ECG dor anesthesiologist

1. ECG clinical application
Dr.Radhwan Hazem Alkhashab
Consultant anaesthesia & ICU
2021

2. An electrocardiogram (ECG) is a medical test that detects
heart problems by measuring the electrical activity generated
by the heart as it contracts.
The electrocardiogram (ECG) was first invented by William
Einthoven in 1906,who used a string galvanogram for his
recordings.
Introduction

3. In the perioperative setting, electrocardiography serves two main functions: diagnosis
and monitoring. In the preoperative period, the standard 12-leads ECG is performed
mainly for risk assessment.
The preoperative ECG may reveal acute or new abnormalities, especially when dealing
with urgent or emergency operations, and in such cases comparing current with
previous ECGs is of extreme importance.
Objectives

4. The small electric currents produced by the electrical activity of cardiac muscle spread
an electrical field through out the body that behaves as a volume conductor, which
allows it to be recorded at various sites on the surface of the body as
electrocardiographic signals. The electrical potentials reaching the skin are recorded
by electrodes (leads) placed at specific locations.

5. The three major types of ECG are:
 Resting ECG : No movement is allowed during the test, as electrical impulses
generated by other muscles may interfere with those generated by your heart. This
type of ECG usually takes 5 to 10 minutes
 Ambulatory ECG (Holter ECG) : patient wear a portable recording device for at least
24 hours. This type of ECG is used for people whose symptoms are intermittent and
may not show up on a resting ECG, and for people recovering from heart attack to
ensure that their heart is functioning properly.
 Exercise stress test (EST) (TMT):This test is used to record your ECG while you ride
on an exercise bike or walk on a treadmill. This type of ECG takes about 15 to 30
minutes to complete.
Types of ECG

6. Each little box is 1 mm tall (vertically). A wave that goes
upward from the baseline is said to be positive. A wave
that goes downward from the baseline is said to be
negative.
The Baseline
The baseline on a 12-lead EKG is an imaginary line that
connects the end of the T wave to the beginning of the
P wave. All measurements of other waves are made
relative to the baseline.
How to Measure Waves on the EKG

7. The ECG is recorded on a graphic paper with standard sized squares.
• The horizontal axis: time measured in seconds. 1 small square (1 mm): 0. 04 seconds 1
large square: 0. 20 seconds.
• The vertical axis: One large box - 0.5 mV
• The standard paper speed is 25 mm/sec.
Standardization
To ensure that the EKG correctly measures and records the amplitude of
waves above and below the baseline, a standardized voltage is inscribed on
every EKG, usually at the right side of the EKG. It should measure exactly 10
little boxes in height.
ECG Paper

8. A lead is formed by a pair of electrodes.
• Frontal Plane ( 6 limb leads) Bipolar Leads: I , II , and III Unipolar leads: a. VR, a. VL, a. VF
• Transverse Plane: Unipolar chest leads: V 1 to V 6
• if depolarization moving towards a +ve leads produces a +ve deflection.
• if depolarization moving in the opposite direction produces a –ve deflection.
12 standard ECG leads

9. Which measure the difference in electrical potential between two points
1. Bipolar Leads: Two different points on the body
2. Unipolar Leads: One point on the body and a virtual reference point with zero
electrical potential, located in the center of the heart
EKG Leads

10. • Lead I: Left arm is +ve, the other is –ve.
• Lead II: The right arm is –ve and the left leg is +ve.
• Lead III: Left arm is –ve, the left leg is +ve.
• The 3 leads arranged as a triangle are known as
Einthoven’s triangle.
Augmented unipolar limb leads , are recordings
between 1 limb and the other 2 limbs.
• aVR (augmented, Voltage, Right arm +ve)
• aVL: uses left arm as +ve.
• aVF: uses left leg as +ve.
Precordial leads

11. • V 1 – Right sternal border, 4 th ICS.
• V 2 – Left sternal border, 4 th ICS.
• V 3 – Halfway between leads V 2 & V 4.
• V 4 – Left mid- clavicular line, 5 th ICS.
• V 5 – Anterior axillary line, 5 th ICS.
• V 6 – Mid axillary line, 5 th ICS.
Chest leads:

12. Anatomic Groups

13. It is waveform components that consist of the electrical
events during one heartbeat
● The waveforms are labeled as P, Q, R, S, T and U.
ECG components

14. Under normal circumstances ,the sinoatrial (SA) node has the most rapid spontaneous
depolarization rate and is therefore the dominant cardiac pacemaker .From the SA
node, the impulse normally spreads to the atrioventricular (AV) node through one
left-sided and two right-sided pathways. The P wave is the result of normal
depolarization of the atria. The anatomically anterior right atrium is activated
earlier, and only later does the signal shift posteriorly as activation proceeds over
the left atrium. Therefore ,the P wave in the right precordial leads (V1 and
,occasionally,V2) is commonly biphasic, a positive deflection followed by a negative
one, whereas in the lateral leads, the P wave is upright and reflects right-to-left
spread of the activation front.
P wave

15. In a normal EKG, the P-wave precedes the QRS complex. It looks like a small bump
upwards from the baseline. The amplitude is normally 0.05 to 0.25mV (0.5 to 2.5
small boxes). Normal duration is 0.06-0.11 seconds (1.5 to 2.75 small boxes). The
shape of a P-wave is usually smooth and rounded.
If P waves are absent and it is an irregular rhythm it may suggest A-Fib
P wave

16. The PR interval is the temporal bridge between atrial and ventricular activation ,during
which the AV node, the bundle of His, the bundle branches ,and the intraventricular
conduction systems are activated
Most of the conduction delay during this segment is due to slow conduction within the
AV node. The normal PR interval is 120 to 200 msec in duration.
PR interval

17. 1.Prolonged PR interval
● Atrioventricular delay (AV block)
● First Degree Heart Block
Delay in the conduction through the conducting system
• Prolong P-R interval
• All P waves are followed by QRS
• Associated with : Digitalis, Beta Blocker, excessive vagal
tone, ischemia, intrinsic disease in the AV junction or bundle
branch system
PR interval

18. 2. Second Degree Heart block
● Mobitz type 1(Wenkebach)
● If the PR interval slowly increases then there is a dropped QRS complex
PR interval ….cont.

19. 3. Second Degree Heart block cont.
● Mobitz type 2
● If the PR interval is fixed but there are dropped beats
● Clarify by the number of dropped beats (2:1, 3:1, 4:1)

20. 4. Third degree Heart Block
● Complete Heart Block
● The P waves and the QRS complex are completely
unrelated

21. PR interval shortens an abnormal pathway that is present in some people.
This pathway connects the atria to the ventricles, bypassing the normal AV
node. As a result, the PR interval is shorter than 0.12 seconds. It is abnormally
short because without the normal AV delay, some part of both ventricles start
to depolarize too early. This produces an early depolarization of the ventricles,
called a delta wave. This short circuit is called an AV bypass tract, short PR syndrome, or
WPW syndrome (named after Drs. Wolff, Parkinson, and White)

22. The short circuit in WPW bypasses the normal
AV node and its safety delay.
If the patient develops atrial fibrillation or atrial
flutter, the ventricles may be bombarded
with impulses at a rate of over 300 bpm
WPW

23. The QRS complex is the manifestation of left and right ventricular muscle depolarization.
Ventricular excitation spreads with in several milliseconds from the bundle branches to the
His-Purkinje fibers, which are dispersed broadly throughout the entire endocardial surfaces
of both ventricles.
The QRS complex, normally beginning with a downward deflection, Q; a larger upwards
deflection, a peak (R); and then a downwards S wave. The QRS complex represents
ventricular depolarization and contraction.
● Amplitude: 5-30 mm high
The QRS complex should be 1.5–2.5 small squares in duration, Duration: 0.06 - 0.10 sec
QRS complex

24. The QT interval represents the time of ventricular
activity including both depolarization and
repolarization.
It is measured from the beginning of the QRS
complex to the end of the T wave. Normally, the
QT interval is 0.36 to 0.44 seconds (9-11 boxes).
The QT interval will vary with patient gender, age
and heart rate.
QT interval

25. Repolarization of the ventricles generates the ST segment and T wave
The T wave is sometimes followed by a small U wave, which may be associated with
hypokalemia or hypomagnesemia.
● T wave is normally a modest upwards waveform representing ventricular repolarization
● Amplitude: 0.5 mm in limb leads
Duration: 0.1 - 0.25 sec
T wave

26. ● To calculate the rate of a regular ECG, simply divide 300 by the number of large
squares between two QRS complexes.
● For irregular rhythms, count the number of complexes between 30 large squares
and multiply by 10 (30 large squares = 6 seconds, assuming standard paper speed
of 25 mm/s).
Rate Estimation

27. Mark out the RR patterns on a piece of paper to see if intervals are the same
Regularly irregular.
Rhythm

28. ST elevation
● It is significant when it is greater than
1 mm (1 small square) in 2 or more
contiguous limb leads or greater
than 2 mm in 2 or more leads
● It is usually caused by complete full
thickness myocardial infarction
The Abnormal Electrocardiogram

29. ST depression
● ST depression > or equal to 0.5 mm in greater than or
equal to 2 contiguous leads, it indicates myocardial
ischemia

30. The T wave indicates the repolarization of the ventricles. It is a slightly asymmetrical
waveform that follows (after a pause), the QRS complex. Take note of T waves
that have a downward (negative) deflection or of T waves with tall, pointed peaks.
The U-wave is a small upright, rounded bump. When observed, it follows the T-wave.
Abnormal T wave

31. BEWARE: T waves are too tall
● >5 mm in the limb leads
● >10 mm in the chest leads, its the same criteria as
small QRS complexes
● You should be thinking of Hyperkalemia or a hyper
acute MI

32. Inverted T waves
● Normally inverted in V1 and inversion in lead III is a
normal variant
● In other leads can be a non specific sign of a variety of
conditions.
Flat T waves
● non specific
● May represent ischemia or electrolyte imbalances

33. A cardiac arrest rhythm with no electrical activity.
There are no P waves or QRS complexes, The heart is not functioning.
Cardiac arrest

34. Initiation of atrial electrical activation from a site other than the SA node occurs in one of
two ways: either as an escape rhythm if the normal SA nodal pacemaker slows or fails
or as an accelerated atrial ectopic rhythm if the automaticity of the ectopic site is
associated with a rate higher than the SA node. Ectopic atrial activation is often
manifested by an abnormal morphology of the P wave (different from the native P).
Most commonly, negative P wave are seen in the leads where the P wave is normally
upright ( leads I,II,Avf,V6) with or without shortening of the PR interval. The exact site
of an ectopic atrial pacemaker is usually of little clinical significance except that left-
sided atrial ectopy is seen more often in association with LV or left heart
valvular abnormalities, whereas right-sided ectopy is more common in patients with
chronic obstructive lung disease or other causes of right heart dysfunction.
Atrial Abnormality

35. Left ventricular hypertrophy (LVH) or enlargement produces changes throughout the
QRST complex. The most characteristic change is increased voltage of the QRS
complex: tall R waves in the left-sided leads (I, aVL, V5, and V6) and deep S waves
in the right-sided leads(V1 and V2). ST-segment and T-wave amplitudes can be
normal or increased
Ventricular Hypertrophy and Enlargement

36. Right ventricular hypertrophy is manifested on the ECG by abnormally tall R waves in the
rightward-directed leads (aVR, V1, and V2), reversal of normal R-wave progression in
the precordial leads, deep S waves with abnormally small R waves
in the left-sided leads (I, aVL, V5, and V6), and marked right axis deviation.
Chronic obstructive pulmonary disease can lead to right ventricular hypertrophy' changes
in the position of the heart within the chest, and hyperinflation of the lungs.
Right ventricular hypertrophy

37. Acute right ventricular pressure overload, such as that caused by pulmonary embolism
can produce a characteristic pattern on the ECG in the right-sided leads, an
S1,Q3,T3, pattern, and an acute incomplete or complete right bundle branch block
(RBBB). However, even the classic S1,Q3,T3,pattern occurs in only about 10%of
cases of acute pulmonary embolism
Pulmonary embolism

38. The ST-T segment ,representing myocardial repolarization ,is the component of the ECG
most sensitive to acute myocardial ischemia.
ST elevation, which may be accompanied by tall positive (hyper acute)T waves, indicates
transmural ischemia and is most often the result of acute coronary artery occlusion
caused by either coronary thrombosis or vasospasm(Prinz metal's variant angina).
Reciprocal ST depression may appear in the contralateral leads. Ischemia confined to the
subendocardial area is usually denoted by ST-segment depression. Subendocardial, ST
depression-type ischemia typically occurs during episodes of symptomatic or
asymptomatic ("silent") stable angina pectoris. It is Characteristic of ischemia occurring
during exercise, tachycardia, or a pharmacologic stress test in patients with significant
but Stable coronary artery disease(CAD)
Myocardial ischemia

40. With prolonged ischemia, there is a risk of developing myocardial Necrosis or myocardial infarction
(MI). The electrocardiographic manifestation of MI includes decreased R-wave amplitude and
pathologic Q waves(>1 mm in depth and >40 msec in duration), which may develop as a result
of loss of electromotive forces in the infarcted area. Transmural infarctions are more likely to
culminate in pathologic a waves, whereas subendocardial (non transmural) infarcts are less
likely to produce Q waves. However, pathologic studies have shown such a wide overlap
between the two entities and their electrocardiographic expression that "Q wave" or "non-Q-
wave" infarction is not synonymous with transmural or non transmural infarction. Pathologic Q
waves usually develop days after the onset of acute MI, and once they develop, they disappear
and serve as an indicator of the location of the infarction. Persistent T-wave inversion may also
be the only sign of chronic ischemia and recent or old MI.
Myocardial Infarction

41. Electrocardiographic leads demonstrating ST-T changes or Q waves may help define the
location and the coronary artery Responsible for the ischemia or MI. For example
,precordial leads V1, to V3 correspond to the anteroseptal or apical walls of the left
Ventricle ;leads V4 to V6 to the apical or lateral LV walls ,
Leads II, III, and aVF to the inferior LV wall and the right-sided leads to the right ventricle.

42. Calcium : hypercalcemia shortens & hypocalcemia prolongs phase 2 of the action
potential duration, thus leading to abbreviation or prolongation of QT interval
respectively.
Severe hypercalcemia (e.g. more than 15 mg/dl) causes decreases in T wave amplitude or
T wave inversion & may cause high take off ST segment in leads V1,V2 simulating
acute ischemia.
Electrolyte Abnormalities

43. Hyperkalemia leads to a distinctive sequence of changes on the ECG, starting with
narrowing and peaking of the T wave and shortening of the QT interval.
Progressive hyperkalemia causes widening of the QRS complex, a low p-wave
amplitude, and prolongation of the PR interval with the possibility of a second- to
third-degree AV block.
Potassium
.Electrocardiographic signs of hyperkalemia
The earliest change with hyperkalemia is
peaking(tenting,,) of the T waves. with
progressive increases in the serum
potassium concentration, the QRS
complexes widen ,the P waves decrease in
amplitude and may disappear, and finally a
sine-wave Pattern leads to asystole unless
emergency therapy is initiate

44. Severe hyperkalemia results in sine-wave ventricular
flutter and eventually asystole .Hypokalemia, in
contrast ,may cause ST depression, flattened T
waves, and a prominent U wave that may sometimes
exceed the amplitude of T waves. Hypokalemia
prolongs repolarization and leads to long QT(u)
syndrome, which predisposes to a torsades de
pointes-type ventricular fibrillation.

45. Mild to moderate hypermagnesemia or hypomagnesemia is not associated with specific
changes on the ECG. Yet severe hypermagnesemia can cause AV and intraventricular
conduction disturbances, including complete heart block and cardiac arrest (Mg >15
mEq/L). Hypomagnesemia is often associated with hypocalcemia or hypokalemia and
may predispose to long QT(U) syndrome & torsades de pointe
Magnesium

46. Arrhythmias are common during & after surgery & have many causes. Postoperative
dysrhythmias are most likely to occur in patients with structural heart disease. The
initiating factors for the arrhythmias after surgery is usually transient insult such as
hypoxemia, cardiac ischemia, catecholamine excess or electrolyte abnormality.
Patients undergoing cardiac surgery obviously have a higher incidence of cardiac
dysrhythmias. The incidence of new onset atrial fibrillation after cardiac surgery
approaches33o/o, such arrhythmias are associated with a worse outcome.
Diagnosis of Arrhythmia

47. 1. General anesthetics : Volatile anesthetics ,such as halothane or enflurane, produce
arrhythmias, probably by a reentrant mechanism .Halothane also sensitizes the
myocardium to endogenous and exogenous catecholamine.
Drugs that block the reuptake of norepinephrine, such as cocaine and ketamine, can
facilitate the development of epinephrine-induced arrhythmias Sevoflurane may cause
Severe bradycardia and nodal rhythm when used in high concentrations during induction in
infants ,and desflurane may prolong the QT within the first minute of Anesthesia in
patients with a normal heart
2. Local anesthetic: Regional anesthesia may cause parasympathetic nervous system
dominance leading to mild to Very severe bradyarrhythmias, especially when the
blockade extends to very high thoracic levels. Inadvertent intravascular injection of a
large dose of local Anesthetic may lead to asystole and cardiac arrest, which
Are very difficult to treat. One proposed treatment is the Administration of 20% Intralipid
Perioperative arrhythmias causes :

48. 3. Abnormal arterial blood gases or electrolyte levels: Excessive hyperventilation,
particularly in the presence of low serum potassium levels, may precipitate severe
cardiac arrhythmia.
4. Endotracheal intubation : this is the most common cause of arrhythmia during
surgery & frequently associated with hemodynamic disturbances.
5. Autonomic reflex may produce sinus Bradycardia and allow ventricular escape
mechanisms to occur. It may also produce AV block or even asystole.
6. Central nervous system stimulation and dysfunction of the autonomic nervous
system: Many electrocardiographic abnormalities can occur in patients with
intracranial disease, especially subarachnoid hemorrhage. These abnormalities are
most commonly ST-T wave changes and may easily mimic myocardial ischemia and
infarction. The mechanism of these arrhythmias appears to be related to changes in
autonomic nervous system tone

49. 7. Preexisting cardiac disease: This is probably the most common background for
arrhythmias during anesthesia and surgery." Patients with a preexisting tendency
for atrial or ventricular arrhythmias are more likely to exhibit them during or after
surgery in response to perioperative stressor secondary to acute withdrawal of oral
antiarrhythmic medications ,most commonly B-blockers.
8. Central venous cannulation: Insertion of catheters or wires into the central
circulation frequently leads to arrhythmias
9. Surgical manipulation of cardiac structures: Arrhythmias are frequently observed
during insertion of atrial sutures or placement of venous cannulas for
cardiopulmonary by pass during cardiac surgery

50. 10. Location of surgery: Dental surgery is often associated with arrhythmias because
profound stimulation of the sympathetic and parasympathetic nervous systems
frequently occurs. junctional rhythms are often seen and may be caused by
stimulation of the autonomic nervous system by the 5th cranial nerve.
The oculo cardiac reflex can leads to severe bradycardia in response to traction of
rectus muscles of the orbit.

51. Sinus bradycardia is diagnosed when the pacemaker site is in the sinus node but the
rate is slower than normal. Etiologic factors include drug effects ,acute inferior MI,
hypoxia, vagal stimulation, and high sympathetic blockade. Sinus bradycardia accounts
for roughly 11% of intraoperative arrhythmias.
Sinus Tachycardia
The pacemaker site in patients with sinus tachycardia is in the sinus node, and the rate
is faster than normal. Sinus tachycardia is the most common arrhythmia in the
perioperative period. It occurs with such frequency that it is not included in most
studies of the incidence of arrhythmias. Common causes include pain, inadequate
anesthesia, hypovolemia, fever, hypoxia, hypercapnia, heart failure, and drug effects.

52. In sinus arrhythmia ,the impulses arise from the SA node, and the rhythm is characterized
by u variable rate. The PR interval is normal ,as is the QRS complex. Most commonly,
but not invariably ,the rate increases with inspiration and decreases with expiration.
This arrhythmia occurs more often in children than in adults.
The heart rate is 60to 100beats/min, the rhythm is irregular, the P/QRS ratio is 1:1, and
the QRS complex has normal morphology. Sinus arrhythmia has little clinical
significance, is considered a normal finding, and requires no treatment
Sinus Arrhythmia

53. An ectopic pacemaker site in the left or right atrium initiates an atrial premature beat
(APB).The shape of the P wave is different from the usual SA node P wave and may
be inverted. The PR interval may be shorter or longer than normal ,depending on the
site of the ectopic focus and the refractoriness of the AV nodal pathway.
Atrial Premature Beats

54. Paroxysmal SVT (PSVT) is characterized by a rapid
regular rhythm, generally with a narrow QRS complex
and lacking the normal SA node P wave .Inclusion of
tachycardia s involving the AV node
Ectopic atrial or ectopic nodal tachycardia are among the
less frequent SVTs.
Paroxysmal Supraventricular Tachycardia

55. Atrial flutter is a regular atrial rhythm characterized by atrial flutter waves.
Lead II frequently demonstrates the classic saw tooth appearance of the flutter
waves, some of which are hidden in the ST segment. Atrial flutter usually is a
regular rhythm at a rate of 240 to 340 with flutter waves
Atrial flutter and fibrillation: Notice the
,,saw tooth“ waves (F waves) with atrial
flutter and the irregular fibrillary waves
(f waves) with atrial fibrillation
Atrial flutter

56. Atrial fibrillation is an excessively rapid and irregular atrial focus with no P waves appearing
on the ECG; instead, fine fibrillatory activity is seen (f waves). This is the most commonly
encountered irregular rhythm. It is often described as irregularly irregular.
The atrial rate is 350 to 500 beats/min, and the ventricular rate is 60 to 170 beats/min.
Clinical significant of AF:
The loss of atrial "kick' from inefficient contraction of the atria may reduce ventricular filling
and significantly compromise cardiac output. After 24 to 48 hours, atrial fibrillation may be
associated with the development of atrial thrombi, possibly resulting in pulmonary
or systemic embolization.
Atrial fibrillation

57. VPBs result from ectopic pacemaker activity arising below the AV junction. The VPB
originates in and spreads through the myocardium or ventricular conducting
system, there by resulting in a wide (>0.12-second), bizarre QRS complex. The ST
segment usually slopes in the direction opposite the main deflection of the
QRS complex. There is no P wave associated with a VPB, but retrograde
depolarization of the atria or blocked sinus beats may obscure the diagnosis.
A VPB often blocks the next depolarization from the SA node, but the following sinus
beat occurs on time. The result is a fully compensatory pause consisting of
the interval from the VPB to the expected normal QRS, which is blocked at the AV
node, plus a normal sinus interval.
Ventricular Premature Beat VPB

58. VPBs are common during anesthesia, where they account for 15%of observed
arrhythmias. They are much more common in anesthetized patients with preexisting
cardiac disease. Other than heart disease, known etiologic factors include electrolyte
and blood gas abnormalities, drug interactions, brainstem stimulation, and trauma to
the heart.
VPB

59. The presence of three or more sequential VPBs defines VT.
VT is classified by its duration and morphology. In duration ,non sustained VT lasts three
beats and up to 30seconds, and sustained VT lasts 30seconds or longer. With
monomorphic morphology ,all complexes have the same pattern, and with
polymorphic morphology ,complexes constantly change patterns. Polymorphic VT
with along QT is also called "torsades de pointes.
Ventricular tachycardia

60. Ventricular fibrillation is an irregular rhythm that results from a rapid discharge of
impulses from one or more ventricular foci or from multiple wandering reentrant
circuits in the ventricles. The ventricular contractions are erratic and are represented
on the ECG by bizarre patterns of various size and configuration. P waves are not
seen. Important causes of ventricular fibrillation include myocardial ischemia, hypoxia,
hypothermia, electric shock, electrolyte imbalance, and drug effect
Ventricular fibrillation

61. Torsade de Pointe (polymophous ventricular tachycardia) is a form of ventricular
tachycardia. The diagnostic hallmark of torsade is a change in direction of the
complexes. the episode of ventricular tachycardia begins with the first three QRS
complexes pointing downward, and the next three pointing upward. This is
associated with long QT interval. Drugs, hypokalemia, and hypocalcemia are
common causes.
Torsade de Pointe

62. Ventricular Pacing
Ventricular pacemaker
rhythm demonstrates a
vertical electrical
artifact (EA) at the
beginning of the QRS.
Pacemakers

63. Atrial Pacing

64. Caused by u serious delay or block of the main left bundle branch or
both of its two fascicles, an LBBB results in a prolonged QRS
duration, abnormal QRS complex, and ST-T wave
abnormalities. A basic requirement is a QRS duration of
120msecor longer. There is also a broad, sometimes notched R
wave in the left-sided leads(I, aVL, V5 V6) with deep S waves in
the right precordial leads and absent septal Q waves.
Left bundle branch block LBBB

65. An RBBB is caused by a conduction delay anywhere in the right-
sided intraventricular conduction system.
The electrocardiographic manifestation of RBBB consists of
prominent and notched R waves with on the right-sided leads
and wide S waves on the left-sided leads, along with QRS
prolongation (>I20 msec)
Right bundle branch block RBBB

66. Thank you