CORONARY ARTERY DISEASE

CARDIAC DISORDERS

CORONARY ARTERY DISEASE

Coronary artery disease (CAD) is a disease characterized by the accumulation of plaque within the layers of the coronary arteries. The plaques progressively enlarge, thicken, and calcify, causing a critical narrowing (75% occlusion) of the coronary artery lumen, resulting in a decrease in coronary blood flow and an inadequate supply of oxygen to the heart muscle.

Acute coronary syndromes (ACS) is a term used to define potential complications of CAD. This syndrome includes unstable angina, non-ST-segment elevation myocardial infarction (MI), and ST-segment elevation MI.

Pathophysiology and Etiology

• The most widely accepted cause of CAD is atherosclerosis (see Box 13-1, page 380).
• Angina pectoris, caused by inadequate blood flow to the myocardium, is the most common manifestation of CAD.
  • Angina is usually precipitated by physical exertion or emotional stress, which puts an increased demand on the heart to circulate more blood and oxygen.
  • The ability of the coronary artery to deliver blood to the myocardium is impaired because of obstruction by a significant coronary lesion (75% narrowing of the vessel).
  • Angina can also occur in other cardiac problems, such as arterial spasm, aortic stenosis, cardiomyopathy, or uncontrolled hypertension.
  • Noncardiac causes include anemia, fever, and thyrotoxicosis.
• ACS is caused by a decrease in the oxygen available to the myocardium due to:
  • Nonobstructive clot on an atherosclerotic plaque.
  • Coronary vasospasm.
  • Atherosclerotic obstruction without clot or vasospasm.
  • Inflammation or infection.
  • Unstable angina due to a non cardiac cause (see angina).
  • Thrombus formation with subsequent coronary artery occlusion (the most common cause). (See MI, page 385.)
• Risk factors for the development of CAD include:
  • Nonmodifiable: age (risk increases with age), male sex (women typically suffer from heart disease 10 years later than men due to the postmenopausal decrease in cardiac-protective estrogen), race (nonwhite populations have increased risk), and family history.
  • Modifiable: elevated lipid levels, hypertension, obesity, cigarette smoking, metabolic syndrome (obesity, hypertension, and diabetes mellitus), sedentary lifestyle, stress.
  • Recent studies have shown that there are also new risk factors that have been associated with the development of CAD. These include increased levels of homocysteine, fibrin, lipoprotein(a), and infection or inflammation (measured by C-reactive protein [CRP]).
  • The American Heart Association (AHA) also lists left ventricular hypertrophy (LVH) as a risk factor.
• The Framingham Scoring Method is used to determine the 10-year risk of development of coronary heart disease (CHD) in men and women based on age, total cholesterol, high-density lipoprotein (HDL) level, systolic blood pressure (BP), presence of hypertension, and cigarette smoking. More information can be found at http://www.nhlbi.nih.gov/guidelines/cholesterol/index.htm.

Clinical Manifestations

See Standards of Care Guidelines, page 381.

Chronic Stable Angina Pectoris

Chest pain or discomfort that is provoked by exertion or emotional stress and relieved by rest and nitroglycerin.

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BOX 13-1 The Pathogenesis of Atherosclerosis

Artherosclerois is the gradual accumulation of plaque within an artery forming an artherosclerotic lesion (artheroma). Plaque consists of lipid-filled macrophages (foam cells), fibrin, cellular waste products, and plasma proteins, covered by a fibrous outer layer (smooth muscle cells and dense connective tissue). Plaque is formed when the endothelium is injured by low density lipoproteins (LDL-C), byproducts of cigarette smoke, hypertension, hyperglycemia, infection, increased homocysteine, hyperfibrinogenemia, and lipoprotein a. An inflammatory response occurs, making the endothelium sticky and thereby attracting other adhesion molecules. Over time, the plaque thickens, enlarges, and calcifies, causing gradual lumen obstruction. Lesions eventually become “complicated” and can cause significant coronary obstruction through hemmorrage and ulceration of the plaque. This artherosclerotic process starts in early childhood and continues throughout life.

Recent studies using intravascular ultrasound (IVUS) have suggested that CAD is not an intraluminal disease but rather an extraluminal one. The accepted view is that atheroma accumulation in the coronary artery wall slowly narrows until symptoms of ischemia occur. IVUS has shown that the lumen does not narrow during the development of the artherosclerotic lesion; instead, narrowing occurs very late in the process.

• Character—substernal chest pain, pressure, heaviness, or discomfort. Other sensations include a squeezing, aching, burning, choking, strangling, and/or cramping pain.
  • Pain may be mild or severe and typically presents with a gradual buildup of discomfort and subsequent gradual fading.
  • May produce numbness or weakness in arms, wrists, or hands.
  • Associated symptoms include diaphoresis, nausea, indigestion, dyspnea, tachycardia, and increase in BP.
• Location—behind middle or upper third of sternum; the patient will generally make a fist over the site of the pain (positive Levine sign; indicates diffuse deep visceral pain) rather than point to it with his finger.
• Radiation—usually radiates to neck, jaw, shoulders, arms, hands, and posterior intrascapular area. Pain occurs more commonly on the left side than the right.
• Duration—usually lasts 2 to 15 minutes after stopping activity; nitroglycerin relieves pain within 1 minute.
• Other precipitating factors—exposure to hot or cold weather, eating a heavy meal, and sexual intercourse increase the workload of the heart and, therefore, increased oxygen demand.

Unstable (Preinfarction) Angina Pectoris

Chest pain occurring at rest; no increase in oxygen demand is placed on the heart, but an acute lack of blood flow to the heart occurs because of coronary artery spasm or the presence of an enlarged plaque or hemorrhage/ulceration of a complicated lesion. Critical narrowing of the vessel lumen occurs abruptly in either instance.

• A change in frequency, duration, and intensity of stable angina symptoms is indicative of progression to unstable angina.
• Unstable angina pain lasts longer than 10 minutes, is unrelieved by rest or sublingual nitroglycerin, and mimics signs and symptoms of impending MI.

NURSING ALERT

Unstable angina can cause sudden death or result in MI. Early recognition and treatment are imperative to prevent complications.

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Silent Ischemia

The absence of chest pain with documented evidence of an imbalance between myocardial oxygen supply and demand (ST depression of 1 mm or more) as determined by electrocardiography (ECG), exercise stress test, or ambulatory (Holter) ECG monitoring

• Silent ischemia most commonly occurs during the first few hours after awakening (circadian event) due to an increase in sympathetic nervous system activity, causing an increase in heart rate, BP, coronary vessel tone, and blood viscosity.

Diagnostic Evaluation

• Characteristic chest pain and clinical history
• Nitroglycerin test—relief of pain with nitroglycerin
• Blood tests
  • Hemoglobin to rule out anemia, which may reduce myocardial oxygen supply
  • Fasting blood glucose, fasting lipid panel to rule out modifiable risk factors for CAD
  • Coagulation studies, CRP (determines inflammation), homocysteine (elevated levels are thought to cause damage to the artery lining), and lipoprotein(a) (increased levels are associated with a two-fold risk in developing CAD)
• Resting ECG—may show LVH, ST-T wave changes, arrhythmias, and Q waves.
• ECG stress testing—progressive increases of speed and elevation walking on a treadmill increase the workload of the heart. ST-T wave changes occur if myocardial ischemia is induced.
• Radionuclide imaging—a radioisotope, thallium 201, injected during exercise is imaged by camera. Low uptake of the isotope by heart muscle indicates regions of ischemia induced by exercise. Images taken during rest show a reversal of ischemia in those regions affected.
• Radionuclide ventriculography (gated blood pool scanning)—red blood cells tagged with a radioisotope are imaged by camera during exercise and at rest. Wall motion abnormalities of the heart can be detected and ejection fraction estimated.
• Cardiac catheterization—coronary angiography performed during the procedure determines the presence, location, and extent of coronary lesions.
• Positron-emission tomography (PET)—cardiac perfusion imaging with high resolution to detect very small perfusion differences caused by stenotic arteries. Not available in all settings.
• Electron-beam CT—detects coronary calcium, which is found in most, but not all, atherosclerotic plaque. It is not routinely used due to its low specificity for identifying significant CAD.

STANDARDS OF CARE GUIDELINES

Chest Pain

• Thoroughly evaluate any complaint of chest pain.
• Be alert to those at highest risk for myocardial infarction—smokers, those with hypertension, diabetes, or hyperlipidemia—but do not discount that MI may occur in those without risk factors.
• Be alert to common alternative presentation of coronary artery disease and MI in women, diabetics, and elderly patients (nausea, indigestion, fatigue).
• Notify health care provider and obtain electrocardiogram for complaint of chest pain.
• For chest pain not relieved by rest or nitroglycerin, assist and advise patient to go to emergency facility immediately. Call 911 for emergency response team if pain is consistent with MI.

Footnote

This information should serve as a general guideline only. Each patient situation presents a unique set of clinical factors and requires nursing judgment to guide care, which may include additional or alternative measures and approaches.

Management

Drug Therapy

Antianginal medications (nitrates, beta-adrenergic blockers, calcium channel blockers, and angiotensin-converting enzyme [ACE] inhibitors) are used to maintain a balance between oxygen supply and demand. Reduction of the workload of the heart decreases oxygen demand and consumption. Coronary vessel relaxation promotes blood flow to the heart, thereby increasing oxygen supply.

• Nitrates—cause generalized vasodilation throughout the body.
  • Nitrates can be administered orally, sublingually, transdermally, or I.V. and provide short- or long-lasting effects.
  • Short-acting nitrates provide immediate relief of acute anginal attacks or prophylaxis if taken before activity.
  • Long-acting nitrates prevent anginal episodes and/or reduce severity and frequency of attacks.
• Beta-adrenergic blockers—inhibit sympathetic stimulation of receptors that are located in the conduction system of the heart and in heart muscle.
  • Some beta-adrenergic blockers inhibit sympathetic stimulation of receptors in the lungs as well as the heart (“nonselective” beta-adrenergic blockers); vasoconstriction of the large airways in the lung occurs; generally contraindicated for patients with chronic obstructive lung disease or asthma.
  • “Cardioselective” beta-adrenergic blockers (in recommended dose ranges) affect only the heart and can be used safely in patients with lung disease.
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• Calcium channel blockers—inhibit movement of calcium within the heart muscle and coronary vessels; promote vasodilation and prevent/control coronary artery spasm.
• ACE inhibitors—have therapeutic effects on the vascular endothelium and have shown to reduce the risk of worsening angina.
• Antilipids—reduce cholesterol and triglyceride levels.
• Antiplatelet agents—decrease platelet aggregation to inhibit thrombus formation.
• Folic acid and B complex vitamins—treat increased homocysteine levels.

Percutaneous Coronary Interventions

• Percutaneous transluminal angioplasty
  • A balloon-tipped catheter is placed in a coronary vessel narrowed by plaque.
  • The balloon is inflated and deflated to stretch the vessel wall and flatten the plaque (see Percutaneous Transluminal Coronary Angioplasty, page 366).
  • Blood flows freely through the unclogged vessel to the heart.
• Intracoronary atherectomy
  • A blade-tipped catheter is guided into a coronary vessel to the site of the plaque.
  • Depending on the type of blade, the plaque is either cut, shaved, or pulverized, and then removed.
  • Requires a larger catheter introduction sheath so its use is limited to larger vessels.
• Intracoronary stent
  • A diamond mesh tubular device is placed in the coronary vessel.
  • Prevents restenosis by providing a “skeletal” support.
  • Drug-eluting stents contain an anti-inflammatory drug, which decrease the inflammatory response within the artery.

Other Interventional Strategies

• Coronary artery bypass graft (CABG) surgery
  • A graft is surgically attached to the aorta, and the other end of the graft is attached to a distal portion of a coronary vessel.
  • Bypasses obstructive lesions in the vessel and returns adequate blood flow to the heart muscle supplied by the artery (see Heart Surgery, page 371).
• Transmyocardial revascularization—by means of a laser beam, small channels are formed in the myocardium to encourage new blood flow.

Primary Prevention

According to the AHA Guidelines for Prevention of Cardiovascular Disease and Stroke (2002 Update)

• Cessation of smoking
• Control of high BP (below 130/85 mm Hg in those with renal insufficiency or heart failure; below 130/80 mm Hg in those with diabetes; below 140/90 mm Hg in all others)
• Diet low in saturated fat (< 10% of calories), cholesterol (< 300 mg/day), trans-fatty acids, sodium (< 6 g/day), alcohol (2 or fewer drinks/day in men, 1 or fewer in women).
• Low-dose aspirin daily for those at high risk
• Physical exercise (at least 30 minutes of moderate intensity exercise most days)
• Weight control (ideal body mass index 18.5 to 24.9 kg/m²)
• Control of diabetes mellitus (fasting glucose < 110 mg/dL and HbA_1C < 7%)
• Control of blood lipids
  • Low-density lipoprotein (LDL) < 160 mg/dL if 1 or less risk factor
  • LDL < 130 mg/dL if 2 or more risk factors and 10-year risk for CHD is < 20%
  • LDL < 100 mg/dL if 2 or more risk factors and 10-year risk for CHD is 20% or greater or has diabetes
  • Triglycerides < 150 mg/dL
  • HDL > 40 mg/dL in men, > 50 mg/dL in women
• Control atrial fibrillation (convert to normal sinus rhythm or anticoagulated)

Complications

• Sudden death due to lethal dysrhythmias
• Heart failure
• MI

Nursing Assessment

• Ask patient to describe anginal attacks.
  • When do attacks tend to occur? After a meal? After engaging in certain activities? After physical activities in general? After visits of family/others?
  • Where is the pain located? Does it radiate?
  • Was the onset of pain sudden? Gradual?
  • How long did it last—seconds? Minutes? Hours?
  • Was the pain steady and unwavering in quality?
  • Is the discomfort accompanied by other symptoms? Sweating? Light-headedness? Nausea? Palpitations? Shortness of breath?
  • How is the pain relieved? How long does it take for pain relief?
• Obtain a baseline 12-lead ECG.
• Assess patient's and family's knowledge of disease.
• Identify patient's and family's level of anxiety and use of appropriate coping mechanisms.
• Gather information about the patient's cardiac risk factors. Use the patient's age, total cholesterol level, HDL level, systolic BP, and smoking status to determine the patient's 10-year risk for development of CHD according to the Framingham risk scoring method (Third Report of the National Cholesterol Education Program (NCEP), 2001) available at http://www.nhlbi.nih.gov/guidelines/cholesterol/index.htm.
• Evaluate patient's medical history for such conditions as diabetes, heart failure, previous MI, or obstructive lung disease that may influence choice of drug therapy.
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• Identify factors that may contribute to noncompliance with prescribed drug therapy.
• Review renal and hepatic studies and complete blood count.
• Discuss with patient current activity levels. (Effectiveness of antianginal drug therapy is evaluated by patient's ability to attain higher activity levels.)
• Discuss patient's beliefs about modification of risk factors and willingness to change.

Nursing Diagnoses

• Acute Pain related to an imbalance in oxygen supply and demand
• Decreased Cardiac Output related to reduced preload, afterload, contractility, and heart rate secondary to hemodynamic effects of drug therapy
• Anxiety related to chest pain, uncertain prognosis, and threatening environment

Nursing Interventions

Relieving Pain

• Determine intensity of patient's angina.
  • Ask patient to compare the pain with other pain experienced in the past and, on a scale of 0 (no pain) to 10 (worst pain), rate current pain.
  • Observe for other signs and symptoms, including diaphoresis, shortness of breath, protective body posture, dusky facial color, and/or changes in level of consciousness (LOC).
• Position patient for comfort; Fowler's position promotes ventilation.
• Administer oxygen if prescribed.
• Obtain BP, apical heart rate, and respiratory rate.
• Obtain a 12-lead ECG as directed.
• Administer antianginal drug as prescribed.
• Report findings to health care providers.
• Monitor for relief of pain, and note duration of anginal episode.
• Take vital signs every 5 to 10 minutes until angina pain subsides.
• Monitor for progression of stable angina to unstable angina: increase in frequency and intensity of pain, pain occurring at rest or at low levels of exertion, pain lasting longer than 15 minutes.
• Determine level of activity that precipitated anginal episode.
• Identify specific activities patient may engage in that are below the level at which anginal pain occurs.
• Reinforce the importance of notifying nursing staff when angina pain is experienced.

Maintaining Cardiac Output

• Carefully monitor the patient's response to drug therapy.
  • Take BP and heart rate in a sitting and a lying position on initiation of long-term therapy (provides baseline data to evaluate for orthostatic hypotension that may occur with drug therapy).
  • Recheck vital signs as indicated by onset of action of drug and at time of drug's peak effect.
  • Note changes in BP of more than 10 mm Hg and changes in heart rate of more than 10 beats/minute.
  • Note patient complaints of headache (especially with use of nitrates) and dizziness.
    • Administer or teach self-administration of analgesics as directed for headache.
    • Encourage supine position to relieve dizziness (usually associated with a decrease in BP; preload is enhanced by this mechanism, thereby increasing BP).
  • Institute continuous ECG monitoring or obtain 12-lead ECG as directed. Interpret rhythm strip every 4 hours for patients on continuous monitoring (beta-adrenergic blockers and calcium channel blockers can cause significant bradycardia and varying degrees of heart block).
  • Evaluate for development of heart failure (beta-adrenergic blockers and some calcium channel blockers decrease contractility, thus increasing the likelihood of heart failure).
    • Obtain daily weight and intake and output.
    • Auscultate lung fields for crackles.
    • Monitor for the presence of edema.
  • Monitor laboratory tests as indicated.
• Be sure to remove previous nitrate patch or paste before applying new paste or patch (prevents hypotension). To decrease nitrate tolerance transdermal nitroglycerin may be worn only in the daytime hours and taken off at night when physical exertion is decreased.
• Be alert to adverse reaction related to abrupt discontinuation of beta-adrenergic blocker and calcium channel blocker therapy. These drugs must be tapered to prevent a “rebound phenomenon”: tachycardia, increase in chest pain, hypertension.
• Discuss use of chromotherapeutic therapy with health care provider (tailoring of antianginal drug therapy to the timing of circadian events).
• Report adverse drug effects to health care provider.

Decreasing Anxiety

• Rule out physiologic etiologies for increasing or new onset anxiety before administering as needed sedatives. Physiologic causes must be identified and treated in a timely fashion to prevent irreversible adverse or even fatal outcomes; sedatives may mask symptoms delaying timely identification and diagnosis and treatment.
• Assess patient for signs of hypoperfusion, auscultate heart and lung sounds, obtain a rhythm strip, and administer oxygen as prescribed. Notify the health care provider immediately.
• Document all assessment findings, health care provider notification and response, and interventions and response.
• Explain to patient and family reasons for hospitalization, diagnostic tests, and therapies administered.
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• Encourage patient to verbalize fears and concerns about illness through frequent conversations—conveys to patient a willingness to listen.
• Answer patient's questions with concise explanations.
• Administer medications to relieve patient's anxiety as directed. Sedatives and tranquilizers may be used to prevent attacks precipitated by aggravation, excitement, or tension.
• Explain to patient the importance of anxiety reduction to assist in control of angina. (Anxiety and fear put an increased stress on the heart, requiring the heart to use more oxygen.) Teach relaxation techniques.
• Discuss measures to be taken when an anginal episode occurs. (Preparing patient decreases anxiety and allows patient to accurately describe angina.)
  • Review the questions that will be asked during anginal episodes.
  • Review the interventions that will be employed to relieve anginal attacks.

Patient Education and Health Maintenance

Instruct Patient and Family About CAD

• Review the chambers of the heart and the coronary artery system, using a diagram of the heart.
• Show patient a diagram of a clogged artery; explain how the blockage occurs; point out on the diagram the location of the patient's lesions.
• Explain what angina is (a warning sign from the heart that there is not enough blood and oxygen because of the blocked artery or spasm).
• Review specific risk factors that affect CAD development and progression; highlight those risk factors that can be modified and controlled to reduce risk.
• Discuss the signs and symptoms of angina, precipitating factors, and treatment for attacks. Stress to patient the importance of treating angina symptoms at once.
• Distinguish for patient the different signs and symptoms associated with stable angina versus preinfarction angina.

Identify Suitable Activity Level to Prevent Angina

Advise the patient about the following:

• Participate in a normal daily program of activities that do not produce chest discomfort, shortness of breath, and undue fatigue. Spread daily activities out over the course of the day, avoid doing everything at one time. Begin regular exercise regimen as directed by health care provider.
• Avoid activities known to cause anginal pain—sudden exertion, walking against the wind, extremes of temperature, high altitude, emotionally stressful situations; these may accelerate heart rate, raise BP, and increase cardiac work.
• Refrain from engaging in physical activity for 2 hours after meals. Rest after each meal if possible.
• Do not perform activities requiring heavy effort (eg, carrying heavy objects).
• Try to avoid cold weather if possible; dress warmly and walk more slowly. Wear scarf over nose and mouth when in cold air.
• Reduce weight, if necessary, to reduce cardiac load.

Instruct About Appropriate Use of Medications and Adverse Effects

• Carry nitroglycerin at all times.
  • Nitroglycerin is volatile and is inactivated by heat, moisture, air, light, and time.
  • Keep nitroglycerin in original dark glass container, tightly closed to prevent absorption of drug by other pills or pillbox.
  • Nitroglycerin should cause a slight burning or stinging sensation under the tongue when it is potent.
• Place nitroglycerin under the tongue at first sign of chest discomfort.
  • Stop all effort or activity; sit, and take nitroglycerin tablet—relief should be obtained in a few minutes.
  • Bite the tablet between front teeth and slip under tongue to dissolve if quick action is desired.
  • Repeat dosage in a few minutes for total of three tablets if relief is not obtained.
  • Keep a record of the number of tablets taken to evaluate change in anginal pattern.
  • Take nitroglycerin prophylactically to avoid pain known to occur with certain activities.
• Demonstrate for patient how to administer nitroglycerin paste correctly.
  • Place paste on calibrated strip.
  • Remove previous paste on skin by wiping gently with tissue.
  • Rotate site of administration to avoid skin irritation.
  • Apply paste to skin; use plastic wrap to protect clothing if not provided on strip.
  • Have patient return demonstration.
• Instruct patient on administration of transdermal nitroglycerin patches.
  • Remove previous patch; wipe area with tissue to remove any residual medication.
  • Apply patch to a clean, dry, nonhairy area of body.
  • Rotate administration sites.
  • Instruct patient not to remove patch for swimming or bathing.
  • If patch loosens and part of it is nonadherent, it should be discarded and a new patch applied.
• Teach patient about adverse effects of other medications.
  • Constipation—verapamil (Calan)
  • Ankle edema—nifedipine (Procardia)
  • Heart failure (shortness of breath, weight gain, edema)—beta-adrenergic blockers or calcium channel blockers
  • Dizziness—vasodilators, antihypertensives
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• Ensure that patient has enough medication until next follow-up appointment or trip to the pharmacy. Warn against abrupt withdrawal of beta-adrenergic blockers or calcium channel blockers to prevent rebound effect.

NURSING ALERT

Instruct patient to go to the nearest health facility if chest pain persists for more than 15 minutes, is unrelieved by three nitroglycerin tablets, or is more intense and widespread than the usual angina episodes. (Patient should not drive self.)

Counsel on Risk Factors and Lifestyle Changes

• Inform patient of methods of stress reduction, such as biofeedback and relaxation techniques.
• Review low-fat and low-cholesterol diet. Explain AHA guidelines, which recommend eating fish at least twice a week, especially fish high in omega-3 oils.
  • Omega-3 oils have been shown to improve arterial health and decrease BP, triglycerides, and the growth of atherosclerotic plaque.
  • Omega-3 oils can be found in fatty fish, such as mackerel, salmon, sardines, herring, and albacore tuna.
  • Suggest available cookbooks (AHA) that may assist in planning and preparing foods.
  • Have patient meet with dietitian to design a menu plan.
• Inform patient of available cardiac rehabilitation programs that offer structured classes on exercise, smoking cessation, and weight control.
• Avoid excessive caffeine intake (coffee, cola drinks), which can increase the heart rate and produce angina.
• Do not use “diet pills,” nasal decongestants, or any over-the-counter medications that can increase the heart rate or stimulate high BP.
• Avoid the use of alcohol or drink only in moderation (alcohol can increase hypotensive adverse effects of drugs).
• Encourage follow-up visits for control of diabetes, hypertension, and hyperlipidemia.
• Have patient discuss supplement therapy (ie, vitamins B₆, B₁₂, C, E, folic acid, and L-arginine) with health care provider.
• For additional information refer to the AHA: http://www.americanheart.org.

Evaluation: Expected Outcomes

• Verbalizes relief of pain
• Blood pressure and heart rate stable
• Verbalizes lessening anxiety, ability to cope
  
  

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