What is an ECG?
A graphical representation of the
electrical events taking place in the
heart during each beat.
The human body is a very good volume conductor and if electrodes are placed on
body surface they will pick up the action potential current and when they are
connected to galvanometer with the help on a conducting wire then these currents
are recoded on a moving paper as the pen needle of galvanometer deflects or
moves.if the wave of depolarization in the heart moves towards the positive electrode
an upward deflection occurs but if wave of depolarization moves away towards
negative electrode then a downward deflection is produced.the needle stays at
neutral point and paper displays an isoelectric line when the myocardium is polarized
(resting), completely depolarized or completely hyperpolarized.Durin these three
conditions there is no movements of electrical charges and therefore no movement of
needle.
Electrocardiogram ECG (EKG)
• Surface electrodes record electrical activity
deep within body - How possible?
• Reflects electrical activity of whole heart not
of single cell!
• EC fluid = “salt solution” (NaCl)  good
conductor of electricity to skin surface
• EKG tracing =  of all electrical potentials
generated by all cells of heart at any given
moment
Recording of ECG
In order to record a standardized ECG ,there
are internationally accepted conventions to
record accurate and standard ECG
• For each 1mv input , there must be 1 cm
deflection of pen or stylus
• Speed of paper ( 25mm/sec)
• Placement of electrodes
The two electrodes connected to a
conducting wire constitute a “ LEAD”
A lead is said to be bipolar if both
electrodes are active and their potential
difference will determine the voltage of
that particular lead. Alead is known as
unipolar if all the current is recorded by
one active electrode and the second is
kept at zero.This is augmentation so all
unipolar limb leads are known as
augmented unipolar limb leads and
written as aVR,aVL,aVF. “a” stands
for augmented.
LEADS
• Bipolar leads , both electrodes are active
V1 – V6
• Unipolar leads , one is active and other is
inactive , aVR ,aVL, aVF.
Einthoven’s Triangle and the 3 Limb Leads:
+
I
RA –
–
Fig 14-19
II
III
+
+
LL
LA
–
• The sum of voltages at the corners of an equilateral triangle
with the source of current (heart) in the center is zero.so if we
know the volatge of two bipolar limb leads the electric
potential of the third lead can be calculated by the
formula:I+III=II this is einthoven’s law.read it from the chapter
11 of guyton with the given example.RA is -0.2mv, LA is+0.3mv
and LF is +1.0mv calculate the voltages of lead I,II and III.
• Mean QRS vector of ventricular depolarization
determines the mean electrical axis of the heart
which is +59 degrees directed to the cardiac apex.the
normal range of cardiac axis is from -30 degree to
+110 degree.
Placement of unipolar precordial chest leads on precordium
• V1 is in right fourth intercostal space along sternal
border
• V2 is in left 4th intercostal space along sternal
border
• V3 is between V2 and V4
• V4 is at the apex
• V5 is in left 5th intercostal space along anterior
axillary line
• V6 is in left 5th intercostal space along mid axillary
line
• V1 and V2 represent right ventricular
activity
• V3 and V4 represent activity of ventricular
septum
• V4 and V5 represent left ventricular activity
ECG PAPER
• Along horizontal axis , time or duration is
represented in seconds
• Along vertical axis amplitude is represented in mv
• Side of one small square vertically is equal to 0.1
mv
• Side of one small square horizontally is 0.04 seconds
• in one second there will be 25 small square
ECG PAPER
• P WAVE
• QRS WAVE
• T WAVE
P WAVE
• +VE wave due to atrial depolarization ,which
occur just before atrial systole
• 0.1-0.2 mv ( 1-2 small square)
• Duration is 0.1 sec( 2.5 square)
• Top coincide with time when cardiac
impulse reaches AV node
QRS COMPLEX
•
•
•
•
Q wave is -ve
R wave is +ve
S wave is -ve
It is due to ventricular depolarization just
before ventricular systole or contraction
• Q wave is due to depolarization of upper
part of ventricular septum
• R wave is due to depolarization of lower
part of septum and apex of heart
QRS COMPLEX
• S wave is due to depolarization of wall and
base of ventricle
• Voltage of QRS from peak of R to bottom
of S is about 1 mv or more than 1 mv
• Duration is 0.08—0.1 sec
• peak of R wave coincide with onset of
ventricular systole
• T wave is +ve wave due to ventricular
repolarization
• Voltage is 0.2-0.3 mv
• Duration is o.25-0.27 sec
Standardized EKG’s
Figure 11-1; Guyton & Hall
• Time and voltage calibrations are
standardized as shown on figure 11-1.
Cardiac Cycle- the timing of mechanical waves with ECG
EKG Concepts
• The P wave immediately precedes atrial
contraction.
• The QRS complex immediately precedes
ventricular contraction.
• The ventricles remain contracted until a few
milliseconds after the end of the T
repolarization wave.
• The atria remain contracted until the atria are
repolarized, but an atrial repolarization wave
cannot be seen on the electrocardiogram
because it is obscured by the QRS wave.
An Electrocardiogram
ECG SEGMENTS
• Segments are isoelectric
• PQ / PR SEGMENT , from end of P wave to
beginning of QRS complex
• ST SEGMENT , from end of S wave to the
beginning of T wave
ECG INTERVALS
• PR/ PQ INTERVAL From beginning of P WAVE
to the beginning of QRS complex
• Represent atrial depolarization and conduction
through AV node
• 0.16 sec average ( 0.12-0.2 )
• QRS INTERVAL , It is duration of QRS complex
• Duration is 0.08-0.1 sec
• VAT,( ventricular activation time ) , From
beginning of Q WAVE to the peak of R
wave
ECG INTERVALS
• QT INTERVAL , From the beginning of Q wave
to the end of T wave .
• it represents ventricular depolarization and
ventricular repolarization
• Duration is 0.36-0.4 sec
• RR INTERVAL it is the interval between two
successive R WAVES ,
• IT is equal to duration of one cardiac cycle . (0.8
sec)
•
•
•
•
It is used to find out heart rate
Heart rate = 60/RR
60/0.8= 75 /MIN
HR= no of small sq in 60 sec/ no of small sq bt
two successive R wave
• HR =no of cardiac cycle x 10
Correlation of plasma K+ level and the
ECG, assuming that the plasma Ca2+
level is normal.
INTRODUCTION TO HEART BLOCKS
• OCCUR WHEN THERE IS A PARTIAL OR
COMPLETE INTERRUPTION IN THE CARDIAC
ELECTRICAL CONDUCTION SYSTEM.
• CAN OCCUR ANYWHERE IN THE ATRIA
BETWEEN THE SA NODE AND THE AV
JUNCTION.
• IN THE VENTRICLES BETWEEN THE AV
JUNCTION AND PURKINJE FIBERS.
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Normal heart rates in children.
•
•
•
•
Newborn: 110 – 150 bpm
2 years: 85 – 125 bpm
4 years: 75 – 115 bpm
6 years+: 60 – 100 bpm
Arrhythmias resulting from block of heart
signals within the intracardiac conduction
pathways.
Sino-atrial block
Incomplete atrioventricular block.
Complete atrioventricular block
Bundle branch blocks
Hemiblocks
Anatomical Basis
• The SA node consists of two main groups of cells:
• A central core of pacemaking cells (“P cells”) that
produce the sinus impulses.
• An outer layer of transitional cells (“T cells”) that
transmit the sinus impulses out into the right atrium.
• Sinus node dysfunction can result from either:
• Failure of the P cells to produce an impulse. This
leads to sinus pauses and sinus arrest.
• Failure of the T cells to transmit the impulse. This
leads to sino-atrial exit block.
Intrinsic causes of sick sinus syndrome.
•
•
•
•
Idiopathic Degenerative Fibrosis (commonest).
Ischaemia.
Cardiomyopathies.
Infiltrative Diseases e.g. sarcoidosis,
haemochromatosis.
• Congenital abnormalities.
Sick sinus syndrome.extrinsic causes.
• Drugs e.g. digoxin, beta-blockers, calcium
channel blockers.
• Autonomic dysfunction.
• Hypothyroidism.
• Electrolyte abnormalitites —
e.g. hyperkalaemia.
ECG abnormalities seen in sick sinus syndrome.
• Sinus Bradycardia.
• Sinus Arrhythmia – associated with sinus node
dysfunction in the elderly in the absence of
respiratory pattern association.
• Sinoatrial Exit Block.
• Sinus Arrest — pause > 3 seconds.
• Atrial fibrillation with slow ventricular response.
• Tachy-brady syndrome.
•
Sino-atrial exit block.
• Sino-atrial exit block is due to failed
propagation of pacemaker impulses beyond
the SA node.
• The sino-atrial node continues to depolarise
normally.
• However, some of the sinus impulses are
“blocked” before they can leave the SA node,
leading to intermittent failure of atrial
depolarisation (dropped P waves).
Causes
•
•
•
•
•
•
Sick sinus syndrome
Increased vagal tone (athletes)
Vagal stimulation (surgery, pain)
Inferior myocardial infarction
Myocarditis
Drugs: digoxin, beta-blockers, calcium channel
blockers, amiodarone.
SA Exit Block.
• There is shortening of PR interval
progressively and suddenly no P wave.
SA EXIT BLOCK.
• Another type of SA block black arrow indicates
dropped P wave as a result the 4th QRS is a junctional
escape beat fllowed by a non conducted P wave.
Sinoatrial exit block.
First Degree Heart Block
Definition
• PR interval > 0.2 sec(five small squares)
• ‘Marked’ first degree block if PR interval >
0.3sec
• Examples
Causes.
•
•
•
•
•
•
•
Increased vagal tone
Athletic training
Inferior MI
Mitral valve surgery
Myocarditis (e.g. Lyme disease)
Hypokalaemia
AV nodal blocking drugs (beta-blockers, calcium
channel blockers, digoxin, amiodarone)
• May be a normal variant
FIRST-DEGREE BLOCK IS NOT A TRUE BLOCK BUT
SIMPLY A DELAY IN THE ELECTRICAL CONDUCTION
SYSTEM.
PROLONGED PRI GREATER THAN 0.20 SECONDS.
THE P WAVE OCCURS BEFORE EVERY QRS BUT THE
PRI IS ALWAYS GREATER THAN 0.20 SECONDS.
P TO P AND R TO R INTERVALS ARE USUALLY
REGULAR DEPENDING ON THE UNDERLYING RHYTHM.
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AV Block: 2nd degree, Mobitz I
(Wenckebach Phenomenon)
Definition
Progressive prolongation of the PR interval culminating in
a non-conducted P wave
The PR interval is longest immediately before the
dropped beat
The PR interval is shortest immediately after the dropped
beat
Other Features
The P-P interval remains relatively constant
The greatest increase in PR interval duration is typically between
the first and second beats of the cycle.
The RR interval progressively shortens with each beat of the cycle.
The Wenckebach pattern tends to repeat in P:QRS groups with
ratios of 3:2, 4:3 or 5:4.
Mechanism
Mobitz I is usually due to reversible conduction
block at the level of the AV node.
Malfunctioning AV node cells tend to
progressively fatigue until they fail to conduct
an impulse. This is different to cells of the HisPurkinje system which tend to fail suddenly
and unexpectedly (i.e. producing a Mobitz II
block).
Causes
Drugs: beta-blockers, calcium channel blockers,
digoxin, amiodarone
Increased vagal tone (e.g. athletes)
Inferior MI
Myocarditis
Following cardiac surgery (mitral valve repair,
Tetralogy of Fallot repair)
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AV block: 2nd degree, “fixed ratio” blocks
• Definition
• Second degree heart block with a fixed ratio of
P waves: QRS complexes (e.g. 2:1, 3:1, 4:1).
• Fixed ratio blocks can be the result of
either Mobitz I or Mobitz II conduction.
MOBITZ II HEART BLOCK
• OCCURS DUE TO AN INTERMITTENT
INTERRUPTION NEAR OR BELOW THE AV
JUNCTION.
• INTERRUPTION IS NOT PROGRESSIVE, BUT
OCCURS SUDDENLY AND WITHOUT
WARNING!!
• P WAVES BEFORE EVERY QRS COMPLEX AND
ALL ARE THE SAME SIZE AND SHAPE.
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2:1 Mobitz type II example.
• THIS OCCURS UNTIL A QRS COMPLEX IS
DROPPED.
• THE QRS MAY BE WIDER IF THE BLOCK
OCCURS NEAR THE BUNDLE OF HIS.
3:1 Mobitz type II-example.
Third degree complete heart block.
• Definition
• In complete heart block, there is complete
absence of AV conduction – none of the
supraventricular impulses are conducted to
the ventricles.
Third degree complete heart block.
• Perfusing rhythm is maintained by
a junctional or ventricular escape rhythm.
Alternatively, the patient may suffer
ventricular standstill leading to syncope (if
self-terminating) or sudden cardiac death (if
prolonged).
• Typically the patient will have severe
bradycardia with independent atrial and
ventricular rates, i.e. AV dissociation.
Third degree heart block.
• P WAVES AND QRS COMPLEXES APPEAR AS WELL AS PR
• INTERVAL THAT ARE CONSTANTLY CHANGING IN LENGTH.
• THE PRI’S DO NOT BECOME PROGRESSIVELY LONGER.
• NO RELATIONSHIP EXISTS BETWEEN THE P WAVES AND
• QRS COMPLEXES.
• NO TRUE PR INTERVAL.
Third degree heart block.
• THE QRS COMPLEXES ARE WIDE AND BIZZARE WITH
A TIME FRAME OF >0.12 SECONDS.
• DEPOLARIZATION IS AT THE INHERENT RATE BUT THE
P TO P AND R TO R INTERVALS ARE NOT EQUAL.
• ATRIAL RATE 60 TO 100 VENTRICULAR RATE 20 TO 40.
• THIS IS A LETHAL DYSRHYTHMIA. CAN LEAD TO
ASYSTOLE.
Example of III degree Complete heart
block.
• No coordination between atria and ventricles.
Causes of complete heart block
• The causes are the same as for Mobitz
I and Mobitz II second degree heart block. The
most important aetiologies are:
• Inferior myocardial infarction
• AV-nodal blocking drugs (e.g. calcium-channel
blockers, beta-blockers, digoxin)
• Idiopathic degeneration of the conducting
system (Lenegre’s or Lev’s disease)
Adams-Stokes (A-S) syndrome
• The association of syncope and convulsions with a
slow pulse, termed the MorgagniAdams-Stokes or
Adams-Stokes (A-S) syndrome, is usually due to
venticular standstill secondary to failure of the
idioventricular pacemaker in advanced or complete
heart block.1 Occasionally the A-S syndrome is due to
extreme sinus bradycardia without heart block, e.g.,
rates below 20 per minute, with consequent
intolerably prolonged cerebral ischemia between
ventricular beats.
BUNDLE BRANCH BLOCK (BBB)
• INTERRUPTION IN THE ELECTRICAL
CONDUCTION SYSTEM OF EITHER THE RIGHT,
LEFT OR BOTH BUNDLE BRANCHES.
• CAUSES A DELAY TO THE VENTRICLES.
• THE INTERRUPTION FORCES THE IMPULSE TO
“DETOUR” AND TAKE ANOTHER ROUTE TO
THE VENTRICLES.
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THIS EXTRA TIME CAUSES THE IMPULSE TO REACH THE
VENTRICLE LATER.
THIS CAUSES TWO SEPARATE DEPOLARIZATIONS.
THE RHYTHM STRIP HAS A NOTCHED QRS REFERRED TO
AS “RABBIT EARS”.
THE QRS MEASURES WIDER THAN 0.12 SECONDS.
IF BOTH BRANCHES ARE BLOCKED THE IMPULSE TAKES
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VENTRICLES.
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PATIENTS ARE MANAGED ONLY IF THEY ARE
HEMODYNAMICALLY SYMPTOMATIC.
THESE ARE SHOCK SYMPTOMS DUE TO LACK OF
CARDIOVASCULAR PERFUSION
• MOBITZ II (2ND DEGREE, TYPE II) – OXYGEN, IV FLUIDS,
• ATROPINE IF OVERALL RATE IS BRADYCARDIC, ARTIFICIAL
• PACEMAKER, DOPAMINE OR EPINEPHRINE.
•
•
IF HEART RATE IS GREATER THAN 100 BUT LESS THAN
150 DILTIAZEM, DIGOXIN, OR BETA BLOCKERS.
•
•
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3RD DEGREE BLOCK – OXYGEN, IV FLUIDS, ATROPINE IF
BRADYCARDIC, DOPAMINE, EPINEPHRINE, OR ARTIFICIAL
PACEMAKER.
•
BBB- PATIENT ASSESSMENT