Coronary artery disease (CAD) is atherosclerosis of the coronary arteries, which produces blockages in the vessels that provide blood flow to the myocardium or heart muscle. Atherosclerosis is a disease of the endothelium, developing from an inflammatory process of the arterial wall, which causes the smooth walls to become jagged and allows plaque to accumulate both in the wall and along the lining of a cardiac artery. A sudden clot formation may occlude the lumen entirely, spasms can cause occlusion, or restricted blood flow may not be able to provide adequate oxygen when increased demand arises from exercise or stress. It is important to remember that over 99% of plaque rupture may be clinically silent. Myocardial ischemia, injury, and death produce ECG changes, a rise in blood markers, and symptoms ranging from mild discomfort to severe pain (angina pectoris) and/or sudden death. This process of cell injury and death can take 3 to 4 hours to progress, making it ever so important to provide timely means to reperfuse the heart muscle, usually with coronary angioplasty and/or percutaneous coronary intervention (PCI) (stent placement) or more invasive coronary artery bypass surgery (Buja, Holmes, & Willerson, 2015). The 2010 ACLS guidelines for acute coronary syndrome (ACS) includes reperfusion therapy mechanically with PCI or with “clot buster” drugs called fibrinolytics or thrombolytics.