Acute Coronary Syndrome

References:

1. Brunner & Suddarth’s Textbook of Medical-Surgical Nursing, 15th Edition, ISBN 978-197-51-6103-3, by Janice L. Hinkle, Kerry H. Cheever, and Kristen J. Overbaugh (Ch. 23)

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Acute coronary syndrome (ACS) is an emergent situation characterized by an acute onset of myocardial ischemia that results in myocardial death (i.e., MI) if definite interventions do not occur promptly. ACS is a spectrum that includes unstable angina, Non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).

1. Unstable Angina: reduced blood flow to a coronary artery occurs, often due to the rupture of an atherosclerotic plaque. A clot begins to form on top of the coronary lesion, but the artery is not completely occluded. This is an acute situation that can result in chest pain and other symptoms that may be referred to as preinfarction angina because the patient will likely have an MI if prompt interventions do not occur.
   • The patient has clinical manifestations of coronary ischemia, but ECG and cardiac biomarkers show no evidence of acute MI.
2. Myocardial Infarction: plaque rupture and subsequent thrombus formation result in complete occlusion of the artery, leading to ischemia and necrosis of the myocardium supplied by that artery. This may also be caused by vasospasm of a coronary artery, decreased oxygen supply, or increased demand for oxygen. In each case, a profound imbalance exists between myocardial oxygen supply and demand.
   • MI can be further defined with its type (NSTEMI, STEMI), location (anterior, inferior, posterior, lateral wall), and point in time within the process of infarction (acute, evolving, or old).
   • A 12-lead ECG can identify type and location. Other ECG indicators such as a Q wave along with patient history, can identify the timing.
   • Regardless of the location, the goals of medical therapy are to relieve symptoms, prevent or minimize myocardial tissue death, and prevent complications. The pathophysiology of CAD and the risk factors involved were discussed earlier.
   • STEMI: The patient has ECG evidence of acute MI with characteristic changes in two contiguous leads on a 12-lead ECG. In this type of MI, there is a significant damage to the myocardium.
   • NSTEMI: The patient has elevated cardiac biomarkers (e.g., troponin) but no definite ECG evidence of acute MI. In this type of MI, there may be less damage to the myocardium.

Assessing for Acute Coronary Syndrome or Acute MI

1. Cardiovascular: (a) chest pain or discomfort unrelieved by nitroglycerin; palpitations; S₃ and S₄ heart sounds, and new onset of murmurs; (b) increased jugular vein distention if heart failure develops; (c) blood pressure may be elevated because of sympathetic stimulation or decreased because of decreased contractility, impending cardiogenic shock, or medications; (d) irregular pulse may indicate atrial fibrillation; (e) tachycardia, bradycardia, or other arrhythmias may be revealed by an ECG.
2. Respiratory: shortness of breath, dyspnea, tachypnea, and crackles if pulmonary congestion has occurred due to MI. Pulmonary edema may be present.
3. Gastrointestinal: nausea, indigestion, and vomiting.
4. Genitourinary: decreased urinary output may indicate cardiogenic shock.
5. Skin: cool, clammy, diaphoretic, and pale appearance due to sympathetic stimulation may indicate cardiogenic shock.
6. Neurologic: anxiety, restlessness, and lightheadedness may indicate increased sympathetic stimulation or a decrease in contractility and cerebral oxygenation. The same symptoms may also herald cardiogenic shock.
7. Psychological: fear with feelings of impending doom, or denial that anything is wrong.

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Clinical Manifestations

The primary manifestation of ACS is chest pain that occurs suddenly and continues despite rest and medication. Some patients experience prodromal symptoms or a previous diagnosis of CAD, but others report no previous symptoms. A combination of these symptoms can appear: chest pain, shortness of breath, indigestion, nausea, anxiety, pale-cool-moist skin, and tachycardia and tachypnea from sympathetic nervous system stimulation.

• Evidently, it is common to find difficulty in distinguishing the signs and symptoms of MI from those of unstable angina; hence, the evolution of the term acute coronary syndrome.

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Diagnostic Findings

A diagnosis of ACS is made symptomatically, while the 12-lead ECG and laboratory tests (e.g., serial cardiac biomarkers) are done to differentiate between unstable angina, NSTEMI, and STEMI.

• Physical examination is always conducted, but a physical examination alone does not confirm the diagnosis.
• Patient History: descriptions of presenting symptoms, history of cardiac and other illnesses, family history of heart disease, and patient risk factors for heart disease.
• Electrocardiogram: rules out or diagnoses acute MI— this should be done within 10 minutes from the time a patient reports pain or arrives in the ED. Continuous monitoring for serial ECG changes can determine the location, evolution, and resolution of an MI.

Expected ECG Changes

• T-wave inversion: alteration and delay of myocardial repolarization causes the T wave to invert. This is found in the zone of ischemia.
• ST-segment elevation: the normally flat ST segment rises as the injured myocardial cells repolarize more rapidly than normal cells. This elevation is found 0.06 to 0.08 seconds after the end of QRS, known as the J point. A finding of elevated ST segment by at least 1 mm in two contiguous leads is a key diagnostic indicator for MI (STEMI). This is found in the zone of injury. During recovery, this is the first change to return to normal.
• Development of an abnormal Q wave: the Q wave depresses because of the absence of depolarization current from the necrotic tissue and opposing currents from other parts of the heart. This is found in the zone of infarction. - A new and significant Q wave is 0.04 seconds or longer and 25% of the R wave depth. The R wave may also be significantly decreased in height in acute MI. - An abnormal Q wave may be present without ST-segment and T-wave changes, which indicates an old, not acute, MI. An old STEMI is usually indicated by an abnormal Q wave or decreased height of the R wave without ST-segment and T-wave changes.

For some patients, there is an absence of an elevated ST segment or other ECG changes. Therefore, an NSTEMI is diagnosed by blood levels of cardiac biomarkers. Cardiac enzymes and biomarkers, which include troponin, creatine kinase (CK), and myoglobin, are used to diagnose an acute MI. Cardiac biomarkers can be analyzed rapidly, expediting an accurate diagnosis. These tests are based on the release of cellular contents into the circulation when myocardial cells die.

1. Troponin is a protein in myocardial cells that regulates the myocardial contractile process. There are three isomers of troponin: C, I, and T. Troponins I and T are specific for cardiac muscle, and these biomarkers are currently recognized as reliable and critical markers of myocardial injury. They can be detected within a few hours during acute MI and remain elevated for a long period, often as long as two weeks. This property allows them to detect recent myocardial damage. It should be noted that troponin rises with other forms of damage to the myocardium, including inflammation and other forms of mechanical stress (e.g., sepsis, heart failure, respiratory failure).
2. Creatine Kinase Isoenzymes also comes in three forms: CK-MM (skeletal muscle), CK-BB (brain tissue), and CK-MB (heart muscle). CK-MB is the cardiac-specific isoenzyme; it is found mainly in cardiac cells and therefore increases when there has been damage to these cells. These increase within a few hours of acute MI and peaks within 24 hours of an infarct.
3. Myoglobin is a heme protein that helps transport oxygen. Like the CK-MB enzyme, myoglobin is found in cardiac and skeletal muscle. The myoglobin level starts to increase within 1 to 3 hours and peaks within 12 hours after the onset of symptoms. An increase in myoglobin is not very specific in indicating an acute cardiac event; however, negative results can be used to rule out an acute MI.

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Medical Management

The goals of medical management are to minimize myocardial damage, preserve myocardial function, and prevent complications. Primary interventions include reducing myocardial oxygen demand and increasing oxygen supply with medications, oxygen administration, and bed rest. These goals are facilitated by the use of guidelines developed by the ACC and the AHA.

Treatment Guidelines for Acute Myocardial Infarction

Use rapid transit once an MI is suspected.

• Obtain a 12-lead electrocardiogram within 10 minutes of the attack, obtain laboratory blood specimens of cardiac biomarkers, including troponin.
• Begin routine medical interventions: (a) supplemental oxygen, (b) nitroglycerin, (c) morphine, (d) aspirin, (e) beta-blockers, (f) angiotensin-converting enzyme inhibitor within 24 hours, (g) anticoagulation with heparin and platelet inhibitors, and (h) statins
• Evaluate for indications for reperfusion therapy: percutaneous coronary intervention, thrombolytic therapy
• Continue therapy as indicated: IV heparin, LMWH, bivalirudin, or fondaparinux, clopidogrel, glycoprotein IIb/IIIa inhibitor, bed rest for a minimum of 12–24 hours, and statins prescribed at discharge.

Equilibrium and Reperfusion

The resolution of pain and ECG changes indicate (a) the equalization of oxygen demand and supply, or (b) reperfusion. To confirm for reperfusion, the visualization of blood flow through an open vessel in the catheterization laboratory is done.

1. The initial management given to a patient with suspected MI is supplemental oxygen, aspirin, nitroglycerin, and morphine.
   • Morphine is the drug of choice to reduce pain and anxiety. It also reduces preload and afterload, decreasing the work of the heart. During administration, the patient is monitored carefully for hypotension or respiratory depression. There are studies associating morphine with adverse patient outcomes, and practitioners are informed to stay up-to-date with changes to clinical guidelines impacting its use.
   • Beta-blockers may also be used if arrhythmias occur. Even if arrhythmias are not present in the initial management period, they should still be introduced within 24 hours of admission, once hemodynamics have stabilized and it is confirmed that the patient has no contraindications.
   • Unfractionated heparin or LMWH may also be prescribed along with platelet-inhibiting agents to prevent further clot formation.
2. Emergent Percutaneous Coronary Intervention is an immediate PCI done in the cardiac catheterization laboratory for patients with STEMI. The procedure is used to open the occluded coronary artery and promote reperfusion to the area that has been deprived of oxygen. It also treats the underlying atherosclerotic lesion. Superior outcomes have been reported with the use of PCI when compared to thrombolytic agents. It is the preferred initial treatment method for acute MI in all age groups. It should ideally be done within 60 minutes of arrival to the ED, referred to as the “door-to-balloon time”, the minimize the number of myocardial cells that die.
3. Thrombolytics: if primary PCI is unavailable or if transport to a PCI-capable hospital is too long, thrombolytic therapy is initiated. These are used to dissolve (“lyse”) the thrombus in a coronary artery, allowing blood to flow through the coronary artery again (reperfusion), minimizing the size of the infarction and preserving ventricular function. This therapy, although effective in dissolving the thrombus, does not affect the underlying atherosclerotic lesion. The patient may be referred for a cardiac catheterization and other invasive procedures following the use of thrombolytic therapy. It should ideally be done within 30 minutes of symptom onset for best results, referred to as the “door-to-needle time”.

Thrombolytic Therapy

Thrombolytic therapy is indicated for patients who (a) have had chest pain for more than 20 minutes, unrelieved by nitroglycerin, (b) have ST-segment elevation in at least two leads that face the same area of the heart, and (c) have been in pain for less than 12 hours.

• Absolute Contraindications: active bleeding, bleeding disorders, history of hemorrhagic stroke, history of intracranial vessel malformation, recent major surgery or trauma, uncontrolled hypertension, and pregnancy

During therapy, the nurse must: minimize skin punctures, avoid IM injections, draw blood for laboratory tests when starting the IV line, avoid continual use of noninvasive blood pressure cuffs, and monitor for acute arrhythmias and hypotension.

• Monitor for reperfusion: resolution of angina or acute ST-segment changes.
• Check for signs and symptoms of bleeding: ↓ Hct, ↓ Hgb, ↓ BP, ↑ heart rate, oozing or bulging at invasive procedure sites, back pain, muscle weakness, changes in level of consciousness, and complaints of headache.
• Treat major bleeding: discontinue thrombolytic therapy and any anticoagulants; apply direct pressure, notify primary provider immediately.
• Treat minor bleeding: apply direct pressure if accessible and appropriate; continue to monitor.

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Cardiac Rehabilitation

An active rehabilitation program is initiated for patients with MI who have returned to a stable condition. It is an important continuing care program for patients with CAD that targets risk reduction by providing patients and family education, offering individual and group support, and encouraging physical activity and physical conditioning.

• The goals of rehabilitation for the patient who has had an MI are to extend life and improve the quality of life. The immediate objectives are to limit the effects and progression of atherosclerosis, return the patient to work and a pre-illness lifestyle, enhance the patient’s psychosocial and vocational status, and prevent another cardiac event.

Phase	Content
Phase I	From the diagnosis of atherosclerosis, which may occur when the patient is admitted to the hospital for ACS. The focus is an the essentials of self-care rather than instituting behavioral changes for risk reduction. The patient is informed that, while CAD is a lifelong disease, they are likely to be able to resume a normal life after an MI. - Learning signs and symptoms that indicate the need to seek emergency assistance. - Learning the medical regimen - Rest-activity balance - Follow-up appointments
Phase II	After discharge. The patient attends sessions three times a week for 4 to 6 weeks but may continue for as long as 6 months. These involve supervised ECG-monitored individualized exercise training, and educational sessions for patients and their families.
Phase III	A long-term outpatient program that focuses on maintaining cardiovascular stability and long-term conditioning. The patient is usually self-directed in this phase and does not require supervision.

Promoting Health After Myocardial Infarction and Other ACSs

To extend and improve the quality of life, a patient who has had an MI must make lifestyle adjustments to promote heart-healthy living. With this in mind, the nurse and patient develop a program to help achieve desired outcomes.

Lifestyle modifications during convalescence and healing includes:

• Avoid any activity that produces chest pain, extreme dyspnea, or undue fatigue.
• Avoid extremes of heat and cold and walking against the wind.
• Lose weight, if indicated.
• Stop smoking and the use of tobacco; avoid secondhand smoke.
• Develop heart-healthy eating patterns and avoid large meals and hurrying while eating. Modify meals to align with AHA dietary recommendations, the Mediterranean diet, or other recommended diets.
• Follow recommendations that ensure that blood pressure and blood glucose are in control.
• Purse activities that relieve and reduce stress.

In addition, the patient needs to undertake a structured program of activity and exercise for long-term rehabilitation. Advise patients to:

• Engage in a regimen of physical conditioning with a gradual increase in activity duration and then a gradual increase in activity intensity.
• Enroll in a cardiac rehabilitation program.
• Walk daily, increasing distance and time as prescribed.
• Monitor pulse rate during physical activity.
• Avoid physical exercise immediately after a meal.
• Alternate activity with rest periods (some fatigue is normal and expected during convalescence).
• Participate in a daily program of exercise that develops into a program of regular exercise for a lifetime.

The patient must learn to recognize and take appropriate action for recurrent symptoms. Make sure that patients know to do the following:

• Call 911 if chest pressure or pain (or prodromal symptoms) is not relieved in 15 minutes by taking 3 nitroglycerin tablets at 5-minute intervals.
• Contact the primary provider if any of the following occur: shortness of breath, fainting, slow or rapid heartbeat, swelling of feet and ankles.

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Nursing the Patient with Acute Coronary Syndrome

In the assessment phase, the patient’s baseline, needs, and priorities are established. A systematic assessment includes a careful history, particularly as it relates to symptoms: chest pain or discomfort, dyspnea, palpitations, unusual fatigue, syncope, or other possible indicators of myocardial ischemia. Each symptom must be evaluated with regard to time, duration, and the factors that precipitate the symptom and relieve it, and in comparison with previous symptoms.

• A focused physical assessment is critical to detect complications and any change in patient status. Refer to Assessing the Patient with Acute Coronary Syndrome for important assessments and possible findings.
• Two IV lines are typically placed for any patient with ACS to ensure that access is available for administering emergency medications, maintained until the patient’s condition stabilizes. IV lines may be changed to a saline lock to maintain IV access in the stable patient.

Nursing Diagnoses

• Acute pain associated with increased myocardial oxygen demand and decreased myocardial oxygen supply
• Risk for impaired cardiac function associated with reduced coronary blood flow
• Risk for hypovolemia
• Impaired peripheral tissue perfusion associated with impaired cardiac output from left ventricular dysfunction
• Anxiety associated with cardiac event and possible death
• Lack of knowledge about post-ACS self-care

Complications

• Acute pulmonary edema
• Heart failure
• Cardiogenic shock
• Arrhythmias and cardiac arrest
• Pericardial effusion and cardiac tamponade

Planning includes relief of pain or ischemic signs (e.g., ST-segment changes) and symptoms, prevention of myocardial damage, maintenance of effective respiratory function, maintenance or attainment of adequate tissue perfusion, reduced anxiety, adherence to the self-care program, and early recognition of complications.

Interventions focus on:

1. Relieving Pain and Other Signs and Symptoms of Ischemia: balancing myocardial oxygen supply with demand is the top priority. Although the medications discussed previously are important, nursing interventions are also important: oxygen therapy (2 to 4 L/min is usually adequate), frequent vital signs assessment as long as the patient remains symptomatic, physical rest with the head of bed elevated or in a supportive chair (cardiac chair). Pain relief also has the effect of decreasing anxiety level, which in turn reduces sympathetic stress response, leading to a decrease in workload of the already stressed heart.

Elevated Head and Torso in ACS

The elevation of the head and torso is beneficial as it (1) improves tidal volume because of reduced pressure from abdominal contents on the diaphragm and better lung expansion, (2) improves the drainage of the upper lung lobes, and (3) decreases venous return to the heart (preload), reducing the heart’s workload.

2. Improving Respiratory Function: regular and careful assessment of respiratory function detects early signs of pulmonary complications. Fluid volume status is closely monitored. Effective ventilation is maintained with deep breathing and frequent repositioning. Pulse oximetry guides the use of oxygen therapy.
3. Promoting Adequate Tissue Perfusion: bed or chair rest reduces oxygen consumption. This limitation is maintained until the patient is pain free and hemodynamically stable. Perfusion is assessed with skin temperature and peripheral pulses.
4. Reducing Anxiety: alleviating anxiety and decreasing fear reduce the sympathetic stress response. This decreases the workload of the heart, which may relieve pain and other signs and symptoms of ischemia. The development of a trusting and caring relationship with the patient is critical in reducing anxiety. The provision of information in an honest and supportive manner encourages the patient to be a partner in care. Other interventions include a quiet environment, avoiding sleep disturbances, and providing spiritual support. Alternative therapies such as pet therapy can help relaxation and reduction of anxiety.
5. Monitoring and Managing Potential Complications: closely monitor changes in cardiac rate and rhythm, heart sounds, blood pressure, chest pain, respiratory status, urinary output, skin color and temperature, mental status, ECG changes, and laboratory values. Any changes in the patient’s condition must be reported promptly to the primary provider and emergency measures instituted when necessary.
6. Promoting Home, Community-Based, and Transitional Care:
   • Self-care is more likely to succeed if the nurse first identifies the patient’s priorities, provide adequate education about heart-healthy living, and facilitate the patient’s involvement in a cardiac rehabilitation program. The most effective treatment plans are made with patient participation.
   • Continuing and Transitional Care is used depending on the patient’s condition, the availability of family assistance. A home health or transitional care nurse can assist with scheduling, appointments, monitoring, and adherence to medication and dietary regimens.

Patient Outcome Evaluation Goals

1. Experiences relief of angina
2. Has stable cardiac and respiratory status
3. Maintains adequate tissue perfusion
4. Exhibits decreased anxiety
5. Adheres to a self-care program
6. Has no complications