Unstable Angina

The chest pain associated with UA is new in onset, occurs at rest, or has a worsening pattern. Myocardial Infarction Severe and persistent chest pain not relieved by rest or nitrate admini stration may mean the patient is having an MI. ■ Unlike any other pain, it is usually described as a heav y, pres-sure, tight, burning, constricted, or crushing feeling. Common locations are the substernal or epigastric area. The pain may radiate to the neck, lower jaw, and arms or to the back. When epigastric pain is present, the patient may relate it to indiges-tion, take antacids without relief, and therefore delay seeking treatment.

■ It may occur while the patient is active or at rest, asleep, or awake. Pain often occurs in the early morning hours. It usually lasts for 20 min or longer.

■ Some patients may not have pain but may have “discomfort,” weakness, nausea, indigestion, or shortness of breath. Some women may have atypical discomfort, shortness of breath, or fatigue.

■ Patients with diabetes may have silent (asymptomatic) MIs because of cardiac neuropathy or have atypical symptoms (e.g., shortness of breath).

■ An older patient may have a change in mental status (e.g., con-fusion), shortness of breath, pulmonary edema, dizziness, or a dysrhythmia. The patient’s skin may be ashen, clammy, and cool (cold sweat). The patient may have nausea and vomiting. Fever occurs within the first 24 hr (up to 100.4°F [38°C])

Description

Acute coronary syndrome (ACS) develops when myocardial isch-emia is prolonged and not immediately reversible. ACS includes the spectrum of non-ST elevation acute coronary syndrome (unsta-ble angina [UA], non-ST segment elevation myocardial infarc-tion [NSTEMI]), and ST segment elevation myocardial infarction (STEMI) (Fig. 1).

Pathophysiology

ACS occurs when a previously stable atherosclerotic plaque rup-tures, releasing the lipid core into the vessel. This causes platelet aggregation and thrombus formation. The vessel may be partially blocked by a thrombus (manifesting as UA or NSTEMI) or totally blocked by a thrombus (manifesting as STEMI). It is unclear what causes the plaque to suddenly become unstable. Systemic inflam-mation (described earlier) may play a role. Patients with suspected ACS need immediate hospitalization.

Unstable Angina

UA is chest pain that is new in onset, occurs at rest, or occurs with increasing frequency, duration, or less effort than the patient’s chronic stable angina pattern. The pain usually lasts 10 min or more. The patient with chronic stable angina may develop UA, or UA may be the first clinical sign of coronary artery disease (CAD). Unlike chronic stable angina, UA is unpredictable and must be treated immediately. ■ The patient with previously diagnosed chronic stable angina describes a significant change in the pattern of angina. It occurs with increasing frequency and is easily provoked by minimal exertion, during sleep, or even at rest.

■ The patient without previously diagnosed angina describes chest pain that has progressed rapidly in the past few hours, days, or weeks, often ending in pain at rest.

Ischemic electrocardiogram (ECG) changes that may be seen

with UA include ST depression and/or T wave inversion. Myocardial Infarction: ST-Elevation and Non-ST-Elevation A myocardial infarction (MI) occurs because of an abrupt stoppage of blood flow through a coronary artery with a thrombus caused by platelet aggregation. This causes irreversible myocardial cell death (necrosis). Serum cardiac biomarkers are released into the blood. Most MIs occur in the setting of preexisting CAD. The loca-tion of an MI correlates with the involved coronary circulation. For example, inferior wall infarctions result from occlusions in the right coronary artery. The majority of MIs affect the left ventricle.

Damage can occur in more than one location (e.g., anterolateral MI, A anteroseptal MI). ■ A STEMI, caused by an occlusive thrombus, creates ST eleva-tion in the ECG leads facing the area of infarction. A STEMI is an emergency. To limit the infarct size, the artery must be opened within 90 min of presentation to restore blood and O2 to the heart muscle and limit the infarct size. This can be done either by percutaneous coronary intervention (PCI) or with thrombolytic (fibrinolytic) therapy. PCI is the first-line treat-ment, if available. Cardiac catheterization confirms which artery has the occlusive thrombus so it can be opened with a balloon and stent. Thrombolytic therapy is done in hospitals that do not have a catheterization laboratory for PCI. If the patient does not seek treatment quickly, the STEMI will evolve.

■ NSTEMI, caused by a nonocclusive thrombus, does not cause ST segment elevation on the 12-lead ECG. The ECG may or may not show ST depression and/or T wave inversion in the leads facing the area of infarction. NSTEMI patients do not need an emergent catheterization but usually undergo the proce-dure within 12–72 hr. Thrombolytic therapy is not a treatment option.

■ Cardiac cells can withstand ischemic conditions for approxi-mately 10 min before cellular death (necrosis) begins. The acute MI process evolves over hours to days. The earliest tissue to become ischemic is the subendocardium (the innermost layer of tissue in the heart muscle). If ischemia persists, it takes around 4–6 hr for the entire thickness of the heart muscle to necrose. If the thrombus is not completely blocking the artery, the time to complete necrosis may be as long as 12 hr.

■ The degree of collateral circulation influences the severity of the MI. A person with a long history of CAD may have developed good collateral circulation to the tissue surrounding the infarc-tion site.

The body’s response to cell death is the inflammatory process.

Within 24 hr, leukocytes infiltrate the area. Enzymes are released from the dead cardiac cells and are important diagnostic indicators (markers) of MI. Proteolytic enzymes from neutrophils and macro-phages remove necrotic tissue by the fourth day. ■ The necrotic zone is identifiable by ECG changes (e.g., ST seg-ment elevation, pathologic Q wave) and by nuclear scanning after the onset of symptoms. The necrotic zone of a STEMI is identified by ECG changes (e.g., lowering of the initially ele-vated ST segments, T wave inversion, and/or a pathologic Q wave) within a day or two.

■ At 10–14 days after MI, the new scar tissue is still weak. The heart muscle is vulnerable to increased stress during this time. At the same time, the patient’s activity level may be increasing, so special caution and assessment are necessary.

■ By 6 weeks after MI, scar tissue has replaced necrotic tissue, and the injured area is considered healed. Changes in the infarcted heart muscle also cause changes in the

unaffected areas. To try to compensate for the damaged muscle, the normal myocardium hypertrophies and dilates. This process is called ventricular remodeling. Remodeling of normal myocardium can lead to the development of late heart failure (HF), especially in the person with atherosclerosis of other coronary arteries and/or an anterior MI. Angiotensin-converting enzyme (ACE) inhibitor drugs are given to limit ventricular remodeling.

Clinical Manifestations Unstable Angina

The chest pain associated with UA is new in onset, occurs at rest, or has a worsening pattern. Myocardial Infarction Severe and persistent chest pain not relieved by rest or nitrate administration may mean the patient is having an MI. ■ Unlike any other pain, it is usually described as a heavy, pres-sure, tight, burning, constricted, or crushing feeling. Common locations are the substernal or epigastric area. The pain may radiate to the neck, lower jaw, and arms or to the back. When epigastric pain is present, the patient may relate it to indiges-tion, take antacids without relief, and therefore delay seeking treatment.

■ It may occur while the patient is active or at rest, asleep, or awake. Pain often occurs in the early morning hours. It usually lasts for 20 min or longer.

■ Some patients may not have pain but may have “discomfort,” weakness, nausea, indigestion, or shortness of breath. Some women may have atypical discomfort, shortness of breath, or fatigue.

■ Patients with diabetes may have silent (asymptomatic) MIs because of cardiac neuropathy or have atypical symptoms (e.g., shortness of breath).

■ An older patient may have a change in mental status (e.g., con-fusion), shortness of breath, pulmonary edema, dizziness, or a dysrhythmia. The patient’s skin may be ashen, clammy, and cool (cold sweat). The patient may have nausea and vomiting. Fever occurs within the first 24 hr (up to 100.4°F [38°C]) and may continue for 4–5 days. BP and pulse rate are elevated ini-tially. The BP may then drop, with decreased urine output, lung crackles, hepatic engorgement, and peripheral edema. Jugular veins may be distended, with obvious pulsations.

Complications Dysrhythmias are the most common complication after an MI and are the most common cause of death in patients in the prehospital period. Dysrhythmias are caused by conditions that affect the myo-cardial cell’s sensitivity to nerve impulses, such as ischemia, elec-trolyte imbalances, and sympathetic nervous system stimulation. Life-threatening dysrhythmias occur most often with anterior wall infarction, heart failure, and shock. Complete heart block is seen in a massive infarction (see Dysrhythmias). ■ Ventricular tachycardia and ventricular fibrillation are lethal dysrhythmias that most often occur within the first 4 hr after the onset of pain. Premature ventricular contrac-tions may precede ventricular tachycardia and fibrillation. Life-threatening ventricular dysrhythmias must be treated immediately.

■ HF occurs when the heart’s pumping action is reduced. Left-sided HF occurs initially with subtle signs, such as mild dys-pnea, restlessness, agitation, or slight tachycardia. Other signs indicating the onset of left-sided HF include pulmonary con-gestion on chest X-ray, S3 or S4 heart sounds on auscultation of the heart, crackles on auscultation of the lungs, paroxysmal nocturnal dyspnea (PND), and orthopnea. Signs of right-sided HF include jugular venous distention, hepatic congestion, and lower extremity edema. (See Heart Failure, XXX)

■ Cardiogenic shock occurs when inadequate oxygen and nutri-ents are supplied to the tissues because of severe left ventricu-lar (LV) failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, or right ventricular infarction. Cardiogenic shock requires aggressive management including control of dysrhythmias, intraaortic balloon pump therapy, and support of contractility with vasoactive drugs. Other complications include papillary muscle rupture, ventricu-lar rupture, ventricular aneurysm, and pericarditis. (See Pericardi-tis, Acute).

Diagnostic Studies

In addition to the patient’s history of pain, risk factors, and health history, the primary diagnostic studies used to determine whether a person has UA or an MI include an ECG and serum cardiac markers. Other diagnostic measures can include coronary angiog-raphy, exercise stress testing, and echocardiogram.

Electrocardiogram ■ When patients first present with chest pain, ST elevations on the 12-lead ECG most likely indicate a STEMI. Compare the new ECG to a previous ECG whenever possible. ST elevation repre-sents myocardial injury that is potentially reversible but, if not treated, will likely evolve to permanent necrosis (tissue death) of the myocardium.

■ A patient with STEMI tends to have a more extensive MI that is associated with prolonged and complete coronary occlusion. A pathologic Q wave develops on the ECG.

■ Patients with UA or NSTEMI may or may not have ST segment depression and/or T wave inversion on the ECG. For patients with chest pain who do not have ST segment elevation or ST–T wave changes on the ECG, it is difficult to distinguish between UA and NSTEMI until we evaluate serum cardiac biomarkers.

■ A patient with UA or NSTEMI usually has transient thrombosis or incomplete coronary occlusion, and the ECG typically does not develop pathologic Q waves.

■ Serial ECGs often reveal the evolution and time sequence of ischemia, injury, infarction, and resolution of the infarction. Cardiac Biomarkers Serum cardiac biomarkers are proteins released into the blood from necrotic heart muscle after an MI. ■ A high-sensitivity cardiac troponin test (hs-cTn) provides more rapid detection of MI compared with the conventional cardiac-specific troponin assays, allowing for a quicker diagnosis. Serum levels of hs-cTn rise within 1 hr of cardiac injury and stay high for 7–14 days. A second hs-cTn is drawn 2–3 hr after the first one if STEMI is ruled out. These markers are highly specific indicators of MI and have greater sensitivity and speci-ficity for myocardial injury than creatine kinase (CK)-MB or myoglobin.

Interprofessional Management

A patient with ACS needs rapid diagnosis and treatment to preserve cardiac muscle. Initial management of the patient with chest pain

most often occurs in the emergency department (ED). ■ Obtain a 12-lead ECG and start continuous ECG monitoring. ■ Position the patient in an upright position unless contraindicated and start O2 by nasal cannula to keep O2 saturation above 93%. ■ Obtain intravenous (IV) access for drug administration

■ Give sublingual nitroglycerin (NTG) and 162–325 mg of chew-able aspirin if not given before arrival at the ED. Morphine is given for pain unrelieved by NTG.

■ A high-dose statin (e.g., atorvastatin [Lipitor]) is given. ■ The patient usually receives ongoing care in a critical care or telemetry unit where continuous ECG monitoring is available and dysrhythmias can be treated.

■ Monitor vital signs, including pulse oximetry, frequently dur-ing the first few hours after admission and closely thereafter. Maintain bed rest and limit activity for 12–24 hr, with a gradual increase in activity unless contraindicated.

■ If the ECG shows ST elevation, the patient with STEMI is taken directly to the cardiac catheterization laboratory in PCI-capable hospitals. Glycoprotein IIb/IIIa inhibitors may be used during PCI for STEMI patients. Thrombolytic therapy is started if the patient is unable to be quickly transported to a PCI capable hospital.

■ If the ECG shows ST depression and/or T wave inversion, the patient is usually transferred to a critical care unit or telemetry unit for ongoing care. Dysrhythmias are treated according to agency protocols.

■ UA and NSTEMI patients are started on heparin. Some patients with UA or NSTEMI start on glycoprotein IIb/IIIa inhibitors (e.g., eptifibatide [Integrilin]) either before catheterization or at the time of PCI.

■ For a patient with UA or NSTEMI, aspirin and heparin (unfrac-tionated heparin [UH] or low-molecular-weight heparin [LMWH]) are recommended. Dual antiplatelet therapy (e.g., with aspirin and clopidogrel) and heparin are recommended for NSTEMI. Cardiac catheterization with possible PCI is consid-ered as treatment for both UA and NSTEMI once the patient is stabilized, or if angina returns or increases in severity.

Traditional coronary artery bypass graft (CABG) surgery places conduits to transport blood between the aorta, or other major arter-ies, and the myocardium distal to the obstructed coronary artery (or arteries). It requires a sternotomy (opening of the chest cavity) and the use of cardiopulmonary bypass (CPB). It is a palliative treat-ment for CAD and not a cure. Newer techniques include minimally invasive direct coronary artery bypass, off-pump coronary artery bypass, totally endoscopic coronary artery bypass (TECAB), and transmyocardial laser revascularization. These surgical procedures and related nursing care are further discussed in Chapter 37 of Harding et al., Lewis’ Medical-Surgical Nursing, ed 12. Drug therapy includes IV nitroglycerin, aspirin, β-adrenergic blockers, and anticoagulation. Systemic anticoagulation may be

achieved with LMWH given subcutaneously or IV UH. If PCI is anticipated, glycoprotein IIb/IIIa inhibitors may be used. ACE inhibitors are added for some patients after an MI. Calcium channel blockers may be used if the patient is already taking adequate doses of β-blockers or does not tolerate these blockers.

Nursing Management Goals The patient with an ACS will experience pain relief, quick and appropriate treatment, and preservation of heart muscle. During the hospitalization, the overall goals include effective coping with illness-associated anxiety, participation in a rehabilitation plan, and reducing risk factors. See eNursing Care Plan 37-1 for the patient with ACS on the website. Interventions

Proper management decreases the O2 needs of the patient’s com-promised myocardium. Institute measures to avoid the hazards of immobility while encouraging rest. ■ Provide nitroglycerin, morphine, and supplemental O2 as needed to eliminate or reduce chest pain.

■ Maintain continuous ECG monitoring while the patient is in the ED and intensive care unit (ICU) and after transfer to a step-down or general care unit. Dysrhythmias need to be identified and treated quickly.

■ If the patient is receiving thrombolytic therapy, monitor for reperfusion dysrhythmias. If signs and symptoms of major bleeding occur (e.g., drop in BP, increase in HR, sudden change in the patient’s mental status, blood in the urine or stool), stop the drug and notify the HCP.

■ In addition to frequent vital signs, evaluate intake and output. Assess lung and heart sounds and inspect for evidence of early heart failure (e.g., dyspnea, tachycardia, pulmonary congestion, distended neck veins).

■ Assess oxygenation status frequently. If the patient is receiv-ing O2, check the nares for irritation or dryness (see Oxygen Therapy).

■ Plan to ensure adequate rest periods free from interruption. There is no evidence for prolonged bed rest for the patient with an uncomplicated MI, but bed rest may be ordered for a few days after a large STEMI.

■ Anxiety is usually present in patients with ACS. Identify the source of anxiety and assist the patient in reducing it. If the patient is afraid of being alone, allow a caregiver to sit quietly by the bedside or check in frequently with the patient.

Patient and Caregiver Teaching The patient will need teaching at every stage of hospitalization and recovery (e.g., ED, telemetry unit, home care). The purpose of teaching is to give the patient and caregiver the tools to make informed health decisions (Table 2). ■ Prepare the patient and caregiver for the usual course of recov-ery and rehabilitation to promote their sense of control.

■ Teach patients to count their HR or use technology (e.g., cell phone applications, fitness trackers) to check their HR. Tell the patient that the HR should return to the resting HR within a few minutes of stopping exercise. Tell the patient to stop exercising and rest if chest pain or shortness of breath occurs.

■ Encourage participation in an outpatient or home-based cardiac rehabilitation program.

■ Include sexual counseling for cardiac patients and their part-ners. Tell the patient that resumption of sex depends on the emo-tional readiness of both the patient and partner and on the health care provider (HCP)’s assessment of recovery. It is generally safe to resume sexual activity 7–10 days after an uncomplicated MI. Sexual activity for most middle-aged men and women with their usual partners is a moderate-energy activity equivalent to climbing two flights of steps or walking briskly.

TABLE 2 Patient and Caregiver Teaching: Acute Coronary Syndrome

Include the following information in the teaching plan for the patient with acute coronary syndrome and the caregiver.

• Signs and symptoms of angina and MI and what to do should they occur (e.g., take nitroglycerin)

• When and how to seek help (e.g., contact ERS) • Anatomy and physiology of the heart and coronary arteries • Cause and effect of CAD • Definition of terms (e.g., CAD, angina, MI, sudden cardiac death, heart failure)

• Identification of and plan to decrease risk • Reasons for tests and treatments (e.g., ECG monitoring, blood tests, cardiac catheterization), activity limitations and rest, diet, and drugs

• Appropriate expectations about recovery (anticipatory guidance) • Resumption of work, physical activity, sexual activity • Measures to promote recovery and health (e.g., cardiac rehabilitation) • Importance of the gradual, progressive resumption of activity

CAD, coronary artery disease; ECG, electrocardiogram; ERS, emergency response system; MI, myocardial infarction.