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IFARCTION
• BY
• DR. ABDUL AZIZ SHAIKH
• ASSTT PROFESSOR
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.
INFARCTION
• NEARELY 99% OF ALL
INFARCTS RESULT FROM
THROMBOTIC OR EMBOLIC
EVENTS, AND ALMOST ALL
RESULT FROM ARTERIAL
OCCLUSION
MORPHOLOGY
• RED (HEMORRHAGIC)
• WHITE(ANEMIC)
• SEPTIC
• BLAND
RED INFARCT
• OVARIAN TORSION
• LOOSE TISSUES(SUCH AS LUNG)
• IN TISSUES WITH DUAL CIRCULATION
SUCH AS LUNG AND SMALL INTESTINE
WHITE INFARCT
• OCCURS WITH ARTERIAL
OCCLUSION
OR IN SOLID ORGANS
SUCH AS HEART,SPLEEN
AND KIDNEY
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
Physical
• The physical exam can often
be unremarkable
• Hypertension
• Hypotension
• Acute valvular dysfunction
may be present
• Neck vein distention
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
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
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
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
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
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
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
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
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
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
Therapy
The goals of therapy in AMI
are the expedient restoration
of normal coronary flow and
the maximum salvage of
functional myocardium
Infarction

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Infarction

  • 1.
  • 2. IFARCTION • BY • DR. ABDUL AZIZ SHAIKH • ASSTT PROFESSOR
  • 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
  • 5. MORPHOLOGY • RED (HEMORRHAGIC) • WHITE(ANEMIC) • SEPTIC • BLAND
  • 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

  1. RED (HEMORRHAGIC) PULMONARY INFARCT, and ANEMIC (WHITE) SPLENIC INFARCT
  2. 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)