MI refers to the process by which areas of myocardial cells in the heart are permanently destroyed. Like unstable angina, MI is usually caused by reduced blood flow in a coronary artery due to atherosclerosis and occlusion of an artery by an embolus or thrombus. 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 for these di-agnoses. Other causes of an MI include vasospasm (sudden con-striction 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, thy-rotoxicosis, or ingestion of cocaine). In each case, a profound im-balance exists between myocardial oxygen supply and demand.
Coronary occlusion, heart attack, and MI are terms used syn-onymously, but the preferred term is MI. The area of infarction takes time to develop. As the cells are deprived of oxygen, ischemia develops, cellular injury occurs, and over time, 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 1 million people have acute MIs; one fourth of these people die of MI (Amer-ican Heart Association, 2001; Ryan et al., 1999). One half of those who die never reach a hospital.
Various descriptions are used to further identify an MI: the lo-cation of the injury to the left ventricular wall (anterior, inferior, posterior, or lateral wall) or to the right ventricle and the point in time within the process of infarction (acute, evolving, or old).
The ECG usually identifies the location, and the ECG and pa-tient history identify the timing. Regardless of the location of the infarction of cardiac muscle, the goal of medical therapy is to pre-vent or minimize myocardial tissue death and to prevent compli-cations.
Chest pain that occurs suddenly and continues despite rest and medication is the presenting symptom in most patients with an MI (Chart 28-6). One study showed that 2% of patients who eventually were diagnosed with an acute MI were incorrectly dis-charged and sent home from the emergency department (Pope et al., 2000). Most of these patients presented with atypical symp-toms such as shortness of breath; they also tended to be female, younger than 55 years of age, of a minority group, and have nor-mal ECGs. The Framingham Heart Study revealed that 50% of the men and 63% of the women who died suddenly of cardio-vascular disease had no previous symptoms (Kannel, 1986). Pa-tients may also be anxious and restless. 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 only for a short time or may not be present, or only some of them may occur. In many cases, the signs and symptoms of MI cannot be distinguished from those of unstable angina.
Diagnosis of MI is generally based on the presenting symptoms, the ECG, and laboratory test results (eg, serial serum enzyme values). The prognosis depends on the severity of coronary artery obstruction and the extent of myocardial damage. Phys-ical examination is always conducted, but the examination alone is insufficient to confirm the diagnosis.
The patient history has two parts: the description of the pre-senting symptom (eg, pain) and the history of previous illnesses and family health history, particularly of heart disease. Previous history should also include information about the patient’s risk factors for heart disease.
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 monitor-ing the ECG 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 (Fig. 28-4). Because infarction evolves over time, the ECG also changes over time. The first ECG signs of an acute MI are from 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 myo-cardium return to the resting state. Myocardial injury also causes ST-segment changes. The injured myocardial cells depolarize nor-mally 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 0.08 seconds after the end of the QRS. If the myocardial injury is on the endocardial surface, the ST segment is depressed 1 mm or more for at least 0.08 seconds. The ST-segment depression is usually horizontal or has a downward slope (Wagner, 2001).
MI is classified as a Q-wave or non-Q-wave infarction. With Q-wave infarction, abnormal Q waves develop within 1 to 3 days because there is no depolarization current conducted from necrotic tissue (Wagner, 2001). 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 (pro-vided the R wave exceeds a depth of 5 mm), or one that did not exist before the event (Wagner, 2001). An acute MI may cause a significant decrease in the height of the R wave. During an acute MI, injury and ischemic changes are also present. An abnormal Q wave may be present without ST-segment and T-wave changes, which indicates an old, not acute, MI. Patients with non-Q-wave MIs do not develop a Q wave on the ECG after the ST-segment and T-wave changes, but symptoms and cardiac enzyme analysis confirm the diagnosis of an MI.
During recovery from an MI, the ST segment often is the first 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 Q-wave MI is usually indicated by an abnormal Q wave or decreased height of the R wave without ST-segment and T-wave changes.
The echocardiogram is used to evaluate ventricular function. It may be used to assist in diagnosing an MI, especially when the ECG is nondiagnostic. The echocardiogram can detect hypo-kinetic and akinetic wall motion and can determine the ejection fraction.
Historically, laboratory tests used to diagnose an MI included creatine kinase (CK), with evaluation of isoenzymes and lacticdehydrogenase (LDH) levels. Newer laboratory tests with faster results, resulting in earlier diagnosis, include myoglobin and tro-ponin analysis. These tests are based on the release of cellular con-tents into the circulation when myocardial cells die. Table 28-5 shows the time courses of cardiac enzymes. An LDH test is now infrequently ordered because it is not useful in identifying cardiac events (Braunwald et al., 2000).
There are three CKisoenzymes: CK-MM (skeletal muscle), CK-MB (heart muscle), and CK-BB (brain tissue). CK-MB is the cardiac-specific iso-enzyme; CK-MB is found mainly in cardiac cells and therefore rises only when there has been damage to these cells. CK-MB assessed by mass assay is the most specific index for the diagnosis of acute MI (Braunwald et al., 2001). The level starts to increase within a few hours and peaks within 24 hours of an MI. If the area is reper-fused (eg, due to thrombolytic therapy or PTCA), it peaks earlier.
Myoglobin is a heme protein that helps to transportoxygen. 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.
The test takes only a few minutes to run. 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. If the first myoglobin test results are negative, the test may be repeated 3 hours later. Another negative test result confirms that the patient did not have an MI.
Troponin, a protein found in the myocardium, regu-lates the myocardial contractile process. There are three isomers of troponin (C, I, and T). Because of the smaller size of this protein and the increased specificity of the troponins I and T for cardiac muscle, these tests are used more frequently to identify myocardial injury (unstable angina or acute MI). The increase in the level of troponin in the serum starts and peaks at approximately the same time as CK-MB. However, it remains elevated for a longer period, often up to 3 weeks, and it therefore cannot be used to identify sub-sequent extension or expansion of an MI.
The goal of medical management is to minimize myocardial dam-age, preserve myocardial function, and prevent complications. These goals are achieved by reperfusing the area with the emer-gency use of thrombolytic medications or PTCA. Minimizing my-ocardial damage is also accomplished by reducing myocardial oxygen demand and increasing oxygen supply with medications, oxygen administration, and bed rest. The resolution of pain and ECG changes are the primary clinical indicators that demand and supply are in equilibrium; they may also indicate reperfu-sion. Visualization of blood flow through an open vessel in the catheterization laboratory is evidence of reperfusion.
The patient with an acute MI receives the same medications as the patient with unstable angina, with the possible additions of thrombolytics, analgesics, and angiotensin-converting enzyme (ACE) inhibitors. Patients should receive a beta-blocker initially, throughout the hospitalization, and a prescription to continue its use after hospital discharge.
Thrombolytics are medications that are usually ad-ministered intravenously, although some may also be given directly into the coronary artery in the cardiac catheterization laboratory (Chart 28-7). 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), minimiz-ing 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 inter-ventions.
Thrombolytics dissolve all clots, not just the one in the coro-nary artery. They should not be used if the patient has formed a protective clot, such as after major surgery or hemorrhagic stroke. Because thrombolytics reduce the patient’s ability to form a stabi-lizing clot, the patient is at risk for bleeding. Thrombolytics should not be used if the patient is bleeding or has a bleeding disorder. All patients who receive thrombolytic therapy are placed on bleeding precautions to minimize the risk for bleeding. This means mini-mizing the number of punctures for inserting intravenous lines, avoiding intramuscular injections, preventing tissue trauma, and applying pressure for longer than usual after any puncture.
To be effective, thrombolytics must be administered as early as possible after the onset of symptoms that indicate an acute MI. They are not given to patients with unstable angina. Hospitals mon-itor their ability to administer these medications within 30 minutes from the time the patient arrives in the emergency department. This is called door-to-needle time (Ryan et al., 1999). The thrombolytic agents used most often are streptokinase (Kabikinase, Streptase), alteplase (Activase), and reteplase (r-PA, TNKase). Anistreplase (Eminase) is another thrombolytic agent that may be used.
Streptokinase increases the amount of plasminogen activator, which then increases the amount of circulating and clot-bound plasmin. Because streptokinase is made from a bacterium, its use also entails a risk of an allergic reaction. Vasculitis has occurred up to 9 days after administration. Streptokinase is not used if the patient has been exposed to a recent Streptococcus infection or has received streptokinase in the past 6 to 12 months.
Alteplase is a type of tissue plasminogen activator (t-PA). In contrast to streptokinase, alteplase activates the plasminogen on the clot more than the circulating plasminogen. Because it does not decrease the clotting factors as much as streptokinase, un-fractionated or low molecular weight heparin is used with t-PA to prevent another clot from forming at the same lesion site. Because t-PA is a naturally occurring enzyme, allergic reactions are mini-mized, but t-PA costs considerably more than streptokinase.
Reteplase is structurally very similar to alteplase and has similar effects. Anistreplase is similar to streptokinase and has similar effects.
The analgesic of choice for acute MI is morphinesulfate (Duramorph, Astramorph) administered in intravenous boluses. Morphine reduces pain and anxiety. It reduces preload, 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 pres-sure, which can be lowered, and the respiratory rate, which can be depressed. Because morphine decreases sensation of pain, ST-segment monitoring may be a better indicator of subsequent ischemia than assessment of pain.
Angiotensin Iis formed when the kidneys release renin in response to decreased blood flow. Angiotensin I is converted to angiotensin II by ACE, a substance found in the lumen of all blood vessels, especially the pulmonary vasculature. Angiotensin II causes the blood vessels to constrict and the kidneys to retain sodium and fluid while excreting potassium. These actions increase circulating fluid and raise the pressure against which the heart must pump, result-ing in significantly increased cardiac workload. ACE inhibitors(ACE-I) prevent the conversion of angiotensin from I to II. Inthe 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 the mortality rate and prevents the onset of heart failure. It is important to ensure that the patient is not hypotensive, hyponatremic, hypovolemic, or hyperkalemic before ACE-I ad-ministration. Blood pressure, urine output, and serum sodium, potassium, and creatinine levels need to be monitored closely.
The patient in whom an acute MI is suspected may be referred for an immediate PCI. PCI may be used to open the occluded coro-nary artery in an acute MI and promote reperfusion to the area that has been deprived of oxygen. PCI treats the underlying atheroscle-rotic lesion. Because the duration of oxygen deprivation is directly related to the number of cells that die, the time from the patient’s arrival in the emergency department to the time PCI is performed should be less than 60 minutes (time is muscle). This is frequently referred to as door-to-balloon time (Smith et al., 2001). To perform an emergent PCI within this short time, a cardiac catheterization laboratory and staff must be available.
After the MI patient is free of symptoms, an active rehabilitation program is initiated. Cardiac rehabilitation is a program that tar-gets risk reduction by means of education, individual and group support, and physical activity. Most insurance programs, in-cluding Medicare, cover the cost of a cardiac rehabilitation pro-gram. However, some studies indicate that only 8% to 39% of patients who are candidates for cardiac rehabilitation services typically participate in these programs (Wenger et al., 1995; Williams et al., 2002).
The goals of rehabilitation for the patient with an MI are to ex-tend and improve the quality of life. The immediate objectives are to limit the effects and progression of atherosclerosis, return the pa-tient to work and a pre-illness lifestyle, enhance the psychosocial and vocational status of the patient, and prevent another cardiac event. These objectives are accomplished by encouraging physical activity and physical conditioning, educating patient and family, and providing counseling and behavioral interventions.
Throughout all phases of rehabilitation, the goals of activity and exercise tolerance are achieved through gradual physical condi-tioning, aimed at improving cardiac efficiency over time. Cardiac efficiency is achieved when work and activities of daily living can be performed at a lower heart rate and lower blood pressure, thereby reducing the heart’s oxygen requirements and reducing cardiac workload.
Physical conditioning is achieved gradually over time. It is not unusual for patients to “overdo it” in an attempt to achieve their goals too rapidly. Patients are observed for chest pain, dyspnea, weakness, fatigue, and palpitations and are instructed to stop exer-cise if any of the symptoms develop. In a monitored program, they are also monitored for an increase in heart rate above the target heart rate, an increase in systolic or diastolic blood pressure more than 20 mm Hg, a decrease in systolic blood pressure, onset or worsening of dysrhythmias, or ST-segment changes on the ECG.
The target heart rate in phase I is an increase of less than 10% from the resting heart rate, or 120 beats per minute. In phase II, the target heart rate is based on the results of the patient’s stress test (usually 60% to 85% of the heart rate at which symptoms oc-curred), medications, and underlying condition. Oxygen satura-tion may also be assessed to ensure that it remains higher than 93%. If signs or symptoms occur, the patient is instructed to slow down or stop exercising. If the patient is exercising in an un-monitored program, he or she is cautioned to cease activity im-mediately if signs or symptoms occur and to seek appropriate medical attention. Table 28-6 identifies conditions in which an unmonitored home exercise program is not recommended.
Patients who are able to walk at 3 to 4 miles per hour are usually able to resume sexual activities. The nurse recommends that the patient be well rested and in a familiar setting; wait at least 1 hour after eating or drinking alcohol; and use a comfortable position. The patient is cautioned against anal sex. Sexual dysfunction or cardiac symptoms should be reported to the health care provider.
Cardiac rehabilitation occurs along the continuum of the disease and is typically categorized in three phases. Phase I may begin with the diagnosis of atherosclerosis, which may occur when the patient is admitted to the hospital for ACS (unstable angina, acute MI). It consists of low-level activities and initial education for the patient and family.
Because of the brief hospital stay, mo-bilization occurs earlier, and patient teaching is prioritized to the essentials of self-care, rather than instituting behavioral changes for risk reduction. Priorities for in-hospital education include the signs and symptoms that indicate the need to call 911 (seek emer-gency assistance), the medication regimen, rest-activity balance, and follow-up appointments with the physician. The nurse needs to reassure the patient that, although CAD is a lifelong disease and must be treated as such, most patients can resume a normal life after an MI. This positive approach while in the hospital helps to motivate and teach the patient to continue the education and lifestyle changes that are usually needed after discharge. The amount of activity recommended at discharge depends on the age of the patient, his or her condition before the cardiac event, the extent of the disease, the course of the hospital stay, and the development of any complications.
Phase II occurs after the patient has been discharged. It usu-ally lasts for 4 to 6 weeks but may last up to 6 months. This out-patient program consists of supervised, often ECG-monitored, exercise training that is individualized based on the results of an exercise stress test. Support and guidance related to the treatment of the disease and education and counseling related to lifestyle modification for risk factor reduction are a significant part of this phase. Short-term and long-range goals are collaboratively deter-mined based on the patient’s needs. At each session, the patient is assessed for the effectiveness of and adherence to the current medical plan. To prevent complications and another hospitaliza-tion, the cardiac rehabilitation staff alerts the referring physician to any problems. Outpatient cardiac rehabilitation programs are designed to encourage patients and families to support each other. Many programs offer support sessions for spouses and sig-nificant others while the patients exercise. The programs involve group educational sessions for both patients and families that are given by cardiologists, exercise physiologists, dietitians, nurses, and other health care professionals. These sessions may take place outside a traditional classroom setting. For instance, a dietitian may take a group of patients and their families to a grocery store to examine labels and meat selections or to a restaurant to discuss menu offerings for a “heart-healthy” diet.
Phase III focuses on maintaining cardiovascular stability and long-term conditioning. The patient is usually self-directed during this phase and does not require a supervised program, although it may be offered. The goals of each phase build on the accomplish-ments of the previous phase.