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At the end of this self study the participant will:
• Describe ACS risk stratification
• List goals of medication therapies
• Describe complications of ACS.
TREATMENT OF ACUTE CORONARY SYNDROMES
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ACS Risk Stratification Findings indicating HIGH likelihood of ACS
Findings indicating INTERMEDIATE likelihood of ACS in absence of high-likelihood findings
Findings indicating LOW likelihood of ACS in absence of high- or intermediate-likelihood findings
History Chest or left arm pain or discomfort as chief symptom
Reproduction of previous documented angina
Known history of coronary artery disease, including myocardial infarction
Chest or left arm pain or discomfort as chief symptom
Age > 50 years
Probable ischemic symptoms
Recent cocaine use
ECG New or presumably new transient ST-segment deviation (> 0.05 mV) or T-wave inversion (> 0.2 mV) with symptoms
Fixed Q waves
Abnormal ST segments or T waves not documented to be new
T-wave flattening or inversion of T waves in leads with dominant R waves
Normal ECG
Serum cardiac markers
Elevated cardiac troponin T or I, or elevated CK-MB
Normal Normal
Taken from http://www.aafp.org/afp/20050701/119.html
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Low Risk Medical Management
• ASA• NTG (PO/NTP)• Consider
– BetaBlocker– Stress Test– Risk factor modification
• Statin• Discharge/Admit to Chest Pain Center
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Intermediate Risk Medical Management
• Oxygen (if O2 sat < 90%)• ASA, Clopidogrel if ASA intolerant/ sensitive• NTG (PO/NTP/Spray)• LMWH/ Unfractionated Heparin -Blocker• ACE inhibitor: EF < 40%• Statin• Consider Echocardiagram, stress test• Admit to Telemetry
Braunwald, et al, http://www.acc.org/clinical/guidelines/unstable/unstable.pdf accessed April 2, 2002.
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• Oxygen (if O2 sat < 90%)• ASA, Clopidogrel if ASA intolerant/ sensitive• Clopidogrel if medical management/ PCI• Enoxaparin • NTG (IV/PO/NTP) -Blocker• ACE inhibitor: ejection fraction <40%• Statins• Consider Echocardiogram• Admit to CCU/Telemetry
Braunwald, et al, http://www.acc.org/clinical/guidelines/unstable/unstable.pdf accessed April 2, 2002.
Medical Management High Risk UA/Non-STEMI
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Aggressive Management High RiskUA/Non-STEMI (Cath, PCI, CABG)
• Oxygen (O2 sat < 90%)• Clopidogrel if ASA intolerant/
sensitive• Clopidogrel in addition to ASA• LMWH or Unfractionated Heparin • NTG (IV/PO/NTP) -Blocker • GP IIb-IIIa Inhibitor for PCI• Cardiac Catheterization
Braunwald, et al, http://www.acc.org/clinical/guidelines/unstable/unstable.pdf accessed April 2, 2002.
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Medical ManagementAcute STEMI
• Oxygen (O2 sat < 90%)• NTG SL• ASA• Unfractionated Heparin • IV Nitroglycerin• IV Morphine Sulfate• Fibrinolytic Therapy (if candidate) or Primary PCI• Consider Beta Blocker; Consider ACE-I• Admit to CCU or Arrange for PCI
*Ryan et al, JACC 1999;34(3):890-911.
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Thrombolytic or Fibrinolytic Agents (start within 30 minutes of “door”)
Goal: break down clots allowing perfusion (remember destroys all clots, not just those in coronary arteries)
Reteplase (rPA)• treatment of MI; double bolus
Tenecteplase (TNK)• treatment of MI; single bolus
Alteplase (tPA)• treatment of ischemic stroke, PE, catheter declotting; bolus followed by
an infusion
Combination Therapy: Fibrinolytic, plus IIb/IIIa inhibitor
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Antiplatelet Agents
• Goal: Prevent further clotting by preventing platelet aggregation
• Salicylates: All ACS– ASA (chewed for acute chest pain)
• ADP-receptor inhibitors: UA, stents– Clopidigrel (Plavix)
• Glycoprotein (GP) IIb-IIIa receptor antagonists: Non-STEMI, UA– Abciximab (ReoPro)– Eptifibatide (intergrelin)– Tirofiban (Aggrastat)
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Antithrombin Agents• Goal: Prevent further clotting by thrombin inhibition,
either directly or indirectly• Heparin -unfractionated heparin (UFH)• Low–molecular-weight heparins (LMWH) with
UA/NSTEMI indications (not indicated for STEMI)– enoxaparin – dalteparin
• Direct-acting antithrombins– Bivalirudin (angiomax)– argatrobran– lepirudin
Incredible Machine. National Geographic Society. 1986. Used by Permission
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Vitamin K Antagonists
• Goal: Prevent clotting through oral therapy
• Coumadin (Warfarin)
– Chronic Atrial Fibrillation– Prosthetic Valves– Mural Thrombus
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Adjunctive Therapy: Beta Blockers-lol drugs
Actions: myocardial 02 demand, heart rate, arrhythmias
Contraindications: avoid in bronchospastic diseases, cardiac failure, severe abnormalities in cardiac conduction, hypotension and insulin dependent diabetics
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Adjunctive Therapy: ACE Inhibitors-pril drugs
Actions: decrease afterload, reduce compensatory LV hypertrophy, improve ejection fraction, limit size of infarct
Contraindications: hypotension, renal artery stenosis, allergy to ACEs
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Adjunctive Therapy: Intravenous Nitroglycerin
Actions: dilates coronary arteries, increases collateral blood flow, decreases preload & afterload
Contraindications: hypotension, marked bradycardia, hypersensitivity to nitrates
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Lipid Lowering Agents
• Lower LDL and increase HDL when combined with Statin
• Niacin, Lopid, Questran, etc.
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STATINSSTATINS
Lowers Low Density Lipoproteins (LDL)Lowers Low Density Lipoproteins (LDL)– May help to decrease accumulation of plaqueMay help to decrease accumulation of plaque– Stabilizes plaqueStabilizes plaque– Reduces chance of plaque ruptureReduces chance of plaque rupture– When combined with Niacin, may increase High When combined with Niacin, may increase High
Density Lipoprotein (HDL).Density Lipoprotein (HDL).– Lipitor, Pravachol, Zocor, etc. Lipitor, Pravachol, Zocor, etc.
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Coronary Artery Bypass Graft (CABG)Coronary Artery Bypass Graft (CABG)• Goal: Surgically enhance circulation• Can use internal mammary artery,
radial artery or sapphenous vein– one end is either sewn to the
aorta or may remain connected to the larger artery where it originated.
– The other end is attached (grafted) beyond the blockage in the coronary artery.
– As a result, blood can flow around the blocked area, increasing the supply of oxygen and nutrients to the heart muscle.
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Post ACS Complications
Left Ventricular Failure• Problem with forward flow (low cardiac output, ejection fraction
drops) • Blood backs up into lungs (respiratory implications)
Cardiogenic Shock• Severe LV failure• Need to intervene early
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Post ACS ComplicationsVentricular Septal Defect• Hole develops in septum causing oxygenated blood to remix with deoxygenated blood in heart• Problem with forward flow• New systolic murmur, decreased pO2, LV failure
Myocardial Rupture• Hole develops in free wall (outside wall)• Problem with forward flow• LV failure, cardiac arrest
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Post ACS Complications
Papillary Muscle Rupture• AV valve (tricuspid or mitral) leaflets float upward
into atria during closure• Blood leaks back into atria during ventricular
contraction• Loud new systolic murmur, pulmonary edema,
cardiogenic shock
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Post ACS Complications
Ventricular Aneurysm and Thrombosis
• Tend to develop with anterior MI• Risk of mural thrombus causing a PE• High risk for stroke if aneurysm in LV• Dx with ECHO• Anticoagulate
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Post ACS ComplicationsRecurrent Ischemia or Infarction• High risk for first 10 days• Especially with non-transmural MI or non Q wave MI• Educate patient about significance of symptoms
Pericarditis• Inflammatory reaction of pericardium• Pain with inspiration, splinting, pericardial rub• Referred to as Dressler’s syndrome if 2 weeks to 3 months post MI
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• 1Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, Jones RH, Kereiakes D, Kupersmith J, Levin TN, Pepine CJ, Schaeffer JW, Smith EE III, Steward DE, & Theroux P. ACC/AHA guidelines for the management of patients with unstable angina and non-ST segment elevation myocardial infarction: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina). J Am Coll Cardiology 2000;36:970-1062.
• 2 The Joint European Society of Cardiology/ American College of Cardiology Committee. Myocardial Infarction Redefined--A Consensus Document of The Joint European Society of Cardiology / American College of Cardiology Committee for the Redefinition of Myocardial Infarction. J Am Coll Cardiol 2000;36:959-969.
References
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