electrophysiology study
Dr. Enas Fathy, MD, PhD
Lecturer of cardiology
Aswan university
South valley university
electrophysiology study
• (EP study) is a test used to evaluate your heart's electrical
system and to check for abnormal heart rhythms.
Properties of cardiac muscle
Arrhythmia
BY
DR. ENAS FATHY, MD, PHD
LECTURER OF CARDIOLOGY
ASWAN UNIVERSITY
SOUTH VALLEY UNIVERSITY
EKG
HEART RATE
-To determine the ventricular rate, count
the QRS complex on a 6 sec paper and
multiply by 10
WAVES
-P wave: atrial depolarization
-QRS complex :ventricular depolarization
-Twave :Ventricular repolarization
INTERVALS
-PR :0.12-0.20 sec
-QRS :under 0.10sec
-QT:under 0.38 sec
How to measure heart rate from ECG
• For regular rhythm
Rate=300/number of large square between two RR
interval
or
=1500/number of small square(more accurate)
• Normal rate = 60-100 beats/minute
• >100beats/minute- tachycardia
• <60 beats/minute- bradycardia
• For irregular rhythm
• 6 seconds rule
• Count number of QRS complex during 6
seconds i.e. 30 large squares and multiply it
by 10.
QRS complex
• It represents ventricular depolarization.
• First negative wave is q or Q wave
• First positive deflection is r or R wave
• Second negative deflection is s or S wave
• Second positive deflection is r’ or R’ wave
• QRS complex normally lasts from 80 to 100
ms.
QRS nomenclature
• QRS: duration <0.12ms, shape, r wave progression
• ST segment: Isoelectric, depressed, raised
• T wave: upright, inverted
• QT interval: 350- 450 ms
Normal
Signal moves rapidly
through the ventricles
Abnormal
Signal moves slowly
through the ventricles
ST Segment Elevation
The Normal ECG
Rate: 50 – 100 bpm
Rhythm : regular
Sinus rhythm:(P present, look alike, P before QRS)
Axis +90o
to –30o
Intervals: PR .12-.20 sec
QRS <.12 sec
ST segment: Isoelectric
T wave: upright
QT : normal
Definition of aRRythmias
• It is any abnormality in the heart rate or rhythm
• including abnormalities of impulse formation
from Sinus Node (SAN), or site of impulse origin
or conduction disturbances.
• This disrupt the normal sequence and direction
of atrial and ventricular activation.
• Normal HR: 60-90 b/m
• Bradycardia <60 b/m Bradycardia
• Tachycardia >90 b/m Tachycardia
Basic arrhythmia
mechanisms
Automaticity
Reentry
Triggered activity
SAN action potential
Mechanism of Arrhthmogensis
1. Disorder of impulse formation.
a) Automaticity.
b) Triggered Activity.
1) Early after depolarization.
2) Delayed after depolarization.
2. Disorder of impulse conduction.
a) Block – Reentry.
b) Reflection.
3. Combined disorder.
Trigger Reentry substrate
Premature beat Two distinctly different pathways in
conduction velocity & RP
2. Re-entry (circus movement) in the form of wave of depolarization
forced to travel around a ring of cardiac tissue. This occurs in cases of
paroxysmal atrial tachycardia, junctional tachycardia, atrial flutter and
fibrillation, AVNRT, AVRT. Sudden onset & offset. Fixed rate.
2. Triggered activity by digitalis, catecholamines or myocardial damage, this
occurs in ventricular arrhythmia or atrial tachycardia induced by digitalis
toxicity.
o Sinus Tachycardia (A)
o Focal Atrial Tachycardia/ extrasystole (PAC) (B)
(C)
o Atrioventricular tachycardia AVRT=
Accessory pathway arrhythmia (D)
AVNRT (E)
(H)
(Narrow QRS tachycardias)
(Wide QRS tachycardias)
⇐Irregular
}Regular
⇐Irregular
⇐Irregular
}Regular
}Atrial
c) AtrioVentricular junctional arrhythmia
Major cardiac arrhythmias
SINUS RYTHMS ATRIAL
RYTHMS
VETRICULAR
RHYTHMS
ATRIO-
VENTRICULAR
(AV) RHYTHMS
SINUS BRADY PREMATURE
ATRIAL
CONTRACTION(PA
C)
PREMATURE
VENTRICULAR
CONTRACTION(PV
C)
1ST
DEGREE AV
BLOCK
SINUS
TACHICARDIA
ATRIAL FLUTTER VENTRICULAR
TACHICARDIA
2ND
DEGREE AV
BLOCK TYPE I
SINUS ARRYTHMIA ATRIAL
FIBRILATION
VENTRICULAR
FIBRILATION
2ND
DEGREE AV
BLOCK TYPE II
SINUS ARREST ASYSTOLE 3RD
DEGREE AV
BLOCK
o Sinus Bradycardia
Etiological Factors
Cardiac
IHD
Structural changes: RHD, CHD, Constrictive pericarditis,
myocarditis, aberrant conduction pathways.
Cardiomyopathies, HF.
Extracardiac
Physiological: pregnancy, exercise, sleep, atheletes, stress.
Pathological: fever, COPD, chest infection, thyrotoxicosis, anemia,
metabolic imbalance (K+, Ca2+, Mg2+, hypoxia, hypercapnia,
metabolic acidosis), excess catecholamine (phaeochromocytomal,
inherited excess catecholamine release, excess caffeine; smoking,
alcohol, coffee).
Genetic causes: inherited channelopathies (Brugada syndrome).
Drugs:
Tests
Laboratory investigations:
FBC (anaemia), renal function, thyroid function, glucose, Ca2+, Mg2+, Na,
K.
ECG monitoring including provocation tests:
1. 12 leads surface ECG
2. Holter (24 hours-7days ECG)
3. Exercise ECG
4. Loop recorder
5. Tilt table test
6. Video recorder
7. Interventional: electrophysiological study (EP study): intracardiac
procedure to determine location of triggering foci.
Echocardiography: to look for structural heart diseases
12 leads surface ECG
Sotalol, Ibutilide
Magnesium, Ivabradine
PHARMACOLOGICAL TREATMENT OF
TACHYARRHYTHMIA
NON PHARMACOLOGICAL TREATMENT OF
TACHYARRHYTHMIA
Pharmacological Treatment of Bradyarrhythmia
• Adrenaline and noradrenaline in case of brady
asystole and in cardiac arrest.
NON PHARMACOLOGICAL TREATMENT OF
BRADYARRHYTHMIA
Atrial Tachyarrhythmia (Narrow QRS Tachycardia)
• Sinus tachycardia
SINUS TACHYCARDIA
• Rate: 101-160/min. P wave: sinus
• QRS: normal
• Conduction: normal
• Rhythm: regular or slightly irregular
• The clinical significance of this dysrhythmia depends on the
underlying cause. It may be normal.
Acute therapy (During attack)
PREAMATURE ATRIAL CONTRACTIONS
• Rate: normal or accelerated
• P wave: usually have a different morphology than sinus P waves
• QRS: normal
• Conduction: normal, however the ectopic beats may have a different P-R interval.
• Rhythm: REGULAR IRREGULARITY, Followed by compensatory pause.
• PAC's occur normally in a non diseased heart.
• However, if they occur frequently, they may lead to a more serious atrial dysrhythmias.
• They can also result from CHF, ischemia and COPD.
Premature Atrial Contractions (PAC)
• These ectopic beats originate in the atria (but not in the SA node),
therefore the contour of the P wave, the PR interval, and the timing
are different than a normally generated pulse from the SA node.
• Etiology: excitation of an atrial cell forms an
impulse that is then conducted normally
through the av node and ventricles.
Premature Ventricular Contractions (PVC)
• Ectopic beats originate in the ventricles resulting in wide and bizarre QRS
complexes.
• When there are more than 1 premature beats and look alike, they are
called “uniform”. When they look different, they are called “multiform”.
• Etiology: One or more ventricular cells are depolarizing and the impulses
are abnormally conducting through the ventricles.
Extrasystole: Premature Atrial and ventricular Contractions
(PAC/PVC)
Supraventricular tachycardia (SVT)
Paroxysmal supraventricular tachycardia (PSVT)
• The heart rate suddenly speeds up, often triggered
by a PAC (not seen here) and the P waves are lost.
• Etiology: there are several types of PSVT but all originate above the ventricles (therefore
the QRS is narrow).
PSVT: Acute Treatment Summary
• Hemodynamically unstable
(shock, pulmonary oedema, chest pain)…
…..DC cardioversion
• Stable: 1) Vagal maneuvers
– 2) Adenosine
– 3) CCB’S
– 4) BB’S
– 5) Amiodarone
– 6) digoxin
– If no response…..DC Cardioversion
PSVT: CHRONIC TREATMENT SUMMARY
Atrioventricular Junctional Arrhythmia
• AVRT (Accessory pathway)
• AVNRT
• Both similar to SVT
Good luck

Electrophysiological study for medical students part 1.pptx

  • 1.
    electrophysiology study Dr. EnasFathy, MD, PhD Lecturer of cardiology Aswan university South valley university
  • 2.
    electrophysiology study • (EPstudy) is a test used to evaluate your heart's electrical system and to check for abnormal heart rhythms.
  • 3.
  • 10.
    Arrhythmia BY DR. ENAS FATHY,MD, PHD LECTURER OF CARDIOLOGY ASWAN UNIVERSITY SOUTH VALLEY UNIVERSITY
  • 17.
    EKG HEART RATE -To determinethe ventricular rate, count the QRS complex on a 6 sec paper and multiply by 10 WAVES -P wave: atrial depolarization -QRS complex :ventricular depolarization -Twave :Ventricular repolarization INTERVALS -PR :0.12-0.20 sec -QRS :under 0.10sec -QT:under 0.38 sec
  • 21.
    How to measureheart rate from ECG • For regular rhythm Rate=300/number of large square between two RR interval or =1500/number of small square(more accurate) • Normal rate = 60-100 beats/minute • >100beats/minute- tachycardia • <60 beats/minute- bradycardia
  • 24.
    • For irregularrhythm • 6 seconds rule • Count number of QRS complex during 6 seconds i.e. 30 large squares and multiply it by 10.
  • 30.
    QRS complex • Itrepresents ventricular depolarization. • First negative wave is q or Q wave • First positive deflection is r or R wave • Second negative deflection is s or S wave • Second positive deflection is r’ or R’ wave • QRS complex normally lasts from 80 to 100 ms.
  • 31.
  • 32.
    • QRS: duration<0.12ms, shape, r wave progression • ST segment: Isoelectric, depressed, raised • T wave: upright, inverted • QT interval: 350- 450 ms
  • 33.
    Normal Signal moves rapidly throughthe ventricles Abnormal Signal moves slowly through the ventricles
  • 34.
  • 35.
    The Normal ECG Rate:50 – 100 bpm Rhythm : regular Sinus rhythm:(P present, look alike, P before QRS) Axis +90o to –30o Intervals: PR .12-.20 sec QRS <.12 sec ST segment: Isoelectric T wave: upright QT : normal
  • 37.
    Definition of aRRythmias •It is any abnormality in the heart rate or rhythm • including abnormalities of impulse formation from Sinus Node (SAN), or site of impulse origin or conduction disturbances. • This disrupt the normal sequence and direction of atrial and ventricular activation. • Normal HR: 60-90 b/m • Bradycardia <60 b/m Bradycardia • Tachycardia >90 b/m Tachycardia
  • 38.
  • 39.
  • 40.
    Mechanism of Arrhthmogensis 1.Disorder of impulse formation. a) Automaticity. b) Triggered Activity. 1) Early after depolarization. 2) Delayed after depolarization. 2. Disorder of impulse conduction. a) Block – Reentry. b) Reflection. 3. Combined disorder.
  • 41.
    Trigger Reentry substrate Prematurebeat Two distinctly different pathways in conduction velocity & RP 2. Re-entry (circus movement) in the form of wave of depolarization forced to travel around a ring of cardiac tissue. This occurs in cases of paroxysmal atrial tachycardia, junctional tachycardia, atrial flutter and fibrillation, AVNRT, AVRT. Sudden onset & offset. Fixed rate.
  • 42.
    2. Triggered activityby digitalis, catecholamines or myocardial damage, this occurs in ventricular arrhythmia or atrial tachycardia induced by digitalis toxicity.
  • 43.
    o Sinus Tachycardia(A) o Focal Atrial Tachycardia/ extrasystole (PAC) (B) (C) o Atrioventricular tachycardia AVRT= Accessory pathway arrhythmia (D) AVNRT (E) (H) (Narrow QRS tachycardias) (Wide QRS tachycardias) ⇐Irregular }Regular ⇐Irregular ⇐Irregular }Regular }Atrial c) AtrioVentricular junctional arrhythmia
  • 44.
    Major cardiac arrhythmias SINUSRYTHMS ATRIAL RYTHMS VETRICULAR RHYTHMS ATRIO- VENTRICULAR (AV) RHYTHMS SINUS BRADY PREMATURE ATRIAL CONTRACTION(PA C) PREMATURE VENTRICULAR CONTRACTION(PV C) 1ST DEGREE AV BLOCK SINUS TACHICARDIA ATRIAL FLUTTER VENTRICULAR TACHICARDIA 2ND DEGREE AV BLOCK TYPE I SINUS ARRYTHMIA ATRIAL FIBRILATION VENTRICULAR FIBRILATION 2ND DEGREE AV BLOCK TYPE II SINUS ARREST ASYSTOLE 3RD DEGREE AV BLOCK
  • 45.
  • 48.
    Etiological Factors Cardiac IHD Structural changes:RHD, CHD, Constrictive pericarditis, myocarditis, aberrant conduction pathways. Cardiomyopathies, HF. Extracardiac Physiological: pregnancy, exercise, sleep, atheletes, stress. Pathological: fever, COPD, chest infection, thyrotoxicosis, anemia, metabolic imbalance (K+, Ca2+, Mg2+, hypoxia, hypercapnia, metabolic acidosis), excess catecholamine (phaeochromocytomal, inherited excess catecholamine release, excess caffeine; smoking, alcohol, coffee). Genetic causes: inherited channelopathies (Brugada syndrome). Drugs:
  • 50.
    Tests Laboratory investigations: FBC (anaemia),renal function, thyroid function, glucose, Ca2+, Mg2+, Na, K. ECG monitoring including provocation tests: 1. 12 leads surface ECG 2. Holter (24 hours-7days ECG) 3. Exercise ECG 4. Loop recorder 5. Tilt table test 6. Video recorder 7. Interventional: electrophysiological study (EP study): intracardiac procedure to determine location of triggering foci. Echocardiography: to look for structural heart diseases
  • 51.
  • 53.
  • 54.
  • 55.
    Pharmacological Treatment ofBradyarrhythmia • Adrenaline and noradrenaline in case of brady asystole and in cardiac arrest.
  • 56.
  • 57.
  • 58.
  • 59.
    SINUS TACHYCARDIA • Rate:101-160/min. P wave: sinus • QRS: normal • Conduction: normal • Rhythm: regular or slightly irregular • The clinical significance of this dysrhythmia depends on the underlying cause. It may be normal.
  • 60.
  • 61.
    PREAMATURE ATRIAL CONTRACTIONS •Rate: normal or accelerated • P wave: usually have a different morphology than sinus P waves • QRS: normal • Conduction: normal, however the ectopic beats may have a different P-R interval. • Rhythm: REGULAR IRREGULARITY, Followed by compensatory pause. • PAC's occur normally in a non diseased heart. • However, if they occur frequently, they may lead to a more serious atrial dysrhythmias. • They can also result from CHF, ischemia and COPD.
  • 65.
    Premature Atrial Contractions(PAC) • These ectopic beats originate in the atria (but not in the SA node), therefore the contour of the P wave, the PR interval, and the timing are different than a normally generated pulse from the SA node. • Etiology: excitation of an atrial cell forms an impulse that is then conducted normally through the av node and ventricles. Premature Ventricular Contractions (PVC) • Ectopic beats originate in the ventricles resulting in wide and bizarre QRS complexes. • When there are more than 1 premature beats and look alike, they are called “uniform”. When they look different, they are called “multiform”. • Etiology: One or more ventricular cells are depolarizing and the impulses are abnormally conducting through the ventricles.
  • 67.
    Extrasystole: Premature Atrialand ventricular Contractions (PAC/PVC)
  • 73.
  • 75.
    Paroxysmal supraventricular tachycardia(PSVT) • The heart rate suddenly speeds up, often triggered by a PAC (not seen here) and the P waves are lost. • Etiology: there are several types of PSVT but all originate above the ventricles (therefore the QRS is narrow).
  • 76.
    PSVT: Acute TreatmentSummary • Hemodynamically unstable (shock, pulmonary oedema, chest pain)… …..DC cardioversion • Stable: 1) Vagal maneuvers – 2) Adenosine – 3) CCB’S – 4) BB’S – 5) Amiodarone – 6) digoxin – If no response…..DC Cardioversion PSVT: CHRONIC TREATMENT SUMMARY
  • 77.
    Atrioventricular Junctional Arrhythmia •AVRT (Accessory pathway) • AVNRT • Both similar to SVT
  • 84.

Editor's Notes

  • #34 A tall peaked T wave (pointed T wave) is not the same thing as ST elevation. It’s important to accurately differentiate when the QRS complex ends (when the S wave begins a change in direction flow, not necessarily when it crosses the isoelectric line) and when the ST segment begins. ST elevation is measured from a point that starts 0.04 seconds (one small box) after the J point (juncture of the QRS complex and the ST segment). Knowing how to measure wave forms is important.