ARRHYTHMIA

Palpitation:
 Definition
o The term “palpitation” refers to any conscious sensation of cardiac activity.
 Arrhythmia
o It is a term used to describe any cardiac rhythm that deviates from the normal sinus
rhythm.
 Normal palpitations occur with exercise, emotions, and stress, or after taking substances
that increase adrenergic tone or diminish vagal activity.
 Abnormal palpitations usually point to a cardiac arrhythmia.
Anatomy of the conducting system:

Heart Physiology:
 P - atria depolarization
 QRS - ventricle depolarization
 PR - conduction A-V
 T - ventricle repolarization
 QT - duration ventricle of repolarization
How tachycardia initiated?
All cardiac tachyarrhythmias are produced by one or more mechanisms, including :
1) Disorders of impulse initiation:
o Triggered activity
o Enhanced automaticity
2) Abnormalities of impulse conduction:
o Re-entry
Automaticity:
 Tissues exhibiting abnormal automaticity that underlie tachyarrhythmias can reside in the
atria, the AV junction, ventricles or vessels that communicate directly with the atria, such
as the vena cava or pulmonary veins.
 The cells with enhanced automaticity exhibit enhanced phase 4 depolarization and,
therefore, an increase in firing rate compared with pacemaker cells.
 If the firing rate of the ectopic focus exceeds that of the sinus node, then the sinus node
can be overdriven and the ectopic focus will become the predominant pacemaker of the
heart. The rapid firing rate may be incessant (ie, more than 50% of the day) or episodic.
o i.e. sinus tachycardia, accelerated idiovent. rhythm.
Triggered activity:
 Triggered activity is a tachycardia mechanism associated with disturbances of recovery
or repolarization.
 Triggered rhythms are generated by interruptions in repolarization of a heart cell called
afterdepolarizations.
 An afterdepolarization of sufficient magnitude may reach “threshold” and trigger an early
action potential during repolarization.
o i.e. TdP, atrial tachycardia, digitalis toxicity.
Re-entry:
 The most common arrhythmia mechanism is re-entry.
 It occurs as repetitive excitation of a region of the heart and is a result of conduction of an
electrical impulse around a fixed obstacle in a defined circuit.
 Initiation of a circus movement tachycardia requires unidirectional conduction block in
one limb of a circuit, which may occur as a result of acceleration of the heart rate or
block of a premature impulse that impinges on the refractory period of the pathway.
 Slow conduction is usually required for both initiation and maintenance of a circus
movement tachycardia.
o i.e. AVNRT and AVRT

1) A wavefront, initiated in a normal fashion in the sinus node, passes around an obstacle
(disc) to electrical activation in a uniform fashion. This obstacle may be formed by an
anatomical feature (fixed conduction block) like the tricuspid annulus, or by a
physiological abnormality (functional conduction block) like an area of ischaemic
myocardium.
2) A premature impulse results in block of conduction on one side of the obstacle while
conduction continues on the other. This is functional block because it is the result of a
short RP which means that the myocardium in this region has not recovered its
excitability in time to conduct the premature beat.
3) This wavefront takes sufficient time to circulate around the obstacle and the area
previously resulting in block recovers its excitability, so that this wavefront continually
encounters excitable tissue and perpetuates as a re-entry circuit .
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
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.
Diagnosis of Arrhythmia:
 Medical history
 Physical examination
 Laboratory test
Therapy Principal:
 Pathogenesis therapy
 Stop the arrhythmia immediately if the hemodynamic was unstable
 Individual therapy
Sinus Arrhythmia:
I.Sinus Rhythms and Sinus Arrhythmias:
 ECG of Sinus Rhythms: HR 60-100bpm
 Sinus rhythm must originate in the sino-atrial node.
1) Regularly recurring sequences of P waves, QRS complexes,and T waves.P-P or R-
R interval establishes a specific interval which should not vary more than 0.12
second.
2) The P wave is upward in lead I,II, avF,V4-5 and downward in lead aVR.
3) The PR interval < 0.12 second.

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
o Needn’t therapy
Sinus Bradycardia:
 Sinus rate < 60 beats/min
 Normal variant in many normal and older people
Causes: Trained athletes, during sleep, drugs (ß-blocker) , Hypothyriodism, CAD or SSS
Symptoms:
1) Most patients have no symptoms.
2) Severe bradycardia may cause dizziness, fatigue, palpitation, even syncope.
o Needn’t specific therapy, If the patient has severe symptoms, planted an pacemaker may
be needed.
Sinus Arrest or Sinus Standstill:
 Sinus arrest or standstill is recognized by a pause in the sinus rhythm.
Causes:
 myocardial ischemia,
 hypoxia,
 hyperkalemia,
 higher intracranial pressure,
 sinus node degeneration and
 some drugs (digitalis, ß-blocks).
Symptoms: dizziness, amaurosis, syncope
Therapy is same to SSS
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.
Divided into three types: Type I, II, III
Only type II SAB can be recognized by ECG.
Sick Sinus Syndrome (SSS):
SSS: The function of sinus node was degenerated. SSS encompasses both disordered SA node
automaticity and SA conduction.
Causes:
 CAD,
 SAN degeneration,
 myopathy,
 connective tissue disease,
 metabolic disease,
 tumor,
 trauma
 congenital disease.

 With marked sinus bradycardia, sinus arrest, sinus exit block or junctional escape
rhythms
 Bradycardia-tachycardia syndrome
Sick Sinus Syndrome (SSS):
EKG Recognition:
 Sinus bradycardia, ≤40 bpm;
 Sinus arrest > 3s
 Type II SAB
 Nonsinus tachyarrhythmia (SVT, AF or Af).
 SNRT > 1530ms, SNRTc > 525ms
 Instinct heart rate < 80bmp
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:
 The term “premature contractions” are used to describe non sinus beats.
 Common arrhythmia
 The morbidity rate is 3-5%

Atrial premature contractions (APCs):

APCs arising from somewhere in either the left or the right atrium.
Causes:
 rheumatic heart disease,
 CAD, hypertension,
 hyperthyroidism,
 hypokalemia
Symptoms:
 many patients have no symptom,
 some have palpitation,
 chest incomfortable.
Therapy:
 Needn’t therapy in the patients without heart disease.
 Can be treated with ß-blocker, propafenone, moricizine or verapamil.
Atrial tachycardia:
Classify by:
 automatic atrial tachycardia (AAT);
 intra-atrial reentrant atrial tachycardia (IART);
 chaortic 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 uncomfortable,
 tachycardia may induce myopathy.
Auscultation: the first heart sound is variable
Automatic atrial tachycardia (AAT):
ECG characters:
 Atrial rate is around 100-200bpm;
 Warmup phenomena
 P’ wave is different from sinus P wave;
 P’-R interval ≥ 0.12”
 Often appear type I or type II, 2:1 AV block;
 EP study: Atrial program pacing can’t induce or terminate the tachycardia
Multifocal atrial tachycardia:
 Always occurs in COPD or CHF,
 Have a high in-hospital mortality ( 25-56%). 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 > 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 induce or terminate the tachycardia

Therapy:
IRAT:
 Esophageal Pulsation Modulation,
 RFCA,
 Ic and
 IV class anti-tachycardia agents
AAT:
 Digoxin,
 IV,
 II,
 Ia and
 III class anti-tachycardia agents; RFCA
CAT:
 treat the underlying disease,
 verapamil or amiodarone.
Associated with SSS: Implant pace-maker.
A. Flutter and Fibrillation:
1. Atrial Flutter
ECG:
1) There are no P waves in ECG
2) Presence of saw-tooth flutter wave.
3) F waves always uniform in size ,shape and frequency.
4) Regular atrial rhythm with a rate of 250-350
5) Ventricular response of 1:1,2:1,3:1,4:1,or higher.
6) Absence of isoelectric line.
Atrial Flutter:
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
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.
Therapy:
1) Treat the underlying disease
2) To restore sinus rhythm:
o Cardioversion,
o Esophageal Pulsation Modulation,
o RFCA,
o Drug (III, Ia, Ic class).
3) Control the ventricular rate:
o digitalis.
o CCB,
o ß-block
4) Anticoagulation
Atrial fibrillation:
Subdivided into three types:
 paroxysmal,
 persistent,
 permanent.
Etiology:
 Morbidity rate increase in older patients
 Etiology just like atrial flutter
 Idiopathic
Mechanism:
 Multiple wavelet re-entry;
 Rapid firing focus in pulmonary vein, vena cava or coronary sinus.
ECG:
1) Absence of P waves
2) P waves replaced by f waves.
3) f waves :
 irregular in size ,shape ,and spacing.
 Rate between 350 and 600
4) Irregularly irregular ventricular rhythm, best seen in II, Avf,V1 or V2.
Atrial fibrillation:
Manifestation:
 Affected by underlying diseases, ventricular rate and heart function.
 May develop embolism in left atrial. Have high incidence of stroke.
 The heart rate, S1 and rhythm is irregularly irregular
 If the heart rhythm is regular, should consider about:
1) restore sinus rhythm;
2) AF with constant the ratio of AV conduction;
3) junctional or ventricular tachycardia;
4) slower ventricular rate may have complete AV block.
Therapy:
1) Treat the underlying disease
2) Restore sinus rhythm:
 Drug,
 Cardioversion,
 RFCA,
 Maze surgery
3) Rate control:
 digitalis.
 CCB,
 ß-block
4) Antithrombotic therapy:
 Aspirine,
 Warfarin
Atrioventricular Junctional arrhythmia:
Atrioventricular junctional premature contractions:
1) A premature AV junction P wave is followed by a QRS and T wave.
2) The AV junction P waves in aVR become upward.
3) The P waves in II,III, and aVF is downward.
4) The PR interval is usually less than 0.12second, if the P waves is before the QRS
complexes.
5) The P waves may appear after the QRS complexes or may be hidden within the QRS
complex.
6) An AV junctional premature beat is followed by a fully compensatory pause.
 Therapy the underlying disease
 Needn’t anti-arrhythmia therapy.

Nonparoxysmal AV junctional tachycardia:

Mechanism: relate to hyper-automaticity or trigger activity of AV junctional tissue
Etiology:
 digitalis toxicity;
 inferior MI;
 myocarditis;
 acute rheumatic fever
 post operation of valve disease
ECG:
 the heart rate ranges 70-150 bpm or more,
 regular,
 normal QRS complex,
 may occur AV dissociation
 wenckebach AV block
Therapy:
 Treat underlying disease; stopping digoxin, administer potassium, lidocaine,
phenytoin or propranolol.
 Not for DC shock
 It can disappear spontaneously. If had good tolerance, not require therapy.
Paroxysmal tachycardia:
 Most PSVT (paroxysmal supraventricular tachycardia) is due to reentrant mechanism.
 The incidence of PSVT is higher in AVNRT (atrioventricular node reentry tachycardia)
and AVRT (atioventricular reentry tachycardia), the most common is AVNRT (90%)
 Occur in any age individuals, usually no structure heart disease.
AVNRT:
• Commonest supraventricular arrhythmia
– ie dependent upon the AV node
AVNRT:

Paroxysmal tachycardia:
Manifestation:
 Occur and terminal abruptly.
 Palpitation, dizziness, syncope, angina, heart failure and shock.
 The severe degree of the symptom is related to ventricular rate, persistent duration
and underlying disease
ECG characteristic of AVNRT:
1. Heart rate is 150-250 bpm, regular
2. QRS complex is often normal, wide QRS complex is with aberrant conduction
3. Negative P wave in II III aVF, buried into or following by the QRS complex.
AVRT:
 Due to an accessory pathway
o Patients can have multiple pathways
 Accessory pathways may conduct
o Antegradely
o Retrogradely
o Combination of the two
 Wolf- Parkinson -White Syndrome
o Short PR interval (<120ms)
o Delta wave
o Palpitations and narrow complex tachycardia
Definitions:
 Orthodromic
o Conduction travels in the normal direction (ie A to V)
 Antidromic
o Conduction travels in an abnormal direction (ie V to A)
 Manifest
o An accessory pathway that conducts antegradely
 Concealed
o An accessory pathway that conducts retrogradely
 Latent
o An accessory pathway that conducts antegradely, but the refractory period exceeds
the sinus cycle length
Paroxysmal tachycardia:
ECG characteristic of AVRT:
1. Heart rate is 150-250 bpm, regular
2. In orthodromic AVRT, the QRS complex is often normal, wide QRS complex is with
antidromic AVRT
3. Retrograde P’ wave, R-P’>110ms.
Wolff-Parkinson-White Syndrome (W.P.W):
ECG criteria:
1. Short P-R interval (less than 0.10 sec to 0.12 sec
2. prolonged QRS complex, 0.12 sec or greater
3. Delta wave in the lower third of the ascending limb of the R wave
4. Type A is characterized by dominantly upright QRS complexes in the right precordial
leads, resulting in tall delta -R waves in leads V1-2.
5. Type B is characterized by dominantly negative QRS complexes in the right precordial
leads, with tall delta -R wave in leads V5-6
Conditions associated with WPW syndrome
1. Atrial fibrillation
2. Atrial flutter
3. Atrial tachycardias
4. Reciprocal tachycardias
AVRT:
Paroxysmal tachycardia:
Therapy:
AVNRT & orthodromic AVRT
1. Increase vagal tone: carotid sinus massage, Valsalva maneuver.if no successful,
2. Drug:
o verapamil,
o adrenosine,
o propafenone
3. DC shock
Antidromic AVRT:
1. Should not use verapamil, digitalis, and stimulate the vagal nerve.
2. Drug:
o propafenone,
o sotalol,
o amiodarone
3. RFCA
Ventricular arrhythmia:
WQRS tachycardia algorithm
Ventricular Premature Contractions (VPCs):
Etiology:
1. Occur in normal person
2. Myocarditis,
3. CAD,
4. valve heart disease,
5. hyperthyroidism,
6. Drug toxicity (digoxin, quinidine and anti-anxiety drug)
7. electrolyte disturbance, anxiety, drinking, coffee
Manifestation:
1. palpitation
2. dizziness
3. syncope
4. loss of the second heart sound
PVCs:
Therapy: treat underlying disease, antiarrhythmia
No structure heart disease:
1. Asymptom: no therapy
2. Symptom caused by PVCs:
o antianxiety agents,
o ß-blocker and
o 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 proarrhythmia and lack of
benefit of prophylaxis
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 (Tdp): 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
Accelerated idioventricular rhythm:
1. Related to increase automatic tone
2. Etiology:
 Often occur in organic heart disease,
 especially AMI reperfusion periods,
 heart operation,
 myocarditis,
 digitalis toxicity
VT:
Manifestation:
1. Nonsustained VT with no symptom
2. Sustained VT: with symptom and unstable hemodynamic,
 patient may feel:
o palpitation,
o short of breathness,
o presyncope,
o syncope,
o angina,
o hypotension and
o 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 dissociation,
fusion or capture beats
3. Tdp: rotation of the QRS axis around the baseline, the rate from 160-280 bpm, QT
interval prolonged > 0.5s, marked U wave
Ventricular Tachycardia:

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
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 isoprenaline, ß-block or pacemaker for long QT patient
3. temporary pacemaker
Ventricular flutter and fibrillation:
 Often occur in severe organic heart disease: AMI, ischemia heart disease
 Proarrhythmia (especially produce long QT and Tdp), electrolyte disturbance
 Anaesthesia, lightning strike, electric 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;
 atrioventricular;
 intra-ventricular
Block degree:
1. Type I: prolong the conductive time
2. Type II: partial block
3. Type III: complete block
Atrioventricular Block:
 AV block is a delay or failure in transmission of the cardiac impulse from atrium to
ventricle.
Etiology:
 Atherosclerotic heart disease;
 myocarditis;
 rheumatic fever;
 cardiomyopathy;
 drug toxicity;
 electrolyte disturbance,
 collagen disease,
 lev’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 symptoms;
 Second degree AV block: palpitation, fatigue
 Third degree AV block: Dizziness, agina, heart failure, lightheadedness, and syncope
may cause by slow heart rate, Adams-Stokes Syndrome may occurs in sever case.
 First heart sound varies in intensity, will appear booming first sound
Treatment:
1. I or II degree AV block needn’t antibradycardia agent therapy
2. II degree II type and III degree AV block need antibradycardia agent therapy
3. Implant Pace Maker
Intraventricular Block:
Intraventricular conduction system:
 Right bundle branch
 Left bundle branch
 Left anterior fascicular
 Left posterior fascicular
Intraventricular Block:
Etiology:
 Myocarditis,
 valve disease,
 cardiomyopathy,
 CAD,
 hypertension,
 pulmonary heart disease,
 drug toxicity,
 Lenegre disease,
 Lev’s disease et al.
Manifestation:
 Single fascicular or bifascicular block is asymptom;
 tri-fascicular block may have dizziness;
 palpitation,
 syncope and
 Adams-stokes syndrome
Intraventricular Block:
Therapy:
 Treat underlying disease
 If the patient is asymptom; no treat,
 bifascicular block and incomplete trifascicular block may progress to complete block,
may need implant pace maker if the patient with syncope
Bundle branch block:
1. Right Bundle Branch Block(RBBB):
ECG:
1. 1QRS 0.12 sec or wider
2. Rsr’(M)pattern in V1 and V2 and deep ,wide S wave in Ⅰ,V5-6.
3. The ST segment is slight depressure with negative T waves
When incomplete RBBB is present ,the pattern is similar, but the QRS width is less than
0.12sec.
Left Bundle Branch Block (LBBB)
ECG:
1) QRS 0.12sec or more .
2) absent q waves in I,V5 and V6
3) wide ,notched,or slurred R waves in V5-6 with depressed ST segments,downward T
waves.
4) wide QS or rS patters with elevated ST segments and upward T waves in V1-2.
When incomplete LBBB in present ,the pattern is similar ,but the QRS width < 0.12
second.
Left anterior fascicular block (LAH)
ECG criteria:
1) Left axis deviation (-30゜to -45゜or greater)
2) Small q wave in lead I
3) Deep s wave in lead II
4) Deeper S wave in lead III
5) S wave in aVF and V6
left posterior fascicular block(LPH) (left posterior hemiblock):
ECG criteria:
1) Right axis deviation of +120 or greater
2) Large S wave in lead I
3) Tall R waves in lead II and III.
Anti-arrhythmia Agents:
 Anti-tachycardia agents
 Anti-bradycardia agents
Anti-tachycardia agents:
Modified Vaugham Williams classification
1) I class: Natrium channel blocker
2) II class: ß-receptor blocker
3) III class: Potassium channel blocker
4) IV class: Calcium channel blocker
5) Others: Adenosine, Digital
Clinical usage:
Anti-tachycardia agents:
Ia class: Less use in clinic
1) Guinidine
2) Procainamide
3) Disopyramide: Side effect: like M-cholinergic receptor blocker
Ib class: Perfect to ventricular tachyarrhythmia
1) Lidocaine
2) Mexiletine
Ic class: Can be used in ventricular and/or supra-ventricular tachycardia and
extrasystole.
1) Moricizine
2) Propafenone
II class: ß-receptor blocker
1) Propranolol: Non-selective
2) Metoprolol:
o Selective ß1-receptor blocker,
o Perfect to hypertension and coronary artery disease patients associated with
tachyarrhythmia.
III class: Potassium channel blocker, extend-spectrum anti-arrhythmia agent.
1) Amioarone: Perfect to coronary artery disease and heart failure patients
2) Sotalol: Has ß-blocker effect
3) Bretylium
IV class: be used in supraventricular tachycardia
1) Verapamil
2) Diltiazem
Others:
1) Adenosine: be used in supraventricular tachycardia
Anti-bradycardia agents:
 Isoprenaline
 Epinephrine
 Atropine
 Aminophylline
Proarrhythmia effect of antiarrhythmia agents:
 Ia, Ic class: Prolong QT interval, will cause VT or VF in coronary artery disease and
heart failure patients
 III class: Like Ia, Ic class agents
 II, IV class: Bradycardia
Non-drug therapy:
 Cardioversion: For tachycardia especially hemodynamic unstable patient
 Radiofrequency catheter ablation (RFCA): For those tachycardia patients (SVT, VT,
AF, AFL)
 Artificial cardiac pacing: For bradycardia, heart failure and malignant ventricular
arrhythmia patients.