ST Elevation Myocardial Infarctionx
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Transcript ST Elevation Myocardial Infarctionx
Management of
ST-Elevation Myocardial Infarction
ST-Elevation Myocardial
Infarction (STEMI)
Myocardial infarction (MI): necrosis of the
myocardium resulting from ischemia
STEMI: acute MI caused by complete
interruption of regional myocardial blood flow
Causes elevation of the ST segment on the
electrocardiogram (ECG)
Managed differently than non–ST-elevation MI
(partial blood flow blockage)
Pathophysiology of STEMI
Blood flow to a region of myocardium is
stopped (platelet plugging and thrombus
formation)
Hydrogen ions accumulate
Local metabolic changes occur
Myocardial injury triggers ventricular
remodeling
Degree of residual cardiac impairment
depends on amount/location of damage
Diagnosis of STEMI
Chest pain
Characteristic ECG changes
Sweating, weakness, sense of impending
doom
Severe substernal, crushing/constricting, down
arm and jaw
20% of patients with STEMI experience no
symptoms
Biochemical markers for MI
Management of STEMI
Routine drug therapy
Oxygen
Aspirin (not NSAIDs)
Morphine
Beta blockers
Nitroglycerin
Management of STEMI
Reperfusion therapy
Primary percutaneous coronary intervention
Fibrinolytic (thrombolytic) therapy
Action: to dissolve clots; converts plasminogen to
plasmin
Management of STEMI
Adjuncts to reperfusion therapy
Heparin
Antiplatelet drugs
Management of STEMI
Thrombolytic drugs
Alteplase, a tissue plasminogen activator
Reteplase
Streptokinase
Tenecteplase
Urokinase
Percutaneous coronary intervention (PCI)
Primary Percutaneous
Coronary Intervention
Primary refers to the use of angioplasty rather
than fibrinolytic therapy
Stents may be placed
Goal: primary PCI within 90 minutes of patient
contact
Success rate with PCI somewhat higher than
with thrombolytics
Fibrinolytic (Thrombolytic) Therapy
Dissolves clots
Converts plasminogen to plasmin (proteolytic
enzyme)
1.
2.
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Alteplase, a tissue plasminogen activator
Reteplase
Streptokinase
Tenecteplase
Urokinase
Fibrinolytic (Thrombolytic) Therapy
Most effective when patient presents early;
not given if pain has been present longer than
12 hours (best if given during first 4–6 hours)
Goal: to improve ventricular function, limit
size of infarct, and reduce mortality
Timely administration = Opening of occluded
artery in 80% of patients
Guidelines suggest 30-minute target time
Best for patients younger than 75 years
Adjuncts to Reperfusion Therapy:
Management of STEMI
Unfractionated heparin used for treatment lasting less
than 48 hours
Low-molecular-weight (LMW) heparin used for
treatment lasting longer than 48 hours
Antiplatelet drugs
Clopidogrel (Plavix)
Glycoprotein (GP) IIb/IIIa inhibitors
Low-dose aspirin
May use concurrently with clopidogrel
Should take indefinitely
Higher dose for PCI patients
Adjuncts to Reperfusion Therapy:
Management of STEMI
Angiotensin-converting enzyme (ACE)
inhibitors and angiotensin II receptor blockers
(ARBs)
Decrease short-term mortality in all patients
Start treatment within 24 hours
ACE inhibitors studied more extensively than
ARBs
Calcium channel blockers
Antianginal, vasodilation, and antihypertensive
actions
Complications of STEMI
Ventricular dysrhythmias
Develop frequently and are major cause of death
after MI
Prophylactic antidysrhythmics not successful
Cardiogenic shock
Results from tissue perfusion reduction
7%–15% of post-MI patients develop shock in first
few days
Complications of STEMI
Ventricular dysrhythmias
Cardiogenic shock
Heart failure
Cardiac rupture
Secondary Prevention of STEMI
Discharge 6–10 days after event
5%–5% of patients have another infarct
in first year
Outcome improved with risk factor reduction
Cholesterol control, smoking cessation, exercise,
blood pressure (BP) control, diabetes control
All post-MI patients should take:
Beta blocker
ACE inhibitor
Antiplatelet drug or anticoagulant