Heart Attack

OR
Myocardial Infarction
BY......... KHUSH
BS CARDIOLOGY
KHYBER MEDICAL UNIVERSITY
 Myocardial infarction
Myocardial infarction (MI), commonly known as a heart attack, occurs
when blood flow decreases or stops to a part of the heart, causing damage
to the heart muscle. These due to ischemia.Ischemia occurs when part of
the heart muscle, the myocardium, is deprived of oxygen and nutrients.
OR
Myocardial infarction (MI) (ie, heart attack) is the irreversible death
(necrosis) of heart muscle secondary to prolonged lack of oxygen supply
(ischemia). Approximately 1.5 million cases of MI occur annually in the
United States.
Diagram showing the blood
supply to the heart by the two
major blood vessels, the left and
right coronary arteries (labelled
LCA and RCA). A myocardial
infarction (2) has occurred with
blockage of a branch of the left
coronary artery (1).
 Common causes of ischemia are:
I. Narrowing or obstruction of a coronary artery.
II. A rapid arrhythmia, causing an imbalance in supply and demand for energy.
III. A short period of ischemia causes reversible effects: The heart cells will be able to
recover. When the episode of ischemia lasts for a longer period of time, heart
muscle cells die. This is called a heart attack or myocardial infarction. That is
why it is critical to recognize ischemia on the ECG in an early stage.
IV. Severe ischemia results in ECG changes within minutes. While the ischemia
lasts, several ECG changes will occur and disappear again. Therefore, it may be
difficult to estimate the duration of the ischemia on the ECG, which is crucial for
adequate treatment.
 Signs and symptoms of myocardial ischemia:
I. Crushing pain on the chest (angina pectoris), behind the sternum,
often radiating to the lower jaw or the left arm
II. Fear of dying
III. Nausea
IV. Shock (manifesting as paleness, low blood pressure, fast weak pulse)
shock
V. Rhythm disturbances (in particular, increasing prevalence of
ventricular ectopia, ventricular tachycardia, AV block)
 Risk assessment of Cardiovascular disease
Narrowing of the coronary artery, leading to a myocardial infarction, usually develops
over several years. An increased risk of cardiovascular disease, which may lead to a
myocardial infarction or cerebrovascular accident, can be estimated using SCORE
system which is developed by the European Society of cardiology (ESC). As shown in the
figure, the most important risk factors for myocardial infarction are:
I. Male sex
II. Smoking
III. Hypertension
IV. Diabetes Mellitus
V. Hypercholesterolemia
 Diagnosis of myocardial infarction
The diagnosis of acute myocardial infarction is not only based on the ECG. A
myocardial infarction is defined as:
Elevated blood levels of cardiac enzymes (CKMB or Troponin T) AND
One of the following criteria are met:
The ECG shows ST elevation or depression.
pathological Q waves develop on the ECG.
So detection of elevated serum cardiac enzymes is more important than ECG
changes. However, the cardiac enzymes can only be detected in the serum 5-7 hours
after the onset of the myocardial infarction. So, especially in the first few hours after
the myocardial infarction, the ECG can be crucial.
 CONTUN.....
Creatine kinase:
Creatine kinase (CK)also known as creatine phosphokinase (CPK) or phospho-
creatine kinaseis an enzyme expressed by various tissues and cell types. CK
catalyses the conversion of creatine and utilizes adenosine triphosphate (ATP) to
create phosphocreatine (PCr) and adenosine diphosphate (ADP). This CK enzyme
reaction is reversible and thus ATP can be generated from PCr and ADP.
Troponin:
Troponin, or the troponin complex, is a complex of three regulatory proteins
(troponin C, troponin I, and troponin T) that is integral to muscle contraction in
skeletal muscle and cardiac muscle, but not smooth muscle .
 Coronary Arteries
The heart is supplied of oxygen and
nutrients by the right and left coronary
arteries. The left coronary artery (the Left
Main or LM) divides itself in the left
anterior descending artery (LAD) and the
ramus circumflexus (RCX). The right
coronary artery (RCA) connects to the
ramus descendens posterior (RDP). With
20% of the normal population the RDP is
supplied by the RCX. This called left
dominance.
 ECG Manifestations of Acute Myocardial Ischaemia
ST elevation:
New ST elevation at the J-point in two contiguous leads with the cut-off points: 0.2 mV in men or
0.15 mV in women in leads V2V3 and/or 0.1 mV in other leads.
ST depression and T-wave changes:
New horizontal or down-sloping ST depression >0.05 mV in two contiguous leads; and/or T
inversion 0.1 mVin two contiguous leads with prominent R-wave or R/S ratio 1
A study using MRI to diagnose myocardial infarction has shown that more emphasis on ST
segment depression could greatly improve the yield of the ECG in the diagnosis of myocardial
infarction (sensitivity increase from 50% to 84%).
Myocardial infarction diagnosis in left or right bundle branch block can be difficultMI diagnosis in
left bundle branch block or paced rhytm.
MI Diagnosis in RBBB.
ST elevation is
measured at the
junctional or J-
point
 The location of the infarct
Myocardial infarction (STEMI) occurs in two distinct arterial territories .The
anterior LAD circulation and postero- inferior RCA/LCX circulation.
An anterior wall myocardial infarction also known as anterior wall
MI, or AWMI, or anterior ST segment elevation MI, or anterior STEMI
occurs when anterior myocardial tissue usually supplied by the left anterior
descending coronary artery 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 myocardial infarction
wall include:
I. ST segment elevation in the anterior
leads (V3 and V4) at the J point and
sometimes in the septal or lateral leads,
depending on the extent of the MI. This
ST segment elevation is concave
downward and frequently overwhelms
the T wave. This is called tombstoning
for obvious reasons; the shape is similar
to that of a tombstone.
II. Reciprocal ST segment depression in the
inferior leads (II, III and aVF).
Posterior Wall Myocardial Infarction
The ECG findings of a posterior wall myocardial infarction are different than the
typical ST segment elevation seen in other myocardial infarctions. A posterior wall MI
occurs when posterior myocardial tissue (now termed inferobasilar), usually supplied
by the posterior descending artery a branch of the right coronary artery in 80%
of individuals acutely loses blood supply due to intracoronary thrombosis in that
vessel. This frequently coincides with an inferior wall MI due to the shared blood
supply.
 The ECG findings of an acute posterior wall MI include:
I. ST segment depression (not elevation) in the septal and anterior precordial leads
(V1-V4). This occurs because these ECG leads will see the MI backwards; the leads
are placed anteriorly, but the myocardial injury is posterior.
II. A R/S wave ratio greater than 1 in leads V1 or V2.
III. ST elevation in the posterior leads of a posterior ECG (leads V7-V9). Suspicion for
a posterior MI must remain high, especially if inferior ST segment elevation is
also present.
IV. ST segment elevation in the inferior leads (II, III and aVF) if an inferior MI is also
present.
An infarction of the inferior wall
will result in ST segment
elevation in leads II, III and AVF.
A lateral wall infarct results in
ST segment elevation in leads I
and AVL. An Anterior wall
infarct results in ST segment
elevation in the precordial leads.
The ST segment elevation points at the infarct location. Inferior MI=ST segment elevation in red
regions (lead II,III and AVF). Lateral MI = ST elevation in blue leads (lead I, AVL, V5-V6).
Anterio MI: ST segment elevation in yellow region (V1-V4). Left main stenosis: ST elevation in
gray area (AVR)
TANKO
F***o