Healthcare Background and Significance
Coronary heart disease (CHD) is the primary health risk for all Americans. The American Heart Association 1 estimates that about 700,000 people experienced a new myocardial infarction (MI) while approximately 500,000 have had a recurrent MI in 2004. The direct costs (hospitalization, nursing home, health professionals, drugs, and home healthcare) and the indirect costs (lost productivity due to morbidity and mortality) of CHD are estimated to be $133.2 billion in 2004. 1Acute coronary syndromes (ACS) is the term used to denote any 1 of 3 clinical manifestations of CHD: unstable angina (UA), non–ST elevation myocardial infarction (NSTEMI), and ST-elevation MI (STEMI) (Fig 1). 2
The major challenge to healthcare providers is the rapid and accurate identification of patients with ACS who would benefit from immediate thrombolysis or percutaneous coronary interventions. In addition, the goals are to prevent premature discharge and reduce unnecessary admissions. Since only 35% to 40% of patients presenting to the emergency department (ED) with chest pain ultimately have a cardiac diagnosis, 3 evaluating the remaining 60% to 65% of people with noncardiac diagnoses in an expeditious and less costly manner is an important goal. Nurses can assist in meeting these goals by completing rapid and accurate triage in the ED and by obtaining a comprehensive clinical history. The purpose of this article, therefore, is to describe the incidence, causes, risk factors, assessment, and diagnosis of patients presenting with ACS as well as current recommendations for nurses who treat patients with ACS.
Pathophysiology of Acute Coronary Syndromes
Unstable angina represents the progression of stable coronary artery disease to unstable disease. The cause is usually the rupture of an atherosclerotic plaque, leading to thrombus formation and a partial occlusion of the involved coronary artery. 4 Non–ST elevation myocardial infarction is closely related to UA and results in a partial occlusion of the coronary artery with minor elevation of cardiac markers and ST segment deviations. 5 ST-elevation MI occurs when an abrupt and complete occlusion of the involved artery leads to acute ischemia and necrosis, resulting in ST elevation and possible Q wave development. 6
Risk Factors for Acute Coronary Syndromes
Nonmodifiable risk factors for CHD include increasing age, male sex, race, and heredity. The major modifiable risk factors for CHD are diabetes, hypertension, smoking, dyslipidemia, physical inactivity, and obesity. Unfortunately, the Centers for Disease Control 7 has declared that the related problems of type 2 diabetes and obesity have reached epidemic levels. These alarming trends in both type 2 diabetes and obesity, in conjunction with an aging population and a lack of risk factor modification in the young, will undoubtedly result in an increase in the incidence of ACS in the future. In an analysis of data from the Framingham Heart Study, Lloyd-Jones 8 determined the risk for developing CHD at age 40 to be 1 in 2 for men and 1 in 3 for women. However, by age 70 women and men are at equal risk. Women's risk of CHD increases after menopause and, on average, women manifest the disease about 10 years later than men. The presence of diabetes confers a higher level of risk for women compared with men. 9
A person's risk for CHD increases if he or she has a male relative who experienced MI before age 55 or a female relative who experienced MI before age 65. 10 While risk factors are helpful in predicting disease and outcomes, many people present with few or no known risk factors. Differences in risks do, however, vary across racial and ethnic groups. The incidence of hypertension is higher in African Americans compared to that in Whites, and their risk for CHD is higher as well. The risk for CHD is also higher for Mexican Americans, American Indians, and Hawaiians.
Symptoms of Acute Coronary Syndromes
The list of symptoms of MI published by the American Heart Association includes chest discomfort in the center of the chest that can feel like pressure, squeezing, fullness, or pain; discomfort in the arms, the back, neck, jaw, or stomach; and associated signs such as shortness of breath, cold sweat, nausea, or lightheadedness. 10 The classic symptoms of MI typically involve precordial or retrosternal chest pain, and the quality of the pain may be described as heaviness, pressure, aching, crushing, burning, or squeezing. The pain may radiate to the jaw, neck, arms, or back. 11 The pain may wax and wane, and usually lasts more than 15 minutes. The presence of associated symptoms such as nausea, vomiting, diaphoresis, and dyspnea help to differentiate the diagnosis from ischemia. 12 The typical symptoms of UA are similar and include substernal chest pain described as pressure, tightness, aching, squeezing, fullness, dullness, or heaviness. In addition, the pain may be poorly localized in the chest, occur with little exertion, or occur at rest. Less typical, but frequently reported, symptoms include dyspnea, nausea, diaphoresis, syncope, or pain in the arms, neck, shoulder, or epigastrium. 5,13,14 It is important to note, however, that the symptoms of UA may be identical to those of MI.
Numerous studies have described the symptoms associated with ACS. 15–19 A number of studies have limited their sample to those patients experiencing MI, 16,17,19–21 while others included patients with all forms of ACS. 15,18,22,23 The most frequently reported symptoms of all forms of ACS in these studies were chest pain, diaphoresis, shortness of breath, and nausea. While these are considered to be typical symptoms, a number of studies listed weakness and fatigue as frequently reported symptoms. 21,24,25 Historically, these symptoms have been considered to be atypical and associated with the prodromal period as opposed to the acute event. 25 McSweeney and colleagues recently published novel research on the prodromal and acute symptoms of MI in women. 26 In that study of a large sample (n = 515) of women interviewed 4 to 6 months after hospital discharge, the most frequently experienced prodromal symptoms were unusual fatigue (70.7%), sleep disturbance (47.8%), and shortness of breath (42.1%). Interestingly, only 29.7% of women reported chest discomfort. The most frequently reported acute symptoms were shortness of breath (57.9%), weakness (54.8%), and fatigue (42.9%). Chest pain/discomfort was present in only 57% of women during the acute period. Mean intensity of discomfort for both prodromal and acute symptoms was mild. 26
Similarly, prior studies have found the incidence of chest pain in patients with ACS to be as low as 67%. 18,22,27–30 This is a disturbing finding because chest pain has been considered the hallmark symptom of ACS, and experiencing chest pain promotes recognition of symptoms as serious and facilitates immediate access to treatment. Those who do not experience chest pain may fail to recognize the seriousness of their symptoms, defer seeking emergency treatment, and experience a delay in treatment when presenting to the ED or be misdiagnosed if they do seek treatment.
Assessing Chest Pain and Associated Symptoms of ACS
The clinical assessment of patients with possible ACS is based on clinical history, electrocardiogram (ECG) findings, cardiac markers, and physical examination. Traditionally, nursing has used the PQRST method to assess symptoms:
- P—the provocative and palliative elements of the symptoms
- Q—the quality of the discomfort
- R—the region (location of discomfort) and radiation
- S—the severity of the discomfort
- T—the temporal quality of the symptoms
Provocative and palliative refer to what brings on the pain and what alleviates or diminishes it. These may include exertion, emotional upset, other stressors, or eating. Often nitrates or rest will relieve chest pain temporarily. Note that the threshold for anginal symptoms may be lower in those who are overweight and/or sedentary. 31 Quality of the discomfort is usually described as pressure, tightness, heaviness, dullness, or squeezing. Typical regions or locations of discomfort are the center or left chest with radiation to the jaw or left arm. Less typical locations are the upper back and shoulders. Women are more likely to experience discomfort in the back, shoulders, and abdomen. Severity of discomfort is assessed on a scale of 0 to 10, 0 being no discomfort and 10 being the worst pain the patient can imagine. In the past, it was believed that the pain of ACS was always severe, but we now know that the pain may be mild and up to 30% of patients suffer no pain at all. 18,22,30 Temporal quality of symptoms refers to when they occur and whether pain begins suddenly or gradually.
The pain of UA is characterized by an increase in severity, pain at rest, and/or episodes that are more frequent or longer in duration than the discomfort of stable angina. The pain of MI is similar to UA but has been described as more severe in some cases. 32 The pain may be triggered by physical exertion, emotional stress, or circadian rhythms. This has been attributed to stimulation of the sympathetic nervous system, the release of catecholamines, and increased platelet aggregation. 31 In a meta-analysis with 83,929 patients who were asked about the onset of MI symptoms, Cohen et al 33 found that the risk of MI increased by 40% between the hours of 6 AM and 12 PM. The value of the symptom assessment cannot be overstated, since early interventions have demonstrated improvement in outcomes and because ACS may not be diagnosed with ECG or cardiac markers alone.
Assessment would be easy if all patients presented with typical symptoms; unfortunately, this is not the case. Many patients experience less typical symptoms and there is evidence that this occurs more frequently in women, the elderly, and people with diabetes, hypertension, prior heart failure, and stroke. 34 In previous studies, women have experienced more lightheadedness, unusual fatigue, and upper back pain than men. 13,15 Older people have reported symptoms that are milder and more ambiguous compared with those of younger people, 34,35 and those aged 75 or older are most likely to present without chest discomfort. 27 Čulić et al 36 found that during MI, patients with diabetes were more likely to experience weakness, dyspnea, and nausea compared to those without diabetes. Unfortunately, prior stroke, heart failure, and diabetes are conditions associated with lack of chest pain, and older people are more likely to have these conditions. 27,37 Pain occurring in locations other than in the chest, and that described as numbness, tingling, stabbing, or burning, or non–chest pain discomfort such as indigestion, lightheadedness, unusual fatigue, or weakness are considered to be less typical. 38 The absence of chest pain is also considered atypical in spite of the fact that up to 33% percent of patients with ACS experience no chest pain. 27,28
TIMI Risk Score for UA/NSTEMI
The TIMI risk score for UA/NSTEMI, is a simple method of risk stratification intended for clinical use following the diagnosis of UA/NSTEMI. The risk score is based on data from the Thrombolysis in Myocardial Infarction IIB trial (Table 1). 39 In that study, incidence of adverse outcomes (death, MI, or urgent revascularization) in the 14 days following an episode of UA/NSTEMI ranged from about 5% in those with 0 or 1 risk factor to 41% in those with 6 or 7 risk factors. The 7 risk factors include age, risk factors for CHD (eg, smoking), amount of coronary stenosis, ST segment deviation, anginal symptoms, aspirin use, and CK-MB elevation.
TIMI Risk Score for STEMI
The TIMI risk score for STEMI, developed by Morrow et al 40 stratifies the risk of mortality in the 30 days following MI. The risk score is based on data obtained from participants in the Intravenous nPA for Treatment of Infarction Myocardium Early II (InTIME-II) trial. 41 The trial compared outcomes in patients receiving the fibrinolytics alteplase (tPA) or lanoteplase (nPA). Ten baseline characteristics are included in the model. Three historical factors—diabetes, hypertension, and angina—were combined, resulting in a list of 8 variables. The final list includes age, history of disease, systolic blood pressure, heart rate, Killup class, weight, ECG changes, and time to treatment (Table 2).
The diagnosis of ACS is based on ECG findings and elevation of cardiac markers in concert with the history and clinical presentation.
In UA, there may be no ECG changes or the ECG may show ST depression in the affected leads. With NSTEMI there is typically ST depression, T wave inversion, or nonspecific ST changes. With STEMI there is ST elevation in the affected leads with reciprocal ST depression. However, these changes may be masked by left bundle branch block (LBBB). Shlipak et al 42 found that the ECG is a poor predictor of MI in patients with LBBB, and this is problematic for the more than 100,000 patients presenting with MI annually who also have LBBB. The investigators concluded that all patients with LBBB should be treated with thrombolytics if their symptoms are consistent with MI. Electrocardiograms identify approximately 40% to 65% of all MIs but may be of little value in diagnosing UA/NSTEMI. 43,44 In a retrospective review of the presenting ECGs of subjects enrolled in the Global Strategies to Open Occluded Arteries in Acute Coronary Syndromes (GUSTO-IIb) trial, Savonitto et al 45 reported that 81% of patients with ST elevation and 89% of those with ST elevation and depression had confirmed MI. They also found that ECG changes were predictive of increases in mortality ranging from 1.7% (for T-wave inversion alone) to 14.4% (for presence of both ST elevation and ST depression).
Until 2000, detection of creatine kinase–MB (CK-MB), an isoenzyme released into the serum following myocardial infarction, was the standard marker for MI. New guidelines for diagnosis of MI adopted by the European Society of Cardiology (ESC) and the American College of Cardiology (ACC) 11 included the measure of the protein marker troponin I or troponin T found in cardiac muscle. Troponins have higher specificity and sensitivity to myocardial damage than CK-MB. 46,47 Troponins can be detected in the serum between 3 and 6 hours after the onset of symptoms, and they remain in the serum for 7 to 10 days. Troponins should be drawn on admission and 6 to 9 hours after onset of symptoms. 48 Since troponin is degraded from contractile proteins in the myocardium, it has a high specificity for irreversible injury. Consequently, elevated troponin levels also contribute to risk stratification. Ottani et al 49 found that patients with elevated troponins had a 9-fold increase in the risk for MI or death in the 30 days following the initial event.
When an urgent diagnosis is needed, such as in the absence of ECG changes, the use of the rapidly appearing myoglobin marker is recommended. Myoglobin is a heme protein found mainly in muscle tissue, where it serves as a reservoir for oxygen. 50 Myoglobin appears in the serum 30 to 60 minutes after the onset of symptoms and falls quickly. Myoglobin lacks the specificity of the troponins but has high sensitivity and may be useful when drawn in conjunction with troponin within 4 to 6 hours after symptom onset. 44,51 Because of its rapid rise and decline, myoglobin levels may also be useful for detecting reinfarction when troponin levels are still elevated, but myoglobin does not contribute to stratification of risk.
While troponin and myoglobin are invaluable in assessing patients during ACS, markers of inflammation, such as C-reactive protein (CRP), are helpful in predicting long-term prognosis for ACS. 52 Findings from the Women's Health Study indicated a direct relationship between CRP levels and risk of cardiovascular disease. 53 C-reactive protein may become routine in the future as more data become available addressing its value.
The physical examination during ACS is often unremarkable, with symptoms often reflecting the amount of cardiac compromise. Vital signs, including blood pressure in both arms, heart rate, and temperature should be recorded. Auscultate the heart for an S3 or S4 gallop, the systolic murmur of mitral regurgitation, and the murmur of aortic stenosis, although it must be emphasized that extra heart sounds might not be present even in the case of severe disease. Auscultate the lungs for rales, which may indicate the onset of pulmonary edema. Peripheral vessels should be examined for pulse deficits or bruits. The physical examination may help rule out other diagnoses such as aortic dissection, pneumothorax, thyrotoxicosis, pericarditis, cardiac tamponade, or congestive heart failure (CHF). 14,53
Patients with confirmed or suspected UA/NSTEMI should be treated with aspirin, enoxaparin (preferred over unfractionated heparin), β-blockers, nitrates, and clopidigrel. 5 Patients with uncomplicated STEMI are treated in a similar fashion with the addition of ACE inhibitors. Thrombolytic therapy should optimally be administered within 30 minutes of symptom onset. Primary percutaneous coronary interventions (PCI) should be performed within 90 minutes of symptom onset. 54
Implications for Practice
The rapid and accurate diagnosis of patients with ACS is a major challenge for nurses. Quick and accurate triage in the ED, the inpatient setting, the clinic, and/or the field is crucial to identifying patients with probable ACS and to initiating emergent care.
Triage begins with the assessment of symptoms. Although the classic symptoms of ACS, chest discomfort, diaphoresis, shortness of breath, and nausea are well known to the general public, other frequently reported symptoms including unusual fatigue and weakness can be vague and attributed to a variety of minor ailments. In one study of patients who presented to the ED and met criteria for reperfusion therapy, 40% had atypical elements in the character of their pain description. 55 McSweeney et al recommended that clinicians assess for chest “sensations” in addition to chest pain. 26
Atypical symptoms should be of concern to nurses for several reasons. First, the general public obtains much of their health related information from the mass media. Frequently, heart attack is depicted as a dramatic event causing severe pain and collapse: “The Hollywood Heart Attack.” 56 Misinformation can lead to erroneous attribution of more mild symptoms of ACS to illnesses such as gastric reflux, flu, or normal aging—especially if chest pain or discomfort is absent. This could lead to a dangerous and potentially fatal delay in seeking emergency care. Furthermore, healthcare providers may also erroneously attribute such symptoms to less acute causes leading to delayed or misdiagnosed ACS and belated treatment.
Another concern is that the general public, and women in particular, often fail to appreciate their risk for ACS. Framingham data demonstrate that the risk for ACS in women is equal to that in men by age 70. Although cardiovascular disease is the leading cause of death for women in the United States, many women believe that they are at higher risk for breast cancer. 57 In a study of adult children of women with premature CHD, Allen and Blumenthal 58 found that even those with a high prevalence of modifiable risk factors did not perceive themselves to be at personal risk for CHD. Martin et al 59 found that women were less likely than men to attribute their prehospital MI symptoms to cardiac causes.
The National Heart, Lung, and Blood Institute (NHLBI), in partnership with others, recently launched a program called “The Heart Truth Campaign: Serious Messages about Women and Heart Disease.” 60 The purpose of the campaign is to make women more aware of their risk for heart disease. In addition, the American Heart Association is sponsoring the Go Red for Women campaign 61 to raise awareness of cardiovascular disease as the leading cause of death for women. The red dress is a symbol and a reminder that too many women are being lost to heart disease and that women are to be encouraged to care for their hearts and their health. Campaigns like these, along with information in the popular press, have helped raise the awareness of vulnerability to heart disease for women. Sharing this information with women may motivate them to modify their risks.
Identifying the symptoms of ACS can have a positive impact on the public, those with a history of ACS, and healthcare providers. Informing the public about what to do in response to symptoms may motivate more people to seek treatment in a timely and appropriate manner. Accurate models of ACS symptoms could put to rest the myth that symptoms are always sudden and severe and could identify the symptoms that are most common to each sex. Identification of symptoms could improve the management of CHD by enabling people to more accurately label symptoms, to seek care when appropriate, and to reduce their delays in seeking care. Unfortunately, an aging population and difficult to modify risk factors mean that the incidence of ACS and its associated complications will grow even larger in the future.
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