Bradyarrhythmias

Classification
Classification:
Disturbances of the initiation and/or
conduction of the electrical impulse
in the SAN
Disturbances of the conductions
system

Etiology
Functional (reversible)
Impairment of the autonomous NS
Intoxication
Dyselectrolytemia

Organic
Ischaemia-necrosis
Inflamation
Fibrosis
Infiltrative diseases
Degenerative diseases

Significance clinical aspects

Symptoms:
Due to cardiac output

cerebral: dizziness-fainting syncope ( Adams-Stokes Sd.)

cardiac: angina
renal: Kussmaul breathing coma
muscular: fatigue

Due to congestion
pulmonary
peripheral

Signs

Of cardiac output
Of congestion

NB!: clinical picture depends on the mechanism of

the bradycardia and substrate
NB!: symptoms can be due to tachyarrhythmia
induced by bradyarrhythmia

Treatment principles and methods

Any intensely symptomatic
bradyarrhythmia requires cardiac pacing
Cardiac pacing
temporary
external
mechanical
electrical

internal

permanent
endocardial
epicardial

Diagnosis
Noninvasive

IHR (Intrinsic Heart Rate)

ECG ,,ladder diagrams
Holter monitoring / external LR / home telemetry
Carotid sinus compression
Tilt-test
ECG exercise test

Invasive
Electrophysiologic study (EPS)
Implantable monitoring devices (implantable
loop recorder)

EPS
SAN function
SAN automaticity: SNRT
Impulse conduction from the SAN: SACT

Conduction system status

Hissian electrogram at rest: HBE
Dynamical behavior: Wenckebach point
retrograde conduction (V-A)

ILR
05:41:41

05:42:09

05:42:23

11:24:04

11:24:14

11:24:24

SAN dysfunction
Sinus bradycardia
Sinus arrests

Sino-atrial conduction block (SAB)

R.V. - Life threatening Brady & Tachy 2016

Treatment
Elimination of the cause
Atropine or other oral belladone
compounds
Permanent cardiac pacemaker
implantation (AAI or DDD if there is
coexisting AVN disease).

Conduction system disturbances

AV block

Intraventricular conduction disturbances

First degree AV block

Delay in AV conduction
ECG: PR interval > 0.20
NB!: PR interval needs to be adjusted by HR (PR
varies with 0,003-0,004 for every 10 bpm
variation of the cardiac rhythm;
Location:
supranodal/intranodal
exceptionally infranodal

Additional criteria:

A PR interval 0,30 sec = always functional

QRS morphology
Narrow QRS - almost always supranodal or intranodal ( AH
or exceptionally PA)
With BBB an EPS is necessary, sometimes sensitized by
procainamide, because in of patients the location of the
block is infranodal ( or x2 of H and/or HV)

Second degree AV block

Mobitz I (with Luciani-Wenkebach periods):

Mobitz II:

Progressive but decremential in PR interval, until one atrial beat is blocked

The first post-block PR interval is equal to the PR of the normal cycle
progressive of RR interval is present.
Narrow QRS almost always supranodal or intranodal
Wide QRS EPS (frequently the block is infranodal)

Constant PR interval, intermittently an impulse is blocked in the AVN

PP that includes the block is a multiple of the basic PP
Usually associated with BBB or bifascicular block (situation in which the block is
almost always intrahissian or infrahissian)
Very rarely associated with narrow QRS (usually also intrahissian or infrahissian)

NB!: in the presence of narrow QRS AV block 2nd degree type Mobitz I with
minimal PR variability is to be suspected

EPS usually confirms the intrahissian or infrahissian location. Differentiating from

type I is important, as type Ii frequently progresses to complete AV block.

Second degree AV block type 2/1:

High degree AV block:

Location of the block can be suggested by the type of the QRS (narrow or large)
and by challenge tests (type I usually responds to i.v. atropine) but most correctly
by a hissiogram.
Block of more than one consecutive impulses (3/1, 4/1)
Similar to type Mobitz II regarding location, can be symptomatic and potentially
progresses to complete AV block much faster
Exceptionally intranodal (associated with narrow QRS)

Third degree AV block

Clinical: extreme bradycardia, cannon heart sounds,
echo systole
ECG:

No relationship between P-waves and QRS complexes,

that succeed regularly, being generated by a replacing
pacemaker (atria and ventricles are dissociated =
transmission of the impulse from the atria to the
ventricles is completely blocked)
Sometimes within the atria an arrhythmia can occur (Afib
or AFlu)
QRS morphology:
A type: narrow complexes, more stable 40-60 bpm rhythm,
the site of the block is intranodal
B type: wide complexes, unstable 20-40 bpm rhythm, risk of
cardiac arrest, site of the block is intrahissian of infrahissian

EPS can precisely indicate the site of the block: V is

preceded by H in the suprahissian type and is
dissociated by H in the infrahisian type.

Cardiac pacing

Chamber
(s) paced

Chamber
Type of
(s) sensed response

Special
functions

Antitachycardia
functions

RVA vs. septal stimulation

R.V. - Life threatening Brady & Tachy 2016

R.V. - Life threatening Brady & Tachy 2016

Tachyarrhythmias

Significance clinical aspects

Symptoms:
Due to cardiac output

cerebral: dizziness-fainting syncope ( Adams-Stokes Sd.)

cardiac: angina
renal: Kussmaul breathing coma
muscular: fatigue

Due to congestion
pulmonary
peripheral

Signs

Of cardiac output
Of congestion

NB!: clinical picture depends on the mechanism of

the tachycardia and on their substrate
NB!: symptoms can be due to bradyarrhythmia
induced by tachyarrhythmia

Preexcitation syndrome

Accessory pathway between atria and ventricules:

Between RA and RV

Between LA and LV

Multiple pathways

Consists of embryonic myocardial tissue:

Not always symptomatic = does not always conduct

Extremely rapid conduction

Atrio-ventricular or ventriculo-atrial conduction

In case of conduction on an accessory pathway the QRS

complex is the fusion result of depolarization through the AVN

and the AP

ECG:

Short PR interval < 0.12 sec

Delta wave

Wide QRS > 0.12 sec

Negative T wave

Pre-excitation + re-entry tachyarrhythmias= WPW SYNDROME

Clinically possible situations in the

presence of AV accessory
pathways
Preexcitation sd. = antegrade conduction through the AP
during SR
Constant permanent delta wave (sometimes variable
concertina effect)

asymptomatic

Intermitent conduction (intermitent delta wave)

Apparently absent eventually for prolonged periods ?? (fusion)

Dependent/associated tachyarrhythmia = WPW SYNDROME:

Ortodromic A-V re-entry
NB!: (sometimes through concealed AP only retrograde V-A conduction)

Antidromic A-V re-entry

Pre-excited AFib

symptomatic

Intermitent delta wave

Permanent pre-excitation

Concertina effect:
delta wave of variable duration

AV re-entrant
tachycardia with
antidromic conduction
Regular tachyarrhythmia with wide QRS
through presence of the delta wave

fast ventricular response > 180-200/min

mechanism:
Antegrade conduction through the AP
Retrograde conduction through the AVN

Differential diagnosis with sustained

monomorphic VT
Increased risk of sudden death -> in case
of Afib -> VFib

SVT in WPW sdr. with antidromic conduction

Regular tachyarrhythmia with wide QRS; no P-waves; dif. dg. with monomoprhic V

WPW sdr. with AFib

Risk of death evaluation in

WPW syndrome
Non-invasive ????:
Intermitent pre-excitation = low risk(??)
Dissapearance of pre-excitation upon procainamide
administration = low risk(?)
Stress-testing (????)
RR interval during AFib
The shorter the RR interval, the higher the risk of death (<250
ms)

Invasive = EPS:
Determining the refractory period of the AP

Treatment of WPW sd.

Pre-excitation syndrome with no tachyarrhythmia (delta wave during SR):
follow-up?
Acute WPW syndrome (pre-excitation with tachyarrhythmia) -> conversion
to SR:
EES if hemodynamically unstable (!!Pre-excited AFib)
Ortodromic tachyarrhythmia, narrow QRS:
i.v. Adenosine

Antidromic tachyarrhythmia, wide QRS:

Class Ia, Ic, III antiarrhythmic drugs

Chronic, profilaxis:
Class Ia, Ic, III antiarrhythmic drugs
RF ablation of the AP/APs

CONTRAINIDICATION:
R.V. - Life threatening Brady & Tachy 2016

R.V. - Life threatening Brady & Tachy 2016

Atrial flutter

Regular tachyarrhythmia with narrow QRS

Through macro-reentry

No P-waves, flutter F waves with 250-350 / min, NO isoelectric line:

Typical AFlu (counter-clockwise): negative in DII, DIII, aVF

Inversed typical AFlu (clockwise): positive in DII, DIII, aVF

Atypical AFlu: >350 / min, variable and/or discordant morphology

AFib with large waves (,,fibrilo-flutter)

Atrial tachycardia (especially PV tachycardias)

Untreated: 2/1 AV conduction (~ 150 / min)

Possibly variable conduction: successive 2/1, 4/1, 3/1

Vagal maneuvers decrease HR stepwise through progressive increase of block degree

1:1 conduction of AFlu

under quinidine
induces quinidine syncope

anticholinergic effect on AVN

decreases the atrial depolarizationR.V.
velocity
- Life threatening Brady & Tachy 2016

Treatment
acute

cardioversion (low energy EES)

Class I i-v antiarrhythmic drugs
i-v CCB
i-v B
vagal maneuvers
overdrive pacing (temporary esophageal or endocavitary
lead)

chronic
profilaxis
Rhythm control

cure?

NB!: risk of embolysm

TEE if onset 48h and/or

uncertaind
anticoagulation

Atrial fibrillation
Absence of P waves
f waves 450-600/min; can be
absent
small waves Afib
large waves AFib

Completely irregular QRS

Variable HR:

Very rapid > 150/min

Rapid > 100 / min
Medium 60 100 / min
Low < 60 / min

Consequences of Afib. Influence on

therapy
1. Loss of atrial systole = Cardiac output
Ao stenosis, OHCM

CONVERSION TO SR

DilCM, RCM, CHT

2. Decrease in dyastole duration = Cardiac output

Mi stenosis, Ao stenosis, OHCM

HR DECREASE

Coronary artery disease

3. Thromboembolic risk

PROFILAXIS OF
SYSTEMIC EMBOLISM

Cardioversion
Candidates:

Hemodynamically unstable EES

First episode
Rare, non-paroxysmal episodes
New-onset/aggravated symptoms due to AFib (ex CHT)
To avoid:
Asymptomatic (especially elderly > 80 ani)
Bleeding risk risky pericardioversion anticoagulation

Predictors of failed cardioversion

Continous AFib 1 an
Extremely dilated LA (transverse > 50 mm)
Elderly >80 ani
Comorbidity (LVD, LVH, HBP, valve disease, thyrotoxicosis, pericarditis)
AFib recurrences in spite of correct AAD therapy

Special problems with

cardioversion
HR control (bB, CCB)
patients confort
May facilitate spontaneous
conversion
!! Underlying cardiopathy

Timing vs anticoagulation
Embolic risk (!! CHA2DS2-VASc)
low <24 h
acceptable <48 h
TEE

HR control
- in permanent AFib or in case of cardioversion contraindications -

1. Acute:
IV Digoxin: first-line in

CHF
Beta-blockers:
Metoprolole: 5-15 mg IV

Propranolole (1-5 mg)

Esmolole

CCBs:
Diltiazem 20-25 mg IV
Verapamile 5-15 mg IV

2. Chronic:
B or CCBs are preferred in

the absence of CHF

B +/- digoxin in CHF; CCBs
are to be avoided
Bronchial spasm: CCBs
Hardly controllable effort HR

Stroke risk in AFib: CHADS2

CHADS2 Score elements:
Congestive Heart Failure: 1 pt
Hypertension: 1 pt
Age: 1 pt
Diabetes: 1 pt

Stroke of transient ischaemic

attack: 2 pt

Rockson SG, Albers GW. JACC 2004;43:929.

Stroke risk in AFib: CHA2DS2-VASc

VENTRICULAR
TACHYARRHYTHMIAS
Wide QRS tachyarrhythmias

VT: definition and ECG

characteristics
Regulated tachyarrhythmia with QRS > 120 msec:
MONOMORPHIC or POLYMORPHIC ASPECT

C.p. 3 successive ventricular depolarizations with > 120/min

Variable duration: 3 QRS > 30 sec (hrs)
AV dissociation
Independent atrial activation or retrograde VA conduction

RISKS:
Unstable hemodynamics
Transition to VFib

VT mechanisms
RE-ENTRY:
PostMI

ABNORMAL AUTOMATICITY:
AMI: unparoxysmal VT (AIVR)

EARLY AND LATE POSTDEPOLARIZATIONS

Digitalis VT
Congenital long QT syndrome
Quinidine

Sustained monomorphic VT
usually RE-ENTRY

R.V. - Life threatening Brady & Tachy 2016

Monomorphic VT: diagnosis

Regular tachyarrhythmia >
120/

Wide QRS > 120 msec

AV dissociation
Fusion beats
Ventricular captured beats
Criterii morfologice

Morphology

leads V1,2 and V6

Rabbit ear sign

RBBB
V1,2

VT

SVT
rsR

R(r)

Monophazic R
qR
RsR cu R>R

V6

qR

rS

rS

R/S > 1
Wellens 1978

R/S < 1

R.V. - Life threatening Brady & Tachy 2016

Morphology
leads V1,2 si V6

LBBB type
V1,2

> 0.03

Wide initial r >30 ms

S wave deflection
slow
noch
bQRS nadir S 60
ms

TV

TSV

> 0.06

Fr q

V6
Q sau QS

Kindwall, 1988

wo RS in precordial leads

yes

no
R S > 100msec ?

VT

yes

No

VT

A-V dissociation?

Yes
VT

VT morphology V1,2 and V6 ?

yes
VT

No

No
SVT with aberancy

TV polimorfa

Polymorphic VT: torsade du pointes

EPD
Fast VT, transition to VFib
through EPD

with long QT or normal QT

Causes:
Long QT syndrome

hipo K, hipo Mg
Type Ia and III AAD
Treatment:
IV MgSO4
Overdrive pacing
Isuprel
Lidocaine, phenytoine
Long QT: AICD, bBlockers,
flecainide, stelectomy.

Dg VT vs. SVT with wide QRS

Wide QRS tachyarrhythmias:

VT

SVT with wide QRS

SVT + pre-existent BBB

SVT with aberrant conduction
SVT + AVRT through antidromic mechanism (WPW)

Dif. Dg. Possible on standard ECG in > 90% of cases

ECG criteria for differentiating VT from wide QRS SVT:

1. Fusion beats; ventricular captured beats
2. AV dissociation

3. VA retrograde conduction (retrograde P-waves)

4. QRS > 140 msec (160 msec = certainly VT)
5. Unique QRS morphology within precordial leads = VT

VT Treatment
VT with no hemodynamical instability: AADs
Lidocaine, Procainamide, Amiodarone, B in some cases
Digitalis VT: phenytoine, lidocaine +/- anti-digitalis antibodies

VT with low BP, LVD, angina, cerebral hipoperfusion:

EES: synchronous > 50 J

Alternative:
Overdrive pacing
thump version

Treatment of correctable or inducing causes:

Acute ischaemia
Hipo K, hipo Mg
Excessive sinus bradycardia

VT termination through overdrive

pacing

Prophilactic treatment of VT
Asymptomatic NSVT on normal/pathological myocardium:
Blockers (EF > 40%) or amiodarone
NO flecainide, encainide, sotalole after CAST

NSVT with hemodynamic deterioration or SVT:

Amiodarone
RF ablation of endocardial foci: palliative(?)
AA surgery
ICD

Ventricular
fibrillation
Fibrillation waves of different amplitude, in the absence of
QRS complexes
Mechanical asystole followed by electrical asystole
Shock, cardiac arrest and death in 3-5 minutes from onset
in the absence of CPR
Causes:
Acute ischaemia in AMI
spontaneous severe
ventricular arrhythmias
Cardiomyopathy (OHCM !)
AFib in WPW
CHT with LVH
COPD hypoxia
Iatrogenic: drug, dyselectrolytemia, cardiac catheterization
QT long syndrome with TdP
asynchronous EES

Preceded or not by VT:

Treatment:
R.V. - Life threatening Brady & Tachy 2016

Treatment of malignant
ventricular arrhythmias: ICD
Indications:
Secondary prophylaxis
Any structural/electrical
cardiomyopathy with one event

(resuscitated SCD, sustained VT,

VFib) in which no reversible cause is
observed

Primary prophylaxis

Anti-tachy and anti-brady pacing

IHD with LVEF < 35-40%

Conversion-defibrillation with energy

Dil. CM with LVEF < 30-35% and

ECG storage

NYHA III

HCM

Technical advantages:

mortality compared to amiodarone in

ARVC

malignant symptomatic ventricular

LQT Sd.

arrhythmias

Brugada Sd.

LQT

R.V. - Life threatening Brady & Tachy 2016

SQT
tip 1: -fx HERG/KCNH2, IKr
tip 2: -fx KVLQT1/KCNQ1, IKs
tip 3: -fx KCNJ2/Kir2.1, IK1; characteristic ECG
High and marked asymmetric T waves
Almost normal ascending slope
Extremely abrupt descending slope

,,overlaping syndromes: -fx Type L Ca2+ chan.

subunit 1 (CACNA1C, QT type 4 Sd.)
subunit (CACNB2b, QT type 5 Sd.)
Mixed phenotype: QTc + ECG Brugada Sd.

Brugada Sd.

Idiopathic VFib
Malignant Early Repolarization Syndrome

ARVC/D

Au. dom. / recessive

Demosomal disease
Fibro-fatty degeneration of RV walls LV
[75%] (relatively preserved IV septum)
Classic (39%): isolated/predominant RV disease
Biventricular (56%): both ventricles implied
Left dominance (5%): LV predominantly

prevalence 1/1000 (possibly

underdiagnosed)
N Italy: 11% of SCD in youths and 22% of
SCD in athletes

ECG