Myocardial infarction

Myocardial infarction

Pathophysiology

In an MI, an area of the myocardium is permanently destroyed. MI is usually caused by reduced blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus. In unstable angina, the plaque ruptures but the artery is not completely occluded. Because unstable angina and acute MI are considered to be the same process but different points along a continuum, the term acute coronary syndrome (ACS) may be used in lieu of these diagnoses. Other causes of MI include vasospasm (sudden constriction or narrowing) of a coronary artery, decreased oxygen supply (eg, from acute blood loss, anemia, or low blood pressure), and increased demand for oxygen (eg, from a rapid heart rate, thyrotoxicosis, or ingestion of cocaine). In each case, a profound imbalance exists between myocardial oxygen supply and demand.

Coronary occlusion, heart attack, and MI are terms used synonymously, but the preferred term is MI. The area of infarction develops over minutes to hours. As the cells are deprived of oxygen, ischemia develops, cellular injury occurs, and the lack of oxygen results in infarction, or the death of cells. The expression “time is muscle” reflects the urgency of appropriate treatment to improve patient outcomes. Each year in the United States, nearly 900,000 people have acute MIs; one fourth of these people die of MI. Half of those who die never reach a hospital.

Various descriptions are used to further identify an MI: the type of MI (ST-segment elevation, non–ST-segment elevation), the location of the injury to the ventricular wall (anterior, inferior, posterior, or lateral wall), and the point in time within the process of infarction (acute, evolving, or old).

The ECG usually identifies the type and location, and other ECG indicators such as a Q wave and patient history identify the timing. Regardless of the location of the infarction of cardiac muscle, the goal of medical therapy is to prevent or minimize myocardial tissue death and to prevent complications. The pathophysiology of heart disease and the risk factors involved were discussed earlier in this chapter.

Clinical Manifestations

Chest pain that occurs suddenly and continues despite rest and medication is the presenting symptom in most patients with an MI . Some of these patients have prodromal symptoms or a previous diagnosis of CAD, but about half report no previous symptoms . Patients may present with a combination of symptoms, including chest pain, shortness of breath, indigestion, nausea, and anxiety. They may have cool, pale, and moist skin. Their heart rate and respiratory rate may be faster than normal. These signs and symptoms, which are caused by stimulation of the sympathetic nervous system, may be present for only a short time or may persist. In many cases, the signs and symptoms of MI cannot be distinguished from those of unstable angina.

Electrocardiogram (ECG)

The ECG provides information that assists in diagnosing acute MI. It should be obtained within 10 minutes from the time a patient reports pain or arrives in the emergency department. By monitoring serial ECG changes over time, the location, evolution, and resolution of an MI can be identified and monitored.

The ECG changes that occur with an MI are seen in the leads that view the involved surface of the heart. The classic ECG changes are T-wave inversion, ST-segment elevation, and development of an abnormal Q wave . Because infarction evolves over time, the ECG also changes over time. The first ECG signs of an acute MI occur as a result of myocardial ischemia and injury. Myocardial injury causes the T wave to become enlarged and symmetric. As the area of injury becomes ischemic, myocardial repolarization is altered and delayed, causing the T wave to invert. The ischemic region may remain depolarized while adjacent areas of the myocardium return to the resting state. Myocardial injury also causes ST-segment changes. The injured myocardial cells depolarize normally but repolarize more rapidly than normal cells, causing the ST segment to rise at least 1 mm above the isoelectric line (area between the T wave and the next P wave is used as the reference for the isoelectric line) when measured 0.06 to 0.08 seconds after the end of the QRS, a point called the J point. This elevation in the ST segment in two contiguous leads is a key diagnostic indicator for MI.

The appearance of abnormal Q waves is another indication of MI. Q waves develop within 1 to 3 days because there is no depolarization current conducted from necrotic tissue. The lead system then views the flow of current from other parts of the heart. An abnormal Q wave is 0.04 seconds or longer, 25% of the R-wave depth (provided the R wave exceeds a depth of 5 mm), or did not exist before the event. An acute MI may also cause a significant decrease in the height of the R wave. During an acute MI, injury and ischemic changes are usually present. An abnormal Q wave may be present without ST-segment and T-wave changes, which indicates an old, not acute, MI. For some patients, there are no persistent ECG changes, and the MI is diagnosed by blood levels of cardiac biomarkers.

Using the above information, patients are diagnosed with one of the following forms of ACS:

Unstable angina: The patient has clinical manifestations of coronary ischemia, but ECG or cardiac biomarkers show no evidence of acute MI.
ST-segment elevation MI: 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 significant damage to the myocardium.
Non–ST-segment elevation MI: The patient has elevated cardiac biomarkers but no definite ECG evidence of acute MI.

During recovery from an MI, the ST segment often is the first ECG indicator to return to normal (1 to 6 weeks). The T wave becomes large and symmetric for 24 hours, and it then inverts within 1 to 3 days for 1 to 2 weeks. Q-wave alterations are usually permanent. An old ST-segment elevation MI is usually indicated by an abnormal Q wave or decreased height of the R wave without ST-segment and T-wave changes.

Laboratory Tests

Laboratory tests called cardiac biomarkers are used to diagnose an MI. Newer laboratory tests with faster results, resulting in earlier diagnosis, include myoglobin and troponin analysis. These tests are based on the release of cellular contents into the circulation when myocardial cells die.

Creatine Kinase and Its Isoenzymes

There are three creatine kinase (CK) isoenzymes: CK-MM (skeletal muscle), CK-MB (heart muscle), and CK-BB (brain tissue). CK-MB is the cardiac-specific isoenzyme; CK-MB is found mainly in cardiac cells and therefore increases only when there has been damage to these cells. Elevated CK-MB assessed by mass assay is an indicator of acute MI; its level begins to increase within a few hours and peaks within 24 hours of an MI. If the area is reperfused (eg, due to thrombolytic therapy or PCI), it peaks earlier.

Myoglobin

Myoglobin is a heme protein that helps transport oxygen. Like 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 are an excellent parameter for ruling out an acute MI.

Troponin

Troponin, a protein found in the myocardium, 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 tests are currently recognized as reliable and critical markers of myocardial injury. An increase in the level of troponin in the serum can be detected within a few hours during acute MI. It remains elevated for a long period, often as long as 3 weeks, and it therefore can be used to detect recent myocardial damage.

Pharmacologic Therapy

The patient with suspected MI is given aspirin, nitroglycerin, morphine, a beta-blocker, and other medications as indicated while the diagnosis is being confirmed. Patients should receive a beta-blocker initially, throughout the hospitalization, and after hospital discharge. Long-term therapy with beta-blockers can decrease the incidence of future cardiac events.

Medical Treatment Guidelines for Acute Myocardial Infarction

Use rapid transit to the hospital.

Obtain 12-lead ECG to be read within 10 minutes.

Obtain laboratory blood specimens of cardiac biomarkers, including troponin.

Obtain other diagnostics to clarify the diagnosis.

Begin routine medical interventions:

Supplemental oxygen
Nitroglycerin
Morphine
Aspirin 162–325 mg
Beta-blocker
Angiotensin-converting enzyme inhibitor within 24 hours

Evaluate for indications for reperfusion therapy:

Percutaneous coronary intervention
Thrombolytic therapy

Continue therapy as indicated:

Intravenous heparin or low-molecular-weight heparin
Clopidogrel (Plavix) or ticlopidine (Ticlid)
Glycoprotein IIb/IIIa inhibitor
Bed rest for a minimum of 12 to 24 hours

1- Thrombolytics

Thrombolytics are usually administered IV, although some may also be given directly into the coronary artery in the cardiac catheterization laboratory. To be effective, thrombolytics must be administered as early as possible after the onset of symptoms that indicate an acute MI, generally within 3 to 6 hours. The purpose of thrombolytics is to dissolve and lyse the thrombus in a coronary artery (thrombolysis), allowing blood to flow through the coronary artery again (reperfusion), minimizing the size of the infarction, and preserving ventricular function. Even though thrombolytics may dissolve the thrombus, they do not affect the underlying atherosclerotic lesion. The patient may be referred for a cardiac catheterization and other invasive interventions.

Administration of Thrombolytic Therapy

Indications

Chest pain for longer than 20 minutes, unrelieved by nitroglycerin
ST-segment elevation in at least two leads that face the same area of the heart
Less than 6 hours from onset of pain

Absolute Contraindications

Active bleeding
Known bleeding disorder
History of hemorrhagic stroke
History of intracranial vessel malformation
Recent major surgery or trauma
Uncontrolled hypertension
Pregnancy

Nursing Considerations

Minimize the number of times the patient's skin is punctured.
Avoid intramuscular injections.
Draw blood for laboratory tests when starting the IV line.
Start IV lines before thrombolytic therapy; designate one line to use for blood draws.
Avoid continual use of noninvasive blood pressure cuff.
Monitor for acute dysrhythmias and hypotension.
Monitor for reperfusion: resolution of angina or acute ST-segment changes.
Check for signs and symptoms of bleeding: decrease in hematocrit and hemoglobin values, decrease in blood pressure, increase in heart rate, oozing or bulging at invasive procedure sites, back pain, muscle weakness, changes in level of consciousness, complaints of headache
Treat major bleeding by discontinuing thrombolytic therapy and any anticoagulants; apply direct pressure and notify the physician immediately.
Treat minor bleeding by applying direct pressure if accessible and appropriate; continue to monitor.

2- Analgesics

The analgesic of choice for acute MI is morphine sulfate administered in IV boluses to reduce pain and anxiety. It reduces preload and afterload, which decreases the workload of the heart. Morphine also relaxes bronchioles to enhance oxygenation. The cardiovascular response to morphine is monitored carefully, particularly the blood pressure, which can decrease, and the respiratory rate, which can be depressed. Because morphine decreases the sensation of pain, ST-segment monitoring may be a better indicator of subsequent ischemia than assessment of pain.

3- Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II. In the absence of angiotensin II, the blood pressure decreases and the kidneys excrete sodium and fluid (diuresis), decreasing the oxygen demand of the heart. Use of ACE inhibitors in patients after MI decreases mortality rates and prevents remodeling of myocardial cells that is associated with the onset of heart failure. It is important to ensure that the patient is not hypotensive, hyponatremic, hypovolemic, or hyperkalemic before administering ACE inhibitors. Blood pressure, urine output, and serum sodium, potassium, and creatinine levels need to be monitored closely.

Nursing Process

The Patient With Myocardial Infarction

Assessment

One of the most important aspects of care of the patient with an MI is the assessment. It establishes the baseline for the patient so that any deviations may be identified, systematically identifies the patient's needs, and helps determine the priority of those needs. Systematic assessment includes a careful history, particularly as it relates to symptoms: chest pain or discomfort, difficulty breathing (dyspnea), palpitations, unusual fatigue, faintness (syncope), or sweating (diaphoresis). 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 precise and complete physical assessment is critical to detect complications and any change in patient status. Two IV lines are typically placed for any patient with ACS to ensure that access is available for administering emergency medications. Medications are administered IV to achieve rapid onset and to allow for timely adjustment. After the patient's condition stabilizes, IV lines may be changed to a saline lock to maintain IV access.

Diagnosis

Nursing Diagnoses

Based on the clinical manifestations, history, and diagnostic assessment data, major nursing diagnoses may include:

Ineffective cardiac tissue perfusion related to reduced coronary blood flow from coronary thrombus and atherosclerotic plaque
Risk for imbalanced fluid volume
Risk for ineffective peripheral tissue perfusion related to decreased cardiac output from left ventricular dysfunction
Death anxiety
Deficient knowledge about post-MI self-care

Collaborative Problems/Potential Complications

Based on the assessment data, potential complications that may develop include the following:

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

Planning and Goals

The major goals for the patient include relief of pain or ischemic signs and symptoms (eg, ST-segment changes), prevention of further myocardial damage, absence of respiratory dysfunction, maintenance or attainment of adequate tissue perfusion by decreasing the heart's workload, reduced anxiety, adherence to the self-care program, and absence or early recognition of complications. Care of the patient with an uncomplicated MI is summarized in the Plan of Nursing Care

Evaluation

Expected Patient Outcomes

Expected patient outcomes may include the following: