricular tachycardia and not PSVT.
Beta Blockers
• Esmolol, a short-acting beta blocker
• given in anintravenous bolus of 0.5 mg per kg over 1
minute or in an infusion at a rate of 0.5 mg per kg per
minute after an initial loading dose of 0.5 mg per kg.
• Short half-life (four to five minutes), compared with
the much longer half-lives (three hours or more) of
most other beta blockers.
• Because of a similar depressive effect on left
ventricular contractility, esmolol should be used with
caution if initial treatment with a calcium channel
blocker is not successful.
Treatment Options for
Supraventricular Tachycardias
Other antiarrhythmic drugs, including quinidine,
procainamide, flecainide (Tambocor), and
amiodarone, may be used in patients if not
responsive to initial therapy.
Selective radiofrequency ablation is rapidly
becoming the treatment of choice in this
situation.
Summary PSVT
• EF Normal
– Ca-blocker> beta-blocker> digoxin> DC
Cardioversion.
– Consider procainamide, sotalol, amiodarone.
– If unstable proceed to cardioversion
• EF < 40%, CHF
– Digoxin or amiodarone or diltiazem.
– If unstable proceed to cardioversion
Atrial Fibrillation/Flutter
Atrial Fibrillation
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Atrial fibrillation is caused by numerous wavelets of depolarization spreading
throughout the atria simultaneously, leading to an absence of coordinated atrial
contraction.
Atrial fibrillation is important because it can lead to:
Hemodynamic compromise
Systemic embolization
Symptoms
Atrial fibrilation
• Affects 3 to 5 percent of patients more than
60 years
• The median age of patients with atrial
fibrillation is 75 years, and the prevalence of
the arrhythmia doubles every 10 years after
the age of 55
A Fib Risk factors
Most risk factors for atrial fibrillation are associated
with structural or ischemic heartdisease.
• Hypertension,
• Left ventricular hypertrophy
• Dilated and restrictive cardiomyopathies
• Coronary artery disease
• Chronic obstructive pulmonary disease
• Diabetes in women
Afib
• The annual risk of stroke in patients with atrial
fibrillation and normal valve function is about
4.5 percent per year.
• Anticoagulation with warfarin (Coumadin)
reduces the risk by about two thirds.
Atrial Fibrillation
EKG Characteristics:
Absent P waves
Presence of fine “fibrillatory” waves which vary in
amplitude and morphology
Irregularly irregular ventricular response
A fib
• The first step in managing a patient with atrial
fibrillation is to decide
– If there is a high likelihood of safe conversion
to sinus rhythm
– Or the patient should be allowed to remain in
atrial fibrillation.
Restoration of Sinus Rhythm.
In General
To Convert
• Within 48 hours of the onset of new atrial
fibrillation are candidates for cardioversion with a
low risk of embolism.
Or Not
• More than 48 hours or for an undetermined
period are more likely to have atrial thrombi and
may develop emboli with immediate electrical or
medical (pharmacologic) cardioversion.
A Fib Conversion
Transesophageal echocardiogram to evaluate
for thrombi
If present anticoagulation is recommended
before cardioversion is attempted .
Anticoagulation can be accomplished using
warfarin, with the dosage adjusted to achieve
an International Normalized Ratio (INR)
between 2.0 and 3.0 for a minimum of 21 days
A Fib
Synchronized cardioversion in appropriately
selected patients, has a success rate of at least
80 percent.
Electrical Cardioversion is preferred in patients
with hypotension, angina, heart failure, or
other evidence of severe compromise.
A Fib
• Amiodarone therapy is successful in 86
percent of patients who have had atrial
fibrillation for less than two years.
• Treatment is also effective in 40 to 60 percent
of patients with long-standing atrial fibrillation
that has been resistant to other agents and to
electrical cardioversion
A Fib Rate Control
• In patients in whom rhythm conversion is not
indicated or those who have new onset atrial
fibrillation with a rapid ventricular response,
treatment may be needed to control the
ventricular rhythm.
• Excessive ventricular rates may result in
diminished cardiac output because of poor
filling time, and in ischemia because of
increased myocardial oxygen demand.
Afib
• Acute management of ventricular rates can
usually be achieved with intravenously
administered
• Calcium channel diltiazem(Cardizem), given in
an initial bolus of 15 to 20 mg(0.25 mg per kg)
over two minutes
• Beta blocker such as propranolol (Inderal),
given in a dose of 0.5 to 1 mg (up to 3 to 5 mg
if needed).
A Fib Rate Control
• Beta blockers are recommended in a consensus
by the American and European societies of
Cardiology and the North American Society of
Pacing and Electrophysiology.
• Propranolol, metoprolol or atenolol are examples
of drugs that have been shown to be effective
• Side effects including hypotension fatigue
depression bronchospasm may prevent use in
some
A Fib Rate Control
• Calcium channel blockers are associated with
better exercise tolerance, may be preferable
to beta blockers.
• Digoxin is associated with a high degree of
exercise intolerance; should be reserved for
use in patients who are
– relatively immobile
– cannot tolerate other treatment options
– who have significant ventricular dysfunction.
Atrial Flutter
Atrial Flutter
Most cases of atrial flutter are caused by a large reentrant circuit in the wall of the right
atrium
EKG Characteristics:
Biphasic “sawtooth” flutter waves at a rate of ~ 300 bpm
Flutter waves have constant amplitude, duration, and
morphology through the cardiac cycle
There is usually either a 2:1 or 4:1 block at the AV node,
resulting in ventricular rates of either 150 or 75
Unmasking of Flutter Waves
In the presence of 2:1 AV block, the flutter waves may not be
immediately apparent.
These can be brought out by administration of adenosine.
Management of atrial flutter
Recommendations for Acute Management of Atrial Flutter
Recommendations for Acute
Management of Atrial Flutter
• Cardioversion should be considered only if the patient
is anticoagulated (INR equals 2 to 3), the arrhythmia is
less than 48 hours in duration, or the TEE shows no
atrial clots.
• Digitalis may be especially useful for rate control in
patients with heart failure.
• Ibutilide should not be taken by patients with reduced
LV function.
• Flecainide, propafenone, and procainamide should
not be used unless they are combined with an AVnodal–blocking agent.
Atrial Flutter
• Atrial flutter is due to a large reentrant circuit
usually originating in the right atrium.
• In the ventricles, reentry may lead to VPBs
and sometimes ventricular tachycardia.
Recommendations for Long-Term Management of Atrial Flutter
Atrial fibrillation/flutter
Summary
• If unstable: proceed more urgently
Cardioversion
• For tachycardia with serious signs and symptoms. Generally not
needed for HR<150.
• If HR>150, prepare for immediate cardioversion. May give brief
drug trial.
• Steps:
– Prepare emergency equipment
– Medicate if possible
– Cardioversion
• monomorphic VT with pulse, PSVT, A fib, A flutter: 100-200-300-360
J* (Synchronized)
– may try 50J first for PSVT or A flutter
– may use equivalent biphasic (biphasic 70, 120, 150, and 170 J)
– if machine unable to synchronize and patient critical, defibrillate
• polymorphic VT: use VT/VF algorithm
Atrial fibrillation/flutter
Summary
Management: Control rate, consider rhythm cardioversion and anticoagulate
depending on physiologic reserve
Normal EF
• Rate control: Ca-blocker or beta-blocker.
• Cardiovert:
– If onset < 48 hours, consider DC cardioversion OR with one of the
following agents: amiodarone, ibutilide, procainamide, (flecainide,
propafenone), sotalol.
– If onset > 48 hours: avoid drugs that may cardiovert (e.g. amiodarone).
Either:
• Delayed Cardioversion: anticoagulate adequately x 3 weeks, then
cardioversion, then anticoagulate x 4 weeks
• Early Cardioversion: iv heparin, then TEE, then cardioversion
within 24 hours, then anticoagulate x 4 weeks
• Anticoagulate if not contraindicated, if A fib > 48 hrs
Atrial fibrillation/flutter
Summary
Management: Control rate, consider rhythm
cardioversion and anticoagulate depending on
physiologic reserve
EF <40% or CHF
• Rate control:
– digoxin, diltizaem, amiodarone (avoid if onset of AF >
48 hours).
– avoid verapamil, beta-blockers, ibutilide,
procainamide (and propafenone/flecainide)
• Cardiovert: Amiodarone.
• Anticoagulate, if A fib > 48 hr.
WPW A Fib
• Suggested by: delta wave on resting EKG, very young
patient, HR>300
• Avoid adenosine, beta-blocker, Ca-blocker, or Digoxin
• If < 48 hour:
– If EF normal: one of the following for both rate control and
cardioversion: amiodarone, procainamide, propafenone,
sotalol, flecainide
– If EF abnormal or CHF: amiodarone or cardioversion
• If > 48 hour
– Medication listed above may be associated with risk of
emboli
– Anticoagulate and DC Cardioversion