copyright © 2013, 2010 by saunders, an imprint of elsevier inc. chapter 53 management of...
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Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc.
Chapter 53
Management of
ST-Elevation Myocardial Infarction
2Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc.
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)
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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
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Diagnosis of STEMI
Chest pain Severe substernal, crushing/constricting, down
arm and jaw Characteristic ECG changes Sweating, weakness, sense of impending
doom 20% of patients with STEMI experience no
symptoms Biochemical markers for MI
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Management of STEMI
Routine drug therapy Oxygen Aspirin (not NSAIDs) Morphine Beta blockers Nitroglycerin
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Management of STEMI
Reperfusion therapy Primary percutaneous coronary intervention Fibrinolytic (thrombolytic) therapy Action: to dissolve clots; converts plasminogen to
plasmin
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Management of STEMI
Adjuncts to reperfusion therapy Heparin Antiplatelet drugs
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Management of STEMI
Thrombolytic drugs Alteplase, a tissue plasminogen activator Reteplase Streptokinase Tenecteplase Urokinase
Percutaneous coronary intervention (PCI)
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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
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Fibrinolytic (Thrombolytic) Therapy
Dissolves clots Converts plasminogen to plasmin (proteolytic
enzyme)1. Alteplase, a tissue plasminogen activator2. Reteplase3. Streptokinase4. Tenecteplase5. Urokinase
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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
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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
13Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc.
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
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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
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Complications of STEMI
Ventricular dysrhythmias Cardiogenic shock Heart failure Cardiac rupture
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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