Transcript Arrythmias and EKGs - Isfahan University of Medical Sciences

Arrhythmias and EKGs
Amirhossein Azhari M.D
Fellowship of electrophysiology
Chamran heart center
Mechanisms of Arrhythmogenesis
Tachycardia
Abnormally rapid heart rhythm
May result from:
Abnormal impulse formation
– Automaticity
– Triggered activity
Abnormal impulse conduction
– Reentry
Tachycardia
Enhanced Normal Automaticity
Basal condition
Increased slope of phase 4 depolarization
Symptoms the following:Include
•Your pulse rate becomes 150 – 200 beats per minute.
•Palpitations (Feeling your heart beat)
•Dizziness, or Feeling Light Headed
•You may become breathless
•If you have angina, then an angina pain may be
• triggered by an episode of SVT
•You may have no symptoms,
• You may only be aware that your
heart is beating fast.
Sinus Tachycardia
Sinus Tachycardia
Is characterized by:
SA node discharge rate of 100 to 180 x m.
Normal P waves and QRS complexes
Most often arises from increased sympathetic
stimulation of the SA node.
Physiologic response to exercise.
Pathologic conditions including fever,
hyperthyroidism and hypoxemia.
Physiologic Sinus Tachycardia:
Treatment
Treatment of sinus tachycardia is directed
at the underlying condition causing the
tachycardia response.
Uncommonly, beta blockers are used to
minimize the tachycardia response if it is
determined to be potentially harmful, as
may occur in a patient with ischemic heart
disease and rate-related anginal
symptoms.
Premature Atrial Complex
(PAC)
V5
Non-Compensatory
Pause
P
P
P
P’
P
Timing of
Expected P
Premature Atrial Complex (PAC):
Alternative Terminology
Premature atrial contraction
Atrial extrasystole
Atrial premature beat
Atrial ectopic beat
Atrial premature depolarization
PACs: Bigeminal
Pattern
P
P’
P
P’
P
P’
PAC with “Aberrant Conduction”
(Physiologic Delay in the His Purkinje
System)
V1
P
P
P’
P
RRbbBBB
PACs with Aberrant
Conduction
(Physiologic RBBB and
LBBB)
V1
RBBB
LBBB
Normal
conduction
Treatment
PACs uncommonly require intervention.
For extremely symptomatic patients who
do not respond to explanation and
reassurance, an attempt can be made to
suppress the PACs with pharmacologic
agents.
Beta blockers are typical first-line therapy.
The repetitive focus can even be targeted
for catheter ablation.
Atrial
Fibrillation
Focal firing
or
multiple
wavelets
Chaotic, rapid
atrial rate at
400-600
beats per min
Atrial Fibrillation
www.uptodate.com
EKG Characteristics:
Absent P waves
Presence of fine “fibrillatory” waves which vary in
amplitude and morphology
Irregularly irregular ventricular response
Atrial Fibrillation: Characteristic
“Irregularly Irregular” Ventricular
Response
II
Atrial Fibrillation with
Rapid Ventricular
Response
II
Irregularity may be subtle
AF is the most common sustained
arrhythmia. It is marked by disorganized,
rapid, and irregular atrial activation. The
ventricular response to the rapid atrial
activation is also irregular.
In the untreated patient, the ventricular
rate also tends to be rapid and is entirely
dependent on the conduction properties of
the AV junction. Although typically the rate
will vary between 120 and 160 beats/min.
The mechanism
multiple wavelets of (micro)reentry.
The drivers appears to originate
predominantly from the atrialized
musculature that enters the pulmonary
veins .
Sustained forms of microreentry as
drivers have also been documented
around the orifice of pulmonary veins;
nonpulmonary vein drivers have also been
demonstrated.
incidence
The incidence of AF increases with age
such that >5% of the adult population over
70 will experience the arrhythmia.
Occasionally AF appears to have a welldefined etiology, such as acute
hyperthyroidism, an acute vagotonic
episode, or acute alcohol intoxication.
Clinical symptoms
clinical importance related to:
(1) the loss of atrial contractility,
(2) the inappropriate fast ventricular
response
(3) the loss of atrial appendage
contractility and emptying leading to the
risk of clot formation and subsequent
thromboembolic events
Acute Management of Atrial
Fibrillation
In emergency department because of AF
generally have a rapid ventricular rate, and
control of the ventricular rate is most
rapidly achieved with intravenous diltiazem
or esmolol.
If the patient is hemodynamically unstable,
immediate transthoracic cardioversion
may be appropriate.
If the AF has been present for more than
48 hours or if the duration is unclear and
the patient is not already anticoagulated,
cardioversion ideally should be preceded
by transesophageal echocardiography to
rule out a left atrial thrombus.
However, a delay in cardioversion may
not be appropriate in the setting of severe
cardiovascular decompensation
If the patient is hemodynamically stable,
the decision to restore sinus rhythm by
cardioversion is based on several factors,
including symptoms, prior AF episodes,
age, left atrial size, and current
antiarrhythmic drug therapy. .
For example, in an elderly patient whose
symptoms resolve once the ventricular
rate is controlled and who already has had
early recurrences of AF despite rhythmcontrol drug therapy, further attempts at
cardioversion usually are not appropriate.
On the other hand, cardioversion usually is
appropriate for patients with symptomatic
AF who present with a first episode of AF
or who have had long intervals of sinus
rhythm between prior episodes.
anticoagulation
Regardless of whether cardioversion is
performed pharmacologically or
electrically, therapeutic anticoagulation is
necessary for 3 weeks or more before
cardioversion to prevent thromboembolic
complications if the AF has been ongoing
for more than 48 hours. If the time of onset
of AF is unclear, for the sake of safety, the
AF duration should be assumed to be
more than 48 hours
Atrial Flutter
(“Typical,”Counterclockw
ise)
Reentrant
mechanism
Atrial flutter (SVT)
Re-entrant loop just above AVN in right atrium
Atrial rate 240-360 without medications
2:1 block, vent rate 150 most common
Regular, fixed; or regularly irregular
Narrow if no aberrancy
Flutter waves, sawtooth pattern--Always visible in lead II
Adenosine can help to diagnose, not treat
Conversion vs. Ventricular slowing
– 50 Joules, Ibutilide/Amiodarone
Atrial Flutter
II
4:1
2:1
Classic
inverted
“sawtooth”
flutter waves
at 300 min-1
(best seen in
II, III and AVF)
V1
Note variable
ventricular
response
Atrial Flutter
2:1
Conduction
(common)
2:1 & 3:2
Conduction
1:1
Conduction
(rare but
dangerous)
V. rate
140-160
beats/min
Multifocal Atrial Tachycardia
EKG Characteristics: Discrete P waves with at least 3 different
morphologies.
Atrial rate > 100 bpm.
The PP, PR, and RR intervals all vary.
Paroxysmal Supraventricular
Tachycardia
Refers to supraventricular tachycardia other
than afib, aflutter and MAT
Occurs in 35 per 100,000 person-years
Usually due to reentry—AVNRT or AVRT
AV Nodal Reentrant Tachycardia
Circuit
F = fast AV
nodal pathway
S = slow AV
nodal pathway
(His
Bundle)
During sinus rhythm, impulses
conduct preferentially
via the fast pathway
Initiation of AV Nodal Reentrant
Tachycardia
PAC
PAC
PAC = premature atrial
complex (beat)
Sustainment of
AV Nodal Reentrant
Tachycardia
Rate 150-250
beats per min
P waves
generated
retrogradely
(AV node
 atria) and
fall within or
at tail of QRS
Sustained AV Nodal Reentrant
Tachycardia
V1
P
P
P
P
Note fixed, short RP interval mimicking r’ deflection of QRS
AVNRT (60% of SVT)
Typical AVNRT: (90% AVNRT)
1. A and V
Simultaneously
2.Pseudo “r” in
V1/AVR
AVNRT Therapy
Acute therapy: Please record ECG at the same time.
1.) Vagal maneuver
2.) Adenosine
3.) Verapamil
Chronic therapy:
1.) RFA (cure >95%, complication rate of <1%,
Mortality < 1/10,000,
heart block 0.5%)
2.) Medications
beta-blocker, calcium channel blocker
Flecainide, propafenone
Accessory Pathway with
Ventricular Preexcitation
(Wolff-Parkinson-White
Syndrome)
Sinus
beat
Hybrid
QRS shape
“Delta” Wave
AP
PR < .12 s
QRS  .12 s
Fusion activation
of the ventricles
Preexcitation
Preexcitation is a condition characterized by an accessory pathway of
conduction, which allows the heart to depolarize in an atypical
sequence.
The most common form of preexcitation is called Wolfe-ParkinsonWhite (WPW) syndrome, in which a direct atrioventricular connection
allows the ventricles to begin depolarization while the standard action
potential is still traveling through the AV node.
ECG Characteristics of WPW:
1. Short PR interval
2. QRS prolongation
3. Delta wave
Varying Degrees of
Ventricular
Preexcitation
Intermittent Accessory Pathway
Conduction
V Preex
V Preex
Normal
Conduction
Note “all-or-none” nature of AP conduction
AV Reentrant Tachycardia (AVRT)
In patients with WPW, a reentrant rhythm can be
generated where the AV node serves as one arm
of the reentrant circuit, and the accessory pathway
as the other.
Types of AVRT
Orthodromic AVRT (More common) – Narrow
complex tachycardia in which the wave of
depolarization travels down the AV node and
retrograde up the accessory pathway.
Antidromic AVRT (Less common) – Wide
complex tachycardia in which the wave of
depolarization travels down the accessory
pathway and retrograde up the AV node.
Mechanism of orthodromic AVRT
Mechanism of antidromic AVRT
Orthodromic AV Reentrant
Tachycardia
Retrograde
conduction
via ac
pathway
(AP)
AP
Anterogade
conduction
via normal
pathway
Initiation of Orthodromic
AV Reentrant Tachycardia
PAC
Atria
AP
AVN
Ventricles
PAC = premature atrial
complex (beat)
Sustainment of
Orthodromic AV
Reciprocating Tachycardia
Atria
Rate 150-250
beats per min
AP
AVN
Ventricles
Retrograde P’s fall
in the ST segment
with fixed, short RP
Orthodromic AV Reentrant
Tachycardia
NSR with
V Preex
SVT:
V Preex
gone
Note
retrograde
P waves
in the
ST segment
AVRT (30% of SVT)
Wolff-Parkinson-White (WPW) pattern: “death pattern”
1. The initial delta wave
2. PR < 120ms
3. The QRS > 100ms
AVRT: orthodromic (95%) and antidromic tachycardia
Normal PR
(short RP SVT)
A fib. in a patient with WPW
1.) can degenerate into V fib (death)
2.) No beta-blocker, calcium channel blocker, digoxin.
3.) drug blocks AP: procainamide, amiodarone, ibutilide, Ic drug
AVRT Therapy
1.) No beta-blocker, calcium channel blocker, digoxin in WPW.
2.) drug blocks AP: procainmide, amiodarone, ibutilide, Ic
But do not reduce SCD risk.
3.) Asymptomatic WPW, EP study if in high risk profession
4.) AVRT in WPW patients needs ESP and likely RFA.
AT 10% (now more)
Normal PR
Can have AVN block
Long RP (most)
Adenosine for SVT
Terminate all AVNRT or AVRT
Terminate 30 AT only
ECG at the same time please!
AT Therapy
1.) More likely to be treated with medications traditionally.
(success rate: 20-50%).
2.) Now more and more ATs are treated with RFA,
(success rate: 70-95%).
PSVT
Initial eval: Is the patient stable?
Determine quickly if sinus rhythm
If not sinus and unstable, cardioversion
Unstable sinus tachycardia---treat cause
Sxs of instability would include: chest pain,
decreased consciousness, short of breath,
shock, hypotension—unstable sxs require shock
SVT
If stable, determine whether regular
rhythm (sinus or PSVT) vs irregular
(afib/flutter, MAT)? p waves (MAT vs. AF)?
If regular, determine whether p waves are
present, if can’t see---At first CSM or other
vagal maneuvers then administer
adenosine (6mg, can give 2 doses)
SVT
CSM or adenosine commonly terminate
the arrhythmia, esp, AVRT or AVNRT
Can also use CCB or beta blockers to
terminate, if available
Counsel to avoid triggers, caffeine, Etoh,
pseudoephedrine, stress
Adenosine
Adenosine interacts with A1 receptors
present on the extracellular surface of
cardiac cells, activating K+ channels (IK.Ach,
IK.Ade) in a fashion similar to that produced
by acetylcholine.
Transient prolongation of the A-H interval
results, often with transient first-, second-,
or third-degree AV node block.
Pharmacokinetics
washout, enzymatically by degradation to
inosine, by phosphorylation to adenosine
monophosphate.
The vascular endothelium and the formed
blood elements contain these elimination
systems, which result in very rapid
clearance of adenosine from the
circulation. Elimination half-life is 1 to 6
seconds.
Dosage and Administration
To terminate tachycardia, a bolus of
adenosine is rapidly injected intravenously
at doses of 6 to 12 mg, followed by a flush.
Pediatric dosing should be 0.1 to
0.3 mg/kg.
When it is given into a central vein and in
patients after heart transplantation or
those receiving dipyridamole, the initial
dose should be reduced to 3 mg.
Transient sinus slowing or AV node block
results, lasting less than 5 seconds. Doses
of more than 18 mg are unlikely to revert a
tachycardia and should not be used.
Indications
Adenosine has become the drug of first choice
to terminate an SVT acutely, such as AV node or
AV reentry .
It is useful in pediatric patients and to judge the
effectiveness of ablation of accessory pathways.
It results in only transient AV block during atrial
flutter or fibrillation and is thus useful only for
diagnosis, not therapy.
Adenosine terminates a group of VTs most
often located in the right ventricular outflow tract.
Calcium
Channel Antagonists
Verapamil
Verapamil, a synthetic papaverine
derivative, is the prototype of a class of
drugs that block the slow calcium channel
and reduce ICa.L in cardiac muscle
In humans, verapamil prolongs conduction
time through the AV node (the A-H
interval) without affecting the P wave or
QRS duration or H-V interval and
lengthens AV nodal anterograde and
retrograde refractory periods.
More commonly, the sinus rate does not
change significantly because verapamil
causes peripheral vasodilation, transient
hypotension, and reflex sympathetic
stimulation.
After intravenous administration, AV nodal
conduction delay occurs within 1 to 2
minutes and A-H interval prolongation is
still detectable after 6 hours.
The elimination half-life of verapamil is 3 to
7 hours, with up to 70% of the drug
excreted by the kidneys.
For acute termination of SVT or rapid
achievement of ventricular rate control
during atrial fibrillation, the most commonly
used intravenous dose of verapamil is
10 mg infused during 1 to 2 minutes while
cardiac rhythm and blood pressure are
monitored.
A second injection of an equal dose may
be given 30 minutes later.
Adverse Effects
Verapamil must be used cautiously in
patients with significant hemodynamic
impairment or in those receiving beta
blockers, as noted earlier. Hypotension,
bradycardia, AV block, and asystole are
more likely to occur when the drug is given
to patients who are already receiving betablocking agents
Hemodynamic collapse has been noted in
infants, and verapamil should be used
cautiously in patients younger than 1 year.
Contraindications
1) advanced heart failure
2) second- or third-degree AV block
without a pacemaker in place
3) atrial fibrillation and anterograde
conduction over an accessory pathway
4) hypotensive states
5) significant sinus node dysfunction
6) Iv B-blocker
Diagnosis ?
Diagnosis ?
What is this arrhythmia?
Antidromic AVRT
Classification Scheme for Arrhythmias
Abnormalities in
Conduction
Bradyarrhythmias
Conduction Block
SA node – SA block
Atria - NA
AV node – AV block
Ventricles – NA
Reentry
Tachyarrhythmias
SA node – SA nodal reentry
Atria – Intraatrial reentrant
tachycardia, a-flutter, a-fib
AV node – AVNRT
Ventricles – Ventricular
tachycardia (common)
Accessory pathways – AVRT
Abnormalities in
Automaticity
Decreased Automaticity
SA node – Sinus bradycardia
Atria – NA
AV node – NA
Ventricles - NA
Increased/Abnormal
Automaticity
SA node – Sinus tachycardia
Atria – Ectopic atrial
tachycardia
AV – Junctional tachycardia
Ventricles – Ventricular
tachycardia (rare)
Additional important arrhythmias: Multifocal atrial tachycardia, torsade de pointes
The end