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Transcript
Acute Myocardial Infarction
Dr. Meg-angela Christi Amores
• one of the most common diagnoses in
hospitalized patients
• mortality rate from AMI is ~30%
• more than half of these deaths occurring
before the stricken individual reaches the
hospital
Acute MI
• usually occurs when coronary blood flow
decreases abruptly after a thrombotic
occlusion of a coronary artery previously
affected by atherosclerosis
• occurs when a coronary artery thrombus
develops rapidly at a site of vascular injury
• Injury facilitated by factors such as cigarette
smoking, hypertension, and lipid
accumulation
Pathogenesis
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•
•
•
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Atherosclerotic plaque disruption
Thrombogenesis
Platelet activation
Platelet aggregation, cross-linking
Coagulation cascade activated
The amount of myocardial damage
depends on:
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•
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•
the territory supplied by the affected vessel
whether or not the vessel becomes totally occluded
the duration of coronary occlusion
the quantity of blood supplied by collateral vessels to
the affected tissue
• the demand for oxygen of the myocardium whose
blood supply has been suddenly limited
• native factors that can produce early spontaneous lysis
of the occlusive thrombus
• the adequacy of myocardial perfusion in the infarct
zone when flow is restored in the occluded epicardial
coronary artery.
Risk factors
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•
•
•
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•
Persons with multiple coronary risk factors
Persons with unstable angina
Hypercoagulability
collagen vascular disease
cocaine abuse
intracardiac thrombi or masses that can
produce coronary emboli
Clinical presentation
• Usually soon after awakening
• PAIN – most common presenting complaint
•
•
•
•
•
•
Deep, visceral
Heavy, squeezing, crushing, stabbing, burning
Similar to angina pectoris but occurs at rest
More severe, lasts longer
Central portion of chest/ epigastrium/ radiates to arm
weakness, sweating, nausea, vomiting, anxiety, and a
sense of impending doom
PE Findings
• anxious and restless
• Pallor, perspiration
• physical signs of ventricular dysfunction
– fourth and third heart sounds, decreased intensity
of the first heart sound, and paradoxical splitting
of the second heart sound
Lab Findings
• Electrocardiogram (ECG)
– ST-segment elevation
• Serum Cardiac Biomarkers
– Proteins released from necrotic heart muscle
– Troponin I
– CKMB
• Cardiac imaging
Management
• Prehospital care
•
•
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•
Recognition of symptoms
Repid deployment of medical team
Expeditious transportation
Implementation of reperfusion therapy
• ER management
• Control of discomfort
• Limitation of infarct size
• O2
Intervention
• Primary percutaneous coronary intervention
– Angioplasty
• Fibrinolysis
– Within 30 mins of presentation
– tPA
– Streptokinase
– rPA (reteplase)
Hospital care
• Should be admitted in the CCU or ICU
• Bed rest for first 12 hours
• Resume upright position with dangling feet
within 24 hours
• NPO in first 4-12 hours
• 50-55% CHO, <30% fats
• Bedside commode, laxative
• Sedation (diazepam)