Arrhythmias

Osama Osman
MD cardiology
Normal Sinus Rhythm

Implies normal sequence of conduction, originating in the sinus node and

proceeding to the ventricles via the AV node and His-Purkinje system.

ECG Characteristics: Regular narrow-complex rhythm

Rate 60 - 90 bpm
Each QRS complex is preceeded by a P wave
P wave is upright in lead II & down going in lead
aVR
 Tachyarrhythmia Bradyarrhythmi

1st degree,
2nd degree
3rd degree
Ventricular Supraventricular
atrial fibrrilation VT
VF Atrial flutter
Paroxysmal SVT
Etiology
● Physiological
● Pathological:
➢Valvular heart disease.
➢Ischemic heart disease.
➢Hypertensive heart diseases.
➢Congenital heart disease.
➢Cardiomyopathies.
➢Carditis.
➢RV dysplasia.
➢Drug related.
➢Pericarditis.
➢Pulmonary diseases.
➢Others (thyroid dis., electrolyte impalance)
Arrhythmia Assessment
● History
● Examination
● ECG
● 24h Halter monitor
● Echocardiogram
● Stress test
● Coronary angiography
● Electrophysiology study
 Clinical Manifestations of
tachyarrhythmias
• Many go unnoticed and produce no symptoms
• Palpitations
• If COP is affected: lightheadedness and syncope, fainting
• Myocardial oxygen demand may increase lead to
ischemia and angina

• Sudden death – especially in the case of an acute MI

• Thromboembolism and systemic embolization
Sinus Tachycardia
● Sinus node is the pacemaker, firing regularly at a rate of greater
than 100 times per minute. Each impulse is conducted normally
to the ventricles .
● Regularity: The R-R intervals are constant; Rhythm is regular
● Rate: Atrial and Ventricular rates are equal; heart rate greater
than 100
● P Wave: Uniform P wave precede every QRS
● PRI: PRI is between 0.12 - 0.20 and constant
● QRS: Normal
●Causes of Sinus Tachycardia:
Physiologic
Exercise
Strong emotion
Pain
Anxiety states
Pathological: fever, hyperthyroidism
Atrial premature contractions (APCs)
● APCs arising from somewhere in either the left
or the right atrium.
● Causes: common in normal persons.
rheumatic heart disease, CAD,
hypertension, hyperthyroidism, hypokalemia
● Symptoms: many patients have no symptom,
some have palpitation, chest uncomfortable.
● Therapy: Need no therapy in patients without
heart disease. Can be treated with ß-blocker,
propafenone or verapamil.
Demographics
● Common; 2.2 million people in U.S.
● Male>Female
● Prevalence increases with age
● Leading cause of embolic strokes
● Associated with increased risk for heart failure and
all cause mortality
Atrial fibrillation pathogenesis
● wavelets propagating in different directions
● disorganised atrial depolarisation without effective
atrial contraction
● f waves 350-600 beats /min.
● ventricular response is grossly irregular at 100-160
beats /min. (in WPW >300/min or VF)
ECG Characteristics of AF

Absent P waves
Presence of fine “fibrillatory” waves which vary in
amplitude and morphology
Irregularly irregular ventricular response
Risk Factors
● Age > 60 (increase in age >80)
● Valvular heart disease (MS)
● Congenital heart disease
● Long standing pulmonary disease (e.g. COPD)
● Hyperthyroidism
● Hypertension
● Coronary disease
● Post CABG surgery
● Drugs: Theophylline, Albuterol, Ephredra, Cocaine,
Methamphetamine
● Lone AF
Symptoms
● Asymptomatic
● Palpitations
● LCO
● Shortness of breath, perhaps syncope
● Thromboembolism
● STROKE
● Symptoms of the cause
❑ Pulse: irregular irregularity, pulse deficit
❑ Neck veins: loss of A wave
❑ Signs of LCO
❑ Signs of the cause
❑ Local cardiac ex:
Signs of the cause
Irregular irregularity of S1 S2
No S4
MANAGEMENT
The first step in management is to determine whether
the patient is stable or not…
-Look for any hemodynamic instability such as
hypotension
-Is the patient responsive?
-Are there any mental status changes?
-are symptoms persistent and unbearable?
RATE VS RHYTHM CONTROL
● Rate Control vs Rhythm Control
● **no clear survival benefit in rate vs rhythm control**
RATE CONTROL
● Agents:
➢Beta Blocker: Metoprolol and bisoprolol
➢Non-dihydropyridine CA blockers: verapamil,
Diltiazem
➢Digoxin
Goal: Rest 60-80 bpm and Activity 80-110
Rhythm Control
● AGENT:
➢III: Amiodarone, Ibutilide, Dofetilide, Sotalol
➢IC: Flecainide, Propafenone
➢IA: Procainamide
ANTICOAGULATION; Which Agent to
Choose?
● CHADS2 SCORE
➢ CHF: 1 point
➢ HTN: 1 point
➢ AGE >75: 1 point
➢ DM: 1 point
➢ Stroke or prior TIA: 2 points
Score:
0=ASA alone
1= either warfarin or ASA
2 or more= warfarin
• Pacemakers not curative and must be worn for life
• Surgical procedures may be effective but are not a
practical solution for the millions of sufferers of AFib
• Catheter ablation is potentially curative

Devices Electrophysiological Surgery

Pacemaker Maze procedure

(single or dual chamber) Catheter ablation
Modified Maze
Internal atrial AV node ablation
defibrillators (mini-Maze)

ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation
J Am Coll Cardiol (2006) 48: 854
PV Antrum Isolation Guided by CARTOMERGE™
Image Integration Software Module

RUPV

LUPV RMPV
LA

AC RLPV
LLPV

Courtesy of Professor Antonio Raviele, Mestre, Italy

Catheter Visualization under Fluoroscopic Guidance
Ablation LASSO®
catheter

LAO RAO
Atrial flutter
● Etiology:
1. It can occur in patients with normal atria or
with abnormal atria.
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 cases have a reentry loop in right atrial
● A single irritable focus within the atria issues an impulse that is conducted in a rapid,
repetitive fashion. To protect the ventricles from receiving too many impulses, the AV
node blocks some of the impulses from being conducted through to the ventricles.

● Regularity: Atrial rhythm is regular. Ventricular rhythm will be regular if the AV node
conducts impulses through in a consistent pattern. If the pattern varies, the ventricular
rate will be irregular

● Rate: Atrial rate is between 250-350 beats per minute. Ventricular rate will depend on
the ratio of impulses conducted through to the ventricles.

● P Wave: there will be "Flutter" waves have a saw tooth appearance.

● PRI: the PRI is not measured in Atrial Flutter.

● QRS: QRS is less than .12 seconds; measurement can be difficult if one or more flutter
waves is concealed within the QRS complex.
 Atrial Flutter

Most cases of atrial flutter are caused by a large reentrant circuit in the wall of the
right atrium

ECG Characteristics: Biphasic “sawtooth” flutter waves at a rate of ~ 300 bpm

Flutter waves have constant amplitude, duration, and
morphology through the cardiac cycle
There is usually either a 2:1 or 4:1 block at the AV node,
resulting in ventricular rates of either 150 or 75
bpm
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: Cardioversion, Drug (III,
Ia, Ic class).
3. Control the ventricular rate: digitalis. CCB, ß-
block
4. Anticoagulation
 PSVT (paroxysmal tachycardia)

● Reentrant arrhythmia at AV node that is spontaneous

in onset
● Narrow QRS with tachycardia
● Occur in any age, usually no structure heart disease.
●Manifestation:

● Occur and terminate abruptly.

●Palpitation, dizziness, syncope,
angina, heart failure and shock.
●The severity of the symptom is
related to ventricular rate, persistent
duration and underlying disease
Treatment
●First line is vagal maneuvers
●Second line is adenosine or
verapamil
●For chronic SVT, class 1A or 1C or
amiodarone or sotalol work well
●Ablation will cure it
 Pre-excitation syndrome

(WPW syndrome)
● There are several types of accessory pathway
1. Kent: adjacent atrial and ventricular
2. James: adjacent atrial and his bundle
3. Mahaim: adjacent lower part of the AVN and
ventricular
● Usually no other structure heart disease.
● Manifestations appear in any age individual
(WPW)
short PR - delta wave - wide QRS
Ventricular arrhythmia
Ventricular Premature Contractions
(VPCs)

● Etiology:
May occur in normal person
Myocarditis, CAD, valve heart disease,
hyperthyroidism, Drug toxicity (digoxin,
quinidine and anti-anxiety drug) electrolyte
disturbance, anxiety, excessive coffee
VPCs
● Manifestation:
1. palpitation
2. dizziness
3. syncope
 PVCs
● Therapy:
1. Asymptomatic: no therapy
2. Symptomatic: antianxiety agents, ß-blocker and
mexiletine to relief the symptom.
● With structure heart disease (CAD, HBP):
1. Treat the underlying disease
2. ß-blocker, amiodarone
3. Class I especially class Ic agents should be
avoided because of proarrhytmia and lack of
benefit of prophylaxis
What is this arrhythmia?

VT
Ventricular tachycardia is usually caused by reentry, and
most commonly seen in patients following myocardial infarction.
 Ventricular Tachycardia

● An irritable focus in the ventricles fires regularly at a rate of 150-250 beats

per minute to override higher sites for control of the heart.
● Regularity: This rhythm is usually regular, although it can be slightly
irregular.
● Rate: Atrial rate cannot be determined. The ventricular rate range is
150-250 beats per minute. If the rate is below 150 bpm, it is considered a
slow VT. If the rate exceeds 250 bpm, its called Ventricular Flutter.
● P Wave: None of the QRS complexes will be preceded by P waves;
dissociated P waves intermittently across the strip.
● PRI: Since the rhythm originates in the ventricles, there will be no PRI.
● QRS: The QRS complexes will be wide and bizarre.
Ventricular tachycardia
● Etiology: often in organic heart disease
CAD, MI, DCM, HCM, HF,
long QT syndrome
Brugada syndrome
● Sustained VT (>30s), Nonsustained VT
● Monomorphic VT, Polymorphic VT
Ventricular tachycardia
● Torsades de points: A special type 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
 VT
● Manifestation:
1. May be asymptomatic (rare) (non sustained)
2. patient may feel palpitation, short of breath,
presyncope, syncope, angina, hypotension and
shock.
 Treatment of VT
1. Treat underlying disease
2. Cardioversion: Hemodynamic unstable VT
(hypotension, shock, angina, CHF) or
hemodynamic stable but drug was no effect
3. Pharmacological therapy: ß-blockers, lidocain
or amiodarone
4. RFCA, ICD or surgical therapy
 Ventricular Fibrillation

● Multiple foci in the ventricles become irritable and generate uncoordinated,

chaotic impulses that cause the heart to fibrillate rather than contract.
● Regularity: There are no waves or complexes that can be analyzed to
determine regularity. The baseline is totally chaotic.
● Rate: The rate cannot be determined since there are no discernible waves or
complexes to measure.
● P Wave: There are no discernible P waves.
● PRI: There is no PRI.
● QRS: There are no discernible QRS complexes.
1- assessment of the pt.
A- heamodynamicaly unstable
B- heamodynamicaly stable

2- according to the type of arrhythmia

3- lines of treatment
A- DC shock
B- Vagal maneuvers
C- Drugs
D- AID
E- Ablation
F- Correction of the cause and precipitating factors