Acute Myocardial Infarction Drug Management: A Review

Mark R. Rasmussen, BA, BSN, RN-C, CCRN
Mark R. Rasmussen, BA, BSN, RN-C, CCRN
Labs are drawn and the cardiology fellow comes down to assess the patient. He determines that this patient meets criteria to go to the cardiac cath lab. The fellow activates the on-call team. The patient is started on a NTG drip at 20 mcg/min, bolused with a weight-based heparin dose and a heparin drip is initiated. The fellow orders a 180-mcg/kg bolus of eptifibatide (Integrilin) followed by a drip at 2 mcg/kg/min. The cath lab RN calls down to the ED and gets a report. The patient arrives at the cath lab hemodynamically stable and on the same amount of drips as he was in the ED. The cath lab team preps the patient, and the fellow(s) get scrubbed. The cath lab RN and CVT/RT hook him up to the NIBP, O2 Sat, and ECG. The heparin drip is stopped and the attending and the fellow(s) get access. The first angiographic shot tells the tale. He has a nasty thrombus sitting in his LAD (left anterior descending) consistent with his ECG. The patient goes on to intervention. The guide engages easily and the wire passes down across the blockage easily. Angioplasty is performed, and after the first balloon inflation, the patient takes a turn for the worst. His HR is now 46 and NIBP has dropped to 88/50 and continues to decrease. The cath lab nurse stops the NTG drip. The MD orders atropine 0.6mg IV and dopamine at 10mcg/kg/min. The nurse quickly administers the atropine. Once that has been flushed in, dopamine is hung at 10 mcg/kg/min. The patient HR comes up to 120 and the NIBP goes up to 144/88. The patient has a drug-eluting stent deployed. Dopamine is titrated down and is shut off by the end of the case. The patient receives 300mg of clopidogrel (Plavix) PO before he is transported to the CCU. This semi-complicated acute MI case may sound familiar. Heparin, eptifibatide, atropine, and clopidogrel are just some of the drugs that are used in a acute coronary case. The above drugs are commonly used at Beth Israel Deaconess Medical Center in Boston, Massachusetts, for the management of an acute MI. This article will review some of the principles and medications described above. Various other drug agents are not discussed in this limited review, but are used in cath labs around the world. Bivalirudin (Angiomax, The Medicines Company) has become more popular in different parts of the country instead of heparin. Abciximab (ReoPro, Eli Lilly and Company) and tirofiban (Aggrastat, Millenium Pharmaceuticals) are other popular IIb/IIIa inhibitor drugs used in different EDs and cath labs instead of eptifibatide. Management of drugs varies continually as a result of ongoing clinical trials around the world. Recently, even the dose of clopidogrel has been changed to 600mg as clinically indicated in some instances. Vasopressors These classes of drugs are the squeezers. These drugs cause vasoconstriction and help increase blood pressures (mean arterial pressure) and perfusion to all organs, most importantly the brain. Vasopressors stimulate various receptors in the body to cause increased heart rate, blood pressure, and more cardiac output. Cardiac output is heart rate multiplied by stroke volume. If I increase my heart rate or stoke volume, I increase my cardiac output. The first treatment of hypotension should be fluid resuscitation. Drugs are more of an adjunct therapy. You have to fix the cause of the problem to cure the issues. There are 4 vasoactive receptors on which these drugs work. They are: Alpha adrenergic. When you think Alpha, think vascular beds and the peripherals. When these are stimulated, they constrict, and cause increased pressure. Think of a pipe going from 4 inches to 2 inches. You get more pressure out of the 2-inch than the 4-inch pipe, given the same volume. Beta-1 adrenergic. Beta-1 is most common in the heart. Beta-1 receptors increase inotropy and chronotropy (squeeze and rate). Beta-2 adrenergic. Beta-2 receptors in blood vessels induce vasodilatation. Dopaminergic. Dopaminergic receptors are found in renal, splanchnic, coronary, and cerebral vascular beds. Stimulation of these receptors can cause either vasodilatation or vasoconstriction, dependent on the amount of dopamine that is infusing. Let's talk about some potent Alpha-1 agents. The big three are usually phenylephrine, norepinephrine, and epinephrine. These drugs provide potent alpha-1 constriction and are used in the management of hypotension. Norepinephrine and epinephrine have Beta-1 stimulation as well. These drugs not only squeeze, they stimulate. Thus, they increase our systemic vascular resistance (SVR) and cardiac output. The effects of dopamine are dose-dependent. At rates of 1.0 to 5.0 mcg/kg/min, dopamine causes vasodilatation of renal and splanchnic beds. At doses of 5.0 to 10.0 mcg/kg/min, you have Beta-1 stimulation, again think heart, and Alpha-1 as well, thus increased CO. Dopamine at ranges of 10.0 to 20.0 mcg/kg/min has moderate Alpha-1 and Beta-1 stimulation. This is the patient with the HR of 120 to 140, and the blood pressure rises quickly. It is not uncommon to use one or two different vasoactive medications. Different receptors are stimulated and depending on the acuity of the patient, higher levels of stimulation may be required. In the case described herein, dopamine was used to elevate the blood pressure by stimulation of the Alpha-1 and Beta-1 receptors. Atropine, vasopressin, lidocaine, and amiodarone are drugs covered in ACLS (Advanced Cardiac Life Support). I do want to touch on atropine briefly, since it was used in our example acute MI case. Atropine is an anticholinergic agent, which means it blocks the action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands and the CNS; increases cardiac output, dries secretions, and antagonizes histamine and serotonin. In simpler terms, it takes the foot off the brake. Heart rate goes up and the patient usually complains of dry mouth. Atropine is used frequently in cath labs, mainly for the treatment of vasovagal reactions (symptomatic bradycardia). Eptifibatide/Heparin Platelets play a key role in the formation of clot. To put it simply, once they become activated, they grow in size, invite their friends and hang out, ultimately forming a nice clot. This ability of platelets to stick to each other is mediated by a surface membrane glycoprotein (GP), one of many. The platelet GP IIb/IIIa receptor is of particular interest because it plays a key role in platelet aggregation. It is this receptor that is stimulated and enables platelets to stick to each other. During an acute MI, the various clotting mechanism are at work, unwittingly causing more harm than good. Drugs like heparin, an indirect thrombin inhibitor, and eptifibatide, a IIb/IIIa inhibitor, can be used to disrupt the clotting process. Heparin is bolused based upon the patient’s weight, as well as eptifibatide. Heparin and eptifibatide may be given in conjunction. The goal is to have an active clotting time (ACT) of greater than 180 seconds. Let’s look at the mechanism of injury, in this case, plaque rupture on an arterial wall. When plaque ruptures, it triggers a release of histamines, stimulates platelet formation, and prevents adequate blood flow through the vessel. To re-establish blood flow, we need to disrupt the clotting mechanisms and open the artery adequately. Aspirin, heparin, and eptifibatide do the first part. The three drugs given together work on the aggregation of platelets. To open the artery, balloon angioplasty is necessary. Once the platelets are unable to stick as well to each other, the hope is that the clot will not increase. Think of platelets as bricks. Eptifibatide and aspirin work on the bricks, while heparin works on the mortar. They also prevent any clots from forming on the wires and balloons used during the angioplasty. More importantly, they prevent thrombus from forming on the newly placed stent. The stent in the artery is a rough surface, especially to a blood platelet. Blood platelets would adhere to the lining of the stent. Patients who have had a stent are placed on clopidogrel, which prevents fibrinogen from binding to ADP receptors, which then in turn prevents platelet adhesion and aggregation. Think of clopidogrel as the super cousin of aspirin. Summary When it comes to cardiac cath lab medications, it is important to remember the art of medicine. Different drugs do different things: some squeeze, some speed the heart up, and some make platelets slippery. Each one has its own benefit. It’s important to remember what you want to achieve and consider the best way to get there. Mark Rasmussen can be reached at mrasmuss@bidmc.harvard.edu
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