3. INFARCTION
• AN INFARCT IS AN AREA OF
ISCHEMIC NECROSIS
CAUSED BY OCCLUSION OF
EITHER THE ARTERIAL
SUPPLY OR THE VENOUS
DRAINAGE IN A
PARTICULAR TISSUE.
4. INFARCTION
• NEARELY 99% OF ALL
INFARCTS RESULT FROM
THROMBOTIC OR EMBOLIC
EVENTS, AND ALMOST ALL
RESULT FROM ARTERIAL
OCCLUSION
6. RED INFARCT
• OVARIAN TORSION
• LOOSE TISSUES(SUCH AS LUNG)
• IN TISSUES WITH DUAL CIRCULATION
SUCH AS LUNG AND SMALL INTESTINE
7. WHITE INFARCT
• OCCURS WITH ARTERIAL
OCCLUSION
OR IN SOLID ORGANS
SUCH AS HEART,SPLEEN
AND KIDNEY
8.
9.
10. History
• Chest Pain- anterior precordium
tightness
• Pain may radiate to jaw, neck and
epigastrium
• Dyspnea- angina equivalent, poor
LV function
• Nausea/abdominal pain with
posterior MI
• Anxiety
11. Physical
• The physical exam can often
be unremarkable
• Hypertension
• Hypotension
• Acute valvular dysfunction
may be present
• Neck vein distention
12. Mechanisms of Myocardial damage
The severity of an MI is dependent
of three factors
• The level of the occlusion in the
coronary
• The length of time of the
occlusion
• The presence or absence of
collateral circulation
13. Cardiac Biomarkers
• Cardiac biomarkers are protein
molecules released into the blood
stream from damaged heart
muscle
• Since ECG can be inconclusive ,
biomarkers are frequently used to
evaluate for myocardial injury
• These biomarkers have a
characteristic rise and fall pattern
14. Troponin T and I
• These isoforms are very specific for
cardiac injury
• Preferred markers for detecting myocardial
cell injury
• Rise 2-6 hours after injury
Peak in 12-16 hours
Stay elevated for 5-14 days
15. Creatinine Kinase ( CK-MB)
• Creatinine Kinase is found in heart muscle
(MB), skeletal muscle (MM), and brain
(BB)
• Increased in over 90% of myocardial
infraction
• However, it can be increased in muscle
trauma, physical exertion, post-op,
convulsions, and other conditions
16. Creatine Kinase (MB)
• Time sequence after myocardial infarction
Begins to rise 4-6 hours
Peaks 24 hours
returns to normal in 2 days
• MB2 released from heart muscle and
converted to MB1.
• A level of MB2 > or = 1 and a ratio of
MB2/MB1 > 1.5 indicates myocardial injury
17. Renal Failure and Renal
Transplantation
• Diagnostic accuracy of serum markers of
cardiac injury are altered in patients with
renal failure
• Cardiac troponins decreased diagnostic
sensitivity and specificity in patients
receiving renal replacement therapy
• Current data show levels of troponin I are
unaltered while levels of troponin T may
be elevated
18. CBC
• CBC is indicated if anemia is suspected as
precipitant
• Leukocytosis may be observed within
several hours after myocardial injury and
returns returns to levels within the
reference range within one week
19. Chemistry Profile
• Potassium and magnesium levels should
be monitored and corrected
• Creatinine levels must be considered
before using contrast dye for coronary
angiography and percutanous
revascularization
20. C-reactive Protein (CRP)
• C- reactive protein is a marker of acute
inflammation
• Patients without evidence of myocardial
necrosis but with elevated CRP are at
increased risk of an event
21. Chest X-Ray
• Chest radiography may provide clues to
an alternative diagnosis ( aortic dissection
or pneumothorax)
• Chest radiography also reveals
complications of myocardial infarction
such as heart failure
22. Therapy
The goals of therapy in AMI
are the expedient restoration
of normal coronary flow and
the maximum salvage of
functional myocardium
Editor's Notes
RED (HEMORRHAGIC) PULMONARY INFARCT, and ANEMIC (WHITE) SPLENIC INFARCT
WEDGE SHAPED SCARRED INFARCT following the distribution of a end artery branch of the renal artery. FIBROSIS implies that it is old (months to years)