unfractionated heparin.

the infusion and administer IV fluid boluses to any

patients with signs of secondary hypotension. Patients

with infarctions that involve the right ventricle are particularly prone to hypotension given their preload dependent condition.

� Morphine

Administer IV morphine to all patients with persistent pain

despite treatment with nitroglycerin. Morphine reduces

myocardial 02 demand by decreasing vascular tone (preload)

ACUTE CORONARY SYN DROMES

and limiting the catecholamine surge that typically accompanies ACS. Avoid the use of morphine in hypotensive

patients.

� Antiplatelet Therapy

Begin immediate treatment with aspirin (ASA) in all patients

with presentations concerning for ACS. Give 2:162 mg of a

non-enteric-coated version. The first dose should be

crushed or chewed to improve absorption and more

quickly reach therapeutic blood levels. Aspirin alone

reduces mortality by 23o/o in STEM! patients. Minor con ­

traindications (remote history of peptic ulcer disease,

vague allergy, etc) should not preclude its use.

Clopidogrel, prasugrel, and ticagrelor all function to

inhibit platelet activation via blockade of the adenosine

diphosphate (ADP) receptors and therefore work in harmony with aspirin therapy. Clopidogrel has been the most

extensively researched of the 3 and, therefore, is the most

commonly used. A loading dose of 600 mg is recommended

for patients with STEM! undergoing emergent PCI, whereas

a 300-mg load is recommended for patients undergoing

reperfusion with thrombolytics and those with UNNSTEMI.

No loading dose is recommended in patients older than

75 years because of a concern for increased bleeding complications. Both prasugrel and ticagrelor produce a more

intense platelet inhibition, but do so at the expense of an

increase in major bleeding complications. Although there is

a legitimate concern for excessive bleeding in patients given

AD P-receptor antagonists who subsequently undergo coronary artery bypass grafting (CABG), the definite benefit of

platelet inhibition in patients with ACS far outweighs the

potential concern for bleeding in the very low number of

patients who actually require emergent CABG.

Glycoprotein lib/Ilia inhibitors represent the third class

of antiplatelet medications and function by inhibiting platelet aggregation via blockade of the surface binding sites for

activated fibrin. There are currently 3 available agents in this

class (abciximab, eptifibatide, and tirofiban), and their use in

patients with ACS has been extensively researched. These

agents have been associated with an increase in major bleed ­

ing complications, and current guidelines recommend their