Document

advertisement
Acute Myocardial
Infarction
Willis E. Godin D.O.,
FACC
Acute Myocardial Infarction
 Definition:
 Decreased delivery of oxygen and nutrients to the
myocardium
 Myocardial tissue necrosis causing irreparable
tissue/cell death
Pathophysiology
 The most frequent cause of an acute MI is a
disruption in the vascular endothelium that is
associated with myocardial plaque
 Plaque occurs over a period of years to
decades
 This combination causes the development of an
intra-coronary thrombus, which causes the
coronary artery to occlude
 Within 20-40 minutes of an occlusion, irreversible
myocardial cell damage/death occurs
Pathophysiology
 2 primary characteristics of plaque development
are 1) a fibromuscular cap and 2) an underlying
lipid rich core.
 The overall loss of structural stability of the
plaque usually occurs at the junction between
the fibromuscular cap and the vessel wall
(shoulder region)
 Thrombus develops (due to the platelet-
mediated activation of the coagulation
cascade) and partial or complete occlusion
occurs causing an acute myocardial infarction.
Pathophysiology
 The severity of an MI depends on three factors
 1) The level of the occlusion in the coronary artery
 Generally, the more proximal the coronary occlusion,
the more extensive the amount of myocardium that
will be at risk of necrosis
 2) The length of time of the occlusion
 The longer the period of vessel occlusion, the greater
the chances of irreversible myocardial damage distal
to the occlusion
 3) The presence or absence of collateral
circulation
Pathophysiology
 STEMI
 “complete” blockage of a coronary artery
 NSTEMI
 “near-complete” blockage of a coronary artery
Pathophysiology
 Left Coronary Artery
 Left Anterior Descending Artery (LAD)
 “widow maker”
 Anterior MI
 Lateral MI
 Left Circumflex Artery (LCx)
 Lateral MI
 Posterior MI
 Right Coronary Artery
 Inferior MI
 RV MI
Prevalence
 Myocardial Infarction is the leading cause of
death in the United States
 Approximately 450,000 people in the US die from
coronary disease per year
 50% of all acute MI’s in the US occur in people
under the age of 65
 No longer considered a “disease of the elderly”
Risk Factors
 Dyslipidemia
 Diabetes Mellitus
 Hypertension
 Tobacco use
 Family History
 Male gender
Diagnosis
 Symptoms (gained by an accurate history)
 Electrocardiogram (ECG)
 Laboratory Tests
 CK
 CK-MB
 Troponin
 Echocardiogram
Symptoms
 Chest pain described as a pressure sensation, fullness, or
squeezing in the midportion of the thorax
 Radiation of chest pain into the jaw or teeth, shoulder, arm,
and/or back
 Associated dyspnea or shortness of breath
 Associated epigastric discomfort with or without nausea and
vomiting
 Associated diaphoresis or sweating
 Syncope or near syncope without other cause
 Impairment of cognitive function without other cause
Electrocardiogram
 ST elevation myocardial infarction (STEMI)
 > 1mm ST elevations in contiguous leads
 Non-ST elevation myocardial infarction (NSTEMI)
 ST depression
 T wave inversions
 No obvious ECG changes
ECG - STEMI
ECG - STEMI
ECG -NSTEMI
ECG - NSTEMI
ECG - NSTEMI
Cardiac Enzymes
 Serial blood draws
 Every 4 hours x 4 sets
 Myoglobin peaks first (detectable in 1-4 hrs)
 Troponin
 peaks last (detectable in 3-12 hrs)
 most specific
 remains detectable in serum the longest
Cardiac Enzymes
Cardiac Enzymes
Imaging (Echocardiography)
 An echocardiogram can be performed to assess
areas of the left ventricle that are not
contracting normally as compared to areas that
are contracting normally
 After normal blood flow is interrupted, the area
of the myocardium affected by the occluded
artery will not function normally.
 This abnormal wall motion can be detected by
echocardiography
Treatment
 Antiplatelets
 Supplemental oxygen
 Nitrates
 Pain control
 Beta Blockers
 Statin Therapy
 Heparin (unfractionated / low-molecular-weight heparin)
 Fibrinolytics
 Angiotensin-Converting Enyme Inhibitors / Angiotensin
Receptor Blockers
 Glycoprotein Iib/IIIa Antagonists
 Aldosterone Antagonists
Other Treatment Options
 Percutaneous Coronary Intervention
 PCI / coronary stenting
 Surgical Revascularization
 CABG
 Implantable Cardiac Defibrillators
 AICD
Treatment Outcomes
 Long-term medications
 Smoking cessation
 Cardiac Rehabilitation
Long-Term Medications
 Most oral medications instituted in the hospital at
the time of acute MI will be continued long term
 Aspirin, beta blockade, and statin therapy is
continued indefinitely in all patients
 ACE inhibitors are continued indefinitely in
patients with CHF, left ventricular dysfunction,
hypertension, or diabetes
 Diet modification, regular exercise
Smoking Cessation
 Smoking is a major risk factor for coronary artery
disease and MI
 For patients who have undergone an MI,
smoking cessation is essential to recovery, longterm health, and prevention of re-infarction
 In one study, the risk of recurrent MI decreased
by 50% after 1 year of smoking cessation
Smoking Cessation
 All STEMI and NSTEMI patients with a history of
smoking should be advised to quit and offered
smoking cessation resources
 Nicotine replacement therapy
 Pharmacologic therapy
 Referral to behavioral counseling or support groups
 Smoking cessation counseling should begin in
the hospital, at discharge, and during follow up
Cardiac Rehabilitation
 Provides a venue for continued education,
reinforcement of lifestyle modification, and
adherence to a comprehensive prescription of
therapies for recovery from MI including exercise
training
 Participation in cardiac rehabilitation programs
after MI is associated with decreases in
subsequent cardiac morbidity and mortality
 Other benefits include improvements in quality
of life, functional capacity, and social support
Summary
 MI results from myocardial ischemia and cell death,
most often because of an intra-arterial thrombus
superimposed on an ulcerated or unstable
atherosclerotic plaque
 Despite advances in therapy, MI remains the leading
cause of death in the United States.
 MI risk factors include hyperlipidemia, diabetes,
hypertension, male gender, and tobacco use.
 Diagnosis is based on the clinical history, ECG, and
blood test results, especially creatine phosphokinase
(CK), CK-MB fraction, and troponin I and T levels.
Summary
 Outcome following an MI is determined by the
infarct size and location, and by timely medical
intervention.
 Aspirin, nitrates, and beta blockers are critically
important early in the course of MI for all
patients.
 Post-discharge management requires ongoing
pharmacotherapy and lifestyle modification.
Download