Nursing

RN/Thomson AHC Home Study Program CE CENTER

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Originally posted February 2005

By Terri Metules, RN, BSN and Jeff Bauer

Terri Metules is the clinical editor, and Jeff Bauer is a senior editor, at RN. As editors on staff at RN, neither author has any financial relationships to disclose.

The most recent guidelines for managing unstable angina recommend invasive treatment for those at highest risk, but they're often unheeded. Here's what the guidelines call for and how to use them to improve your care.

Of the more than 8 million patients with chest pain who visit an ED each year, 1.4 million have unstable angina (UA).^1,2 Up to half of patients with UA will develop an MI within hours of arriving at the ED.¹ Unfortunately, many of them don't receive the proven treatments recommended in the latest guidelines from the American College of Cardiology (ACC) and the American Heart Association (AHA), which were last updated in 2002.

Part of the reason these guidelines aren't always followed may have to do with how rapidly our understanding of UA and MI is evolving. Previously, clinicians believed that only patients with chest pain whose EKG revealed ST segment elevation were having an MI; those without ST segment elevation were assumed to be having angina and were managed with a more conservative approach.³

Over the last 10 years, however, we have come to recognize that UA is actually the beginning of a process that can also lead to a non-ST segment elevation MI (NSTEMI). In addition, we now know that high-risk patients with this condition do better with earlier, more aggressive intervention.

Research suggests that some clinicians have been slow to embrace the latest treatment strategies.¹ An analysis of more than 56,000 high-risk UA/NSTEMI patients, performed by CRUSADE, a national quality improvement organization for UA/ NSTEMI patients, found that only 36% of eligible patients received a drug (a platelet glycoprotein [GP] IIb-IIIa inhibitor) recommended by the ACC/AHA guidelines that significantly reduces the risk of death in these patients.⁴ The use of other medications recommended by the guidelines ranged from 80% - 92%.⁵

Other CRUSADE research indicates that the use of recommended therapies has increased slightly in recent years.⁶ But the increases have been small, and there is still much room for improvement.⁶

Diagnostic uncertainty may be another reason some clinicians are not readily using the guidelines. When a patient first presents with chest pain, it's often hard to tell if the pain is reflective of UA or NSTEMI or caused by some other condition.

To best care for patients with UA or NSTEMI, you need to be able to spot their signs. You also need to know what the current ACC/AHA guidelines call for, and why.

Understanding the ACS continuum

Acute coronary syndrome (ACS) is an umbrella term used to describe all of the conditions caused by myocardial ischemia, including angina, NSTEMI, and ST segment elevation MI (STEMI). ACS is a major cause of morbidity and mortality in the United States.¹ While stable angina is chest pain that occurs predictably on exertion, UA is chest pain that occurs more often and with less exertion, possibly even when the patient is at rest. Like stable angina, UA is the result of reduced blood flow through the coronary arteries, though it is more severe.

The hallmark sign of acute MI is ST segment elevation in the EKG leads facing the injury. We know that ST segment elevation occurs when the large arteries that supply oxygen to the heart muscle, such as the left main or left anterior descending artery, become completely blocked. Patients with STEMI should receive standard treatment for MI.

What we now know is that, like ST elevation, the ischemic changes that show up on a patient's EKG as ST depression, flat or inverted T waves, or non-specific ST segment changes can signal an impending infarction as well. These changes are caused either by partially blocked arteries, in which case the patient has UA, or complete occlusion of a small vessel?most likely the left circumflex?or the distal portion of a large vessel, in which case he is having an NSTEMI. The infarction that occurs in NSTEMI may start out small, but it can extend, and therefore should be treated as aggressively as STEMI, according to the ACC/AHA guidelines.

The difference between UA and NSTEMI is the severity of injury, as measured by markers of myocardial injury.⁷ If a patient with chest pain has detectable levels of these cardiac biomarkers, then he is having an NSTEMI; if not, he's got UA.⁷

Start by determining the patient's risk

When a patient with chest pain arrives in the ED, treat him according to your facility's chest pain protocol, which should direct you to immediately obtain an EKG, assess the chest pain, provide supplemental oxygen, and administer nitrates and/or morphine sulfate as ordered.

Assess the pain by asking the patient to rate his chest pain on a scale of one to 10, and inquire about the frequency, radiation, duration, and triggers of the pain.¹ As is the case with STEMI, the most common form of chest pain in UA/NSTEMI is substernal pain, which the patient might describe as squeezing, tightness, aching, dullness, fullness, heaviness, or pressure.² However, UA/NSTEMI patients might also present with dyspnea, nausea, diaphoresis, syncope, or pain in the arms, epigastrium, shoulder, or neck; these symptoms are more common among patients 65 and older.²

Take the patient's history and perform a physical exam. Assess him for the classic cardiac risk factors such as diabetes, hypertension, hyperlipidemia, and smoking. Determine if he has a non-cardiac condition?such as a panic disorder, chest trauma, or a musculoskeletal disorder?that might be causing his symptoms.

Because an EKG is one of the best ways to evaluate a patient with chest pain, the guidelines call for a 12-lead EKG to be done within 10 minutes of arrival.⁷

If the initial EKG shows an ST segment that's depressed or normal with inverted T waves, draw blood to check for four markers of cardiac injury: creatine kinase-myocardial band (CK-MB), troponin I (TnI), troponin T (TnT), and myoglobin.¹ If your facility has a central lab, results should be available within 60 minutes, and preferably within 30 minutes.⁷ Testing for the cardiac-specific troponins?TnI and TnT?is preferred because these proteins are not normally detectable in the blood of healthy patients; their presence indicates that myocardial cells have died within a few hours of injury.¹

Testing for CK-MB is an acceptable alternative, but low levels of this marker may be detected in the blood of healthy patients, which limits its usefulness.⁷ Myoglobin, though it is not cardiac-specific and therefore cannot be relied upon to diagnose MI, can be detected as early as one to two hours after the onset of myocardial necrosis.⁷ It can be used to quickly rule out an MI; a negative result on myoglobin testing means the patient's chest pain isn't cardiac-related.⁷

High-risk patients get invasive treatment

Based on the results of the history, exam, EKG, and biomarker testing, patients are classified as low, intermediate, or high risk for death or MI. Low-risk patients are those who don't have angina at rest or at night and have a normal EKG.⁷ High-risk patients have at least one of the features (See “Deciding who's high risk.”) ⁷ All other patients are considered intermediate risk.⁷

There are two types of treatment strategies for UA/NSTEMI: early conservative and early invasive.¹ Early conservative treatment consists of immediate anti-ischemic, antiplatelet, and antithrombotic drug therapy, and continuous monitoring. It's recommended for low-risk patients. These patients should undergo further testing, such as a stress or treadmill test, either before discharge or within 72 hours of discharge as an outpatient.⁷

Early invasive treatment is recommended for high-risk patients. It calls for the same drug therapies, followed by diagnostic catheterization, and revascularization, (typically percutaneous coronary intervention [PCI] or coronary artery bypass grafting [CABG]) as indicated by angiographic findings, within 24 - 48 hours. Intermediate-risk patients can be treated with either strategy.¹

While your patient awaits invasive treatment, your goal is to provide immediate relief of his ischemia and related symptoms.⁷ Assign patients with ongoing pain at rest to bed rest, and provide continuous EKG monitoring. Give supplemental oxygen as needed, and use pulse oximetry to confirm that the patient has adequate arterial oxygen saturation.⁷

You'll give nitroglycerin?first 0.4 mg as a sublingual tablet or spray, and then an IV infusion starting at 10 mcg/min.⁷ For patients who have hypotension or have taken sildenafil (Viagra), tadalafil (Cialis), or vardenafil (Levitra) in the past 24 hours, IV nitroglycerin is contraindicated.⁷

Administer morphine sulfate IV to any patient whose symptoms do not resolve after receiving nitroglycerin or who has acute pulmonary congestion or severe agitation. Patients with ongoing chest pain should also receive a beta-blocker, such as metoprolol (Lopressor). Angiotensin converting enzyme (ACE) inhibitors are used for patients with left ventricular (LV) dysfunction or congestive heart failure whose hypertension persists despite treatment with nitroglycerin and a beta-blocker.⁷

Patients should also receive antiplatelet drug therapy immediately, to prevent platelet activation. Aspirin is the first choice. Unless there are contraindications, all UA/NSTEMI patients?high risk or not?should receive an initial dose of 160 - 325 mg as soon as they arrive in the ED.⁷ The patient should continue to receive a daily dose of 75 - 325 mg.⁷

Clopidogrel (Plavix) should be administered in addition to aspirin and continued for at least one month in all patients except those for whom CABG is planned. Clinical trials of this drug have used a loading dose of 300 mg, followed by 75 mg daily.⁷ For patients who will undergo CABG, clopidogrel should be withheld for five to seven days before surgery.⁷ Patients who can't take aspirin because of allergy or major GI intolerance, such as significant bleeding from a peptic ulcer, should receive clopidogrel alone.

Platelet GP IIb-IIIa inhibitors are often overlooked

The third type of drug administered as part of antiplatelet therapy is a GP IIb-IIIa inhibitor. These relatively new agents prevent platelet aggregation by keeping fibrinogen from binding to the GP IIb-IIIa receptors on the platelet surface.⁷ The use of a GP IIb-IIIa inhibitor within 24 hours of admission significantly reduces UA/NSTEMI patients' risk of death while hospitalized, but only a little over a third of eligible patients receive it.⁵

The three GP IIb-IIIa inhibitors approved for use in the United States fall into two categories. Eptifibatide (Integrilin) and tirofiban (Aggrastat) belong to a category called small-molecule agents, while the third drug, abciximab (ReoPro), is a monoclonal antibody fragment.¹ Eptifibatide and tirofiban are more specific for the GP IIb-IIIa receptor than abciximab, but platelet aggregation returns to normal four to eight hours after these two drugs are stopped while the effects of abciximab can last for weeks.¹

The guidelines call for the administration of a GP IIb-IIIa inhibitor to high-risk patients who will undergo catheterization or PCI.¹ Ideally, the drug should be given as soon as possible; it may be given just before PCI if not administered sooner.

Patients who will be undergoing PCI may receive any one of the GP IIb-IIIa inhibitors. Those who won't can be given eptifibatide or tirofiban, but not abciximab.¹ The GP IIb-IIIa inhibitors are contraindicated for patients with bleeding diathesis (an unusual susceptibility or predisposition to bleeding), acute abnormal bleeding or history of stroke within the last month, any history of hemorrhagic stroke, or severe hypertension that is not controlled by drug therapy.¹ Renal dialysis, a history of major surgery within the last six weeks, or a platelet count <100,000 mm³ are also contraindications.¹ In addition to antiplatelet therapy (and the anti-ischemic therapy provided early on), your UA/NSTEMI patient will also need an antithrombotic. Heparin is the most commonly used anticoagulant for these patients. It blocks thrombin formation by accelerating the action of circulating antithrombin, an enzyme that inactivates factors needed to produce thrombin.⁷

Unfractionated heparin (UFH), administered IV, may be used, but the low molecular weight heparin enoxaparin (Lovenox), given subcutaneously, is preferred.⁷ Enoxaparin has a longer half-life than UFH, which means it provides more predictable and sustained anticoagulation and can be administered once or twice a day.

However, because the anticoagulation effect of UFH can be reversed more quickly than that of enoxaparin, UFH is the preferred form of heparin for patients who will undergo CABG within 24 hours.⁷ Contraindications for both forms of heparin include hypersensitivity to heparin, previous heparin-induced thrombocytopenia, severe current thrombocytopenia, uncontrollable active bleeding, and the inability to monitor platelet counts.¹

Patient care continues after revascularization

In addition to giving the recommended drugs, you'll prepare your high-risk patient for diagnostic coronary angiography, which will provide detailed information about the size and distribution of coronary vessels, the location and extent of obstruction, and how suitable the vessels are for revascularization.⁷ If indicated, revascularization?PCI or CABG?should be performed as soon as possible. By improving blood flow through the obstructed coronary arteries, revascularization can relieve symptoms, prevent complications, and improve cardiac function.

Before deciding to progress from angiography to revascularization, the physician will consider the condition of the patient's coronary vessels, the severity of his symptoms, his ventricular function, his life expectancy, and comorbidity.⁷ Which procedure the patient will undergo?PCI or CABG?depends on how many vessels are blocked, the degree of LV dysfunction, and other factors.⁷

Patients who undergo successful PCI are usually discharged the next day, while those who have uncomplicated CABG remain in the hospital for four to seven days.⁷ Most patients will need to continue taking the drugs that were started in the ED, including aspirin, clopidogrel, and ACE inhibitors.⁷ Whether a patient needs to take other medications as well will depend on his risk factors. For example, patients with hypertension will need antihypertensives, and those with high cholesterol levels may need lipid-lowering agents.

Teach your patients about the proper use of any prescribed medications. Address lifestyle modifications that reduce the risk of having another MI, such as quitting smoking, switching to a low-fat diet, and exercising. Teach the patient to recognize the symptoms of an MI and what to do if he experiences such symptoms. Make sure high-risk patients are scheduled for a follow-up visit within two weeks.⁷

Overall, caring for a high-risk UA/NSTEMI patient is similar to caring for one who is having a STEMI. Both types of patients need immediate treatment and continuous monitoring to prevent complications and death. By providing UA/ NSTEMI patients with the early, evidence-based care the guidelines call for, you'll improve their chances of survival and recovery.

REFERENCES

1. The CRUSADE Executive Committee. "A practical guide to understanding the 2002 ACC/AHA guidelines for the management of patient with non-ST segment elevation acute coronary syndromes." 2002. www.crusadeqi.com/Main/Ecab/QIToolbox/ EITO453_Monograph.pdf (10 Nov. 2004).

2. Braunwald, E. (2003). Application of current guidelines to the management of unstable angina and non-ST-elevation myocardial infarction. Circulation, 108(16 Suppl 1), III28.

3. CRUSADE National Quality Improvement Initiative. "Can risk stratification of unstable angina patients suppress adverse outcomes with early implementation of the ACC/AHA Guidelines: The CRUSADE national quality improvement initiative. www.crusadeqi.com/Main/Ecab/ CRUSADEOverview.pdf (16 Nov. 2004).

4. CRUSADE National Quality Improvement Initiative."AHA and ACC annual meeting presentations." 2004. www.crusadeqi.com/Main/Ecab/Newsletters/ NL4_FINAL_PRINTREADY_03MAR04.pdf (16 Nov. 2004).

5. CRUSADE National Quality Improvement Initiative. "Focus on acute care: Use of GP IIb-IIIa inhibitors." 2003. www.crusadeqi.com/Main/Ecab/Newsletters/ focus_on_qi_20NOV2003.pdf (16 Nov. 2004).

6 CRUSADE National Quality Improvement Initiative. "CRUSADE national report." 2003. www.crusadeqi.com/Main/Ecab/NationalReports/ National_Report_Nov03.pdf (16 Nov. 2004).

7. American College of Cardiology and the American Heart Association. "ACC/AHA 2002 guideline update for the management of patients with unstable angina and with non-ST segment elevation myocardial infarction." 2002. www.acc.org/clinical/guidelines/unstable/ unstable.pdf (10 Nov. 2004).

Deciding who's high risk

How you'll treat a patient with unstable angina (UA) or non-ST segment MI (NSTEMI) will depend upon whether he's considered low, intermediate, or high risk for death or MI, as determined by his history, exam, EKG, and biomarker testing. High-risk patients will need what the ACC/AHA guidelines call early invasive treatment, which includes anti-ischemic, antiplatelet, and anticoagulant drug therapy, and diagnostic catheterization and revascularization as needed within 24 - 48 hours.

To be classified as high risk, a patient needs to have a least one of the following features:

History

• Accelerating tempo of ischemic symptoms within the past 48 hours

Character of pain

• Pain at rest that lasts >20 minutes

Clinical findings

• Pulmonary edema
• New or worsening mitral regurgitation murmur, an S₃ gallop, or rales
• Hypotension (systolic BP <100 mm Hg)
• Bradycardia (pulse <60 bpm)
• Tachycardia (pulse >100 bpm)
• Age >75 years

EKG findings

• ST segment depression greater than or equal to 0.5 mm
• Transient ST elevation greater than or equal to 0.5 mm
• New, or presumed new, bundle-branch block
• Sustained ventricular tachycardia
• Cardiac markers
• Troponin I or troponin T >0.1 ng/ml
• Elevated CK-MB (normal is 0% - 4%)

Sources: 1. The CRUSADE Executive Committee. "A practical guide to understanding the 2002 ACC/AHA guidelines for the management of patient with non-ST segment elevation acute coronary syndromes." 2002. www.crusadeqi.com/Main/Ecab/QIToolbox/ EITO453_Monograph.pdf (10 Nov. 2004). 2. American College of Cardiology and the American Heart Association. "ACC/AHA 2002 guideline update for the management of patients with unstable angina and with non-ST segment elevation myocardial infarction." 2002. www.acc.org/clinical/guidelines/unstable/ unstable.pdf (10 Nov. 2004).