Transcript Atrial fibrillation

Arrhythmia and
conduction disorders
http://www.uzhnu.edu.ua/uk/infocentre/2006
ІІ
Taras V. Chendey, MD, PhD, Ass. Prof.
Chair of hospital therapy
Cardiac arrhythmias (dysrhythmias)
Disorders of frequency (rate), regularity
and/or sequence of heart excitation and
contraction.
 Arrhythmias may occur at any age, they
may affect either healthy subjects or
patients with heart disease or other
disease.
 Arrhythmias vary from benign to fatal;
they are amongst major causes of sudden
death.

Arrhythmology’s basics:
action potential
Refractory
period
Arrhythmology’s basics:
automaticity
S. bradycardia (<50')
SА-node:
50-100'
AV-junction:
40-50'
NSR
S. tachycardia (>100')
Junctional rhythm
Accelerated J. rhythm (50-100')
J. tachycardia (>100')
Bundle
branches:
15-20'
ІІ
Idioventricular rhythm
Accelerated I. rhythm (50-100')
Ventricular tachycardia (>100')
Mechanisms of arrhythmias
Disorders of automaticity
 Re-entry
 Triggered activity
 Conduction block

Re-entry concept
Triggered activity
Vaughan-Williams antiarrhythmic drug
classification
Class І: Na-channels blockers:
-Class Іа: quinidine, procainamide
-Class Іb: mexiletine
-Class Іс: propafenone, etacizine,
flecainide
Class Ia
Class Ib
Class ІІ: beta-blockers
Class ІІІ: Potassium channels
blockers – amiodarone, sotalol,
dronedarone
Class IV: non-DHP Са-channel blockers
(verapamil)
Class Ic
Class III
Class IV (action
potential of AV-node
Other AAD: glycosides, ATP, potassium and magnesium salts,
sympatomimetics, atropine
Classification of arrhythmias
I.
II.
III.
IV.
V.
Disorders of impulse formation
Disorders of impulse conduction
Combined disorders of impulse
formation and conduction
Diseases, syndromes and phenomena
Arrhythmias in normal or altered
function of different types of artificial
pacemakers.
Etiology of arrhythmias
Disorders of cardiovascular system
 Internal and neurological disease
 Electrolyte disorders (K, Ca, Mg)
 Certain drugs
 Genetic causes (LQTS, SQTS, Brugada
syndrome etc.)

Extrasystoles
Extrasystole (ectopy, premature beat) – premature
depolarization of the heart
Site of origin:
Other characteristics:
•Supraventricular:
•Single (isolated), pair (two
in a row), group (3-triplet or
4)
•atrial
•junctional (u/, m/, l/p)
•Ventricular (from LV, RV)
•Allorhythmic (bi-, tri-,
quadrigemini)
•early (R on T)/ late
•interpolated
Atrial premature beats
0,92 сек




0,52 сек
1,0 сек
Premature occurrence of QRS complex with preceding
deformed/wide P wave of non-sinus origin, often superimposed on
preceding T-wave.
Extrasystolic PQ may be prolonged due to incomplete recovery of
AV-junction after prior sinus cycle.
Exrtrasystolic QRS width may normal (<120 msec), it may be wide
and deformed, resembling a bundle branch block due to incomplete
recovery of bundle branch (aberrant conduction).
Distance between R wave of sinus complex before APB and R wave
of sinus complex after APB less than double normal RR interval –
“incomplete post-extrasystolic pause”.
Junctional premature beats
JPB w/prior atrial excitation
А
JPB w/simult. ex. of
atria and ventr.
V
JPB w/prior
ventricular excitation
Ventricular premature beats
Premature appearance of wide (≥120 msec), deformed ventricular complex with
ST segment and T wave shifted discordantly relative to QRS.
No P-wave before VPB.
“Complete” post-extrasystolic pause.
No complete pause in interpolated VPBs, which occur in sinus bradycardia.
Ventricular trigeminy
Ventricular pairs and groups
V1,2
V5,6
In right ventricular premature beat QRS complex resembles left BBB (positive
complexes in left chest leads).
In left ventricular premature beat QRS complex resembles right BBB (positive
complexes in right chest leads).
Right bundle branch block
– Deep and wide S-waves in limb and left
chest (V5,6) leads.
– Wide and deformed QRS complex (rSR')
in right chest leads (V1,2).
– Reciprocal ST-T changes (i.e. ST
depression and T-wave inversion) in
right chest leads.
– Prolonged activation time in right chest
leads.
– Clinical significance: mostly benign
finding associated with normal heart
function. Almost always present in
dilatation/ hypertrophy or failure of
right heart chambers.
– In classical type of RBBB heart
electrical axis shifted rightwards or
normal in Wilson type electrical axis
deviated leftwards.
Left bundle branch block





Wide (>120 msec) and deformed
QRS in limb and left chest leads.
Deep and wide S-waves in right
chest leads (“cut sward” sign).
ST-T moves discordantly (in the
opposite direction) from the QRS
complex – ST elevated in right chest
leas and depressed in left chest
leads.
Prolonged activation time in left
chest leads.
Clinical significance: always
associated with heart dysfunction.
Left anterior fascicular block
Extreme left axis deviation, when α<60°which is characterized by SII>RII,
RaVR≥QaVR, deep SIII deep, tall RaVL>RI.
 Clinical significance: always associated with
heart dysfunction.

Posterior fascicular block
AV-blocks – impairment of impulse
conduction from atria onto ventricles via AVjunction
 First-grade AV-block: all implulses are being
conducted onto ventricles with some and same
delay. ECG: prolonged PQ(R) interval (> 0.2
sec). HR unaffected, and there is a P-wave
before each QRS complex.
PQ=0,4"
Second-degree AV-block – more pronounced

impairment of AV-conduction in which NOT ALL
impulses are being conducted to ventricles.
2nd degree AV-block type Mobitz-I
(Wenckebach block) : progressive prolongation of
PQ(R) in consecutive cycles with non-conducted
subsequent P and no QRS. (Wenckebach periods).

This block caused by the alteration at the level of
AV-node (nodal block).
2nd grade AV-block type
Mobitz-II

Constant (normal or prolonged) PQ(R) interval
with irregular sequence of conducted and nonconducted P-waves (no Wenckebach periods)
High-grade AV-block (Mobitz-ІІІ)

Normal PQ(R) interval with regular
sequence of conducted and nonconducted P-waves (mostly 2:1 or 3:1)
3rd grade AV-block (complete): no conduction from
atria to ventricles

AV-dissociation – rhythm of P-waves independent from the

Proximal (nodal) complete block: escape pacemaker located in

rhythm of QRS complexes
His bundle and produces 30-40 narrow (<120 msec) QRS complexes
per minute (junctional escape rhythm).
Distal (infranodal): escape pacemaker located in the left or right
bundle branch and produces 20-30 wide QRS complexes per minute
(idioventricular escape rhythm).
Treatment of complete AV-block

Implantation of artificial pacemaker
Tachyarrhythmias
arrhythmias with HR>100'
QRS width
Narrow QRS
(<120 мс)
Regularity
Wide QRS
(>120 мс)
Regular
Irregular
Narrow-complex tachycardia


Sinus
tachycardia
Paroxysmal
supraventricular
tachycardia
HR 188/min

Atrial
fibrillation
Wide-complex tachycardia: ventricular
tachycardia
Atrial fibrillation
Supraventricular tachycardia with irregular
ventricular response
 Most common chronic arrhythmia


AFib linked to increased risk of heart failure,
embolism (mostly embolic stroke) and death
Common causes/favoring conditions in AFib:
IHD (all forms)
Мyоcarditis
Cardiomyopathies
Valvular heart disease (esp. mitral stenosis)
Thyrotoxicosis
Sick sinus syndrome
Atrial fibrillation: classification and
terminology
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Paroxysmal – normal sinus rhythm restores
spontaneously without intervention; usually lasts up to
48 hours.
Persistent – restoration of NSR requires pharmacological
or electrical intervention (cardioversion); lasts up to
several days or weeks.
Permanent – restoration of NSR is not possible or not
feasible.
Primary and recurrent atrial fibrillation
Isolated atrial fibrillation
Tachy- and normosystolic atrial fibrillation
Mechanisms of Atrial Fibrillation
Left atrial microreentry near
pulmonary veins
ostia
 Daughter wavelets
of re-entry
 Irregular ventricular
response due to
physiologic AVblock

2
1
4
ECG-signs of AFib:
1) absence of
P-waves
2) irregular ventricular
rhythm
3) f-waves
4) electrical alternation
3
Atrial flutter
F F F F
Regular tachyarrhythmia with HR 150/min
F-waves at rhe rate of 300/min
Conduction F/QRS = 2:1
Treated atrial flutter
Regular rhythm with HR 75 bpm
F-waves at the rate of 300/min
Conduction F/QRS = 4:1
Patient with AF
Restoration and attainment
of NSR
(“rhythm control”)
Class Іс drugs
Class ІІІ drugs
Electrical cardioversion
Ablation
Attainment of normal HR
(“rate control”)
Class ІІ drugs
Class ІV drugs
Digoxin
AV-node destruction +
pacemaker
Thromboembolism
prevention
Aspirin
Vit. K antagonists
Novel anticoagulants
Left atrial appendage
isolation
Stroke risk assessment in atrial fibrillation –
CHA2-DS2-VaSc score
C
H
A2
D
S2
Va
Sc
Cardiac failure – 1 point
Hypertension – 1 point
Age > 65 – 1 point, >75 yrs – 2 points
Diabetes – 1 point
S2 Stroke or TIA – 2 points
Vascular disease – MI/PAD – 1 point
Sex category – female sex – 1 point
Total score: 0-9
0-1 point – low risk (1,9-2,8% per year) → aspirin 150 mg/d
≥2 points – high risk (>4% per year) → VKAs (warfarin)
or novel anticoagulants
Rationale for the therapeutic range of INR
Thrombosis
Bleeds
Target range
INR