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Pembesaran Atrium Jantung

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2. Pembesaran Ventrikel Jantung

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• Right ventricular hypertrophy (RVH) occurs when the right
ventricular wall thickens due to chronic pressure overload.

• ECG : R-S ratio of > 1 in lead V1 in the absence of other causes

or if the R wave in lead V1 is > 7 mm tall.

• The strain pattern occurs when the right ventricular wall is quite
thick and the pressure is high as well.

• Strain causes ST segment depression and asymmetric T wave

inversions in leads V1 - V3.

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Pembesaran ventrikel kanan akan
menggeser aksis jantung ke kanan

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Contoh RVH-strain
Indikasi kematian sel miokard
irreversibel
 Diagnosis infark miokard
Otot jantung mati  arus listrik mati daerah infark mati
 seluruh arus listrik jantung akan menjauhi area
infark  defleksi negatif yg dalam  gelb Q
• Melibatkan permukaan posterior.
• Oklusi a. koroner dekstra.
• Dx dibuat dgn melihat
perubahan resiprok lead
anterior, khususnya V1.
• Melibatkan permukaan
anterior ventrikel kiri.
• Oklusi a. anterior sinistra
desenden.
• Tjd perubahan lead
precordial (V1-V6)
• Melibatkan permukaan
dinding lateral.
• Oklusi a. sirkumfleksi sinistra.
• Perubahan terjadi pd lead
lateral kiri I, aVL, V5 dan V6.
• Melibatkan permukaan
diafragmatik jantung.
• Oklusi a. koroner
dekstra atau cabang
desendennya.
• Perubahan pada lead
inferior II, III, aVF
• Occurs when the left anterior descending coronary artery (LAD) suffers injury
due to lack of blood supply.
• When an AWMI extends to the septal and lateral regions as well, the culprit
lesion is usually more proximal in the LAD or even in the left main coronary
artery. This large anterior myocardial infarction is termed an "extensive
anterior".

• The ECG findings of an acute anterior wall myocardial infarction include:

• 1. ST segment elevation in the anterior leads (V3 and V4) and sometimes in
septal and lateral leads depending on the extent of the myocardial
infarction. This ST elevation is concave downward and frequently overwhelms
the T wave. This is called "tombstoning" due to the similarity to the shape of
a tombstone.
• 2. Reciprocal ST segment depression in the inferior leads (II, III and aVF).
Note: To distinctly say that an old anterior wall myocardial infarction is present on
the ECG, there must be no identifiable R wave in lead V1 and usually V2 as well. If
there is an R wave in V1 or V2, the term poor R wave progression can be used, but
not an old anterior wall myocardial infarction.
• Occurs when the right coronary artery (RCA), is injured due to
thrombosis.
• When an inferior myocardial infarction extends to posterior regions
as well, an associated posterior wall myocardial infarction may occur.
• The ECG findings:
1. ST segment elevation in the inferior leads (II, III, and aVF).
2. Reciprocal ST segment depression in the lateral and/or high lateral
leads (I, aVL, V5 and V6).

• Note: If the reciprocal ST depressions are not present, consider

alternative causes of ST segment elevation such as pericarditis.
• Inferior myocardial infarctions have multiple potential complications
and can be fatal.
The ECG findings:
1. ST segment elevation in the inferior leads (II, III, and aVF).
2. Reciprocal ST segment depression in the lateral and/or high
lateral leads (I, aVL, V5 and V6).
• Occurs when posterior myocardial (inferobasilar) tissue, usually supplied
by the posterior descending artery (a branch of the right coronary artery
in 80% of individuals), acutely loses blood supply.
• This frequently coincides with an inferior wall myocardial infarction.
• The ECG findings:
1. ST segment depression (not elevation) in the septal and anterior
precordial leads (V1 to V4). This occurs since these ECG leads will see
the MI backwards (since the leads are placed anteriorly, but the
myocardial injury is posterior).
2. The ratio of the R wave to the S wave in leads V1 or V2 is > 1.
3. ST elevation in the posterior leads of a posterior ECG (leads V7 to V9).
4. ST elevation in the inferior leads (II, III, and aVF) may be seen if an
inferior MI is also present.
Joan, 62 year old business executive. Early morning in hotel when she goes to business trip,
she is awakened with shortness of breath and severe chest pressure that radiates into her
jaw and left arm. Feeling somewhat dizzy and nauseated, she sits down and phones doctor,
who immediately orders ambulance to take her to the local emergency room. She arrives
there only 2 hours after the onset of her symptoms, which haved continued unabated despite
3 sublingual NTG tablet given in ambulance. A 12 lead EKG reveals:
The EKG shows ST segment elevation in leads V2-V5,
there are no Q waves.
Joan is in the throes of an Acute Myocardial Infarction.
Joan is an excellent candidate for either thrombolytic therapy or acute coronary
angioplasty. Unfortunately, she relates that only 1 month ago she suffered a mild
hemorrhagic stroke, leaving her with some weakness in her left arm and leg, and making
the risks of thrombolytic therapy prohibitive. In addition, acute angioplasty is not
available at this small community hospital, and the nearest large medical center is
several hours away. Joan admitted to ICCU and she is given morphine, i.v NTG, i.v beta
blocker, and aspirin also. Anticoagulant agents are withheld.
Late on the first night of her hospital stay, one of the nurses notices peculiar beats on her
EKG:

There is a run of three consecutive PVCs. In the setting of an acute

infarction, antiarrhythmic therapy is often given immediately because
these PVCs can trigger ventricular tachycardia and fibrillation.
The next morning, Joan’s EKG looks like this: What has
changed?

All ventricular ectopy has been suppressed. It also shows new Q waves in
the anterior leads, consistent with full evolution of an anterior infarct.
Later in the afternoon, joan begins to experience chest pain. A repeat EKG is taken.
What has changed?

Joan is extending her infarct. New ST elevation can be seen in the left lateral leads.
A few hours later she complains of light-headedness, and another EKG is performed:
Now what do you see?

Joan has gone into third-degree AV block. Serious conduction blocks are commonly seen in
anterior infarctions. Her ligh-headedness is due to inadequate cardiac output the face of a
ventricular escape rhythm of approximately 35 beats per minute. Pacemaker insertion is
mandatory
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