Beat the Clock

Abstract

The initial evaluation of chest pain is a challenge that emergency department (ED) nurses face every day, and they do so more frequently than do other health professionals because they’re often the first ones to deal with the patient. Acute coronary syndromes (ACS), which include non–Q wave myocardial infarction (MI), Q wave MI, and unstable angina, are particularly challenging because they require an awareness of typical, atypical, and multisystem signs and symptoms. Non–Q wave MI, also known as nontransmural infarct, involves damage to the subendocardium, the intramural myocardium, or both. Non–Q wave MI doesn’t usually progress to a Q wave MI, as seen on an electrocardiogram (ECG) reading. Q wave MI, which is a transmural infarct, involves extensive necrosis or nearly full thickness of the ventricular wall. In this case, the ECG shows ST-segment and Q wave evolving. In unstable angina, the ECG shows normal or no ST elevation, yet it can progress across the spectrum of acute coronary syndromes to Q wave MI. Of the three acute coronary syndromes, unstable angina is particularly difficult to diagnose because of the lack of ECG changes and cardiac marker elevations. Patients with unstable angina present with chest pain resulting from myocardial ischemia, with no evidence of myocardial necrosis. Unstable angina may progress to Q wave MI. This acute ischemic syndrome falls between chronic stable angina and acute MI in the clinical spectrum of coronary artery disease (CAD). However, biologically, unstable angina represents the disease in a potentially dangerous form. Patients with unstable angina are at risk for developing ST-segment depression, T-wave inversion, or ST-segment elevation indicative of acute MI requiring rapid reperfusion and pharmacologic modalities. 1 According to Mayme Roettig, RN, it’s imperative to obtain a 12-lead ECG every 30 minutes for a two-hour period in those patients whose conditions fall into the difficult pattern between stable angina and acute MI. 1 Unstable angina is often difficult to assess because the 12-lead ECG shows normal or non–ST-segment elevation (nondiagnostic ECG). Hence, a diagnosis of unstable angina results from a combination of patient history, clinical assessment, serial ECGs, and cardiac markers. SIGNS AND SYMPTOMS Patients with chest pain may not have the typical clinical complaints of substernal chest tightness, pressure, heaviness, or squeezing. Some may present with more subtle signs, such as nausea, syncope, diaphoresis, dyspnea, or weakness. Those most often presenting with chest pain of an atypical nature are women, the elderly, and people with diabetes. Atypical symptoms may also include abdominal pain (especially in women), fatigue, and muscle weakness. It’s important to note that in some cases a patient also may present with multisystem complaints that further complicate triage. For example, a female patient with diabetes who presents with epigastric pain, weakness, and diaphoresis needs to be evaluated for possible MI. Other symptoms to note are neck, jaw, and shoulder pain that may accompany any of the above-mentioned symptoms. Most patients don’t seek medical advice until two hours or longer after the onset of symptoms. Many wait 12 hours or longer. In general, reperfusion therapy after 12 hours may confer little benefit on the patient’s recovery. 1 Factors that may cause delays of treatment after the onset of symptoms may be patient-related, either a failure to recognize the significance of the symptoms or a delay in seeking care. Other delays may be caused by the length of time taken for prehospital evaluation and transport, as well as by inherent delays within the hospital for diagnosis and treatment. Usually patient-related delays are the longest, and yet the other factors mentioned each contribute to the patient getting further away from the time when the effect of treatment may not be as beneficial. Effective early intervention cannot occur without the patient’s and his family’s vigilance in regard to the significance of chest pain and their immediate action upon its onset. 2 TRIAGE It’s the triage nurse’s primary goal to appropriately assess the patient and to facilitate treatment. Triage of any patient with complaints of chest pain must be completed within three to five minutes. During triage the nurse takes vital signs, and also rates the patient’s level of pain on a scale of 0 to 10. Traditionally, on this scale, 0 indicates no pain at all and 10 the worst pain imaginable. The nurse might also consider using the term “discomfort” rather than “pain,” since some patients present with pressure or squeezing that might not be interpreted as pain. A brief history of the patient’s presenting complaint, risk factors, and family history also must be obtained. A 12-lead ECG must be performed and serves to provide necessary information for the treating physician as well as the ED team in the event that the patient must be reperfused. In some urban emergency departments, the triage nurse or the emergency department technician performs the ECG and draws stat baseline cardiac markers prior to transferring the patient to the main ED. Additionally, a clinical pathway ensures that the patient presenting with cardiac complaints will be triaged according to the appropriate algorithm. It’s especially important that the nurse be knowledgeable in the various signs and symptoms of chest pain. The clinical pathway is an algorithm that guides the nurse to the track appropriate to the patient with chest pain, facilitates care and treatment, and helps decrease the time for diagnostic testing and admission. (See Chest Pain Overview, page 12.) Once the nurse’s triage assessment is complete, she consults the physician and the charge nurse and proceeds to transfer the patient to the appropriate patient care area in the ED. DIAGNOSIS The ED nurse must be knowledgeable in the recent trends and guidelines of the American College of Cardiology–American Heart Association (ACC–AHA) when assessing patients with ischemic chest pain. Decisions made according to the initial evaluation can have clinical consequences such as increased length of stay. 3 Physician clinical assessment. Using an algorithm such as the Chest Pain Overview as a guide, she places the patient in the appropriate track. Track 1 describes patients with acute MI with ST-segment elevation in two contiguous leads with typical symptoms or left bundle branch block. Track 2 describes a patient presumed to be at high risk (that is, with unstable angina, non–Q wave MI) with ST-segment depression. This patient presents with a history of CAD or risk factors such as smoking, positive family history, diabetes, and persistently or frequently recurring chest pain correlated to unstable angina. Track 3 describes patients who have normal ECG or unspecific changes and are presumed to be at moderate risk although still with cardiac risk factors and classic presentation. Track 4 patients (possible unstable angina) have a history of atypical chest pain, are at the time asymptomatic, and have an ECG that is not diagnostic. Track 5 describes those with noncardiac chest pain symptoms and a normal ECG. ECG. Patients presenting with complaints of either ischemic chest pain or a history of CAD must receive a 12-lead ECG within 10 minutes. The ECG is one of the critical tools in risk stratification. It not only can lend support to the clinical assumption of CAD, it also provides prognostic information based on the pattern and magnitude of the abnormalities. 3 A rhythm strip obtained or 12-lead ECG performed during an episode of the presenting symptoms is particularly valuable. In some emergency medical systems (EMS), a patient’s complaints of chest pain prompts the paramedic to notify the ED before transporting the patient there. The information is then relayed to the nursing and medical staff, which expedites the management of patients with ACS. The rhythm strip obtained by the EMS helps in determining the management of patient care as well as the pharmacologic intervention. Additionally, continuous ST-segment monitoring or repeated ECGs are recommended for patients with ischemia whose conditions may progress to a high-risk category. Cardiac markers are biochemical analyses acquired by serum collection. Since 50% of patients with acute MI don’t show ST-segment elevation, these markers are used to establish both the diagnosis of myocardial necrosis and an approximate prognosis. 1,3 There are various types of cardiac markers. The ones used most often are: CK-MB, or creatine kinase-myocardial band, is an isoform of CK found in the heart muscle. Considered a “late riser,” this marker begins to rise within three to nine hours of infarction. Myoglobin is a newer marker that rises within one to two hours of infarction. However, myoglobin is not specific to cardiac muscle and may give a false-positive result in patients with skeletal muscle and renal disease. Myoglobin is a low-weight protein present in both cardiac and skeletal muscle. Because it is sensitive for myocardial death within the first two to four hours, it is not specific for it. Cardiac troponins I (cTnI) and T (cTnT) are the best markers for diagnosing acute MI. Additionally, troponin confers an advantage over the CK-MB marker because it’s able to predict an increased risk of death in patients with non–Q wave MI or unstable angina. 4 Troponin levels begin to rise above normal within three to nine hours after infarction. Cardiac marker analyses can be acquired by two different methods, either by point-of-care instrumentation or by central laboratory processing. Point-of-care instrumentation provides rapid results in 15 minutes and is readily available at the bedside. However, point-of-care testing presents some disadvantages. For example, there are regulatory issues in place in some states limiting who may perform the test. It’s especially helpful in determining the pathway of unstable angina. Central laboratory processing provides an analysis report in one to two hours. Compared with point-of-care instrumentation, central laboratory processing may pose a disadvantage because of the length of time required to obtain test results. Portable chest X-ray is another diagnostic tool used in the immediate care of patients with chest pain. It determines whether the patient has pulmonary infiltrates, cardiomegaly, or congestive heart failure. Patients must sit up when the radiograph is obtained in order to get the best image of the heart. If the chest X-ray is unremarkable, further chest roentgenograms are usually not necessary. 5 Oxygen therapy. This is initiated routinely when patients arrive in the ED. Those presenting with chest pain are often found to be hypoxic and require supplemental O 2 . Oxygen may also relieve some of the chest pain from ischemia. TREATMENTS Aspirin is the first choice for antiplatelet therapy. It’s the least expensive and safest antiplatelet agent shown to be effective in acute MI and ACS. 6 Thienopyridine derivatives (ticlopidine, clopidogrel) can be used as a substitute in patients who are hypersensitive to aspirin or who have major gastrointestinal intolerance to it. Nitrates are also used to reduce the oxygen demand of the myocardium. The nurse should administer a direct-acting vasodilator such as nitroglycerin (NTG). If the patient’s symptoms are not relieved by 3 sublingual tablets or a metered-dose spray of it, the administration of a β-blocker before intravenous NTG is necessary if no contraindications exist. Morphine is also recommended for patients whose symptoms are not relieved after three doses of NTG tablets. Intravenous unfractionated heparin, or subcutaneous low-molecular-weight heparin (LMWH) such as enoxaparin, must be added to antiplatelet therapy. Enoxaparin has been extensively researched as a possible replacement for unfractionated heparin in patients with unstable angina and other ACSs. The antithrombotic activity of LMWH stabilizes the plaque. Eptifibatide, a glycoprotein IIb–IIIa receptor blocker, is indicated for patients with unstable angina and non–Q wave MI, including both patients who are to be managed medically and those undergoing percutaneous coronary intervention (PCI). Tirofiban and abciximab are glycoprotein IIb–IIIa receptor blockers for patients with unstable angina and ST-segment depression on an ECG and those with non–Q wave MI. The nurse must be aware of the complications and risk factors associated with the administration of these drugs. She must observe for hypotension when administering nitrates to patients. Continuous pulse oximetry monitoring must be instituted when administering oxygen therapy. Antiplatelet therapy indicates the necessity of monitoring partial thromboplastin time and hemoglobin and hematocrit values. It’s important to remember that bleeding is the most common complication seen in the use of abciximab, eptifibatide, or tirofiban. Nurses must discuss the treatment plan and what is to be expected of it with the patient and family. While continuously monitoring and stabilizing the patient, the nurse can begin to prepare the patient for admission to the intensive care unit, the telemetry unit, or a chest pain observation unit, according to the diagnosis. The chest pain unit, if available, may be used to facilitate a more definitive evaluation of the diagnosis while avoiding unnecessary hospital admissions of patients who fall in the categories of “possible ACS” or “low-risk ACS.” The chest pain unit may produce a reduction in both misdiagnosis and the premature discharging of patients with active myocardial ischemia without ST-segment elevation. Serial cardiac markers with 12-lead ECGs may be performed every three to four hours, depending on institutional policies and procedures. Patients at a low risk for UA may be given a stress test. In some instances, they may require more invasive treatments such as cardiac catheterization, placement of an intraaortic balloon pump, or even both. In essence, all patients must be monitored carefully and consistently and the appropriate treatment given. The ED nurse is an integral part of this process. FIGUREFigure: Chest Pain Overview Adapted with permission of Dr. Michael Washington, clinical director, Emergency Department, Howard University Hospital, Washington, DC.