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Mechanisms of Arrhythmias
• Altered automaticity
• Normal, enhanced normal, abnormal
• Triggered activity
• Reentry
2. Triggered Activity
Afterdepolarization reaches threshold
Early: interrupt repolarization
Congenital or acquired long QT syndrome: altered K+ and Na+
currents during phase 2 can produce dangerous V-tach
Delayed: after completion of AP.
3. Reentry (circus movement, reciprocal or echo beat, reciprocating
tachycardia)
Anatomic: nodal tissue, Purkinje, BB, accessory path
Example: WPW
Functional
Local differences in conduction velocity and membrane characteristics
Anisotropic:
circuit determined by difference in conduction velocity through length of
fiber
Reflection
Parallel pathways with depressed segments
3. Reentry (circus movement, reciprocal or echo beat, reciprocating
tachycardia)
Requires: available circuit, unidirectional block, and different
conduction speed in limbs of circuit
Conditions that depress conduction velocity or shorten refractory period
promote functional block
Exp: WPW reciprocating tachycardia, AV-nodal reentry, V-tach due to
bundle branch reentry, infarcted area.
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Electrical Impulse
Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery
Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery
Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery
Atrio-Ventricular Re-entry
• Wolf Parkinson White
• supraventricular tachycardia
Clinical Manifestations of Arrhythmias
• many go unnoticed and produce no symptoms
• palpitations – ranging from “noticing” or “being aware” of ones heart
beat to a sensation of the heart “beating out of the chest”
SP FP
Rate of 78 bpm
Sinus bradycardia
Fig 3
RAA LAA
SN * * *
CT
RAFW
PV
CSO
LAFW
IVC
20 yr woman with post-partum congestive heart failure
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Specific Diagnostic Evaluation
Ectopic atrial focus
Since the rhythm is initiated by enhanced
automaticity of a single focus, the first ectopic
and the subsequent P-wave morphology are
identical.
The rate at onset varies and gradually accelerates
as the focus "warms up."
AV nodal block may exist.
Specific Diagnostic Evaluation
Vagal maneuvers do not terminate the rhythm,
although they may produce AV block and thus, reduce
heart rate
The PR interval is related to the rate of tachycardia.
The vector of the ectopic P wave is usually normal with
upright P waves in leads II, III, and aVF, although the P
wave appear slightly different from the normal P wave.
Atrial tachycardia
Multifocal Atrial Tachycardia
The rate is usually 100 to 150/min with at least
three P waves of at least three different
morphologies identified in a single lead. The
atrial rate is slightly irregular, and the PR interval
also varies.
MAT
Atrial fibrillation and
flutter
Atrial Fibrillation
Pneumonia Congenital
Pulmonary embolism Multiple sclerosis
Sudden emotion Muscular dystrophy
Thyrotoxicosis Pheochromocytoma
Trauma Right atrial cold injections
Rare Swallowing
Acute hypovolemia Tyramine foods
Atrial Fibrillation
Mechanism is activation of
multiple wavelets within the
right and left atrium
AF
originating
in LSPV
Atrial Fibrillation
Clinical Classification
Paroxysmal
Persistent
Permanent
Introduction
Paroxysmal AF
Short lasting < 1 hour
Long lasting >1; < 48 hours
AF interspersed with periods of sinus rhythm & usually terminates
spontaneously
Persistent AF
Occur between 2days - weeks
Intervention is needed to restore the sinus rythum
Chronic or permanent AF
Persists for months to years
No spontaneous conversion
Interventions to restore sinus rythum are either ineffectual or not tried
Atrial Fibrillation
Atrial Fibrillation
ECG:
1).Absence of P waves
2).P waves replaced by f waves.
3).f waves : irregular in size ,shape ,and spacing.
Rate between 350 and 600
4). Irregularly irregular ventricular rhythm, best seen in
Ⅱ,Ⅲ,Avf,V1 or V2.
Variable RR intervals
No clear p waves
Atrial Fibrillation
Mechanisms
Type – I --- Activation consisted of single, broad wavefronts
propagating without conduction delay & either only short arcs of
conduction block or small areas of slow conduction that did not disrupt
the main course of propagation
Atrial Flutter
Reentry Circuit of Common
Atrial Flutter
Dependent upon:
– AV node conduction properties
– Usually a 2:1, 4:1 fixed conduction ratio
Ablation in
cavo-
tricuspid
isthmus
(CTI)
Atrioventricular Nodal Reentrant Tachycardia
(AV Node Reentry or AVNRT)
• Most common cause
of paroxysmal SVT in
the young adult
• Occurs over a small
reentrant circuit located
near the AV node
• The circuit consists of
a fast and slow pathway
connected by a common
top and bottom pathway
Supraventricular Tachycardia Due to AV
Nodal Reentry(AVNRT)
This supraventricular tachycardia with a regular
ventricular rate varying between 160 to 260
beats per minute is due to AV nodal reentry.
Mechanism- Dual pathway
physiology in AV node
Specific Diagnostic Evaluation
Examination of a 12-lead electrocardiogram may reveal a
retrograde P wave buried in the QRS complex or immediately
following the QRS complex,
P waves may fall on terminal part of S wave in V1, so as to produce
pseudo R’ wave in V1
P waves may fall in terminal part of R waves in lead II, so as to
produce a pseudo S wave
The PAC initiating AV nodal tachycardia has a long PR interval as a
result of antegrade conduction down the slow-conducting
alpha pathway.
The rhythm may be initiated and terminated by a PAC or PVC.
Vagal maneuvers may slow and then abruptly terminate the rhythm
AVNRT
Adenosine conversion of AVNRT
to SR
Retrograde p waves
RP = 60 msec
PR interval is short
(80 to 90 msec)
QRS is wide
(over 120 msec)
Dr Dattatreya
Ventricular Tachyarrhythmias
Classification
A. VPC
1. Unifocal
2. Multi focal
3. Monomorphic
4. Poly morphic
B. Ventricular tachycardia
1. NSVT
2. Sustained VT
3.Mnomorphic VT
4. Polymorphic VT
C. Ventricular flutter
D. Ventricular fibrillation
Ventricular Beats & Rhythms
R on T
phenomemon
“R on T phenomenon”
time
Dilated cardiomyopathy
Non-sustained VT
Episodes last at least 6 beats but < 30 seconds
Premature Ventricular
Contraction
PVC
Ectopic beat in the ventricle that can occur singly
or in clusters
Caused by electrical irritability
Drug intoxication
Classification
Ventricular Tachycardia
Monomorphic
Idiopathic VT
Bundle branch reentry tachycardia
Ventricular flutter
Ventricular fibrillation
Polymorphic
Torsades de pointes (TdP)
Monomorphic VTs
Monomorphic VT
Heart rate: 100 bpm or greater
Rhythm: Regular
Mechanism
Reentry
Abnormal automaticity
Triggered activity
Recognition
Broad QRS
Stable and uniform beat-to-beat appearance
ECG Recognition
Treatment options:
Pharmacologic therapy (beta blockers, verapamil)
RF ablation
ECG Recognition
Treatment: Cardioversion
Ventricular Fibrillation
Heart rate: Chaotic, random and asynchronous
Rhythm: Irregular
Mechanism: Multiple wavelets of reentry
Recognition:
No discrete QRS complexes
Treatment:
Defibrillation
ECG Recognition
Recognition:
Wide QRS with phasic variation
Torsades de pointes
ECG Recognition
Early afterdepolarizations
Sotalol
Ibutilide
Physical
Ischemia
Electrolyte abnormalities
Treatment
Pharmacologic therapy:
Potassium
Magnesium
Isoproterenol
Ventricular Tachycardia
SVT with aberrancy (functional bundle branch
block)
SVT with underlying bundle branch block
SVT with pre-excitation
Additional Mimimics of Wide
Complex Tachycardias
Step 2. Is the interval from the onset of the R wave to the nadir of the S
wave greater than 100 msec in any precordial leads?
V1 V6
Monophasic R wave QS or QR
QR or RS R/S <1
V1or V2 V6
Notched downstroke
S wave.
Adapted from Brugada et al. A new approach to the differential diagnosis of regular tachycardia with a wide QRS complex.
Circulation 1991; 83:1649-59.
Therapy for Ventricular
Tachycardia
Clinical condition of patient
Unstable requires DC cardioversion
Stable may be treated with Drugs or Cardioversion
Presence or absence of Left ventricular Dysfunction
determines choice of pharmacologic therapy
Amiodarone 150 mg I.V. over 10 minutes may be RX of
choice maximum 2.2 gm/24 hours class IIA recommendation