Dr Mohamed A.

Fathi
Cardiology specialist and
Tutor
GMCHRC
 What is Arrhythmia??
 Definition of Arrhythmia:
It is abnormal Origin, Rate,
Rhythm, Conduct velocity and
sequence of heart activation.
Anatomy of the conducting system
 Pathogenesis and Inducement
of Arrhythmia
 Some physical condition
 Pathological heart disease
 Other system disease
 Electrolyte disturbance and
acid-base imbalance
 Physical and chemical factors or
toxicosis
 Mechanism of Arrhythmia
 Abnormal heart pulse
formation
1. Sinus pulse
2. Ectopic pulse
3. Triggered activity
 Abnormal heart pulse
conduction
1. Reentry
2. Conduct block
Classification of Arrhythmia
 Abnormal heart pulse formation
1. Sinus arrhythmia
2. Atrial arrhythmia
3. Atrioventricular junctional arrhythmia
4. Ventricular arrhythmia
 Abnormal heart pulse conduction
1. Sinus-atrial block
2. Intra-atrial block
3. Atrio-ventricular block
4. Intra-ventricular block
 Abnormal heart pulse formation
and conduction
 Diagnosis of Arrhythmia
 Medical history
 Physical examination
 Laboratory test
Sinus Arrhythmia
Sinus Arrhythmia
 Sinus tachycardia
 Sinus rate > 100 beats/min (100-
180)
 Causes:
1. Some physical condition: exercise,
anxiety, exciting, alcohol, coffee
2. Some disease: fever,
hyperthyroidism, anemia,
myocarditis
3. Some drugs: Atropine, Isoprenaline
• Needn’t therapy
Sinus tachycardia
 Sinus Bradycardia
 Sinus rate < 60 beats/min
 Normal variant in many normal and older pe
ople
 Causes: Trained athletes, during sleep, drug
s (ß-blocker) , Hypothyriodism, CAD or SSS
 Symptoms:
1. Most patients have no symptoms.
2. Severe bradycardia may cause dizziness, fati
gue, palpitation, even syncope.
 Needn’t specific therapy, If the patient has s
evere symptoms, planted an pacemaker may
be needed.
Sinus Bradycardia
 Sinoatrial exit block (SAB)
 SAB: Sinus pulse was blocked so
it couldn’t active the atrium.
 Causes: CAD, Myopathy,
Myocarditis, digitalis toxicity, et
al.
 Symptoms: dizziness, fatigue,
syncope
 Therapy is same to SSS
 Sinoatrial exit block (SAB)
 Divided into three types: Type I,
II, III
 Only type II SAB can be
recognized by EKG.
Sinoatrial exit block (SAB)
 Sinus Arrest or Sinus
Standstill
 Sinus arrest or standstill is recognize
d by a pause in the sinus rhythm.
 Causes: myocardial ischemia, hypoxi
a, hyperkalemia, higher intracranial
pressure, sinus node degeneration a
nd some drugs (digitalis, ß-blocks).
 Symptoms: dizziness, amaurosis, syn
cope
 Therapy is same to SSS
Sinus Arrest or Sinus Standst
ill
Sick Sinus Syndrome (SSS)
 SSS: The function of sinus node was degen
erated. SSS encompasses both disordered
SA node automaticity and SA conduction.
 Causes: CAD, SAN degeneration, myopathy
, connective tissue disease, metabolic dise
ase, tumor, trauma and congenital disease
.
 With marked sinus bradycardia, sinus arre
st, sinus exit block or junctional escape rh
ythms
 Bradycardia-tachycardia syndrome
Sick Sinus Syndrome (SSS)
 Sick Sinus Syndrome (SSS)
 Therapy:
1. Treat the etiology
2. Treat with drugs: anti-
bradycardia agents, the effect
of drug therapy is not good.
3. Artificial cardiac pacing.
Atrial arrhythmia
 Premature contractions
 Common arrhythmia
 The terms “premature beat"," p
remature contraction"," premat
ure systole", or “extra systole” i
ndicate that the atria ,AV juncti
on, or ventricle are stimulated p
rematurely.
Atrial premature contractions (A
PCs)
1).A premature P wave is present .It
may be superimposed on the preceding
T wave because it is premature. The pr
emature P wave is usually followed by
a QRS complex and a T wave. Occasion
ally, it is not followed by a QRS comple
x and a T wave .(blocked atrial premat
ure beat).
2).The QRS and T waves that follow th
e premature P waves usually resemble
the other QRS and T waves in the lead.
Atrial premature contractions (A
PCs)
 3).The P-R interval of the atrial prema
ture beat is usually longer than the no
rmal PR intervals in the ECG.
4).An atrial premature beat is often fo
llowed by a noncompensatory pause.
5).The ventricular complex is usually
normal but may be aberrant in from if
the premature atrial beat coincides wi
th the refractory phase of the previou
s ventricular beat .The aberrant QRS i
s called aberrant conduction.
Atrial premature contractions (A
PCs)
 Atrial premature contractions
(APCs)
 Causes: rheumatic heart disease, CAD, hy
pertension, hyperthyroidism, hypokalemi
a
 Symptoms: many patients have no sympt
om, some have palpitation, chest incomfo
rtable.
 Therapy: Needn’t therapy in the patients
without heart disease. Can be treated wit
h ß-blocker, propafenone, moricizine or v
erapamil.
 Atrial tachycardia

 Classify by automatic atrial tachycardia

(AAT); intra-atrial reentrant atrial
tachycardia (IART); chaotic atrial
tachycardia (CAT).
 Etiology: atrial enlargement, MI; chronic
obstructive pulmonary disease; drinking;
metabolic disturbance; digitalis toxicity;
electrolytic disturbance.
 Atrial tachycardia

 May occur transient; intermittent;

or persistent.
 Symptoms: palpitation; chest unco
mfortable, tachycardia may induce
myopathy.
 Auscultation: the first heart sound
is variable
 Intra-atrial reentry tachycardia
(IART)
 ECG characters:
1. Atrial rate is around 130-150bpm;
2. P’ wave is different from sinus P wave;
3. P’-R interval ≥ 0.12”
4. Often appear type I or type II, 2:1 AV
block;
5. EP study: atrial program pacing can
induce and terminate tachycardia
 Automatic atrial tachycardia
(AAT)
 ECG characters:
1. Atrial rate is around 100-200bpm;
2. Warmup phenomena
3. P’ wave is different from sinus P wav
e;
4. P’-R interval≥ 0.12”
5. Often appear type I or type II, 2:1 A
V block;
6. EP study: Atrial program pacing can’t
induce or terminate the tachycardia
 Chaotic atrial tachycardia
 (CAT) atrial tachycardi
Also termed “Multifocal
a”.
 Always occurs in COPD or CHF,
 Have a high in-hospital mortality ( 25-5
6%). Death is caused by the severity of
the underlying disease.
 ECG characters:
1. Atrial rate is around 100-130bpm;
2. The morphologies P’ wave are more tha
n 3 types.
3. P’-P’, P’-R and R-R interval are different.
4. Will progress to af in half the cases
5. EP study: Atrial program pacing can’t in
duce or terminate the tachycardia
 Therapy
 IRAT: Esophageal Pulsation Modula
tion, RFCA, Ic and IV class anti-tach
ycardia agents
 AAT: Digoxin, IV, II, Ia and III clas
s anti-tachycardia agents; RFCA
 CAT: treat the underlying disease, v
erapamil or amiodarone.
 Associated with SSS: Implant pace-
maker.
 Atrial flutter
 Etiology:
1. It can occur in patients with
normal atrial or with abnormal
atrial.
2. It is seen in rheumatic heart
disease (mitral or tricuspid valve
disease), CAD, hypertension,
hyperthyroidism, congenital heart
disease, COPD.
3. Related to enlargement of the atria
4. Most AF have a reentry loop in
right atrial
 Atrial flutter
 Symptoms: depend on underlying
disease, ventricular rate, the
patient is at rest or is exerting
 With rapid ventricular rate:
palpitation, dizziness, shortness
of breath, weakness, faintness,
syncope, may develop angina
and CHF.
 Atrial flutter
 Therapy:
1. Treat the underlying disease
2. To restore sinus rhythm: Cardio
version, Esophageal Pulsation M
odulation, RFCA, Drug (III, Ia, I
c class).
3. Control the ventricular rate: digi
talis. CCB, ß-block
4. Anticoagulation
 Atrial fibrillation
 Subdivided into three types:
paroxysmal, persistent, permanent.
 Etiology:
1. Morbidity rate increase in older
patients
2. Etiology just like atrial flutter
3. Idiopathic
 Mechanism:
1. Multiple wavelet re-entry;
2. Rapid firing focus in pulmonary
vein, vena cava or coronary sinus.
 Atrial fibrillation
 Manifestation:
 Affected by underlying diseases, ventricular
rate and heart function.
 May develop embolism in left atrial. Have hig
h incidence of stroke.
 The heart rate, S1 and rhythm is irregularly i
rregular
 If the heart rhythm is regular, should consid
er about (1) restore sinus rhythm; (2) AF wit
h constant the ratio of AV conduction; (3) ju
nctional or ventricular tachycardia; (4) slow
er ventricular rate may have complete AV bl
ock.
 Atrial fibrillation
 Therapy:
1. Treat the underlying disease
2. Restore sinus rhythm: Drug, Car
dioversion, RFCA, Maze surgery
3. Rate control: digitalis. CCB, ß-bl
ock
4. Antithrombotic therapy: Aspirin
e, Warfarin
Atrioventricular Junctional
arrhythmia
Atrioventricular junctional prematur
e contractions

 Etiology and manifestation is like

APCs
 Therapy the underlying disease
 Needn’t anti-arrhythmia therapy.
Nonparoxysmal AV junctional tachycardi
a
 Mechanism: relate to hyper-automat
icity or trigger activity of AV junctio
nal tissue
 Etiology: digitalis toxicity; inferior M
I; myocarditis; acute rheumatic feve
r and postoperation of valve disease
 ECG: the heart rate ranges 70-150 b
pm or more, regular, normal QRS co
mplex, may occur AV dissociation an
d wenckebach AV block
Nonparoxysmal AV junctional tachycardi
a
 Therapy:
 Treat underlying disease; stoppi
ng digoxin, administer potassium
, lidocaine, phenytoin or propran
olol.
 Not for DC shock
 It can disappear spontaneously.
If had good tolerance, not requir
e therapy.
 Paroxysmal tachycardia
 Most PSVT (paroxysmal supraventricular t
achycardia) is due to reentrant mechanism
.
 The incidence of PSVT is higher in AVNRT
(atrioventricular node reentry tachycardia)
and AVRT (atioventricular reentry tachycar
dia), the most common is AVNRT (90%)
 Occur in any age individuals, usually no str
ucture heart disease.
 Paroxysmal tachycardia
 Manifestation:
 Occur and terminal abruptly.
 Palpitation, dizziness, syncope,
angina, heart failure and
shock.
 The sever degree of the
symptom is related to
ventricular rate, persistent
duration and underlying
disease
 Paroxysmal tachycardia
 ECG characteristic of AVNRT
1. Heart rate is 150-250 bpm, regular

2. QRS complex is often normal, wide

QRS complex is with aberrant condu
ction
3. Negative P wave in II III aVF, burie
d into or following by the QRS compl
ex.
4. AVN jump phenomena
 Paroxysmal tachycardia
 ECG characteristic of AVRT
1. Heart rate is 150-250 bpm, regul

ar
2. In orthodromic AVRT, the QRS co

mplex is often normal, wide QRS

complex is with antidromic AVRT
3. Retrograde P’ wave, R-P’>110ms

.
 Paroxysmal tachycardia
 Therapy:
 AVNRT & orthodromic AVRT
1. Increase vagal tone: carotid sinus mas
sage, Valsalva maneuver.if no successf
ul,
2. Drug: verapamil, adrenosine, propafen
one
3. DC shock
 Antidromic AVRT:
1. Should not use verapamil, digitalis, and
stimulate the vagal nerve.
2. Drug: propafenone, sotalol, amiodaron
e
 RFCA
 Pre-excitation syndrome
(W-P-W syndrome)
 There are several type of accessory
pathway
1. Kent: adjacent atrial and ventricular
2. James: adjacent atrial and his bundl
e
3. Mahaim: adjacent lower part of the
AVN and ventricular
 Usually no structure heart disease,
occur in any age individual
 WPW syndrome

 Manifestation:
 Palpitation, syncope, dizzine
ss
 Arrhythmia: 80% tachycardi
a is AVRT, 15-30% is AFi, 5
% is AF,
 May induce ventricular fibrill
ation
 WPW syndrome
 Therapy:
1. Pharmacologic therapy: orthodr
ome AVRT or associated AF, AFi,
may use Ic and III class agents.
2. Antidromic AVRT can’t use digox
in and verapamil.
3. DC shock: WPW with SVT, AF or
Afi produce agina, syncope and
hypotension
4. RFCA
Ventricular arrhythmia
Ventricular Premature Contractio
ns (VPCs)
 Etiology:
1. Occur in normal person
2. Myocarditis, CAD, valve heart di
sease, hyperthyroidism, Drug to
xicity (digoxin, quinidine and an
ti-anxiety drug)
3. electrolyte disturbance, anxiety,
drinking, coffee
 VPCs
 Manifestation:
1. palpitation
2. dizziness
3. syncope
4. loss of the second heart
sound
 PVCs
 Therapy: treat underlying disease, antiarrh
ythmia
 No structure heart disease:
1. Asymptom: no therapy
2. Symptom caused by PVCs: antianxiety agen
ts, ß-blocker and mexiletine to relief the sy
mptom.
 With structure heart disease (CAD, HBP):
1. Treat the underlying diseas
2. ß-blocker, amiodarone
3. Class I especially class Ic agents should be
avoided because of proarrhytmia and lack o
f benefit of prophylaxis
 Ventricular tachycardia
 Etiology: often in organic heart di
sease
CAD, MI, DCM, HCM, HF,
long QT syndrome
Brugada syndrome
 Sustained VT (>30s), Nonsustain
ed VT
 Monomorphic VT, Polymorphic VT
 Ventricular tachycardia
 Torsades de points (Tdp): A special t
ype of polymorphic VT,
 Etiology:
1. congenital (Long QT),
2. electrolyte disturbance,
3. antiarrhythmia drug proarrhythmia
(IA or IC),
4. antianxiety drug,
5. brain disease,
6. bradycardia
 Ventricular tachycardia
 Accelerated idioventricular rhyth
m:
1. Related to increase automatic to
ne
2. Etiology: Often occur in organic
heart disease, especially AMI rep
erfusion periods, heart operation
, myocarditis, digitalis toxicity
 VT
 Manifestation:
1. Nonsustained VT with no sym
ptom
2. Sustained VT : with symptom
and unstable hemodynamic, p
atient may feel palpitation, sh
ort of breathness, presyncope
, syncope, angina, hypotensio
n and shock.
 VT
 ECG characteristics:
1. Monomorphic VT: 100-250 bpm, occur and
terminate abruptly,regular
2. Accelerated idioventricular rhythm: a runs
of 3-10 ventricular beats, rate of 60-110
bpm, tachycardia is a capable of warm up
and close down, often seen AV dissociatio
n, fusion or capture beats
3. Tdp: rotation of the QRS axis around the b
aseline, the rate from 160-280 bpm, QT int
erval prolonged > 0.5s, marked U wave
 Treatment of VT
1. Treat underlying disease
2. Cardioversion: Hemodynamic u
nstable VT (hypotension, shock
, angina, CHF) or hemodynamic
stable but drug was no effect
3. Pharmacological therapy: ß-blo
ckers, lidocain or amiodarone
4. RFCA, ICD or surgical therapy
 Therapy of Special type VT
 Accelerated idioventricular rhythm:
 usually no symptom, needn’t therapy.

 Atropine increased sinus rhythm

 Tdp:
1. Treat underlying disease,
2. Magnesium iv, atropine or isoprenalin
e, ß-block or pacemaker for long QT p
atient
3. temporary pacemaker
Ventricular flutter and fibrillation
 Often occur in severe organic hear
t disease: AMI, ischemia heart dise
ase
 Proarrhythmia (especially produce
long QT and Tdp), electrolyte distu
rbance
 Anaesthesia, lightning strike, elect
ric shock, heart operation
 It’s a fatal arrhythmia
Ventricular flutter and fibrillation
 Manifestation:
Unconsciousness, twitch, no
blood pressure and pulse, going
to die
 Therapy:
1. Cardio-Pulmonary Resuscitate
(CPR)
2. ICD
 Cardiac conduction block
 Block position:
Sinoatrial; intra-atrial; atrioven
tricular; intra-ventricular
 Block degree
1. Type I: prolong the conductive t
ime
2. Type II: partial block
3. Type III: complete block
 Atrioventricular Block
 AV block is a delay or failure in tra
nsmission of the cardiac impulse fr
om atrium to ventricle.
 Etiology:
Atherosclerotic heart disease; my
ocarditis; rheumatic fever; cardio
myopathy; drug toxicity; electrolyt
e disturbance, collagen disease, le
v’s disease.
 AV Block

 AV block is divided into three

categories:
1. First-degree AV block
2. Second-degree AV block: further
subdivided into type I and type
II
3. Third-degree AV block: complete
block
 AV Block
 Manifestations:
 First-degree AV block: almost no symptom
s;
 Second degree AV block: palpitation, fatig
ue
 Third degree AV block: Dizziness, agina, h
eart failure, lightheadedness, and syncope
may cause by slow heart rate, Adams-Sto
kes Syndrome may occurs in sever case.
 First heart sound varies in intensity, will a
ppear booming first sound
 AV Block
 Treatment:
1. I or II degree AV block needn’
t antibradycardia agent therap
y
2. II degree II type and III degr
ee AV block need antibradycar
dia agent therapy
3. Implant Pace Maker
 Intraventricular Block
 Intraventricular conduction syst
em:
1. Right bundle branch
2. Left bundle branch
3. Left anterior fascicular
4. Left posterior fascicular
 Intraventricular Block
 Etiology:
 Myocarditis, valve disease, cardiom
yopathy, CAD, hypertension, pulmon
ary heart disease, drug toxicity, Le
negre disease, Lev’s disease et al.
 Manifestation:
 Single fascicular or bifascicular bloc
k is asymptom; tri-fascicular block
may have dizziness; palpitation, syn
cope and Adams-stokes syndrome
 Intraventricular Block
 Therapy:
1. Treat underlying disease
2. If the patient is asymptom; no tre
at,
3. bifascicular block and incomplete t
rifascicular block may progress to
complete block, may need implant
pace maker if the patient with syn
cope