LIFE-THREATENING

ARRHYTHMIAS
Alexandru Deaconu
Senior Lecturer UMF Carol Davila
Cardiologist
 LIFE-THREATENING
ARRHYTHMIAS

• Bradyarrhythmias:
• Infra-nodal AV block

• Tachyarrhythmias:
• Malignant ventricular arrhythmias
 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 arrhythmia and

substrate
BRADYARRHYTHMIAS
 CLASSIFICATION -
BRADYARRHYTHMIAS
HEAR RATE <50 bpm

•Disturbances of the initiation and/or

conduction of the electrical impulse in the
SAN (Sick Sick Syndrome (SSS))

•Disturbances of the conductions system

(atrioventricular block (AVB))

Where is the P?
ILR
 QUESTION:
WHAT IS THE DIAGNOSIS?

A.SSS
B.AVB
C.Both
D.Don’t know…
(only one answer please)
 SAN DYSFUNCTION

• Sinus bradycardia

• Sinus arrests

• Sino-atrial conduction block (SAB)

 QUESTION:
WHAT IS THE DIAGNOSIS?

A.SSS
B.AVB
C.RBBB
D.Don’t know…
(multiple answers possible)
 CONDUCTION SYSTEM
DISTURBANCES

• AV blockNodal
Or
• First degree
• Second degree: Mobitz 1/Mobitz 2
Infranodal
• Third degree (complete)

• 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
½ 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):
• 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 )
• Mobitz II:
• 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 2 nd 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:
• 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 .
• High degree AV block:
• 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)
 QUESTION
DIAGNOSIS?
A. SSS
B. 1st degree AVB
C. Mobitz 1
D. Mobitz 2
 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.
 QUESTION
DIAGNOSIS?

A. SSS
B. 1st degree AVB
C. Mobitz 2
D. Complete AVB
 QUESTION
DIAGNOSIS?

A. SSS
B. 1st degree AVB
C. Mobitz 2
D. Complete AVB
 SO – BOTH CAVB BUT…
IS THERE A DIFFERENCE?

A. Yes
B. No
 ETIOLOGY

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

• Organic
• Ischaemia-necrosis
• Inflamation
• Fibrosis
• Infiltrative diseases
• Degenerative diseases
 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)
 CARDIAC PACING

Chamber Chamber Type of Special Antitachycardia

(s) paced (s) sensed response functions functions

V V I R P

A A T
D D D
RVA VS. SEPTAL STIMULATION
 PACEMAKERE

AD - Curs ECG normala - UMFCD/SCUB 06/10/24

AD - Curs ECG normala - UMFCD/SCUB 06/10/24
AD - Curs ECG normala - UMFCD/SCUB 06/10/24
AD - Curs ECG normala - UMFCD/SCUB 06/10/24
 CARDIOSTIMULARE VVI –
NORMOFUNCTIONALA?

A.Deaconu - Provocari in aritmologie Lipsa de captura ventriculara 06/10/24

TACHYARRHYTHMIAS
 TACHYARRHYTHMIAS

• Supraventricular
• WPW
• Atrial flutter
• Atrial fibrillation

• Ventricular
 TACHYARRHYTHMIAS

• If hemodynamically unstable

=> Urgent electrical cardioversion

 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)

• Intermitent conduction (intermitent delta wave)

• Apparently absent – eventually for prolonged periods ?? (fusion) asymptomatic

asymptomatic

• 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
symptomatic
INTERMITENT “DELTA” WAVE
PERMANENT PRE-EXCITATION
AV RE-ENTRANT
TACHYCARDIA WITH
ANTIDROMIC
CONDUCTION
 Regular
 Regular tachyarrhythmia
tachyarrhythmia with
with wide
wide QRS
QRS

through”
through” presence
presence of
of the
the delta
delta wave
wave

 fast
 fast ventricular
ventricular response
response >
> 180-200/min
180-200/min

 mechanism:
 mechanism:

 Antegrade
Antegrade conduction
conduction through
through the
the AP
AP

 Retrograde
 Retrograde conduction
conduction through
through the
the AVN
AVN

 Differential
 Differential diagnosis
diagnosis with
with sustained
sustained

monomorphic
monomorphic VT
VT

 Increased
 Increased risk
risk of
of sudden
sudden death
death ->
-> in
in case
case

of
of Afib
Afib ->
-> VFib
VFib
 SVT IN WPW SDR. WITH ANTIDROMIC CONDUCTION

Regular
Regular tachyarrhythmia
tachyarrhythmia with
with wide
wide QRS;
QRS; no
no P-waves;
P-waves; dif.
dif. dg.
dg. with
with monomoprhic
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:
• Digoxin
• Calcium blockers
 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 SVT VT
• V1,2
rsR’ R(r’)
• Monophazic R
• qR
• RsR’ cu R>R’

• V6 qR rS
• rS

R/S > 1 R/S < 1

Wellens 1978
 MORPHOLOGY
LEADS V1,2 SI V6
TSV TV
• LBBB type
• V1,2 > 0.03

• Wide initial r >30 ms

• S wave deflection
• slow
• noch > 0.06

• bQRS  nadir S ≥ 60 ms Fără q q

• V6
• Q sau QS

Kindwall, 1988
 wo RS in precordial leads

yes no

VT R – S > 100msec ?

yes No

VT A-V dissociation?

Yes
No

VT
VT morphology V1,2 and V6 ?

yes
No

VT
SVT with aberancy
TV POLIMORFA
POLYMORPHIC VT: TORSADE DU
POINTES
•• Fast
Fast VT,
VT, transition
transition to
to VFib
VFib
•• through
through EPD
EPD
•• with
with long
long QT
QT or
or normal
normal QT
QT
•• Causes:
Causes:
•• Long
Long QT
QT syndrome
syndrome
•• hipo
hipo K,
K, hipo
hipo Mg
Mg
•Type
•Type Ia
Ia and
and III
III AAD
AAD
•• Treatment:
Treatment:
•• IV
IV MgSO4
MgSO4
•• “Overdrive
“Overdrive pacing”
pacing”
•• Isuprel
Isuprel
•• Lidocaine,
Lidocaine, phenytoine
phenytoine
•• Long
Long QT:
QT: AICD,
AICD, bBlockers,
bBlockers,
flecainide,
flecainide, stelectomy.
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:
• EES 200-300 J CPR, OTI
• Bicarbonat EV daca CPR > 60 sec Lidocaina, bretiliu, amiodaron EV
• Corectarea cauzei
R.V. - Life threatening Brady & Tachy 2016
• Profilactic: DI sau amiodaron
 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
• Technical advantages:
• IHD with LVEF < 35%
• Anti-tachy and anti-brady pacing
• Dil. CM with LVEF < 30-35% and NYHA ≥
III • Conversion-defibrillation with  energy

• HCM • ECG storage

• ARVC
•  mortality compared to amiodarone in
• LQT Sd.
malignant symptomatic ventricular arrhythmias
• Brugada Sd.

• SQT Sd.
 CLINICAL CASE
• 70 year-old man with diabetes collapses shortly after presenting to the
ER for palpitations
• HR 200 bpm, BP 60/40 mmHg
 WHAT DO YOU DO?

A.Begin BLS followed by ALS

B.External electrical shock
C.Adenosine iv
D.Amiodarone iv

(only one answer please)

 SO….
LIFE-THREATENING ARRHYTHMIAS

• Bradyarrhythmias:
• Infra-nodal AV block

• Tachyarrhythmias:
• Malignant ventricular arrhythmias
Thank you!