2. PALPITATION
Definition
The term “ palpitation” refers to any conscious sensation of
cardiac activity.
Arrhythmia
It is a term used to describe any cardiac rhythm that deviates from
the normal sinus rhythm.
3. PALPITATION
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.
4. Anatomy of the conducting system
SA Node – “pacemaker” of
the heart (60-100bpm)
AV Node – junction of the
atria and ventricles (40-
60bpm)
Bundles – Bundle of His
connects the AV node to the
bundle branches (20-40bpm)
5. Pacemakers of the Heart
•SA Node - Dominant pacemaker with
an intrinsic rate of 60 - 100 beats/minute.
•AV Node - Back-up pacemaker with an
intrinsic rate of 40 - 60 beats/minute.
•Ventricular cells - Back-up pacemaker
with an intrinsic rate of 20 - 45 bpm.
8. What Is In Each Beat?
(the cardiac cycle in waves, complexes, and
intervals)
P Wave: atrial contraction or depolarization, (usually upright)
QRS Complex: time for ventricular contraction or
depolarization
(usually upright) (0.04 - 0.12sec) (delays in the bundle branches will widen
the QRS)
T Wave – ventricular repolarization “recharging” (usually
upright)
9. What Is In Each Beat?
PR Interval: time between atrial depolarization to
ventricular
depolarization (beginning of P wave to beginning of QRS)(0.12 -
0.20sec)
(prolonged PR = delays in the AV node conduction)
QT Interval: represents one complete ventricular
depolarization and repolarization (beginning of QRS to the end of the
T wave) (0.32 – 0.44sec)
(disturbances are usually due to electrolyte disturbances or
drug effects)
10. ECG Paper and related Heart Rate & Voltage
Computations
11. PATHOGENESIS AND INDUCEMENT
OF ARRHYTHMIA
Some physical condition
Pathological heart disease
Other systemic disease
Electrolyte disturbance and acid-base
imbalance
Physical and chemical factors or toxicosis
12. HOW TACHYCARDIA INITIATED?
All cardiac tachyarrhythmias are produced by one or more
mechanisms, including
1) Disorders of impulse initiation
Triggered activity
Enhanced automaticity
2) Abnormalities of impulse conduction.
Re-entry
13. 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.
14. AUTOMATICITY
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.
i.e. sinus tachycardia, accelerated idiovent. rhythm.
15. 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.
16. TRIGGERED ACTIVITY
An afterdepolarization of sufficient magnitude may reach
“threshold” and trigger an early action potential during
repolarization.
i.e. TdP, atrial tachycardia, digitalis toxicity.
17. RE-ENTRY
The most common arrhythmia mechanism.
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.
18. RE-ENTRY
Slow conduction is usually required for both initiation and maintenance
of a circus movement tachycardia.
i.e. AVNRT and AVRT
19. (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 ischemic
myocardium.
Re-entry
20. (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.
Re-entry
21. (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 .
Re-entry
27. Step 1: Calculate Rate
Option 1 –Count the # of R waves in a 6 second rhythm strip,
then multiply by 10.
Interpretation? 9 x 10 = 90 bpm
3 sec
3 sec
Option 2–Find a R wave that lands on a bold line.
–Count the # of large boxes to the next R wave.
If the second R wave is 1 large box away the rate is 300, 2
boxes - 150, 3 boxes - 100, 4 boxes - 75, etc. (cont)
R wave
3
0
0
1
5
0
1
0
0
7
5
6
0
5
0
Approx. 1 box less than 100 = 95
28. Step 2: Determine regularity
•Look at the R-R distances (using a caliper or
markings on a pen or paper).
•Regular (are they equidistant apart)? Occasionally
irregular? Regularly irregular? Irregularly irregular?
Interpretation? Regular
29. Step 3: Assess the P waves
•Are there P waves?
•Do the P waves all look alike?
•Do the P waves occur at a regular rate?
•Is there one P wave before each QRS?
Interpretation?
Normal P waves with 1 P wave for every QRS
34. SINUS RHYTHM 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 sec.
2) The P wave is upward in I,II, aVF,V4-5 and downward in aVR.
36. 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.
Needn’t specific therapy, If the patient has severe symptoms, planted
an pacemaker may be needed.
37. 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
38. 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
39. 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 and congenital disease.
With marked sinus bradycardia, sinus arrest, sinus exit block or
junctional escape rhythms
Bradycardia-tachycardia syndrome
41. 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.
43. PREMATURE CONTRACTIONS
The term “premature contractions” are used to describe
non sinus beats.
Common arrhythmia
The morbidity rate is 3-5%
44. 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.
46. ATRIAL TACHYCARDIA
May occur transient; intermittent; or persistent.
Symptoms: palpitation; chest uncomfortable, tachycardia may
induce myopathy.
Auscultation: the first heart sound is variable
47. AUTOMATIC ATRIAL TACHYCARDIA (AAT)
ECG characters:
1. Atrial rate is around 100-200bpm;
2. Warmup phenomena
3. P’ wave is different from sinus P wave;
4. P’-R interval ≥ 0.12”
5. Often appear type I or type II, 2:1 AV block;
6. EP study: Atrial program pacing can’t induce or
terminate the tachycardia
48. MULTIFOCAL ATRIAL TACHYCARDIA
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
49. 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.
50. 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
52. 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.
Flutter and Fibrillation
54. 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.
55. ATRIAL FLUTTER
Therapy:
1. Treat the underlying disease
2. To restore sinus rhythm: Cardioversion, pacing, RFCA,
Drug (III, Ia, Ic class).
3. Control the ventricular rate: digitalis. CCB, ß-block
4. Anticoagulation
56. ATRIAL FIBRILLATION
Subdivided into three types: paroxysmal, persistent, permanent.
(lone Af)
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.
57. ATRIAL FIBRILLATION
2. Atrial Fibrillation 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.
58. 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.
61. ATRIOVENTRICULAR JUNCTIONAL
PREMATURE CONTRACTIONS
1).A premature AV junction P wave is followed by a QRS & T
wave.
2).The AV junction P waves in aVR become upward .The P
waves in II,III, and aVF is downward. The PR interval is
usually less than 0.12second , if the P waves is before the
QRS complexes. The P waves may appear after the QRS
complexes or may be hidden within the QRS complex.
3).AV junctional premature beat is followed by a fully
compensatory.
Therapy the underlying disease Needn’t anti-arrhythmia therapy.
62. NON PAROXYSMAL AV JUNCTIONAL
TACHYCARDIA
Mechanism: relate to hyper-automaticity or trigger activity of AV
junctional tissue
Etiology: digitalis toxicity; inferior MI; myocarditis; acute rheumatic
fever and post-operation of valve disease
ECG: the heart rate ranges 70-150 bpm or more, regular, normal QRS
complex, may occur AV dissociation and wenckebach AV block
63. NONPAROXYSMAL AV JUNCTIONAL
TACHYCARDIA
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.
64. 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.
66. PAROXYSMAL TACHYCARDIA
Manifestation:
Occur and terminate 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
67. 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 conduction
3. Negative P wave in II III aVF, buried into or
following by the QRS complex.
68. AVRT
Due to an accessory pathway
Patients can have multiple pathways
Accessory pathways may conduct
Antegradely
Retrogradely
Combination of the two
69. DEFINITIONS
Orthodromic
Conduction travels in the normal direction (ie A to V)
Antidromic
Conduction travels in an abnormal direction (ie V to A)
Manifest
An accessory pathway that conducts antegradely
Concealed
An accessory pathway that conducts retrogradely
70. 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.
72. 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
Wolff-Parkinson-White Syndrome (W.P.W)
73.
74. PAROXYSMAL TACHYCARDIA
Therapy:
AVNRT & orthodromic AVRT
1. Increase vagal tone: carotid sinus massage,
Valsalva maneuver.if no successful,
2. Drug: verapamil, adrenosine, propafenone
3. DC shock
Antidromic AVRT:
1. Should not use verapamil, digitalis, and
stimulate the vagal nerve.
2. Drug: propafenone, sotalol, amiodarone
RFCA
78. Morphological criteria (if the above criteria are inconclusive)
LBBB pattern
Initial R more than 40ms? Yes => VT
Slurred or notched downwards leg of S wave in leads V1 or
V2
Yes => VT
Beginning of Q to nadir QS >60 ms in V1 or V2? Yes => VT LR >50:1
Q or QS in V6? Yes => VT LR >50:1
79. RBBB pattern
Monofasic R or qR in V1? Yes => VT
R taller than R' (rabbit-ear sign)? Yes => VT
rS in V6? Yes => VT
82. If the distance traveled on the Y axis in the initial 40ms of the QRS
complex is smaller than that traveled in the terminal 40ms of the QRS
complex, a VT is much more likely
83.
84.
85. VENTRICULAR PREMATURE
CONTRACTIONS (VPCS)
Etiology:
1. Occur in normal person
2. Myocarditis, CAD, valve heart disease,
hyperthyroidism, Drug toxicity (digoxin, quinidine
and anti-anxiety drug)
3. electrolyte disturbance, anxiety, drinking, coffee
Manifestation:
1. palpitation
2. dizziness
3. syncope
4. loss of the second heart sound
86.
87. PVCS
Therapy: treat underlying disease,
antiarrhythmia
No structure heart disease:
1. Asymptom: no therapy
2. Symptom caused by PVCs: antianxiety agents,
ß-blocker and mexiletine to relief the symptom.
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 of
benefit of prophylaxis
89. 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
90. VENTRICULAR TACHYCARDIA
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
91. VT
Manifestation:
1. Nonsustained VT with no symptom
2. Sustained VT : with symptom and unstable hemodynamic,
patient may feel palpitation, short of breathness,
presyncope, syncope, angina, hypotension and shock.
92.
93. 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
3. Tdp: rotation of the QRS axis around the
baseline, the rate from 160-280 bpm, QT interval
prolonged > 0.5s, marked U wave
95. 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
96. 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
97. 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
98. VENTRICULAR FLUTTER AND
FIBRILLATION
Manifestation:
Unconsciousness, twitch, no blood pressure and pulse, going to
die
Therapy:
1. Cardio-Pulmonary Resuscitate (CPR)
2. ICD
99. 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
100. 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.
101. 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
102. 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
103. AV BLOCK
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
109. Complete AV block
•No atrial activity conducts to the ventricles
•AV dissociation is present. The atria and ventricles are
controlled by independent pacemakers.
•Ventricular focus is usually located just below the site
of block.
•Higher sites are more stable with a more faster escape
rate.
111. INTRAVENTRICULAR BLOCK
Etiology:
Myocarditis, valve disease, cardiomyopathy, CAD, hypertension,
pulmonary heart disease, drug toxicity, 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
112. INTRAVENTRICULAR BLOCK
Therapy:
1. Treat underlying disease
2. If the patient is asymptom; no treat,
3. bifascicular block and incomplete trifascicular block may progress to
complete block, may need implant pace maker if the patient with
syncope
113. 1. Right Bundle Branch Block(RBBB)
ECG:
1).QRS 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.
Bundle branch block
114. 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.
Bundle branch block
115. 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).Decper S wave in lead
III
5).S wave in aVF and V6
Bundle branch block
116. 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.
Bundle branch block
118. 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
119. CLINICAL USAGE
Anti-tachycardia agents:
Ia class: Less use in clinic
1. Quinidine
2. Procainamide
3. Disopyramide: Side effect: like M-cholinergic receptor
blocker
121. Anti-tachycardia agents:
Ic class: Can be used in ventricular and/or supra-ventricular
tachycardia and extrasystole.
1. Moricizine
2. Propafenone
3. Flecainide
122. ANTI-TACHYCARDIA AGENTS:
II class: ß-receptor blocker
1. Propranolol: Non-selective
2. Metoprolol: Selective ß1-receptor blocker, Perfect to hypertension
and coronary artery disease patients associated with
tachyarrhythmia.
123. ANTI-TACHYCARDIA AGENTS:
III class: Potassium channel blocker, extend-spectrum anti-arrhythmia
agent.
Amioarone: Perfect to coronary artery disease and heart failure
patients
Sotalol: Has ß-blocker effect
Bretylium
Ibutilide
124. ANTI-TACHYCARDIA AGENTS:
IV class: be used in supraventricular
tachycardia
1. Verapamil
2. Diltiazem
Others:
Adenosine: be used in supraventricular
tachycardia
