ECG IN CHAMBER

ENLARGEMENTS

ATRIAL ENLARGEMENTS

Can be caused by:

volume-overload (e.g. mitral/tricuspid valve
insufficiency)
pressure overload (e.g. mitral/tricuspid valve
stenosis)

RIGHT ATRIAL ENLARGEMENT

(RAE)

Etiology: stenosis/ insufficiency of the tricuspid valve;

increased pressure in RV; RV failure.
Atrial depolarization: the RA has a larger mass,
determines a larger depolarization vector, and the
resultant atrial vector is moved downwards
(verticalized) or even towards right. The depolarization
time of RA is increased, but usually it doesnt increase
the total atrial depolarization time (because the left
atrium starts to activate later).

RIGHT ATRIAL ENLARGEMENT

(RAE)
On ECG: normal duration of P wave.
In frontal plane:
Tall P wave in inferior leads (DII, aVF, DIII), with
amplitude > 2.5 mm in at least one of these 3 leads;
this aspect = P pulmonale
P wave axis is deviated downward (around +90).
(Sometimes it is even deviated towards right).
In horizontal plane:
In V1 and/or V2 the first component of the P wave, the
positive one, is taller; it is significant for diagnosis is P
wave is taller than 2 mm in V1 or V2.

LEFT ATRIAL ENLARGEMENT

(LAE)

Etiology: stenosis (e.g. post-rheumatic), regurgitation of

the mitral valve; increased pressure in LV; LV failure.

Atrial depolarization:
Normal RA depolarization.
LAE generates a larger vector => the global
depolarization vector is more horizontal than normal
(the electrical axis of atrial depolarization is deviated
towards left); also it needs more time for depolarization
and because the LA begins its depolarization after the
right atrium this determines a longer global atrial
depolarization time.

LEFT ATRIAL ENLARGEMENT

(LAE)

On ECG: A larger duration of P wave: P wave 0.12

In frontal plane:
P wave is positive and bifid in DI, aVL, DII. This aspect
and the P wave duration 0.12 = P mitrale
P wave axis is oriented towards 0.
In horizontal plane:
In V1 and/or V2 the second part of the biphasic P wave,
the negative one, is larger than the first positive one; it is
significant for diagnosis if the negative phase of the P
wave has a duration 0.04 and amplitude > 1mm.
In V5 and V6 it is a similar aspect with DI.

***In biatrial chamber enlargement the ECG will feature

characteristics of LAE in frontal plane and RAE in horizontal
plane.

VENTRICULAR ENLARGEMENTS

Can be caused by:

pressure overloads (e.g. aortic stenosis);
volume overloads usually dilations (eventually)
occurs (e.g. aortic regurgitation).
primary/secondary cardiomyopathies associated
either with hypertrophy, either with dilation.

LEFT VENTRICULAR ENLARGEMENT (LEFT

VENTRICULAR HYPERTROPHY = LVH)
Etiology: aortic stenosis/ insufficiency, mitral
regurgitation, high systemic arterial blood pressure.

Ventricular depolarization: The LV depolarization

vectors are larger than normal. Because there is more
LV mass, the depolarization time of the LV (and the
total ventricular depolarization time) can be increased.

Ventricular repolarization: can be also affected: if the

stimulus has a long way from subendocardial to
subepicardial cells, the subendocardial cells have the
opportunity to repolarize first so the repolarization
vector is inverted.

LEFT VENTRICULAR HYPERTROPHY =

LVH
On ECG: the most important criteria are the voltage
criteria;
Voltage criteria:
In frontal plane:
R in aVL > 13 mm
White-Block index = R in DI + S in DIII - (S in DI + R
in DIII) > +17 mm
In horizontal plane:
R in V5 or V6 > 25 mm
S in V1 or V2 > 25 mm
S in V1 + R in V5/V6 > 35 mm (Sokolov-Lyon index)

LEFT VENTRICULAR HYPERTROPHY =

LVH
Other criteria:
Left QRS axis deviation (usually around -30)
QRS duration 0.10 - 0.12 sec.
Delayed intrinsicoid deflection > 0.05 sec. in V5, V6
Secondary repolarization changes: depressed ST
segment (but with J point on isoelectric line) and
negative, asymmetrical T waves in left leads, where
the QRS complex is predominantly positive.
LA enlargement.

THE ROMHILT-ESTES POINT SCORE SYSTEM

("DIAGNOSTIC" >5 POINTS; "PROBABLE" 4 POINTS):
ECG Criteria
S in V1 or V2 25 (30)mm or R in V5 or V6 25
(30)mm

Points
3

ST-T vector opposite to QRS in V5, V6, D1, aVL

P mitrale

Left axis deviation (QRS of -30 or more)

QRS duration >0.10 sec

Delayed intrinsecoid deflection in V5 or V6 (>0.05

sec)

LEFT VENTRICULAR HYPERTROPHY

= LVH

LEFT VENTRICULAR HYPERTROPHY =

LVH
DD:
LBBB (left bundle branch block)
Left anterior fascicular block
Anterior MI
WPW syndrome type B
Left positional axis without cardiac pathologies
(horizontalised heart)

** In V1 the QRS aspect can be QS

REPOLARIZATION CHANGES:
In ventricular hypertrophies, intraventricular conduction
blocks, WPW syndrome secondary to the depolarization
abnormalities there can be present repolarization changes;
they are called secondary repolarization changes. Typically
secondary repolarization changes are: ST and T are opposed to
QRS (= where QRS complex is predominantly positive, ST is
depressed and T is negative); j point is isoelectric; the
depressed ST is descending; T wave is asymmetrical.
We name ECG primary repolarization changes those that
appear as a result as a primary repolarization abnormality :
ST depression or elevation, and T symmetrical negative or
positive (as it happens in ischemic heart disease: the earliest
affected are the repolarization processes).
Sometimes the patient has multiple cardiac modifications: e.g.
LVH and ischemic heart disease; and the changes of
repolarization are so-called mixed repolarization changes.

RIGHT VENTRICULAR ENLARGEMENT (RIGHT

VENTRICULAR HYPERTROPHY = RVH)

Etiology: pulmonary hypertension primary/secondary

(e.g. long-standing mitral stenosis with narrow
orifice); tricuspid regurgitation, stenosis of pulmonary
artery; congenital heart defects; cardiomyopathies.
Ventricular depolarization: larger RV vectors that
counterbalance the left normal ones; usually the
enlarged mass of RV is smaller than the normal mass
of left ventricle, so although the depolarization time
for RV is longer, the total ventricular depolarization
time is normal.
Ventricular repolarization can be affected secondary
to depolarization disturbances: secondary
modifications of ST-T.

RIGHT VENTRICULAR HYPERTROPHY =

RVH

Voltage criteria (can be present 1 criterion or more):

In frontal plane:
White-Block

index = R in DI + S in DIII - (S in DI + R in
DIII) < - 14 mm

Horizontal plane:
R

in V1 > 7 mm
R in V1 + S in V5 or V6 > 11 mm (Sokolov-Lyon index)
R/S ratio > 1 in V1 and/or V2
R/S ratio < 1 in V5 and/or V6

RIGHT VENTRICULAR HYPERTROPHY

= RVH

Other criteria: if there are present, they are additional

criteria for diagnosis; but their absence doesnt exclude
the LVH diagnosis based on voltage criteria!
Right QRS electrical axis deviation between 90and 150
TIDI 0.04 sec in V1 and/or V2
Secondary repolarization changes. (ST and T wave in
opposition to QRS complex).
P pulmonale

RIGHT VENTRICULAR HYPERTROPHY

= RVH

DD:
Left posterior fascicular block
Posterior wall MI
WPW syndrome type A

**Usually QRS duration is normal.

RIGHT VENTRICULAR HYPERTROPHY

= RVH

COR PULMONALE
= alteration in structure and function of the RV secondary to a respiratory
disease/affliction that determines an increase in the pressure in pulmonary
circulatory system.
Cor pulmonale can be acute (e.g. in pulmonary thromboembolism = PTE) or
chronic (e.g. in COPD).
In cor pulmonale some aspects of ECG can be suggestive, but arent highly
specific or sensitive:
S1Q3T3 pattern = deeper S wave in DI, q wave in DIII, negative T wave in
DIII (+/- ST segment slightly elevated in DIII) DD with inferior MI
T wave inversion (= negative T waves) in anterior precordial leads
RV overload, incomplete/complete RBBB, RA overload
Sinusal tachycardia; other arrhythmias.
Right/extreme right axis deviation for QRS electrical axis
S1S2S3 pattern = preeminent S waves in DI, DII, DIII
Other repolarization changes: nonspecific ST-T changes; ST elevation in DIII,
aVF, V1