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    Critical care update

    CE Center

    RN/DREXEL Home Study Program

    CE credit is no longer available for this article. Expired May 2005

    Sponsored by an unrestricted educational grant from Aventis Pharmaceuticals.

    Originally posted May 2003

    Refining our approach to acute coronary syndrome
    Preventing venous thromboembolism
    The changing winds of healthcare

    Refining our approach to acute coronary syndrome


    CATHERINE SANIUK is the program coordinator for critical care education and a research study coordinator at Brigham and Women's Hospital, Boston.

    KEY WORDS: percutaneous coronary intervention (PCI), unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI), acute coronary syndrome (ACS), risk stratification, low molecular weight heparin, unfractionated heparin, anticoagulation

    When patients present with chest pain, we don't always have all the answers. But research and evidence-based guidelines are helping us find them.

    A patient complains of mid-sternal chest pain radiating down his left arm and his electrocardiogram (EKG) shows ST-segment elevation. You administer oxygen, aspirin, nitroglycerin, morphine, and heparin, and you prepare him for thrombolysis or percutaneous coronary intervention (PCI)—angioplasty with or without stenting—to open up the coronary artery.

    Your plan of action is relatively clear-cut when patients present with ST-segment elevation myocardial infarction (STEMI). But when chest pain patients have no ST-segment elevation, things get a bit murkier.

    In the early stages, it's often difficult to determine whether someone is having unstable angina (UA) or a non-ST-segment elevation MI (NSTEMI), and that makes clinical decision making difficult: Should the patient be admitted— Should the patient be managed conservatively—with medication—or more aggressively—with PCI— Which combination of drugs is most appropriate— Should the patient go to the cath lab and, if so, when—

    There's no one best way to manage all patients with acute coronary syndrome (ACS), particularly UA/NSTEMI. Research and evidence-based guidelines are constantly refining our approach to these patients. If you work in the emergency department (ED) or in cardiac care, here are some of the trends you're probably noticing—and the reasons for them.

    Early risk stratification is essential

    When a patient presents with chest pain without ST-segment elevation, rapid assessment is followed immediately by risk stratification so that the patient gets the most appropriate treatment. One way of accomplishing this is with the TIMI (Thrombolysis in Myocardial Infarction) risk scoring system.

    The TIMI system is simple to use, easy to remember, and doesn't require a calculator. Give your UA/NSTEMI patient one point for each of the prognostic variables listed in the "Risk stratification using the TIMI system" box, then add up those points to get the score. Each score corresponds to a risk percentage, so it can be used to determine the prognosis and guide treatment decisions.

    The score tells you the likelihood that the patient will have a first or recurrent MI, develop ischemia severe enough to require urgent revascularization, or die over the next 14 days.1 The higher the score, the higher the risk and, generally, the more aggressive the treatment that's indicated. A patient with a score of 3 or less would typically be managed medically, while PCI would probably be considered for a patient with a score of 4 or higher.

    Keeping the clot from evolving

    Though some UA/NSTEMI patients will be managed conservatively and others invasively, certain aspects of treatment apply across the board. The American College of Cardiology (ACC) and the American Heart Association (AHA) strongly recommend that patients receive antiplatelet therapy right away. Aspirin is indicated, unless the patient is allergic to it. In this case, clopidogrel bisulfate (Plavix) is used. Clopidogrel is indicated in addition to aspirin in high-risk patients.

    Some patients, depending upon their degree of risk and whether PCI is planned, will need a glycoprotein (GP) IIb/IIIa inhibitor, such as eptifibatide (Integrilin) or tirofiban HCl (Aggrastat).2 And all patients should get heparin—either low molecular weight heparin subcutaneously (SQ) or unfractionated heparin intravenously (IV).2

    The most recent version of the AHA/ACC's Guidelines for the Management of Patients With Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction says that one type of low molecular weight heparin—enoxaparin—is preferred over unfractionated heparin, except in patients who will undergo coronary artery bypass graft (CABG) surgery within 24 hours.2 This recommendation was graded Class IIa, meaning that the weight of evidence or opinion was in its favor, although conflicting evidence or divergent views exist.2

    Several types of low molecular weight heparin are being studied with respect to acute coronary syndrome. However, only enoxparin sodium (Lovenox) has been FDA-approved to prevent ischemic complications of UA and non-Q-wave MI, when administered together with aspirin. The approved dosing regimen is 1 mg/kg SQ every 12 hours. The drug should be given for at least two days, until the patient is clinically stable.3 A typical regimen is two to eight days, though the optimum duration of therapy hasn't been determined.

    Two large, randomized, controlled, multicenter clinical trials—ESSENCE and TIMI IIB—compared the safety and efficacy of enoxaparin and unfractionated heparin in the treatment of UA/NSTEMI. In both trials, the enoxaparin groups had significantly fewer deaths, nonfatal MIs, and severe ischemia requiring urgent revascularization than the unfractionated heparin groups. These benefits were still evident one year after treatment. During acute therapy, however, there was a higher incidence of minor bleeding in the enoxaparin groups.4,5,6,7

    When PCI is necessary

    Concerns have arisen when low molecular weight heparin is used instead of unfractionated heparin in patients headed for PCI. The patient must be adequately anticoagulated during the procedure but sufficiently coagulated when it's time to pull the catheter sheath.

    With IV unfractionated heparin, the degree of anticoagulation can be monitored during the procedure using activated clotting time (ACT), a point-of-care test. And, the heparin's effects can be easily reversed with protamine sulfate, if needed, which is especially important if the patient requires emergency surgery.

    Until recently, low molecular weight heparin couldn't be monitored at the point of care, although plasma anti-Xa levels have been used for this purpose. (In fact, monitoring isn't normally required because low molecular weight heparin, which is typically given SQ, produces a relatively predictable and consistent anticoagulation response.) However, a new point-of-care tool, the ENOX test, recently received FDA clearance for monitoring the anticoagulant effects of enoxaparin.

    An issue that remains, however, regarding low molecular weight heparin and PCI is that patients going for this procedure usually receive a GP inhibitor. Giving these two types of drugs together is still relatively new territory.

    The results of clinical trials are allaying some of these concerns. The SYNERGY trial will look at rates of death and non-fatal MI in 10,000 high-risk patients with non-ST-segment elevation ACS who are going for early invasive treatment. Patients will receive a GP inhibitor plus either enoxaparin or unfractionated heparin.8

    The NICE 1 and NICE 4 trials have already shown that PCI can be performed safely and effectively in patients receiving enoxaparin IV, with or without the GP inhibitor abciximab (Reopro).9 And, the INTERACT trial compared the safety and efficacy of enoxaparin and IV heparin in high-risk NSTEMI patients receiving the GP inhibitor eptifibatide: The enoxaparin group had a higher rate of minor bleeding, but a lower rate of MI and death.10

    In the meantime, the manufacturer of enoxaparin recommends that if a PCI patient has received enoxaparin, the catheter sheath be left in place until six to eight hours after the last dose. After PCI, don't give enoxaparin until six to eight hours after the sheath has been removed.3

    Who gets to go to the cath lab?

    A TIMI risk score can help you anticipate which patients are most likely to need PCI. The AHA/ACC has recommendations, too, regarding who should be sent to the cath lab early on. They strongly recommend an early invasive strategy—angiography with possible revascularization—for UA/NSTEMI patients who have any of the following:2

    — recurrent angina/ischemia at rest or with low-level activity, despite intensive anti-ischemic therapy (nitroglycerin, morphine, oxygen, etc.),

    — elevated troponin (TnT or TnI) levels,

    — new ST-segment depression,

    — recurrent angina/ischemia with symptoms of congestive heart failure, an S3 gallop, pulmonary edema, worsening rales, or new or worsening mitral regurgitation,

    — high-risk (positive) findings on noninvasive stress testing,

    — depressed left ventricular function (e.g., ejection fraction less than 0.40),

    — hemodynamic instability (e.g., hypotension), or

    — sustained ventricular tachycardia.

    These are just some of the many issues being addressed by experts and researchers with respect to UA/NSTEMI. Keeping up with the latest developments and recommendations ensures that our practice reflects not only the tried and true, but the best and most current information that science has to offer.


    1. Antman, E. M., Cohen, M., et al. (2000). The TIMI risk scored for unstable angina/Non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA, 284(7), 835.

    2. Braunwald, E., Antman, E. M., et al. (2002). ACC/AHA 2002 guidelines update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction—summary article: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. (Committee on the Management of Patients with Unstable Angina). J Am Coll Cardiol, 40(7), 1366.

    3. Lovenox. "Prescribing information. Dosage and administration. Adult dosage. Unstable angina and non-Q-wave myocardial Infarction." November 2001. www.aventispharma-us.com/PIs/lovenox_TXT.html (12 Dec. 2002).

    4. Cohen, M., Demers, C., et al., for the Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q-Wave Coronary Events Study Group. (1997). A comparison of low-molecular-weight heparin with unfractionated heparin for unstable coronary artery disease. N Engl J Med, 337(7), 447.

    5. Cohen, M., Demers, C., et al. (1998). Low-molecular-weight heparin in non-ST-segment elevation ischemia: The ESSENCE Trial. Efficacy and safety of subcutaneous enoxaparin versus intravenous unfractionated heparin, in non-Q-wave coronary events. Am J Cardiol, 82(5B), 19L.

    6. Antman, E. M., McCabe, C. H., et al. (1999). Enoxaparin prevents death and cardiac ischemic events in unstable angina/non Q-wave myocardial infarction: Results of the Thrombolysis in Myocardial Infarction (TIMI) IIB trial. Circulation, 100(15), 1593.

    7. Antman, E. M., Cohen, M., et al. (2002). Enoxaparin is superior to unfractionated heparin for preventing clinical events at 1-year follow-up of TIMI IIB and ESSENCE. Eur Heart J, 23(4), 308.

    8. The SYNERGY Executive Committee. (2002). The SYNERGY trial: Study design and rationale. Am Heart J, 143(6), 952.

    9. Kereiakes, D. J., Grines, C., et al. (2001). NICE 1 and 4 Investigators. National Investigators Collaborating on Enoxaparin. Enoxaparin and abciximab adjunctive pharmacotherapy during percutaneous coronary intervention. J Invasive Cardiol, 13(4), 272.

    10. Williams, E. S., & Miller, J. M. (2002). Results from late-breaking clinical trial session at the American College of Cardiology 51st Annual Scientific Session. J Am Coll Cardiol, 40(1), 1.

    Risk stratification using the TIMI system

    Getting chest pain patients the most appropriate treatment requires risk stratification. The TIMI (Thrombolysis in Myocardial Infarction) risk scoring system is one way to do that. Give your unstable angina/non-ST-segment elevation MI patient one point for each of the prognostic variables listed below. Then take the total number of points (the score) and check it against the grid below. The corresponding risk percentage can be used to determine a patient's prognosis and to guide treatment decisions.

    • Age 65 or older
    • Three or more risk factors for coronary artery disease (CAD) (elevated cholesterol levels, family history of coronary artery disease, hypertension, diabetes mellitus, smoking)
    • Previous CAD (stenosis of 50% or more)
    • Aspirin use over the last seven days
    • Two or more anginal episodes over the last 24 hours
    • ST-segment deviation on presentation
    • Elevated creatine kinase MB band (CK-MB) or troponin levels

    Score Risk of death, MI or severe ischemia in the next 14 days
    0 — 1 5%
    2 8
    3 13
    4 20
    5 26
    6 — 7 41

    Source: Antman, E. M., Cohen, M., et al. The TIMI risk scored for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA, 284(7), 835.

    Preventing venous thromboembolism


    SUSAN SHEEHY is associate director of clinical research, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, and the author of numerous articles and textbooks on emergency nursing. She's currently conducting research on the role early nursing intervention plays in the reduction and elimination of venous thromboembolic disease.

    KEY WORDS: venous thromboembolic (VTE) disease, deep vein thrombosis (DVT), pulmonary embolism (PE), unfractionated heparin, low molecular weight heparin

    Despite a variety of prophylactic options, venous thromboembolism kills 60,000 patients in the United States each year. Are we doing all we can to protect our patients?

    Nearly 200 years ago, a French pathologist, Jean Cruveilhier, believed that phlebitis was the cause of most diseases. Although his theory was later disproved by a colleague, Rudolf Virchow, the work of these two men opened the door to our understanding of a problem that still challenges us today: venous thromboembolism (VTE).

    Consider these facts: Two million patients a year in the United States develop deep vein thrombosis (DVT),1,2 the most prevalent form of venous thromboembolic disease. In eight out of 10 cases, the hallmark signs—extremity pain, redness, and swelling—are absent,1,2 and the patient and practitioner may be unaware that there's a problem.

    Without treatment, the clot is more likely to break loose from the vein, travel via the bloodstream through the right side of the heart, and lodge in the lungs as a pulmonary embolism (PE). This happens in close to a third of all patients with DVT—about 600,000 patients a year.1,2 If the PE is large enough, it obstructs the pulmonary vessel and blocks blood flow to the lungs, causing shock, cardiac arrest, and death. In fact, PE kills one in 10 of its victims,1,2 and autopsy reports show that it may be a contributing factor in as many as 25% of all hospital deaths.1,2

    Preventing DVT is essential to reducing mortality from PE, and nurses are the key to accomplishing this goal. Because we frequently see patients first, early, and often, we're in an ideal position to identify risk factors for DVT early on, and to initiate prophylactic measures right away.

    Who's at risk? Or rather, who isn't?

    Essentially, any patient with venous stasis, vascular wall damage, or a clotting abnormality is at risk for DVT. If you work in acute care, chances are most of your patients have at least one of these three conditions.

    Venous stasis results from decreased venous blood flow due to bed rest, paralysis, a long car or plane ride, a leg cast?essentially anything that renders a patient or body part immobile. Another cause of venous stasis is vessel obstruction—from a tumor, fracture, or peripheral vascular disease. Vessel dilation, which can occur because of immobility, congestive heart failure, incompetent vascular valves, pregnancy, or obesity, can lead to venous stasis as well.

    In patients with stasis, the decreased blood flow damages the endothelial lining of the vessels. Poor venous emptying leads to hypoxia because the stagnant blood doesn't return to the lungs. As the blood pools in the veins, clotting factors accumulate in the stasis area, leading to thrombus formation.

    Vascular wall injury promotes DVT formation because it promotes clotting at the site of the injury. Causes of vascular wall injury include trauma from burns, crush injuries, fractures, sepsis, recent surgery, or tight bandages.

    Other causes of vascular wall injury include IV drug abuse, central lines, and venous dilation. Venous dilation results from anything that decreases vascular tone, such as general anesthesia.

    Clotting abnormalities obviously contribute to DVT formation, by increasing the level of clotting factors in the blood, lowering clot inhibitor levels, or decreasing the blood's fibrinolytic components. Clotting abnormalities may be inherited, as in antithrombin III, protein C, and protein S deficiencies; or, they can be triggered by events, such as trauma, burns, acute myocardial infarction, or surgery. Postop patients, for example, are at highest risk for clotting three days after surgery, when their fibrinolytic capacities are the lowest.

    Primary and secondary risk factors for VTE are listed in the "Risk factors for VTE" box. When assessing patients, bear in mind that age is a primary risk factor for DVT. Patients older than 40 are at greater risk than younger patients.3

    Options for preventing venous thrombosis

    Hospitalization is a risk factor for DVT: We admit patients, assign them a bed, help them into it, give them a TV, and send them the message—albeit unintentionally—that they should stay put.

    Outpatients are no exception: Emergency department (ED) patients sometimes lie on a bed or stretcher for hours waiting to go for the next test or be seen by the next practitioner. And same-day surgery patients have been known to show up in the ED with signs and symptoms of DVT or PE several days after the procedure.

    For some patients, the risk of developing DVT will be low. Take someone who is younger than 40 and, except that he's hospitalized, has no other risk factors for venous thromboembolism. He may need only routine nursing intervention to ward off unwanted clots—adequate hydration, early ambulation, and frequent repositioning and range-of-motion exercises. Yes, these things do help; however, the majority of acute care patients have multiple risk factors, so they'll need more aggressive prophylaxis—probably, a combination of things.

    The type and number of risk factors a patient has will help determine the appropriate regimen. You'll need to consider things like his medical condition, the surgery—if any—he is to undergo, his risk of bleeding, the types of prophylaxis available in your institution, and your hospital protocol, if there is one. Many hospitals have protocols for preventing DVT in specific groups of patients—patients going for hip or knee surgery, for example—but few, if any, have protocols that could be easily and appropriately applied to all patients in general.

    The American Academy of Chest Physicians (AACP) has published evidence-based guidelines for preventing venous thromboembolism in various groups of patients.4 For example: For general medical patients with risk factors for VTE, the AACP recommends low-dose unfractionated heparin or low molecular weight heparin,4 which are two of the several options available for DVT prophylaxis. Other options include graduated compression stockings, such as TED or Jobst; intermittent pneumatic compression (IPC) boots, such as Venodyne or Aircast VenaFlow; and warfarin sodium (Coumadin). Here's a brief rundown of each.

    Graduated compression stockings—also referred to as elastic stockings—help prevent DVT by decreasing venous stasis. Make sure they're thigh high, not knee high, so they promote adequate circulation in the popliteal and proximal leg veins as well as the calf veins. DVTs of the upper leg veins are more dangerous than lower leg DVTs; they are more likely to develop into life-threatening PEs.

    Also make sure the stockings fit correctly. Measure the patient's leg and follow the manufacturer's instructions. Explain to patients why the stockings are necessary and tell them not to roll them down. Elevate the patient's legs as well, to help with venous return.

    IPC boots—or compression boots—decrease venous stasis, reduce venous distention, and enhance blood flow in the deep veins of the legs. You can use them along with graduated compression stockings.

    Compression boots have no known side effects and are an option for patients for whom anticoagulation is contraindicated. However, if a patient has been immobile and without any form of DVT prophylaxis for more than three days or so, it's a good idea to have lower extremity Doppler studies done before putting on the boots. That way, you won't have to worry about dislodging a clot that could already be forming.

    Unfractionated heparin is a well-established option for preventing DVT. It may be ordered intravenously (IV) or subcutaneously (SQ), depending upon the patient's reason for admission and his degree of risk for DVT.

    Unfractionated heparin prevents thrombi from forming by combining with antithrombin III, thereby inhibiting the activation of thrombin and factor Xa—both of which play a role in clot formation. It also inhibits platelet aggregation.

    As you know, when given as an IV infusion, unfractionated heparin requires hospitalization and frequent monitoring of activated partial thromboplastin time (aPTT). However, when given in low doses—5,000 units SQ every eight to 12 hours—aPTT monitoring isn't required.

    Unfractionated heparin binds nonspecifically with a multitude of blood components, such as plasma proteins, platelets, osteoclasts, and endothelial cells. This decreases its bioavailability and produces an unpredictable, or variable, anticoagulation response; patients respond differently to it. In some patients, it causes heparin-induced thrombocytopenia (HIT). With long-term use—greater than 10,000 units per day for three months or longer—it can cause osteoporosis.

    Low molecular weight heparin is an alternative to unfractionated heparin. It is given SQ and affects clotting factors higher up in the clotting cascade so it's more specific to what it's meant to do.

    Low molecular weight heparin stimulates antithrombin III's ability to inhibit coagulation. It has greater activity against factor Xa and a longer half-life than unfractionated heparin. All this translates into a more predictable and constant anticoagulation response. And, because low molecular weight heparin is less likely to bind to platelets and osteoclasts, the risk of bleeding, HIT, and osteoporosis is lower than with standard heparin.

    The three types of low molecular weight heparin on the market for DVT prevention are approved for specific groups of patients: ardeparin sodium (Normiflo) for knee surgery patients; dalteparin sodium (Fragmin) for hip replacement or abdominal surgery; and enoxaparin sodium (Lovenox) for hip, knee, or abdominal surgery.

    In addition, enoxaparin is approved for patients at risk for VTE because of severely restricted mobility during acute illness. It's the only low molecular weight heparin approved for DVT prevention in nonsurgical patients.

    Be aware that the three types of low molecular weight heparin that are used for DVT prevention are different fragments of the longer heparin chain, so they are not interchangeable. You cannot simply switch from one to another. And all are contraindicated in active peptic ulcer disease, active bleeding, and pregnancy.

    Warfarin is used for very high-risk patients who require long-term DVT prevention. As you know, it's given orally, and it takes at least three days to produce a therapeutic effect. Ideally, it should follow a short course of low molecular weight heparin. You will need to check the international normalized ratio (INR) daily while the patient is in the hospital, then every two to three days as an outpatient until the INR stabilizes, then every two to four weeks. Treatment typically lasts six to eight weeks. The goal is an INR of 2 to 3.

    Vena caval filters are used to prevent PE in patients who are at high risk for DVT and can't be anticoagulated. They don't prevent DVT, but they trap embolized fragments so they don't reach the lungs.

    Risk assessment and prevention protocols

    Preventing venous thromboembolism requires a multidisciplinary effort. Hospitals need protocols so that nurses can do a quick risk assessment on all patients and get an appropriate prophylactic regimen in place right away.

    At my hospital, we are working to develop a scoring system for risk factor assessment so that, at triage, we can check off what risk factors a patient has and evaluate his or her degree of risk on the spot. In the meantime, we try to initiate DVT prophylaxis right away, as soon as the patient hits the ED. We make sure that patients who will be in our ED for more than 18 hours or so get either IPC boots or some form of heparin.

    Obviously, when it comes to DVT prevention, we cannot underestimate the value of basic nursing care, including patient teaching. Here are some gentle reminders: Do not tether the patient to the bed unnecessarily—either physically or emotionally. For example, you should use saline locks instead of IVs, or a mobile chest drain instead of a more cumbersome chest drainage unit, so that the patient feels more comfortable moving about.

    Unless bed rest is absolutely indicated, make sure patients know it's OK—in fact, it's beneficial—to get out of bed and walk around. And, when appropriate, take a minute to teach patients range-of-motion exercises, or show the family how to provide them.

    Venous thromboembolism is a risk management issue. It can kill patients. We need to treat it the way we treat patient falls and medication errors—aggressively and before the fact.


    1. Heit, J. A., Silverstein, M. D., & Mohr, D. M. (2000). Risk factors for DVT/PE: A population-based control study. Arch Intern Med, 160(9), 809.

    2. Goldhaber, S. Z. (2000). Prevention of venous thromboembolism in medical and surgical patients. 5th Congress of the European Haematology Association. 25 — 28 June 2000. Birmingham, UK. Session 9 — Clinical management of thrombosis.

    3. Clagett, G. P., Anderson, F. A., et al. (1995). Prevention of venous thromboembolism. Chest, 108(Suppl. 4), 312S.

    4. Geerts, W. H., Heit, J. A., et al. (2001). Prevention of venous thromboembolism. The Sixth (2000) ACCP guidelines for antithrombotic therapy for prevention and treatment of thrombosis. Chest, 119(Suppl. 1), 132S.

    Risk factors for VTE

    Major surgery in the past three months
    Acute myocardial infarction (MI)
    Major trauma, especially of the pelvis, hip, knee, or femur
    Spinal cord injury
    Age (40 or older)
    History of venous thromboembolism

    Congestive heart failure
    Chronic respiratory disease
    Hematological disorders
    Nephrotic syndrome
    Family history of venous thromboembolism
    Indwelling central line
    Alcohol abuse
    Human immunodeficiency virus infection
    Varicose veins
    Oral contraception or estrogen use
    Systemic lupus erythematosus
    Presence of a lower extremity cast
    Intravenous drug use
    Recent history of a long car or plane ride

    Sources: 1. Clagett, G. P., Anderson, F. A., et al. (1998). Prevention of venous thromboembolism. Chest, 114(5 Suppl), 531s. 2. Elder, A. (1999). Applying risk assessment models in non-surgical patients: Effective risk stratification. Blood Coagulation & Fibrinolysis, 10(suppl 12), s91. 3. Samama, M. M., Cohen, A. T., et al. (1999). A comparison of enoxaparin with placebo for the prevention of venous thromboembolism in acutely ill medical patients. N Eng J Med, 341(11), 793.

    The changing winds of healthcare


    SANDRA SIECK is director of cardiovascular development at Providence Hospital in Mobile, Ala., where she developed the emergency department's Chest Pain Center and the hospital's Early Heart Attack Care Program. She is also the president and owner of Sieck HealthCare Consulting, LLC, and author of the ACS Best Practice Guide.

    KEY WORDS: chest pain, fee-for-service, Ambulatory Payment Classifications (APCs), reimbursement, acute coronary syndrome, cost avoidance

    Prior to 1997, a financial model was driving clinical outcomes. But that's evolving. A new focus on chest pain management and reimbursement illustrates how.

    Chest pain accounts for approximately 8 million visits to U.S. emergency departments (EDs) each year and leads to 5 million hospital admissions. Of these 5 million in-patients, 13% — 15%—about 700,000—are truly having a heart attack. Those who aren't cost the system at least $600 million.1

    Of the 3 million patients discharged from the ED, 4% — 5%—about 135,000—have chest pain that's due to undiagnosed myocardial infarction (MI). In as many as 22% of these cases, the MI is fatal.1

    These numbers send us an important message: We have an opportunity to improve care and cut cost. Early risk stratification and the use of evidence-based medicine will help us to accomplish both.

    Outpatient risk stratification allows us to admit the high-severity patients and assess the low-severity patients further in outpatient departments such as chest pain centers or observation units, where fixed operating costs are lower. It also ensures that patients receive the most appropriate treatments that ultimately optimize clinical and financial outcomes. Here's how.

    A brief history of chest pain

    As you know, chest pain does not always signal a full-blown, ST-segment elevation MI. Other possibilities include unstable angina and non-ST-segment elevation MIs. In addition, there is chest pain that's cardiac but not caused by coronary artery disease, and there is chest pain that's not cardiac at all. It takes time and technology to distinguish one from the others. Observation plays a vital role, and that's something that hospitals weren't always reimbursed for.

    Until the Balanced Budget Act of 1997, our healthcare delivery system was at least 80% fee-for-service. That means we were paid for essentially whatever we did. If we used a pump, we charged for a pump. If we ran a test, we billed for it and were paid.

    Initially, outpatient care was still reimbursable on a fee-for-service payment system, while inpatient diagnosis-related groups (DRGs) fell within the bundled prospective payment system. The Centers for Medicare & Medicaid Services (CMS) then developed an outpatient system of bundled services comprised of Ambulatory Payment Classifications (APCs). Fee-for-service reimbursement essentially disappeared from the outpatient side as well.

    The changes didn't end there. Soon we were no longer able to bill separately for outpatient observation. Without observation, how can you distinguish one type of acute coronary syndrome from another? The majority of chest pain patients were admitted, thereby overburdening the system, instead of discharging them and facing possible medical and legal ramifications. We admitted many patients so that we would not miss the true MIs; we had no financial incentive to do otherwise. We flooded our inpatient departments, even though we didn't have the nurses there to care for them.

    In a fee-for-service system, where hospitals are reimbursed for diagnostic tests, admitting patients regardless of their acuity made financial sense. But in today's era of cost avoidance, and with current reductions in DRG reimbursement, it no longer did. Patient flow shifted back to the ED, where reimbursement was better.

    Hospitals lobbied Washington for an increase in reimbursement and, in April of last year, hospitals obtained it—in the form of APC 0339. Now, hospitals get an additional $350 for each chest pain, asthma, or congestive heart failure patient who comes to the ED; that money is to be used for risk stratification.

    The additional dollars are linked to certain requirements. In the case of chest pain, we are required to do two sets of cardiac enzymes and two sequential electrocardiograms in the outpatient area before we decide to admit or discharge the patient. These tests, along with nuclear studies and stress tests, help us admit the patients who truly need to be admitted and discharge the patients who do not.

    Evidence-based practice optimizes outcomes

    The American College of Cardiology and the American Heart Association stress the importance of early risk stratification in their Guidelines for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction.2 When care is driven by evidence-based guidelines like these, costs and lengths of stay go down and quality and revenue go up.

    The chest pain arena is one area in which clinical and financial outcomes are becoming inextricably intertwined. Treatment will be benchmarked to criteria such as how long it took to open up that coronary artery and whether we gave that aspirin or that beta-blocker. Reimbursement will be tied to those outcomes.

    The door that separates the clinical from the financial is open, perhaps wider than ever before. Administrators are asking nurses, physicians, and other clinicians for their input. No longer are clinical and financial goals separate. Maybe clinical is now driving finance. Maybe ...


    1. Health Care Financing Administration. National Health Expenditures Projections. www.hcfa.gov/stats/nhe-proj/ (19 Feb. 2002).

    2. Braunwald, E., Antman, E. M., et al. (2002). ACC/AHA 2002 guidelines update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction—summary article: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. (Committee on the Management of Patients with Unstable Angina). J Am Coll Cardiol, 40(7), 1366.