This document discusses cardiac dysrhythmias and their electrophysiological interpretation. It begins by defining heart block and describing different types including first, second and third degree heart block. It then discusses bundle branch blocks, atrial and ventricular enlargements, ischemia, injury and infarction patterns on ECG. Various cardiac arrhythmias and abnormalities are related to their characteristics on ECG tracings. Investigation methods and management of arrhythmias are also summarized.

1. CARDIAC DYSRHYTHMIA
Electrophysiological Interpretation
PART 2
By DR. QAZI IMTIAZ RASOOL

2. LEARNING OBJECTIVES
By the end of the session, the students should be able to;-
1. Describe abnormal cardiac rhythms resulting from heart blocks.
2. Describe the characteristics of atrial and ventricular hypertrorhies
3. Relate all these abnormal rhythms to changes in ECG
REF;- 1. HARRISSON’S PRINCIPLE IF INTERNAL MEDICINE 18 TH ED. CH 228,231-233
2. Medical physiology 3rd edition walter f. Boron, emile l. Boulaep international edition 483-493
3.Guyton and Hall, Textbook of Medical Physiology, 2 edition South Asia Edition CH 33,34
4. Compherensive textbook of medical physiology as per new MCI curriculum Vol 1 G.K.PAL Section 35 Part C pg 382--390

3. Definition of Heart block
-is a disturbance of impulse conduction that can be permanent or transient
owing to anatomical or functional impairment.
Mechanism ;-
PHYSIOLOGICAL CAUSE
disturbance of impulse Conduction
caused by physiological refractoriness
.
Normal sinus rhythm of heart

4. A. Transverse blockade:
1.Sinus
2.Atria
3.Atrioventricular ( partial, full)
4. Blockade of BB’s (incomplete,complete).
B. Longitudinal blockade:
A. 1.LBBB
a) Anterior or left ant.hemiblock
b) Posterior. hemiblock
2. RBBB
B.Combined longitudinal blockade: Bi or Trifasicular block
1. SА
2
3

5. First Degree Heart Block (1º)
SA Node – normal P wave +
MEC:- AVN and beyond conducts more slowly than
normal
RESULT;-1.Prolonged PR Interval > 0.20 sec
2. Without disruption of atrial to ventricular conduction
Clinical significance;- None
Treatment None
Note – can progress to 2º or 3º heart block

6. Conduction through the AV Node – progressively delayed until a drop beat is seen
1. PR Interval prolongs with each beat until a dropped beat is seen
2. PR Interval is NOT constant
3. After each dropped beat, cycle starts again,1ST beat after has the shortest interval
P-R P-R P-R- Dropped beat
Second Degree Heart Block (2º) MobitzTypeI (Wenkebach)
-Symptoms e.g.. Lethargy, Confusion
• Treatment - Pacemaker if during day & /or symptoms
- No treatment if at night
• Note – this can progress to 3º Heart Block

7. P=R P-R DROPPED BEAT P-R
Second Degree Heart Block (2º) MobitzTypeII
• ConductIon through AVnode Is constant,block is below in HBE.
• PR Interval Is normal and constant
• QRS are wide usually but not always
• Occasionally dropped beat Is seen
• ClInIcal SIgnIfIcance – more sIgnIfIcant dIsease
• Treatment– pacemaker
• Note– thIs can progress to 3º Heart Block

8. 1. Complete failure of the AV Node
2. No impulses from Sinus Node will pass through to
the ventricles
3. Some part if the conducting system will take over as
pacemaker of the heart (even a myocardial cell 10-
15 bpm)
Third Degree Heart Block (3 º) Complete

9. CRETERIA’s
-P wave rate – normal
PR interval is not constant
P wave may overlap on T wave or QRS complex
Rate usually less than 40 .
QRS complex usually wide and sometimes normal
-Ventricular rate – slow-Idioventricular rhythm
Complete dissociation between P waves & QRS
P P P
P
QRS QRS
Clinical significance;- STOKE-ADAM’s
SYNDROMESymptoms LOC, Confusion, Dizziness, Low BP
• Can lead to standstill, VT or VF
Treatment - Pacemaker
>

10. BBB
either a complete or a partial interruption of the electrical pathways inside the wall of the heart
between the two lower chambers (ventricles)
SYMPTOMS;-
1. RBBB can occur who otherwise seem normal. If it happens with a heart attack, it can be a sign
of serious heart muscle damage.
2. RBBB may cause an ECG to be distorted
3. LBBB can be benign and not cause problems. However, it always interferes with using an ECG
to diagnose heart disease.
Treatments 1.Usually no treatment is done for BBB directly.
2. Implanting a pacemaker isn't beneficial with exceptions to this.

11. LBBB
1. QRS > 120 msec. at lead V1
2. Absence of Q wave in leads I, V5 and V6
3. Monomorphic R wave in I, V5 and V6
4. ST and T wave displacement opposite to
the major deflection of the QRS complex

12. RBBB
Criteria;-
1. QRS > 120 msec.
2. rsR' “bunny ear” pattern
in the anterior precordial
leads (leads V1-V3)
3. Slurred S waves in leads
I, aVL and frequently V5
and V6.

13. ATRIAL ENLARGEMENTS
RAE;- Lead 2 for Tall Peaked P Waves, Arrow
head P waves Amplitude is 4 mm ( 0.4 mV) –
(P=PULMONALE)
Causes;-
Pulmonary Hypertension, Tricuspid Stenosis, Regurgitation
Pulmonary Valvular Stenosis Pulmonary Embolism,Atrial Septal
Defect with L to R shunt
LAE;- Lead 2 and V 1 for Biphasic P Waves, Prolonged s
P wave 0.16 sec, ↑ Downward component
(M= MITRALE)
Causes;-
Systemic Hypertension, MS and or MR Aortic Stenosis and
Regurgitation Left ventricular hypertrophy with dysfunction
Atrial Septal Defect with R to L shuntL

14. Right Ventricular Hypertrophy
1. Tall R in V1 with R >> S, or R/S ratio > 1
2. Deep S waves in V4, V5 and V6
3. Anti-clock wise rotation of Heart
4. RAD+ RAE
5. Deep T inversions in V1, V2 and V3
6. Absence of Inferior MI

15. Left Ventricular Hypertrophy
1. High QRS voltages in limb leads
2. Cornell Voltage criteria, Estes point scoring
- R in Lead I + S in Lead III > 25 mm
- S in V1 + R in V5 > 35 mm
- 24 ♂, > 20 ♀
3. Deep symmetric T inversion in V4, V5 & V6
4. QRS duration > 0.09 sec
5. LAD+ LAE

17. Ischemia, Injury & Infarction
1. Ischemia produces ST segment
depression with or without T
inversion
2. Injury causes ST segment
elevation with or without loss of
R wave voltage
3. Infarction causes deep Q waves
with loss of R wave voltage.SILENT
ELECTRIAC WINDOW
PATHOPHYSIOLOGY;- wedge shaped from epicardium inwards. because of absence of
colletral

18. 18
Ischemia and Infarction
TRANSMURAL Injury ST
Elevation

19. 2 CELL MODULE IN INFARCTION

20. CONVENTINAL ELECTRIC THEORIES
DIASTOLIC AND SYSTOLIC (Extracellularly, current )
Defect in Infarcted Cells Current Flow
Decreased resting membrane potential
Into infarct
Delayed depolarization
Out of infarct
Rapid repolarization
Out of infarct

21. IONIC ELECTRONs THEORY

22. 22
ST Segment Depression
1. Upward sloping depression of ST segment is not indicative
of IHD
2. It is called J point depression or sagging ST seg
3. Downward slopping or Horizontal depression of ST segment
leading to T↓is significant of IHD
T WAVE INVERSION
Repolarization abnormality MI include:
1. ST elevation followed by peaked and
inverted T waves
2. Dominant R wave and ST depression
in V1-V3

23. 23
Pathological Q wave
Notice the deep & wide
Infarction Q in Lead I

24. 24
Blood Supply - MI - Leads
ANTERIOR LATERAL INFERIOR POSTERIOR
LAD LAD or LCx RCA RCA + LCx
V1, V2, V3, V4 V5, V6, L1, aVL L2, L3, aVF V1, V2 Mirror

25. What are the Investigations ?
1. Resting 12 Lead ECG, Chest X-Ray
2. Tread Mill Test (TMT) – Provocative stress tests
3. Troponins (bed side), LDH, CPK isoenzymes
4. Echocardiography and Doppler
5. Calcium scoring and CT angiography
6. Exercise Echo, Dobutamine challenge
echocardiography
7. Perfusion – Stress Thalium, Sistemibi, Dipyridamole
8. 3D Coronary Cartography (CCG), PET scan
9. Coronary Angiography (Gold Standard)

26. MANAGEMENT OF ARRHYTHMIAS
Treat Cause Stable Vs Unstable’;-
1. Do Nothing
2. Pharmacological therapy.
3. Cardioversion.
4. Pacemaker therapy.
5. Surgical therapy e.g. aneurysmal excision.
6. Interventional therapy “ablation”.