Transcript Chapter 16 Cholinesterase Inhibitors

Chapter 53
Management of
ST-Elevation Myocardial Infarction
Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc.
ST-Elevation Myocardial
Infarction (STEMI)
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Myocardial infarction (MI): necrosis of the
myocardium resulting from ischemia
STEMI: acute MI caused by complete
interruption of regional myocardial blood flow
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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
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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
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Chest pain
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Characteristic ECG changes
Sweating, weakness, sense of impending
doom
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Severe substernal, crushing/constricting, down
arm and jaw
20% of patients with STEMI experience no
symptoms
Biochemical markers for MI
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Management of STEMI
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Routine drug therapy
 Oxygen
 Aspirin (not NSAIDs)
 Morphine
 Beta blockers
 Nitroglycerin
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Management of STEMI
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Reperfusion therapy
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Primary percutaneous coronary intervention
Fibrinolytic (thrombolytic) therapy
Action: to dissolve clots; converts plasminogen to
plasmin
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Management of STEMI
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Adjuncts to reperfusion therapy
Heparin
Antiplatelet drugs
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Management of STEMI
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Thrombolytic drugs
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Alteplase, a tissue plasminogen activator
Reteplase
Streptokinase
Tenecteplase
Urokinase
Percutaneous coronary intervention (PCI)
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Primary Percutaneous
Coronary Intervention
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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
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Dissolves clots
Converts plasminogen to plasmin (proteolytic
enzyme)
1.
2.
3.
4.
5.
Alteplase, a tissue plasminogen activator
Reteplase
Streptokinase
Tenecteplase
Urokinase
Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc.
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Fibrinolytic (Thrombolytic) Therapy
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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
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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
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Clopidogrel (Plavix)
Glycoprotein (GP) IIb/IIIa inhibitors
Low-dose aspirin
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May use concurrently with clopidogrel
Should take indefinitely
Higher dose for PCI patients
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Adjuncts to Reperfusion Therapy:
Management of STEMI
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Angiotensin-converting enzyme (ACE)
inhibitors and angiotensin II receptor blockers
(ARBs)
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Decrease short-term mortality in all patients
Start treatment within 24 hours
ACE inhibitors studied more extensively than
ARBs
Calcium channel blockers
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Antianginal, vasodilation, and antihypertensive
actions
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Complications of STEMI
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Ventricular dysrhythmias
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Develop frequently and are major cause of death
after MI
Prophylactic antidysrhythmics not successful
Cardiogenic shock
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Results from tissue perfusion reduction
7%–15% of post-MI patients develop shock in first
few days
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Complications of STEMI
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Ventricular dysrhythmias
Cardiogenic shock
Heart failure
Cardiac rupture
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Secondary Prevention of STEMI
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Discharge 6–10 days after event
5%–5% of patients have another infarct
in first year
Outcome improved with risk factor reduction
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Cholesterol control, smoking cessation, exercise,
blood pressure (BP) control, diabetes control
All post-MI patients should take:
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Beta blocker
 ACE inhibitor
 Antiplatelet drug or anticoagulant
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