Advanced Clinical Insights & Practice: Acute Coronary Syndrome

Advanced Clinical Insights & Practice: Acute Coronary Syndrome

Article Jun 30, 2008

CEU Review Form Advanced Clinical Insights & Practice: Acute Coronary Syndrome (PDF) Valid until September 5, 2008

     Advanced Clinical Insights & Practice is an ongoing series designed to provide continuing education to an ever-expanding realm of paramedicine that needs more of it: the critical care transport paramedic. Second, and equally important, are the benefits that can be reaped by other certification levels reading this feature. For EMT-Basics and Intermediates, it will provide a great enhancement to your core knowledge, although most of the interventions discussed will be beyond your traditional scope. For paramedics, it will augment both your pathophysiological understanding and clinical assessment/management skills of diseases and injuries discussed. Ultimately, it is hoped that anyone who reads these articles will become a better clinician. The next article will appear in the October issue.

     This article provides the critical care paramedic with a review of the ongoing management of a patient with an acute coronary syndrome (ACS). In the March issue, we focused on the management and critical care transport of an unstable ACS patient from a small outlying community hospital back to the cath lab. In this article, we focus on the same patient as she progresses through the catheterization lab with complications. It is important to remember that, due to the instability of the precipitating condition, not all patients have a successful outcome with catheterization, and the critical care transport crew may be summoned again for transport.

     It's around 0930 hours, and you and your partner have arrived at your program's sister hospital where you are to transfer a "stable cardiac patient" back to the main campus for ongoing definitive treatment after she received emergent cardiac catheterization. Upon arrival, you find the patient still in cath lab #3 and immediately detect distress in everyone present. From your vantage point behind the lead wall and viewing glass, you can see the patient lying supine on the table, where the cardiologist is frantically working with catheters in her groin, another care provider is assisting the patient's ventilations with a bag-valve mask, and two nurses are regulating IV drips and administering medications. Your RN partner turns to you and says, "I thought this was supposed to be a routine transport." "Me too," you whisper back quietly, as you watch the situation unfolding before your eyes. In the following article, we will return to this case study to provide additional information as it pertains to the discussion.

     In many of today's EMS systems, advancements have been made that allow EMS providers to identify patients at risk for acute coronary syndromes or an AMI event through a thorough history and physical examination, and by obtaining and transmitting a 12-lead ECG to the hospital. This information allows the emergency department physician or a cardiologist to activate the cardiac catheterization team. With this ability, some EMS systems have developed a protocol to allow prehospital providers to bypass the ED and proceed directly to definitive treatment in the cath lab. In fact, there is ongoing research into a combination of therapies, where prehospital providers administer low-dose fibrinolytics to STEMI patients and then deliver them to the cath laboratory.

     It is important to note that treatment rendered by the prehospital and ED providers is not ineffective. It's just that many interventions done in the emergency setting (both prehospital and ED) are geared to minimize or halt the active infarction and deal with other cardiovascular complications, but they do not provide true repair to the damaged blood vessel. It's with this mind-set the critical care provider must remember the old saying that "time is muscle."

     Angioplasty is composed of the Greek words aggeios, meaning "vessel" and plastos, meaning "formed." Over the years, this technique has undergone several name changes, although the basic premise is the same. The most current reference for this procedure is "percutaneous coronary intervention" (PCI), which previously has been referred to as "angioplasty," "percutaneous transluminal coronary angioplasty" (PTCA), or simply "balloon angioplasty."

     This technique for opening coronary arteries, introduced in the late 1970s, is currently performed on more than one million people in the United States annually. The procedure has greatly reduced the number of cardiac bypass graft surgeries (open heart surgery), and reduced overall morbidity and mortality of infarction patients. PCI is an invasive procedure that can allow the cardiologist to identify the location of a stenosis/lesion in the coronary artery and provide definitive treatment/therapy via dilatation of the obstructive plaque or dilatation with stenting. With the obstruction removed, blood flow distal to the lesion can again resume and the heart muscle is preserved. Although "clot-busting" agents have also been used to reopen vessels, studies have shown that patients treated with thrombolytics or fibrinolytics versus PCI in the cath lab have an increased morbidity and mortality owing to the reocclusion of the vessel after "medical therapy" is complete, but research is ongoing.

     As mentioned previously, information gained from the prehospital and/or emergency department regarding the patient with an acute coronary syndrome will initiate the cath lab team, which is commonly comprised of one or two nurses, a radiology technician and the interventional cardiologist. After being alerted, much like trauma team alerts, the team proceeds to the cath lab and begins setting up the suite to receive the patient.

     PTCA is performed by guiding a number of thin catheters into the coronary arteries, usually through the large femoral artery. Another approach involves cannulation through the brachial artery, although this is typically more time-consuming and does not allow as large a sheath to be introduced. This process is not without risks, as perforation of the cannulated vessel can result in substantial and life-threatening hemorrhage. Of even more concern is that patients are first anticoagulated with heparin, aspirin and often a glycoprotein IIb/IIIa inhibitor prior to the procedure to decrease the risk of reocclusion following angioplasty.

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     Once the artery is catheterized with a 5–8 French sheath (similar to the large-bore central lines inserted into trauma patients for fluid resuscitation), a flexible guidewire is introduced into the vessel and navigated cephalad through the abdominal and thoracic aorta to a point just before the aortic valve. The coronary arteries are the first vessels to branch off the aorta just distal to the aortic valve. From here, the guidewire is guided into the coronary circulation with the help of an injected radiopaque dye. Once the dye is injected, the patient's vascular system is illuminated with fluoroscopy, which allows the physician to see a "road map" of the coronary vasculature.

     Since the area of obstruction from a thrombus or embolism prevents blood flow distally, the absence of dye in the distal vasculature will illustrate the lesion. Once identified, the first treatment is to thread a very thin guidewire through the occluded vessel. Once it's through, dye is again injected past the obstruction to verify distal circulation. A flexible balloon catheter is then guided over the wire, centering itself in the middle of the occlusion. Once centered, the balloon is inflated to a predetermined pressure (3–12 atmospheres) and for a predetermined time (usually 1—2 minutes), causing the plaque to compress onto itself and allowing the vessel lumen to enlarge. Ideally, the dilatation will allow blood to again flow to the areas distal to the obstruction.

     One potential complication of PTCA therapy is that during balloon inflation a weakened coronary artery may rupture, resulting in uncontrollable hemorrhage and decreased blood supply to distal myocardium. For this reason, the institution must be prepared to perform an emergent coronary artery bypass graft (CABG) or transfer the patient to an institution that can perform this procedure to prevent significant morbidity or mortality.

     Initial dilatation is successful in 75%–95% of the cases, depending on a number of factors. Because the development of plaque is multi-factoral, more complex lesions will oftentimes reocclude. One newer technique that helps prevent this involves the original PCI. Once the vessel is "opened," a small stent (resembling a small coil or spring) is inserted into the coronary artery at the lesion site to prevent further occlusion. The stent is often coated with a material that will help diminish subsequent plaque adhesion.

     The cardiologist looks worried and is attempting to thread a catheter farther down the left anterior descending artery. You can see on the next fluoroscopy that he has already inserted at least two stents in the very proximal LAD. The patient's BP has fallen to 72/40, her heart rate is 104, and an anesthesiologist is preparing to intubate. The physician asks the nurses to call the receiving facility and speaks with the cardiothoracic surgeon on the overhead intercom system. He relays the patient's current clinical state; hemodynamic status, including an ejection fraction calculated via the catheterization of approximately 24%; notes that the left circumflex is over 80% occluded, with no distal flow to the apex of the heart; and reports significant occlusions to the right marginal artery. The decision is made to attempt to stabilize the patient in the cath lab and transfer her to the receiving facility for emergent CABG surgery.

     Ejection fraction (EF) is the amount of blood that the heart expels with each contraction. A normal EF is considered to be >60%. Any patient who has a low EF, say less than 30%, has a significantly diminished cardiac output. Providing critical care transport to a patient with a poor EF from an acute myocardial infarction or some other etiology causing hemodynamic instability can be very challenging. Essentially, every treatment in your armamentarium has benefits and risks. The astute critical care paramedic needs to realize this prior to using additional medications rather than after. As such, a brief review of basic hemodynamics is warranted here.

     Systolic perfusion pressure (blood pressure) equals cardiac output multiplied by systemic vascular resistance (BP=COxSVR). Whereas cardiac output refers to how much blood the heart ejects over one minute, SVR (systemic vascular resistance) is a function of the degree of arterial vasoconstriction or vasodilation (see Table I). As a general principle, if cardiac output increases or decreases, so will the patient's blood pressure. Similarly (but to a point), if the patient's SVR changes due to vasoconstriction or vasodilation, there will also be a change in systolic pressure.

     Cardiac output, the volume of blood the heart pumps over one minute, is obviously an important component of systolic blood pressure; understanding it is also important when it comes to patient management. The two determinants of cardiac output are heart rate (HR) and stroke volume (SV). Heart rate is predisposed to certain rates according to the normal decaying properties of automaticity cells (intrinsic pacemaker sites), as well as being influenced extrinsically by the two branches of the autonomic nervous system: the sympathetic and parasympathetic. The second determinant, stroke volume, refers to the amount of blood ejected by the ventricles per contraction, and is itself determined by ventricular preload, contractility of the heart and afterload (see Tables II and III). Almost all of these independent determinants of cardiac output and systolic pressure can be manipulated by medications. The goal of this is to maintain a good forward movement of blood out of the left ventricle with the smallest expenditure of cardiac reserves, and to ensure adequate perfusion pressure to the body's organs. Most important, myocardial workload must be balanced with maintaining adequate blood pressure to the brain, heart, lungs, kidneys and other end organs. As a critical care paramedic, it is important to remember the aforementioned discussion on the body's hemodynamic parameters, and, before administering any vasoactive drug or one that affects the heart rate, ask yourself, "BP=COxSVR; CO=SVxHR…which component is the problem with my patient, and which one am I about to affect with this drug?" Even if your protocol requires a consultation with medical control before administering a medication, you should already have a treatment plan thought out and use the medical control consultation to approve the plan.

     Along with oxygen, a common medication administered to a patient suffering an acute ischemic event is nitroglycerin. Nitroglycerin predominantly dilates capacitance vessels (venous); however, it is unique in that it also dilates coronary vessels through activation of nitric oxide in the endothelium of the blood vessel. This dilatation allows increased perfusion to the distal ischemic regions of the myocardium. This benefit, however, must be balanced with the fact that vasodilatation of the venous system will result in diminished blood return to the right atrium. By decreasing preload to the right side of the heart, the heart instinctively attempts to compensate by increasing its rate and systemic vascular resistance. This increase in heart rate, if significant, causes an increase in myocardial oxygen consumption, possibly increasing ischemia and the size of the infarct.

     Another medication commonly used during an ACS is the beta blocker. When preparing to transport a patient with a diagnosed ACS from the emergency department, providing the patient's systolic pressure is not extremely low and he is not bradycardic, consider asking if he has received full doses of beta blockade prior to transport. Common practice in AMI management is to "beta block" the patient to reduce myocardial oxygen consumption by decreasing the heart rate. This is often done with metoprolol at 5mg doses IVP (max 15 mg). Ideally, the heart rate should be controlled between 50–60 bpm.

     Complications that arise on the cath table may also be from poor cardiac contractility (inotropic activity). If the heart rate is normalized, the next step to maintaining perfusion pressure is typically addressed by evaluating the inotropic status of the heart. Inotropic medications increase the contractile force of the heart by stimulating the adrenergic beta 1 receptors in the heart. Stimulation of beta 1 receptors causes an increase in adenyl cyclase activity in the cellular walls, which in turn promotes the conversion of ATP into cyclic adenosine monophosphate (cAMP). As intracellular levels of cAMP rise, the desired sympathomimetic response is gained. If needed, common positive inotropic medications given via infusion in critical care are dopamine hydrochloride, dobutamine hydrochloride and epinephrine hydrochloride. Dobutamine hydrochloride is the only "pure" beta agonist and is a good choice, since it increases contractile force without increasing SVR by stimulating alpha receptors.

     Milrinone lactate is a phosphodiesterase inhibitor that can also be used as a positive inotropic agent. Phosphodiesterase is an intracellular enzyme that breaks down cAMP, thereby eliminating the adrenergic response. If this enzyme is blocked by the action of milrinone lactate, the levels of cAMP intracellularly will remain elevated and promote continued beta 1 stimulation. This translates not only to increased contractile force in the myocardium, but also smooth muscle relaxation in the vascular structures of the heart and arterial bed. This is ideal with the patient in acute left ventricular failure who has an elevated SVR due to the body's release of catecholamines in an attempt to compensate for a low cardiac output state. Overall, this drug will promote a slight decrease in SVR while increasing the heart's contractile force. The heart can pump more efficiently, increase coronary perfusion pressure, decrease myocardial ischemia and increase end-organ perfusion.

     Finally, increasing the SVR pharmacologically may be a consideration in low-perfusion states to elevate systolic pressure, but it must be matched by an increase in the contractile force of the left ventricle in order to maintain normal/adequate cardiac output. If this additional strain on the left ventricle is too high, it will place the patient in overt left ventricle failure. Usually, this is not the care option for managing hypotension in the face of an MI. Inotropic and chronotropic agents are usually employed first.

     During the ongoing management of an unstable ACS patient, the cath lab team may utilize pharmacological therapies such as nitroglycerin, milrinone lactate and dobutamine hydrochloride in an attempt to maintain the patient's cardiac output, blood pressure and heart rate. If these interventions fail to work, as evidenced by continually diminishing blood pressure, rising heart rate and ECG evidence of the infarction spreading (by increasing ST segment elevation), the cardiologist may decide to place an intra-aortic balloon pump (IABP) catheter through the femoral sheath. The IABP is designed to increase myocardial perfusion and decrease the afterload the left ventricle has to overcome in order to pump blood into the systemic circulation. Along with the IABP balloon, the cardiologist will insert an arterial pressure line to manage inflation and deflation of the balloon. The result is a possible increase in blood pressure, decrease in heart rate and increase in the patient's SpO2.

     The critical care transport crew may then be called upon to transport the patient should surgical capabilities for a CABG not be immediately available and will need to maintain this fine balance during transport. The concerns of understanding and managing the patient receiving IABP therapy during transport will be the focus of the next Advanced Clinical Insights & Practice article in the October issue.

     Where the first article in this series in the March issue discussed the critical care management and transport of an unstable MI patient from either the prehospital or outlying facility to the cardiac catheterization laboratory, this article addresses what happens in the cath lab during a PCI intervention, as well as complications that may arise. In this setting, the critical care paramedic may once again be called upon to provide emergent transport of the patient to a facility where ongoing treatment (such as CABG surgery) may be better rendered. The patient in this scenario may be more critically unstable than what is commonly seen, and requires the critical care team to remain abreast of common pharmacological management utilized in support of her heart rate, blood pressure and coronary perfusion. As stated earlier, the goal is to maintain good forward movement of blood with the smallest expenditure of cardiac reserves, and to ensure adequate perfusion pressure to the body's organs. Most important, myocardial workload must be balanced with maintaining an adequate blood pressure to the brain, heart, lungs, kidneys and other end organs.

CEU Review Form Advanced Clinical Insights & Practice: Acute Coronary Syndrome (PDF) Valid until September 5, 2008

Andersen HR, Nielsen TT, Rasmussen K, et al. A comparison of coronary angioplasty with fibrinolytic therapy in acute myocardial infarction. N Engl J Med 349:733–742, 2003.
Braunwald E, Zipes DP, Libby P, eds. Heart Disease: A Textbook of Cardiovascular Medicine, 6th edition. W.B. Saunders, 2001.
Crawford M, DiMarco JP, et. al. Cardiology. Mosby, 2001.
Fink MP, Abraham EV, Jean-Louis, Kochanek PM, eds. Textbook of Critical Care, 5th edition. Elsevier Saunders, 2005.
Hensley FA, Martin DE, Gravlee GP, eds. A Practical Approach to Cardiac Anesthesia, 3rd edition. Lippincott Williams and Wilkins, 2003.

Randall W. Benner, Med, MICP, NREMT-P, is an instructor in the Department of Health Professions at Youngstown (OH) State University, and has over 20 years' experience in the delivery of prehospital medicine, critical care transport medicine and prehospital education. He currently serves as director of the Emergency Medical Technology Program at Youngstown State University, where he is responsible for all levels of prehospital EMS and critical care educational programs. While still functioning actively as a prehospital provider and flight paramedic in Ohio, he is also completing his PhD in Education.

Matthew S. Zavarella, RN, NREMT-P, MS, CFRN, CCRN, CEN, SRNA, a practicing paramedic/nurse, has been involved with EMS, EMS education, publishing and aeromedical critical care transport for 15 years. He holds a bachelor's in Health Sciences from YSU and a master's in Science from the University of Mississippi Medical Center. He's also nearing completion of a second master's degree in Nursing Anesthesia from the Excela Health School of Anesthesia in Latrobe, PA. He works part time as a critical care nurse and a critical care flight nurse.

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