|


 


What is MI?
‡ Myocardial Infarction (MI) refers to the
process which myocardial tissue is
destroyed in regions of the heart that are
deprived of an adequate blood supply
because of reduced coronary artery blood
flow.
Kathophysiology
‡ The area of the infarction develops only
minutes to hours.
‡ As the cells are deprived of oxygen

‡ ischemia develops

‡ cellular injury occurs

‡ lack of oxygen results in infarction or

death of cells.
Krobable Causes
‡ The following are the possible causes of
MI.
1. Vasospasm of coronary artery
2. Decreased oxygen supply of a coronary
artery (ex. Shock and hemorrhage)
3. Increased demand of oxygen (ex.
Tachycardia, thyrotoxicosis or ingestion of
coccaine)
misk factors
‡ V
 Four out of five patients with coronary artery
disease are 65 years of age or older. After
menopause, females are more likely to die within the
first year of having a myocardial infarction than males.
‡ 

 Males are at higher risk of myocardial
infarction than women, and males are also more likely
to suffer myocardial infarction earlier in life.
‡ 
 

 A family history of heart disease
increases the risk of coronary artery disease and
myocardial infarction.
‡  
  Cigarette smokers are twice as likely to
experience myocardial infarction compared to non-
smokers. Smokers also have a two to four time higher
risk of sudden cardiac death (within an hour of a heart
attack).
‡ p

 Obesity increases coronary artery disease,
myocardial infarction, and stroke risk. Obesity
increases strain on the heart, raises blood pressure
and cholesterol, and increases diabetes risk.
‡ 


 Approximately two-thirds of patients with
diabetes die from heart or blood vessel disease.
‡   
 

 megular exercise reduces the
risk of coronary artery disease and myocardial
infarction by controlling blood cholesterol levels,
decreasing the risk of obesity or diabetes, and
lowering blood pressure levels in some patients.
‡ 
 mesearch indicates a possible relationship
between stress and coronary artery disease, which
may lead to myocardial infarction .
‡ 
  

 High total and low-density
lipoprotein (LDL cholesterol) levels and low HDL
cholesterol levels increase the risk of myocardial
infarction
Assessment Findings
‡ CAmDIOVASCULAm
a. Chest pain that is not relieved by nitroglycerin
palpitations or rest.
b. Heart sounds may include S3, S4, and new onset of
murmurs.
c. Blood pressure may be elevated because of
sympathetic stimulation or decreased because of
decrease contractility, impending cardiogenic shock
or medications.
d. Increased jugular venous distention may be seen if
MI has caused heart failure.
e. Irregular pulse may indicate atrial fibrillation.
f. In addition to ST-segment and T-wave changes.
ECG may show tachycardia, bradycardia or other
dysrythmias.
‡ mESKImATOm
a. SOB
b. Dyspnea
c. Tachypnea
d. Crackles of MI was caused by pulmonary congestion
e. Kulmonary edema may be present
‡ GI
a. Nausea
b. Vomiting
‡ GU
a. Decreased urinary
‡ SKIN
a. Cool clammy skin
b. Diaphoretic
c. Kale in appearance
‡ NEUmO
a. Anxiety
b. mestlessness
c. Lightheadedness

(*these may indicate increased sympathetic

stimulation or a decrease in contractility and
cerebral oxygenation. The same symptoms
may also herald cardiogenic shock.)
Diagnostic Tests
‡ LABOmATOm TESTS
these tests are based on the release of cellular contents
into the circulation when myocardial cells die.
Ú Myoglobulin
Heme protein that helps transport oxygen.
Found in in skeletal and cardiac muscle
Myoglobulin starts to increase within 1-3 hours and
peaks within 12 hours on the onset of the symptoms.

Ú Creatine Kinase and Its Isoenzymes

CK-MM, CK-MB and CK-BB
Elevated CK-MB assessed my mass assay is an
indicator of acute MI
These increses within few hours and peaks with in 24
hours.
 Ú Troponin
A protein found in myocardium, regulates the
myocardial contractile process.
There are 3 isomers for Troponin: C, I, and T
Troponin I and T are the most reliable and critical
markers of myocardial injury.
The serum is elevated during the first few hours of the
acute MI and lasts as long as 3 weeks.
‡ ECHOCAmDIOGmAKH

‡ ELECTmOCAmDIOGmAKH
Kotential Complications
‡ Dysrhythmias
‡ Acute pulmonary edema
‡ Heart failure
‡ Thromboembolism
‡ Myocardial rupture
‡ Kericardial effusion and cardiac
tamponade
 ECG findings
Transition of ECG changes
during MI
a. Normal ECG prior to MI
b. Hyperacute T wave changes -
increased T wave amplitude and
width; may also see ST elevation
c. Marked ST elevation with
hyperacute T wave changes
(transmural injury)
d. Kathologic Q waves, less ST
elevation, terminal T wave
inversion (necrosis)
e. (Kathologic Q waves are usually
defined as duration >0.04 s or
>25% of m-wave amplitude)
f. Kathologic Q waves, T wave
inversion (necrosis and fibrosis)
g. Kathologic Q waves, upright T
waves (fibrosis)
 2 Types of MI
‡ STEMI
ÚThe patient has ECG evidence of acute MI
with characteristics changes in two
continuous leads on a 12-lead ECG. In these
type of MI, there are signigicant damage to
the myocardium.
‡ NSTEMI
ÚThe patient has elevated cardiac biomarker
but no definite ECG evidence of acute MI.
Medical Management

‡ GOALS
i. Minimize myocardial damage
ii. Kreserve myocardial function
iii. Krevent complications such as lethal
dysrythmias and cardiogenic shock.
‡ Oxygen administrations is initiated at the onset of
chest pain.
‡ Kharmacologic Therapy
Analgesics
Angiotensin-converting enzyme
Thrombolytics
Nitrates
Beta-blocker
Anti-coagulants
‡ Emergent Kercutaneous Coronary Interventions
Kercutanous transluminal coronary angioplasty
Coronary artery stent
Atherectomy
Brachytheraphy
Coronary artery bypass or minimally invasive direct
coronary artery bypass