LEFT BUNDLE BRANCH BLOCK, RIGHT BUNDLE

BRANCH BLOCK, POLYSEROSITIS

Diajukan Untuk Memenuhi Syarat Kepaniteraan Klinik Senior
SMF ILMU KESEHATAN ANAK
RSUD CIAMIS JAWA BARAT

Pembimbing :
dr. Hj. Suherjati Setiyadi, Sp. A

Disusun Oleh :
Ania Mutmainah 10310045
Mochamad Basri 10310241

KEPANITERAAN KLINIK SENIOR SMF ILMU KESEHATAN ANAK

RSUD CIAMIS JAWA BARAT
FAKULTAS KEDOKTERAN UNIVERSITAS MALAHAYATI
BANDAR LAMPUNG

Left Bundle Branch Block (LBBB) ECG

The ECG criteria for a left bundle branch block (LBBB) include:
1. QRS duration of > 120 milliseconds.
2. Absence of Q wave in leads I, V5, and V6.
3. Monomorphic R wave in I, V5, and V6.
4. ST and T wave displacement opposite to the major deflection of the QRS complex.
A simple way to diagnose a left bundle branch in an ECG with a widened QRS complex (>
120 ms) would be to look at lead V1. If the QRS complex is widened and downwardly
deflected in lead V1, a left bundle branch block is present. If the QRS complex is widened
and upward deflected in lead V1, then a right bundle branch block is present. Below shows
the typical findings of a left bundle branch block in the precordial ECG leads:

Note: If the QRS duration is between 100-119 milliseconds with criteria 2, 3, and 4 of the
above, an incomplete left bundle branch block is present.
A rate dependent left bundle branch block can occur at times of fast heart rates. This may be
caused by myocardial ischemia or refractoriness of the left bundle at faster heart rates. A rate
dependent left bundle branch block, when occurring at heart rates greater than 100 beats per
minute, can at times be difficult to distinguish from ventricular tachycardia since both cause a
wide complex QRS complex. The Brugada Criteria for diagnosing ventricular tachycardia is

helpful to make this distinction. The below ECG strip shows normal sinus rhythm, then atrial
fibrillation with a rapid ventricular response develops. With the faster heart rate the QRS
complex morphology changes to that of a left bundle branch block. As sinus rhythm restores
and the ventricular rate slows, the QRS morphology returns to normal.

Sgarbossa Criteria
The Sgarbossa criteria is used in the diagnosis of an acute myocardial infarction when a left
bundle branch block is present.
The Sgarbossa criteria is used in the diagnosis of an acute myocardial infarction when a left
bundle branch block is present.
Traditionally it has been taught that myocardial infarction is not able to be diagnosed via
ECG in the presence of a left bundle branch block (LBBB), however Sgarbossa et al in 1996
described some ECG changes seen in those with LBBB and concomitant myocardial
infarctions and devised a point scoring system. This is called the Sgarbossa criteria.
1) ST elevation > 1 mm and in the same direction (concordant) with the QRS complex. 5
points
2) ST depression > 1 mm in leads V1, V2, or V3. 3 points
3) ST elevation > 5 mm and in the opposite direction (discordant) with the QRS. 2 points
A score of 3 points is required to diagnose an acute myocardial infarction. Criteria #3 is under
debate as to its usefulness, so basically you need to have either criteria 1 or criteria 2. Our
patient just made 1 mm ST elevation in lead V5 and about 0.5 mm ST elevation in V6. This
ECG was indeed from a patient with an acute left anterior descending thrombosis.

Note: The Cabrera's sign and Chapmans sign have been used to diagnose acute myocardial
infarction in the setting of a left bundle branch block as well. Also, examining the T wave in
leads V5-V6 can be helpful. In the Sgarbossa study there was a 26% sensitivity to detect
acute MI when the T wave was upright instead of inverted (see image above).

Right Bundle Branch Block ECG

The ECG criteria for a right bundle branch block include:
1.

QRS duration of > 120 milliseconds

2.

rsR' "bunny ear" pattern in the anterior precordial leads (leads V1-V3)

3.

Slurred S waves in leads I, aVL and frequently V5 and V6.

Remember that T wave inversions and ST segment depression is normal in leads V1 - V3 in

the presence of a RBBB, thus technically myocardial ischemia can not be easily determined
in these leads. However, unlike in the presence of a left bundle branch block, myocardial
ischemia and infarction can easily be detected on ECG when a RBBB is present. Below is a
RBBB with an anterior ST elevation MI followed by some other examples:

Anterior Wall ST elevation MI with RBBB (Example 1)

Anterior Wall ST elevation MI with RBBB (Example 2)

Inferior Wall MI with RBBB (Example 1)

Inferior Wall MI with RBBB (Example 2)

Some variations of right bundle branch blocks can occur. There are times where a QRS
complex may appear in a right bundle branch block pattern intermittently such as premature
ventricular contractions that arise from the left ventricle (takes time to travel to the right
ventricle and thus has a RBBB QRS morphology) or in the setting of an "Ashman beat"
which is a premature atrial contraction or supraventricular beat that occurred when the right
bundle was refractory. This causes the beat to conduct with a RBBB pattern. An example is
below:

There is not always a typical "bunny-ear" pattern present in a RBBB since the R or the R'
may be very small. Thus, do not rely on identifying the "bunny-ear" pattern to diagnose a
RBBB. Below is an example of a QRS complex with a RBBB pattern, but without the typical
rsR' pattern:

Also, a "rate dependent" right bundle branch block can occur during times of fast heart rate.
When the heart rate slows, then the narrow QRS complex returns. A rate dependent right
budnel branch block can be mistaken at times for ventricular tachycardia. Using the Brugada
Criteria as discussed below can help distinguish these two entities.
Lastly, ventricular tachycardia itself can sometimes have a right bundle branch block pattern
if it arises from the left ventricle. If there is tachycardia present (heart rate > 100
beats/minute) in a right bundle branch block pattern, then ventricular tachycardia should be
considered. The QRS morphology criteria to diagnose ventricular tachycardia with a RBBB
include:

A monophasic R or biphasic qR complex in V1.

If an RSR pattern (bunny-ear) is present in V1 or V2 with the R peak being higher

in amplitude than the R peak, then VT is present (see image below).

A rS complex in lead V6 favors VT

Polyserositis

Definition is inflammation of the serous membranes simultaneously several cavities (pleura,

pericardium, peritoneum, sometimes joints). Polyserositis most commonly found in
tuberculosis and rheumatism, sometimes with systemic lupus erythematosus, sepsis,
pneumonia, uremia.
The clinical course of the disease may be acute (in exudative polyserositis) and chronic (with
adhesive polyserositis).

Polyserositis (Polyserositis) inflammation of the serous membranes lining the large body
cavity (pleura, pericardium, peritoneum, sometimes joints).
Found, in particular, panserozit (panserositis) simultaneous inflammation of serous
membranes of all cavities. Polyserositis is a manifestation or complication of another
disease. The most common AP tuberculosis and rheumatic origin. More rarely it occurs in
sepsis, pneumonia, typhoid fever, systemic lupus erythematosus, visceral syphilis. P. also
exhibit at azotemicheskoy uremia, scurvy. Described polyserositis unexplained so called
periodic disease, family repetitive P. Major role in the occurrence of P. is serous membranes
hyperergic reaction to infection or toxic exposure, which causes an increase in vascular
permeability and inflammation in serous cavities. Poliserozita are exudative and adhesive. In
the first case dominated exudative inflammation. Serous fluid in the cavity can be serous,
sero-fibrinous, hemorrhagic, or purulent. When adhesive P. dominated productiveproliferative processes in the form of proliferation of connective tissue, which leads to
shrinkage of the serous membranes.
The clinical course of the disease may be acute (in exudative AP) and chronic (with adhesive
PP). In most cases, adhesive PP are the result of exudative process. The clinical picture
depends on the PA primary disease. For acute P. characterized by pain in the chest, the heart
or the stomach, raising the temperature to 38-40 , the gradual accumulation of fluid in the
cavities.

When a bit of fluid in the cavities, then it is possible to listen to the pleural rub, pericardium
or peritoneum. When a cluster of significant amounts of fluid phenomena develop
compression relevant authorities (see pericarditis, peritonitis, pleurisy). Duration exudative
poliserozita from several weeks to several months. After the liquidation of exudative
process are more or less extensive adhesions or process becomes chronic adhesive
polyserositis.
The clinical picture of periodic disease (see) is dominated by symptoms of acute peritonitis,
usually disappear within a day. The intervals between the attacks from several days to
several months. With a very serious events occurs described MN Akhutin acute infectious
diplostreptokokkovy AP observed in young people in the Far East and ends, usually death.
Adhesive polyserositis characterized by a gradual increase in adhesions and wrinkling of the
peritoneum, pleura, pericardium. These processes lead to a violation of the motor function of
the intestine to the partial or complete obstruction, cirrhosis of the liver, chest wall deformity,
shift of the mediastinum, swelling of the neck veins, heart failure, development of a large
ascites.
Poliserozita diagnosis is based on clinical symptoms of pleurisy, pericarditis, or peritonitis,
and typical radiographic changes. The differential diagnosis of symptoms should be guided
by the underlying disease. Laboratory tests (blood tests, punctate) help establish the etiology.
Prognosis for life is dependent on the underlying disease, and the chronic form on the
extent of adhesions and the dysfunction of the relevant authorities. Treatment of the
underlying disease in the first place, as a rule, complex. Nonspecific infectious poliserozita
prescribe broad spectrum antibiotics with the sensitivity of the isolated cultures to antibiotics.
When P. tubercular etiology on combined specific treatment streptomycin (1 g per day),
Pasco

(12

g),

ftivazid

(1.5

g).

When

polyserositis

rheumatic

etiology

antirheumatic treatment (Salicylates, antibiotics).

GP with symptoms that accompany tuberculosis, rheumatic fever, lupus erythematosus,
effective use of ACTH and 60 units, 50-75 mg of cortisone, prednisolone or prednisone 20
mg daily, reduces allergic and exudative processes. Displaying restorative treatment
(vitamins, diet, etc.). With a significant accumulation of fluid in the serous cavities
puncture.
Periodic disease treatment (aspirin, gistoglobin, nivahin) is ineffective. When conservative
cohesion P. treatment the same, but it gives a less pronounced effect. With significant
adhesions and dysfunction of surgical treatment (eg, perikardektomiya).