Online Nursing Continuing Education CEU CE Contact Hour

Online Nursing CEU Course

Pharmacological Managagement of Acute Coronary Syndrome (ACS) in the Acute Care Setting
By: Dr. Jeffrey Ruff, PharmD, R.Ph., C.Ph. and Travis Thomas, RN, BSN, BA

CEU hour(s)/CE Contact Hour(s): 1.0
Awarded by the Florida Board of Nursing
Cost: $7.00 (USD)


Intended audience: Nurses practicing in the acute care setting and all areas requiring cardiac monitoring.


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ACS Introduction

Acute coronary syndromes (ACS) result from the acute obstruction of one or more coronary arteries. The possible consequences of ACS depend on the degree of vessel obstruction. Once diagnosed with ACS, a patient’s condition is further classified into one of the following categories representing a spectrum of severity and clinical significance: Unstable Angina (UA), Non –ST-segment Elevation Myocardial Infarction (NSTEMI), non-Q wave and Q-wave Myocardial Infarction, ST Elevation MI (STEMI) and Sudden Cardiac Death. Symptoms are similar in each of these syndromes and can include chest pain, dyspnea, nausea, and diaphoresis. Treatment is aimed at reducing myocardial ischemia/infarction and allowing reperfusion of affected myocardium as soon as possible. This treatment includes the use of anti-ischemic therapies, antiplatelet drugs, anticoagulants and, for STEMI, emergency reperfusion with thrombolytic drugs, percutaneous intervention (PCI), or coronary artery bypass graft surgery (CABG). Healthcare professionals can effectively address ACS by recognizing and reporting recognizable symptoms and providing patients with timely administration of appropriate medications. Nurses are in a unique position, as those administering medications to patients, to assist doctors and pharmacists in an ongoing effort to ensure compliance with core measures and standards of care, all with the end goal of achieving optimal outcomes for patients affected by ACS.

The following discussion will highlight the pharmacological treatment of ACS in the acute care setting with specific application to UA and N-STEMI.

ACS General Pathophysiology and Treatment

Pathophysiology:
As indicated above, ACS results from the acute obstruction of coronary arteries. This obstruction may be a severe narrowing of an artery due to plaque formation or spasm, the rupture of a plaque formation, or formation of a clot. These obstructions decrease or completely block coronary artery blood flow thus reducing oxygen delivery to varying areas of the myocardium. The resulting decrease in oxygen delivery causes ischemia and potential infarction (death) of myocardial tissue.

Treatment:
Treatment of ACS is aimed at rapidly reestablishing coronary artery blood flow and/or reducing myocardial oxygen demands to decrease ischemia and/or infarction. Intervention with pharmacology utilizes varying drug classes in combination to provide anti-ischemic, antiplatelet, and anticoagulant therapies. Anti-ischemic therapy is aimed at increasing blood flow and oxygen delivery, and reducing the oxygen demand of the myocardium. Antiplatelet and anticoagulant therapies are used to prevent further clots from forming.

Anti-Ischemic Therapies

Anti-ischemic therapy:
Anti-ischemic therapy consists of bed rest, oxygen, morphine, nitroglycerin (NTG), beta-blockers (BB), calcium channel blockers (CCB), and angiotensin converting enzyme inhibitors (ACEI). Bed rest reduces myocardial oxygen demand. Oxygen increases the supply of oxygen in the body.

•Morphine
Morphine is a potent analgesic and anxiolytic that reduces heart rate and causes vasodilation. The dose of Morphine is 1-5mg IV Q 5-30mins for chest pain that is unrelieved by nitroglycerin.

•Nitroglycerin
Nitroglycerin is a vasodilator that decreases preload and afterload. It reduces myocardial oxygen demand while simultaneously enhancing myocardial oxygen delivery. Nitroglycerin comes as a sublingual tablet or spray (0.4mg). Doses may be repeated every five minutes for a total of 3 doses. If symptoms are unrelieved, then IV Nitroglycerin should be initiated. IV therapy should be initiated at 10-20mcg/min and can be increased in 10-20mcg increments until symptoms are relieved or until desired blood pressure effect is achieved. When stable, patients should be switched to an oral or topical dosage form of Nitroglycerin.

Beta-blockers (BB):
BB’s decrease heart rate and blood pressure. They reduce myocardial contractility, sinus node rate, and AV node conduction velocity. Through this action they blunt heart rate and contractility to stimuli. They also decrease systolic blood pressure and reduce myocardial oxygen demand. These agents should be started early in all patients without contraindications. For high risk patients or those with ongoing chest pain IV therapy should be initiated first followed by oral therapy. For intermediate or low risk patients, oral therapy may be initiated first. Initial BB choices include metoprolol, atenolol, or propranolol.

•Metoprolol
The dose for metoprolol is 5 mg slow IVP initially which can be titrated up to 15 mg. Oral therapy should be initiated 15 minutes after the last IV dose with 25-50mg Q6H for 48 hours followed by 100mg twice daily.

•Atenolol
The dose for atenolol is 5mg IV followed in 5 minutes with another 5mg IV. Oral therapy should be initiated at 50-100mg daily given 1-2 hours after the last IV dose.

Calcium Channel Blockers (CCB):
CCB’s also decrease heart rate and blood pressure. CCBs work by inhibiting the contractile process of myocardial smooth muscle, resulting in dilation of coronary and systemic arteries with improved oxygen delivery to myocardial tissue. Total peripheral resistance, systemic blood pressure, and afterload are decreased with an increase in coronary blood flow. They should be used in patients where ischemia continues or recurs frequently and BBs are contraindicated as initial therapy in the absence of LV dysfunction or other contraindications. They may also be added to the regimen in patients with recurrent ischemia even though BBs and NTG are fully used and the patient has no contraindications to the use of CCBs. They may be used in an extended release form in place of a BB. There is some evidence that CCBs may be beneficial in ACS and even in patients with LV dysfunction. The initial choices for CCBs include diltiazem and verapamil.

•Diltiazem (Oral regular release formulation):
Initial dose of 30-60mg PO four times daily. Dosage may be increased up to 360mg a day (some patients require 480mg a day) in divided doses 3-4 times a day. Once stable the patient may be converted to a long acting product.

•Verapamil (Oral regular release formulation)
Initial dose of 80-120mg PO every 8 hours. May increase up to 480mg daily in 3-4 divided doses.

Angiotensin Converting Enzyme Inhibitors (ACEIs):
The main mechanism ACEIs is to decrease BP. ACEI’s work by inhibiting the conversion of angiotensin I, to angiotensin II, which is a potent vasoconstrictor. They cause arterial dilation, thereby reducing total peripheral resistance. There is no change in heart rate or cardiac output, although in heart failure patients an increase in cardiac output may be observed. They should be instituted when hypertension persists despite use of NTG and BBs in patients with LV dysfunction, CHF or ACS patients with diabetes. They have also been shown to reduce mortality not only in the previously mentioned patient types but also in a wide spectrum of patients with high risk chronic CAD. Angiotensin receptor blockers (ARBs) are now considered an appropriate alternative to ACEIs. They block angiotensin receptors and decrease systemic vascular resistance. Some examples of ACEI’s are enalapril (Vasotec®) 10-40mg daily, lisinopril (Prinivil®, Zestril®) 10-40mg daily and fosinopril (Monopril®) 10-40mg daily. Examples of ARB’s are valsartan (Diovan®) 80-320mg daily, losartan (Cozaar®) 50-100mg daily and olmesartan (Benicar®) 20-40mg daily.

Antiplatelet Therapies

Antiplatelet Therapy:
This therapy decreases platelet aggregation, thereby helping to prevent further clot formation. These agents do not dissolve clots. The prevention of clot formation allows for continued blood flow and oxygen delivery. The agents have different mechanisms of action and may be used alone or in combination with each other.

Oral Antiplatelet Therapy:
•Aspirin (ASA)
Aspirin should be started immediately and continued indefinitely.
The doses of ASA are 81-325mg daily.

•Clopidogrel (Plavix®)
Clopidogrel should be started in patients who do not tolerate
ASA. Clopidogrel should be loaded with a one time dose of 300mg then
given as 75mg daily maintenance dose. If an early nonintervention approach is planned, clopidogrel should be added to ASA as soon as possible and continued for at least 1 month and up to 9 months. If PCI is planned, clopidogrel should be started and continued as above as long as the patient is not at high risk for bleeding.

IV Antiplatelet Therapy – Glycoprotein (GP) IIb/IIIa Inhibitors:
GP IIb/IIIa inhibitors block the attachment of fibrinogen to platelets thereby inhibiting platelet aggregation and formation of a thrombus (clot). GP IIb/IIIa therapy should be added, in addition to ASA and heparin, to patients with planned intervention (catheterization or PCI), and to patients with ongoing ischemia, elevated troponin, or with other high-risk features in whom intervention is not planned. Therapy may be started just prior to intervention.

•Integrilin
The initial choice of GP IIb/IIIa inhibitor is eptifibatide (Integrilin).
For ACS a loading dose of 180mcg/kg IV bolus (max 22.6 mg) should be given followed by a 2mcg/kg/min IV infusion maintenance dose (max 15mg/h). If undergoing PCI infuse up to 96 hours otherwise infuse up to 72 hours. Infuse 18-24 hours post procedure. For PCI give the same loading and maintenance doses. Begin the infusion and then repeat the loading dose 10 minutes after the first bolus. In renal impairment (CrCL <50 mL/min) give half of the usual maintenance infusion (1mcg/kg/min with a max of 7.5mg/h).

Anticoagulation Therapies

Anticoagulation Therapy:
Therapy with anticoagulants prevents further clot formation from occurring. These agents do not dissolve clots. The “heparins”, Unfractionated Heparin (UFH), and Low Molecular Weight Heparin (LMWH) work at different sites of the coagulation cascade to reduce the incidence of further clot formation. This action allows for continued blood flow and oxygen delivery. Anticoagulation therapy with subcutaneous LMWH or intravenous UFH should be added to Oral Antiplatelet Therapy. The anticoagulant drugs below should NOT be used together.

Anticoagulation Therapy – Unfractionated Heparin:
UFH accelerates antithrombin III (ATIII) to inactivate thrombin. Doses are based on a weight based dosing regimen which varies with specific institutional guidelines. UFH should be given with a 60 units/kg loading dose then a 14 units/kg maintenance dose. Doses should be adjusted based on partial thromboplastin time (aPTT).

Anticoagulation Therapy – Low Molecular Weight Heparin:
LMWH is a smaller molecule than UFH. It is more specific for clotting factor Xa. The anti-Xa activity of LMWH increases clotting time. There is no monitoring necessary as there is with UFH. The initial choices of LMWH are enoxaparin (Lovenox) and dalteparin (Fragmin).

•Enoxaparin
The dose of enoxaparin is 1mg/kg Q12H subcutaneously. In renal impairement (CrCL < 30mL/min) give 1mg/kg daily.

•Dalteparin:
The dose of dalteparin is 120 units/kg (max 10,000 units) Q12H subcutaneously. Consider use of UFH in patients with renal impairment (CrCl < 30ml/min)

Anticoagulant Therapy – Direct Thrombin Inhibitors:
Direct thrombin inhibitors directly inhibit thrombin formation thereby reducing clot formation. Initial choices include argatroban (Argatroban), lepirudin (Refludan), and bivalirudin (Angiomax). Bivalirudin is the most commonly used agent is ACS of the direct thrombin inhibitors. These agents are used in place of heparin (LMWH or UFH) with or without GPIIb/IIIa inhibitors in patients undergoing PCI.

•Bivalrudin
A loading dose of 0.75mg/kg IV bolus followed by 1.75mg/kg IV infusion for the remainder of the procedure (PCI).

Long-term Therapy

Long term medical therapy:
ASA can be given in 81-325mg daily doses. Clopidogrel can be given in doses of 75mg daily when ASA is not tolerated. ASA and clopidogrel can be used in combination for 9 months post UA/NSTEMI. Beta-blockers, lipid lowering agents, and ACEIs can also be used long term.

ACS Conclusion

Conclusion:
It has been well documented for years that coronary artery disease is the number one cause of death in the United States. Thus, the early recognition and treatment of cardiac complications is crucial if we are to lower these statistics. In acute care settings, nurses need to be aware of the signs and symptoms of varying forms of ACS, including UA and N-STEMI. This knowledge, coupled with appropriate use of pharmacology and other indicated therapies, can aid in the reduction of morbidity and mortality associated with ACS.

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Bibliography:
1. American Heart Association. “Acute Coronary Syndrome- What is acute coronary Syndrome?” http://www.americanheart.com/presenter.jhtml?identifier=3010002 Last accessed on 8/8/07
2. American Heart Association. “Heart Attack, Stroke and Cardiac Arrest Warning Signs.” http://www.americanheart.org/presenter.jhtml?identifier=3053; Last accessed on 8/8/07
3. Field, John M, Hazinski Mary Fran, & Gilmore, David. Handbook of Emergency Cardiovascular Care for Healthcare Providers (January 2006). 2006 American Heart Association.
4. Clinical Pharmacology Gold Standard Media. http://cpip.gsm.com Last accessed on 8/8/07
5. Braunwald, Eugene, Antman, Elliot M., et al. ACC/AHA 2002 Guideline Update for the Management of Patients With Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction. 2002. (PDF version of document last downloaded August 9, 2007).

The Florida Board of Nursing recognizes Synergy Group, Inc. as an authorized continuing education unit provider and approves this online course offering. The appropriate number of CEU/CE Contact Hour(s) will be easily visible on certificates generate upon course completion.