copyright © 2013, 2010 by saunders, an imprint of elsevier inc. chapter 53 management of...

Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc.

Chapter 53

Management of

ST-Elevation Myocardial Infarction

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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

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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