2. DEFINITIONS
Myocardial infraction also know as heart attack when
disruption of blood supply occur to part of the heart
damaging heart muscles.
Heart muscle death
Blockage/ obstructions of coronary arteries by clot
formations
3. SYMPTOMS
Chest pain = typical radiate pain-
Pain radiate to back , neck vertebra , jaws, left hand and
five fingers
High intensity pain, severe pain under sternum
Squeezing or heaviness, shortness of breath
Nausea, vomiting, weakness, Diaphoresis, syncope
4. RISK FACTOR
Age (more than 45 yrs)
Smoking and alcohol and poor diet
High blood pressure
High cholesterol
Diabetes
Obesity
Stress
Lack of physical activity
5. PATHOPHYSIOLOGICAL
There is disruption of an atherosclerotic plaque in an
epicardial coronary artery, which leads to a clotting
cascade or occlusion of the artery.
Plaque rupture is believed to be triggering mechanism
for the development of clot , at the site that can occlude
blood flow resulting myocardial infractions
6.
7. Irreversible damage to the myocardium can begin as early as 20
to 40 minutes after interruption of blood flow.
The dynamic process of infarction may not be completed,
however, for several hours.
Necrosis of tissue appears to occur in a sequential fashion about
5-6 hours
Reimer and associates demonstrated that cellular death occurs
first in the subendocardial layer called Subendocardial infraction
and spreads like a “wavefront” throughout the thickness of the
wall of the heart called Transmural infraction.
8. a substantial amount of myocardial tissue can be salvaged if flow is
restored within 6 hours after the onset of coronary occlusion.
The cellular changes associated with an MI can be followed by:
= The development of infarct extension (new myocardial necrosis)
= Infarct expansion (a disproportionate thinning and dilation of the
infarct zone)
= Ventricular remodeling (a disproportionate thinning and dilation
of the ventricle).
10. INVESTIGATIONS/DIAGNOSIS
1st Test – ECG = ST Elevations
Blood test, Cardiac Marker (CKMB levels) {(+ve in MI) or
(-ve in case of angina)}
Cardiac Troponin
History
11. ECG
Very specific and a good test, particularly
helpful if positive:
– Should be done within 10 minutes of
arrival on anyone with suspected ACS
– Observation
ST elevation
- In the normal ECG, the ST segment should not be elevated
more than 1 mm in the standard leads or more than 2 mm in the
precordial leads. With an acute injury, the ST segments in the leads
facing the injured area are elevated. It occur due to premature
repolarization.
12. . Pathological Q wave
-They are the result of absence of electrical activity.
A myocardial infarction can be thought of as an electrical 'hole' as
scar tissue is electrically dead and therefore results in pathologic
Q waves. Pathologic Q waves are not an early sign of myocardial
infarction, but generally take several hours to days to develop.
Once pathologic Q waves have developed they rarely go away
15. Patients with MI describe as heaviness, squeezing, chocking or
smothering sensation.
Or sensations as someone were crush my chest.
Substernal pain can radiate to neck, left arm, back or jaws
Pain of MI is more often prolonged and unrelieved by rest or
sublingual nitroglycerin
Gastrointestinal complaints are related to severity of pain and
resulting vagal stimulations.
16. PHYSICAL EXAMINATIONS
Patients usually appear restless and in distress
and skin is warm and moist
Breathing may be labored and rapid, fine crackles or
rhonchi may be heard when auscultating the lung
When the patient placed in the left lateral decubitus
position, abnormalities of the precordial pulsations can
be felt. These abnormalities includes a lack of point of
maximal impulse or the presence of diffuse contractions
.
17. On auscultations, the first heart sound may be diminished as a
result of dec contractility
A fourth heart sound is heard in almost all patients with MI,
Whereas a third heart sound is detected in only about 10% to 20 %
of patients
Transient systolic murmurs may be heard
After about 48 to 72 hrs , many patients acquire a pericardial
friction rub
18. CARDIAC MARKER
Creatine kinase –MB (CKMB)
CK-MB appears in the serum in 6 to 12 hours, peaks between 12
and 28 hours, and returns to normal levels in about 72 to 96
hours.
Serial samplings are performed every 4 to 6 hours for the first 24
to 48 hours after the onset of symptoms
Myoglobin
Myoglobin is an oxygen-binding protein found in skeletal and
cardiac muscle. Myoglobin’s release from ischemic muscle occurs
earlier than the release of CK
19. The myoglobin level can elevate within 1 to 2 hours of acute MI
and peaks within 3 to 15 hours.
Because myoglobin is also present in skeletal muscle, an
elevated myoglobin level is not specific for the diagnosis of MI.
consequently, its diagnostic value in detecting an MI is limited
Troponin (troponin T and troponin I):
Troponin I levels rise in about 3 hours, peak at 14 to 18 hours,
and remain elevated for 5 to 7 days.
Troponin T levels rise in 3 to 5 hours and remain elevated for 10
to 14 days
20. TREATMENT
Time is Muscle: Every 10 minute delay to Percutaneous
Coronary Intervention (PCI) results in a 1% change in
mortality.
Fibrinolytic agent -streptokinase-PA
Aspirin and anti-platlet drugs
beta-blockers- metoprolol, carvidalol
ACE inhibitors
Coronary artery bypass graft
