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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)
3Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. 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
4Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. 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
5Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. Management of STEMI Routine drug therapy Oxygen Aspirin (not NSAIDs) Morphine Beta blockers Nitroglycerin
6Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. Management of STEMI Reperfusion therapy Primary percutaneous coronary intervention Fibrinolytic (thrombolytic) therapy Action: to dissolve clots; converts plasminogen to plasmin
7Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. Management of STEMI Adjuncts to reperfusion therapy Heparin Antiplatelet drugs
8Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. Management of STEMI Thrombolytic drugs Alteplase, a tissue plasminogen activator Reteplase Streptokinase Tenecteplase Urokinase Percutaneous coronary intervention (PCI)
9Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. 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
10Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. Fibrinolytic (Thrombolytic) Therapy Dissolves clots Converts plasminogen to plasmin (proteolytic enzyme) 1.Alteplase, a tissue plasminogen activator 2.Reteplase 3.Streptokinase 4.Tenecteplase 5.Urokinase
11Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. 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
12Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. 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
14Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. 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
15Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. Complications of STEMI Ventricular dysrhythmias Cardiogenic shock Heart failure Cardiac rupture
16Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. 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
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