Dr. Bernhard Arianto Purba, M.Kes., AIFO
ECG
Textbooks• Guyton, A.C & Hall, J.E. 2006. Textbook of Medical
Physiology. The 11th edition. Philadelphia: Elsevier-Saunders: 918-930, 961-977.
• Brooks, G.A. & Fahey, T.D. 1985. Exercise Physiology. Human Bioenergetics and Sts Aplications. New York : Mac Millan Publishing Company: 122-143.
• Foss, M.L. & Keteyian, S.J. 1998. Fox’s Physiological Basis for Exercise and Sport. 4th ed. New York : W.B. Saunders Company: 471-491.
• Astrand, P.O. and Rodahl, K. 1986. Textbook of Work Pysiology, Physiological Bases of Exercise. New York : McGraw—Hill.
• Braunwald, Pauci, et al.2008. Harrison's PRINCIPLES OF INTERNAL MEDICINE. Seventeenth Edition. New York : McGraw—Hill: Chapter 332, 333, 338.
• Jardins, Terry Des. 2002. Cardiopulmonary Anatomy & Physiology. The 4th edition. USA: Delmar, A Division of Thomson Learning Inc.
ELECTROCARDIOGRAPHY
(ECG)
ECG
A Brief introduction to ECG
• The electrocardiogram (ECG) is a time-varying signal reflecting the ionic current flow which causes the cardiac fibers to contract and subsequently relax. The surface ECG is obtained by recording the potential difference between two electrodes placed on the surface of the skin. A single normal cycle of the ECG represents the successive atrial depolarisation/repolarisation and ventricular depolarisation/repolarisation which occurs with every heart beat.
• Simply put, the ECG (EKG) is a device that measures and records the electrical activity of the heart from electrodes placed on the skin in specific locations
What the ECG is used for?
• Screening test for coronary artery disease, cardiomyopathies, left ventricular hypertrophy
• Preoperatively to rule out coronary artery disease• Can provide information in the precence of metabolic
alterations such has hyper/hypo calcemia/kalemia etc.• With known heart disease, monitor progression of the
disease• Discovery of heart disease; infarction, coronal
insufficiency as well as myocardial, valvular and cognitial heart disease
• Evaluation of ryhthm disorders• All in all, it is the basic cardiologic test and is widely
applied in patients with suspected or known heart disease
Each small box = 1 mm
= .04 Sec.
5 small boxes = 1 large
box = 0.2 Sec.
MEASURING ECG
ECG commonly measured via 12 specifically placed leads
Lead Configurations for ECG Measurement
Bipolar Leads Augmented Leads Chest (V) Leads
Bipolar Leads: lead I
+ _
vo
+
_
Bipolar Leads: lead II
+ _
vo
+
_
Bipolar Leads: lead III
+ _
vo
+
_
ECG Limb Leads
Augmented Leads: aVR
+ _
vo
+
_
Augmented Leads: aVL
+ _
vo
+
_
Augmented Leads: aVF
+ _
vo
+
_
ECG Augmented Limb Leads
Unipolar Chest Leads
v1 v2
v3
v4
v5 v6
v1: fourth intercostal space, at right sternal margin. v2: fourth intercostal space, at left sternal margin. v3: midway between v3 and v4. v4: fifth intercostal space, at mid clavicular line. v5: same level as v4, on anterior axillary line. v6: same level as v4, on mid axillary line.
Unipolar Chest Leads (cont.)
+ _ +
_
ECG Precordial Leads
Current Lead Placement Conventions(22 Electrodes)
V3R
V4RV5RV6R
E
H
I
3R
5R
V9V8
V7
I
E
M
6R
Current clinical conventions may use 22 different leads
ECG Lead Color Codes
C (brown)
LA (black)
LL (red)RL (green)
RA (white)
Surface Cardiac Potentials
taken at t = to suggests an equivalent dipole located within the heart
Eindhoven’s Triangle-very crude solution to inverse problem using bipolar limb leads:
RA LA
LL
_
_
+
_
++
lead II
lead I
lead III
NORMAL HEARTBEAT AND ATRIAL ARRHYTHMIA
Normal rhythm Atrial arrhythmia
AV septum
Ventri-culardepola-rization
Ventri-culardepola-rization(cont’d)
Ventri-culardepola-rization(cont’d)
++
++
++
++ + +
++
+
++
++
+
+
+
--
--
--
- ---
-
--
--
--
--
--
--
-
Ventri-cularrepola-rization
Lead I
Lead II
Lead III
LimbLeads(bipolar)
Lead I
Lead II
Lead III
aVR
aVL
aVF
aVR
aVL
aVF
Uni-polarLead
Normalvalues
PR interval0.12-0.20”
P wave00.8-0.11”
QRS duration0.06-0.10”
Intrinsicoid deflection
< 0.05”
U wave
ST segmentStd: > 1mmPre : > 2mm
T wave
QT segmentMen < 0.39”Wo < 0.40”
Pre-cordialleads
V1 V2
V4
V5
V3
V6
Hori-zontalvsVerti-cal heart
Hori-zontalvsVerti-cal heart
Clock-wisevsCounterclock-wiserotation
Viewed from below the heart looking towards the apex in vertical heart
13
2
4
13 2
4
13
2
4
1
3
24
P wave
V1
AtrialEnlargement
V1
P mitralWide and notch
Biphasic with(-) terminalcomponent
Left atrialenlargement
AtrialEnlargement(cont’d)
V1
Tall and peakedP wave
Right atrialenlargement
Tall and peakedP wave
Elec-tricalaxis
Lead I
aVF
qRS = +3
qRS = +1
TheQRS
Bundle of His
LBB
Anterosuperiordivision
Posteroinferiordivision
RBB
TheQRS
13
2
V1
V6
4
QRS vectors:• Initial depolarization• Terminal depolarization• S-T segmen• Re-polarization
Myo-cardial injury
Electrical forces are directed away from a injured area
A B C D E
Normal Minimal Subendocard Transmural Subepicard
Myo-cardial injury
A B C D E
Normal Minimal Subendocard Transmural Subepicard
ST segment deviated towards the surface of injured tissue
Myo-cardialinfarction
Zones of myocardial infarction:• Necrosis• Injury• Ischaemia
2
13 1
2
34
1
2
3
4
Myo-cardialinfarction(cont’d)
ECG parameters of myocardial infarction:• Necrosis• Injury• Ischaemia
13
V1
V6
2
4
Myo-cardialinfarction(cont’d)
Phases of myocardial infarction:
• Hyperacute phase- Slope elevation of the ST sement- Tall widened T wave- Increased ventr. activation time
• Fully evolved phase- Pathological Q wave- Coved, elevated ST segment- Inverted symetrical T wave
• Old infarction- Pathological Q wave- ST segment and T wave return to normal
Myo-cardialinfarction(cont’d)
Localization of infarcted areas
2
13
II, III, aVF
IaVLV4 V5
V6
V1 V2
V3
Rightventricularhypertrophy
1
2
V1
V6
4
3
Leftventricularhypertrophy
1
2
V1
V6
4
3
Diatolic overload
Leftventricularhypertrophy
1
2
V1
V6
4
3
Systolic overload
RBBB
12
V1
V6
4
3
LBBB
1a2
V1
V6
43
1b
QTinterval
QTc= QT
R-R
Prolonged QTc
• Hypocalcemia• Acute rheumatic carditis
Shortened QTc
• Hypercalcemia• Digitalis effect• Hyperthermia• Vagal stimulation
Normal QT does not exclude the diagnosis of
• Acute myocardial infarction• Acute myocarditis of any causes• Sympathetic stimulation• Procain effect
AtrialSeptalActiva-tion
Sinus rhythms• Sinus arrythmia• Sinus tachycardia• Sinus bradycardia
AV nodal rythms• AVn extrasystole• Paroxysmal AVn tachycardia• Idionodal tachycardia
Ectopic atrial rythms• Atrial extrasystole• PAT• Atrial fibrilation• Atrial flutter
Ventricular rhytms• V-extrasystole• V-tachycardia• V-flutter• V-fibrilation• Idioventricular tachycardia
Disturbances of impulse formation
Arrhythmias
Disturbances of impulse conduction
S-A blockA-V block
WPW syndrome(Wolf-Parkinson-White)LGL syndrome(Lawn-Ganong-Levin)
Reciprocal rythms
Arrhythmias
2nd disorders of rythms
Atrial escape
Ventricular escape
AVn escape
A-V dissociation
Aberrant ventricular conduction
Arrhythmias
Diagnostic approach
To be continued next weekInsyaa Allah
Arrhythmias
1
2
V1
V6
4
3
Arrhythmias
1
2
V1
V6
4
3
Arrhythmias
1
2
V1
V6
4
3
Arrhythmias
1
2
V1
V6
4
3
Arrhythmias
1
2
V1
V6
4
3
Electrocardiogram
The WavesP wave
atrial depolarization
duration 0.11s
amplitude < 3mm
detects atrial functionSA node
Electrocardiogram
The WavesQRS Complex
ventricular depolarization duration 0.10s
detects ventricular functionQ wave
first downward strokeR wave
first upward strokeS wave
any downward stroke preceded by an upward stroke
T waveventricular repolarization
Intervals and Segments
PR segmentend of P wave to start of
QRSmeasures time of
depolarization through AV node
PR intervalstart of P wave to start of
QRSmeasures time from start of SA conduction to end of
AV node conductionnormal 0.12-0.20s
Intervals and Segments
ST segmentend of QRS complex to start
of T wavemeasures start of ventricular
repolarizationelevated in MI’s
ST intervalend of QRS to end of T waverepresents complete time of
ventricular repolarization
QT intervalstart of QRS to end of T wave
duration of ventricular systole
< 1/2 of the RR interval
Intervals and Segments
Intervalsthe timing for
depolarizations/repolarizations can be interpreted from the EKG
P-R 0.12-0.2 secmeasures the time between the start
of atrial depolarization and the start of ventricular depolarization
a long P-Q interval is a sign of AV node dysfunction
QT interval, about 0.4 secstart of QRS to end of T wave
QRS 0.08-0.1 secwider with ventricular dysfunction
ST segment (don’t worry about time)elevated with acute MI
Electrocardiogram
The wavesmore on the QRS
note that the Q or the R or the S wave is not always
presentname according to direction
of first deflection, second, etcQ waves are often absent
lead V1no Q
small Rlarge S
lead V2no Q
large Rsmall S
Heart Rate
Heart Ratedefined as beats per
minuteeasy way to estimate ratefind an R wave on a thick
linecount off on the thick
lines 300, 150, 100, 75, 60,
50until you reach another
R wave
in our example the middle R wave falls on the dark
linethe next R falls just before the 75, so
estimate about 80 bpm
300
150
100
75
Normal Sinus Rhythmheart rate between 60-100
bpm pacing by SA node.
QRS after every P waverhythm is regular
Sinus Tachycardiaheart rate > 100 bpm
p wave is there but hidden by the T wave
regular QRS rhythmSinus Bradycardia
heart rate < 60 bpmQRS after every P wave
regular rhythm
Heart Rate
ST segment elevation
ischemia
Q wavein some leads may indicate ischemia and
necrosis
T wave inversionlate sign of
necrosis and fibrosis
Wave Abnormalities
Atrial Fibrillationmultifocal areas in atria firing
no p waves and irregular heart rate
Rhythm Abnormalities
Complete (3rd degree) AV Block AV node cannot conduct impulsep waves and QRS not connected
irregular heart rate
Rhythm Abnormalities
Premature Ventricular Contractionsventricles pace early
early heart beatlarge QRS
Rhythm Abnormalities
Ventricular Tachycardiarapid ventricular pacing
rapid, regular ratewide QRS
Rhythm Abnormalities
Ventricular Fibrillationmultifocal
ventricular beatsirregular
won’t last long
Rhythm Abnormalities
0
+90
180
-90
Axis
QRS AXISanother name for the vector of
depolarizationan axis is measured in degrees the axis is measured by adding
the positive deflection and subtracting the negative
deflectionoverall + is left axis directionoverall - is right axis direction
for lead one most of the QRS is positive, therefore it has a
leftward axisif an MI caused the QRS to be
mostly negative the lead would have a rightward axis
—— ++
QRS AXISlead II
positive on left legnegative on right arm
looking at the tracing we see that the QRS is
mostly positivewhat does this mean?0
+90
180
-90
——
++
Axis
QRS AXISlead III
positive on left legnegative on left arm
looking at the tracing we see that the QRS is
mostly positivewhat does this mean?0
+90
180
-90
——
++
Axis
QRS AXISlead I
leftward axislead II
downward axisfrom this we can see that a
normal QRS axis lies somewhere in between 0 and +90 degrees
remember that infarction will cause the axis to shift rightward
(>+90) and that hypertrophy will shift the axis upward
(between 0 and -90)
0
+90
180
-90
——
++
++
Axis
The Anatomy of the Heart
The Blood Supply to the Heart• Coronary circulation meets heavy demands
of myocardium for oxygen, nutrients• Coronary arteries (right, left) branch from
aorta base• Anastomoses (arterial interconnections)
ensure constant blood supply• Drainage is to right atrium
• Great, middle cardiac veins drain capillaries• Empty into coronary sinus
• Arteries include the right and left coronary arteries, marginal arteries, anterior and posterior interventricular arteries, and the circumflex artery
• Veins include the great cardiac vein, anterior and posterior cardiac veins, the middle cardiac vein, and the small cardiac vein
Blood Supply to the Heart
SA node activity and atrial activation begin.
Stimulus spreads across the atrial surfaces and reaches the AV node.
There is a 100-msec delay at the AV node. Atrial contraction begins.
The impulse travels along the interventricular septum within the AV bundle and the bundle branches to the Purkinje fibers.
The impulse is distributed by Purkinje fibers and relayed throughout the ventricular myocardium. Atrial contraction is completed, and ventricular contraction begins.
Time = 0
SA node
AV node
Elapsed time = 50 msec
Elapsed time = 150 msec
AV bundle
Bundle branches
Elapsed time = 175 msec
Elapsed time = 225 msec Purkinje fibers
Coronary Circulation
Coronary Circulation
Coronary Circulation
Figure 20.9a, b
Coronary Circulation
Figure 20.9c, d
HOLTER MONITOR
Technology• 5 electrodes• 2-3 leads• Derived 12 lead available• Digital or analog recording• Digital transmission to analyzer• Requires removal of Holter monitor to
scan recording
Uses:• Patients experiencing daily symptoms• Precise quantification of arrhythmias
Positives:• 24-48 hours full disclosure available• Heart rate and AF burden graphs• Arrhythmia counts (ex., 10 PVCs per
hour)
HOLTER MONITOR