ECG EXAMINATION

Seminary of pathophysiology

Pavel Maruna
Electrical conduction in heart

SA node
(= pacemaker)

AV node

Bundle of His

Right and left

bundle branches

Purkynje fibres
 Cellular depolarization
• What do we measure?
• What is positive and negative vector?
 12-lead ECG examination

Limb leads

aVL
aVR

Bipolar leads
I, II, III

Pseudounipolar leads aVF

aVR, aVL, aVF
 12-lead ECG examination

Chest leads
Unipolar leads
12-lead ECG examination
 QRS axis
(Axis of QRS complex depolarization)

- 30° to + 105°
initiation of impulse in the SA
node
initiation of impulse in the SA
node

atrial depolarization
initiation of impulse in the SA
node

atrial depolarization

depolarization of AV
nodus and bundle of His
septal depolarization
septal depolarization

early ventricular
depolarization
septal depolarization

early ventricular
depolarization

late ventricular
depolarization
ventricular systole
ventricular systole

ventricular repolarization
ventricular systole

ventricular repolarization

repolarization of bundle
of His
PR (PQ) interval QTc interval
(0,12 - 0,20 s) (to 0,44 s)
QRS complex
(0,06 - 0,10 s)
 What to see on the curve?
• Rhythm?
• P wave
• Intervals
• QRS complex
• ST segment
• T wave (U wave)
 P wave

Electrical impulse originates in the SA node

Impulse triggers atrial depolarization

Physiology:
• positive orientation (possible biphasic in I lead)
• duration < 0,11 s, amplitude < 2,5 mm

Pathology:
• hypertrophy of left or right atrium
• abnormal conduction (SVES)
 P wave
P mitrale

High P amplitude due to left

atrial hypertrophy
 PR (PQ) interval

depolarization of AV node and bundle of

His

It represents the physiological delay in conduction from

atrial depolarization to the beginning of ventricular
depolarization. It is electrically neutral.
Limits: 0,12 - 0,20 s

Physiological importance:
1. synchronization of both atrial and ventric. systoles
2. protection against the transmission of supraventricular
tachyarrhythmia to vetricular tachycardia
 PR (PQ) interval
AV blockade
1st = prolongation of PR interval

2nd = partial blockade (transmission of selected

impulses)
- Wenckenbach

- Mobitz
 PR (PQ) interval
AV blockade

3rd = complete blockade

 QRS complex

Depolarization of the ventricles

Physiology:
• duration 0,06 - 0,10 s
• Q < 0,04 s, < 25 % of R wave
• Sokolow index (S in V2 + R in V5) < 35 mm (< 45 mm for
young)
• axis of ventricular depolarization -30 to +105 °
 QRS complex

Physiology:
• duration 0,06 - 0,10 s
• Q < 0,04 s, < 25 % of R wave
• Sokolow index (SV2 + RV5) < 35 mm (< 45 mm for young)
• axis of ventricular depolarization -30 to +105 °
• VAT (ventricular activation time) of LV < 0,04 s, RV < 0,03 s
 QRS complex
Both QRS complex duration and shape is depend on:
1. Physiology of His-Purkine´s system or aberrant signal
passing

VES
 QRS complex
Both QRS complex duration and shape is depend on:
1. Physiology of His-Purkine´s system or aberrant signal
passing

Intraventricular
blockades

RBBB ......................
(QRS prolongation, rSR´ in V1, negative T wave)

V1
RBBB
 QRS complex
Both QRS complex duration and shape depend on:
2. Myocardial mass

LV hypertrophy

RV hypertrophy

cardiomyopathy
 QRS complex
wide QRS
complex
Both QRS complex duration and shape is depend on: high sharp
T wave
3. Factors affecting signal velocity - metabolic, endocrine,
and pharmacological

hyperkalemia
 QRS complex
Both QRS complex duration and shape is depend on:
3. Factors affecting signal velocity - metabolic, endocrine,
and pharmacological

digitalis
 QRS complex
Prolongation Shortening

diffuse alteration
LV, RV hypertrophy
(amyloid, fibrosis)

hyperkalemia, digoxin artificial factors

(obesity, pericard. effusion)

intraventricular blockade
VES
 QRS complex
Pathological Q wave
Q wave prolongation (> 0,04 s) and depression (> 25 % R)
Manifestation of transmural myocardial necrosis
„Cavity potential“
Patological Q
 ST segment
The length between the end of the S
wave (end of ventricular depolarization)
and the beginning of repolarization

• From „J point“ on the end of QRS complex, to inclination

of T wave
• Normally, all cells have the same potential = ST segment is
electrically neutral (on isolectric line)
 ST segment
Physiological changes
sympathicus ... ST depression, „anchor-like“ curve
parasympathicus (vagus) ... ST elevation
syndrome of an early repolarization

Artificial changes
depend on lead localization, chest malformation etc.

Patological changes
electric potential of destroyed myocardial area
 ST segment
Ischemic focus has a different electric potential
= electric vector leads to this area

1. subendocardial ischemia
(non-Q MI, AP paroxysm)
... ST depresssion
 ST segment
Ischemic focus has a different electric potential
= electric vector leads to this area

2. subepicardial ischemia
(Q-MI, spastic form of AP, aneurysma)
... elevation of ST segment
 T wave
Ventricular repolarization

Normally: a repolarization directs from epicardium to

endocardium = T wave is concordant with QRS complex
Ischemic area: a repolarization is delayed, an action potential is
extended

Vector of repolarization is directed from ischemic area:

- subendocardial ischemia ... to epicardium ... T wave elevation
- subepicardial ischemia ... to endocardium ... T wave inversion
 T wave
•LV overload Nonspecific changes
•neurocirculatory asthenia
•sympathetic system
•hypokalemie Diffuse T changes,
T wave
•hyperglycemia asymmetric
•myxoedema or biphasic

•pancreatitis
•pneumotorax
 T wave
Ischemia Nonspecific changes

Diffuse T changes,
Localized T changes
T wave
T wave - symmetric
asymmetric
negativity
or biphasic
K+ influence on cardiac conductivity
 Refractory period
1. Absolute = Absolutely no stimulation
can cause another action potential
2. Relative = It is possible to cause
another action potential, but the intensity
of the premature contraction will be
relative to the time in this period.
„R on T“ phenomena
„Malignant VES“: R wave of the next beat falls in
certain portions of the previous T-wave
... Serious and life-threatening arrhythmia
 Holter monitoring
24-h ECG recording
Ambulatory ECG device
Analysis of mean, maximal, and minimal HR,
occurrence and frequency of major arrhythmia
Confrontation of record and subjective
difficulties (patient activity log)

Indications:
1. syncope or palpitation of unclear origin
2. an unveiling of latent ischemia
3. an antiarrythmic therapy control
4. a pacemaker control
 Holter monitoring

Patient No. 1
Finding of atrial fibrillation.
Pauses > 2 s
Rare ventricular ES
 Holter monitoring

Patient No. 2
Ventricular fibrillation
 Holter monitoring

Patient No. 3
Ventricular
tachycardia
 Ergometry, exercise ECG
Gradual load increase in 4-min. intervals, basic level 25 -
75 W
Stopping - submaximal load or complications (accelerated
hypertension, polytopic VES, blockades, ST elevation ST,
ST depression > 2 mm, T inversion
Coincidence of chest pain + ST changes
= confirmation of ischemia

Indications:
1. specification of ischem. disease prognosis
2. suspicion on ischemic disease
3. examination of functional capacity
Q myocardial infarction
ECG changes

Martin Vokurka
 Acute anterior myocardial infarction
ST elevation in the anterior leads V1 - 6, I and aVL
reciprocal ST depression in the inferior leads
 Acute inferior myocardial infarction
ST elevation in the inferior leads II, III and aVF
reciprocal ST depression in the anterior leads
RBBB and bradycardia are also present
 Old inferior myocardial infarction
Q wave in lead III wider than 1 mm (1 small square) and
Q wave in lead aVF wider than 0.5 mm and
Q wave of any size in lead II
 Old inferior MI (note largest Q in lead III, next
largest in aVF, and smallest in lead II)
Inferior MI
Pathologic Q waves and evolving ST-T changes in leads
II, III, aVF

Q waves usually largest in lead III, next largest in lead

aVF, and smallest in lead II

Example: frontal plane leads with fully evolved inferior

MI (note Q-waves, residual ST elevation, and T
inversion in II, III, aVF)
Anteroseptal MI
Acute anterior or anterolateral MI (note Q's
Q, QS, or qrS complexes in leads V1-V3 (V4)
V2-6 plus hyperacute ST-T changes)
Evolving ST-T changes

Example: Fully evolved anteroseptal MI

(note QS waves in V1-2, qrS complex in V3,
plus ST-T wave changes)
 | | |
chronické organ. změny srdce

prodloužení vedení zpomalení vzruchu

arytmogenní substrát

nehomogenní nehomogenní repolarizace

depolarizace

dg.: disperze QT intervalu

alternans T vlny

reverzibilní vegetativní
ischemie dysbalance
dg.: pozdní potenciály
dg.: senz. baroreflexu, variabilita fr.

maligní arytmie
(nejčastěji komor.| re-entry)

náhlá smrt
častější u mužů, etiol. kardiální 30% (ve stáří 80-90%), z kardiálních příčin: 80% tachyarytmie
Nové metody predikce kardiální náhlé smrti (predikce arytmogeneze):
disperze QT intervalu
alternans T vlny spontánní variabilita voltáže T vlny
pozdní potenciály v závěru QRS a během ST
senzibilita baroreflexu index f/TK po farmakol.stimulaci nebo spontánně
variabilita frekvence periodicita respirační, baroreflexní, termoregulační atd.,
oplošťuje se s věkem, sympatikotomií
(její snížení tedy odráží vyšší riziko maligních dysrytmií)
Atrial extrasystole Compensatory pauses
Ventricular extrasystole
Atrial flutter Atrial fibrillation
SV tachycardia
Ventricular tachycardia
Ventricular fibrilation (or flutter)
Acute situation, hemodynamic arrest –
0 cardiac output, 0 pulsation, coma,
resuscitation
AV block 2rd degree
 AV block 3rd degree

Preexcitation,
WPW syndrome
Bundle branch blocks

LBBB RBBB
Left anterior fascicular block