Acute Coronary Syndrome Case Study

ANSWERS

Patient E is a 54-year-old man who came to his primary care physician’s office complaining of chest pain. When he arrived at the primary care physician’s office, he had no chest pain. A 12-lead ECG was performed, which revealed no differences from previous ECGs. The patient’s vital signs were stable and within normal limits: blood pressure was 135/78 mm Hg, heart rate was 68 beats per minute and regular, and respirations were 16 breaths per minute and unlabored. He was inebriated.

Comments and Rationale: Anyone presenting to a healthcare facility with a complaint of chest pain should be evaluated for the presence of signs and symptoms of ACS. Vital signs and a 12-lead ECG are appropriate assessment measures for changes that could indicate ischemia or an infarct. On arrival, Patient E had no chest pain, his ECG showed no acute ischemic changes, and his vital signs were stable. Further evaluation by a healthcare provider is advised.

The doctor inquired about Patient E’s chest pain episodes. About a week ago, the patient said he was having his “usual” occasional chest pain when he “worked too long, too hard in the yard.” However, in the last week, his chest pain attacks had become more severe, necessitating more sublingual nitroglycerin tablets for relief. He had a prolonged episode of chest pain at rest the night before and decided to seek medical attention.

Comments and justification: Stable angina is defined as chest pain that occurs in a predictable pattern, is generally triggered by the same level of exertion and is easily relieved by rest and sublingual nitroglycerin. Stable angina is a common symptom of CHD, but it is rarely associated with acute myocardial ischemia. However, increased frequency, severity, or the need for additional nitroglycerin tablets to achieve relief and severe chest pain at rest are signs that the patient’s angina has become “unstable.” Medication evaluation and intervention are required right away.

The physician reviewed Patient E’s medical record and discovered that he had had CABG surgery five years before. Patient E needed a drug-eluting stent placed two years ago to open a blockage in one of his prior CABG saphenous vein grafts. Patient E was also prescribed dyslipidemia medication; his most recent laboratory tests revealed that his LDL was borderline high at 135 mg/dL. He had quit smoking two years prior, following the placement of the stent. The patient weighed about 30 pounds too much. When the doctor mentioned his need to lose weight, the patient’s usual response was, “Either the weight or the smoking is to blame. I cannot do both.”

Comments and Rationale: A thorough history and physical examination can provide the information needed to triage patients who present with chest pain and stratify their risk for serious outcomes such as acute MI. Known history of CHD, a history of occlusions that required intervention to restore blood flow and oxygen supply, and the presence of modifiable risk factors such as obesity, dyslipidemia, smoking, and hypertension are all major risk factors for ACS.

Given the patient’s known CHD, prior history of CABG and PCI with stents, and ongoing risk factors, the physician directed Patient E to the local hospital’s emergency department. The patient refused emergency medical services transport and insisted on driving to the hospital.

Comments and Rationale: According to ACCF/AHA guidelines, people who may have ACS should be transported to the hospital by emergency medical services. Transport by emergency medical services allows skilled healthcare providers to assess the patient, obtain an immediate ECG, and administer aspirin and other medications as needed. Furthermore, emergency medical services can notify the receiving emergency department that the patient is expected, allowing immediate triage and evaluation. ACCF/AHA guidelines strongly discourage people with ACS from driving or asking friends or family members to drive them to the emergency room.

Patient E presented to the emergency department with chest pain. He rated the pain as a ten on a ten scale, located on the left side of his chest, in the substernal region. He was slightly diaphoretic with a blood pressure of 170/90 mm Hg and a heart rate of 110 beats per minute.

Comments and Rationale: Severe, intense chest pain in the left substernal area of the chest, combined with diaphoresis and changes in vital signs, is a strong indicator of ACS.

The emergency physician initiated the chest pain protocol. Patient E was given 325 mg of aspirin and told to chew it before swallowing. He was also given sublingual nitroglycerin, and supplemental oxygen at 2 liters per nasal cannula was started. A 12-lead ECG and blood work, including troponin T levels, were performed.

Comments and rationale: Aspirin is administered immediately in ACS to reduce the risk of thrombus formation. Sublingual nitroglycerin acts as a vasodilator, reducing myocardial workload while increasing oxygen supply to the heart. It also aids in the reduction of high blood pressure.

Nonspecific ST-segment and T-wave changes were seen on the 12-lead ECG. The patient reported 10/10 chest pain five minutes after taking one sublingual nitroglycerin tablet, and his blood pressure was 140/88 mm Hg. A second sublingual nitroglycerin tablet was administered; five minutes later, Patient E reported his pain to be 8/10 and his blood pressure to be around 140/88 mm Hg. A third sublingual nitroglycerin tablet was administered, and the patient reported that his pain level was 5/10 minutes later. His blood pressure was found to be 132/80 mm Hg. The doctor prescribed 2 mg of morphine IV.

Nonspecific ST-segment and T-wave changes are concerning in patients with clinical symptoms of ACS. Serial ECGs may be recommended to detect the presence of a developing MI. If the patient does not become hypotensive, sublingual nitroglycerin can be given every five minutes for up to three doses. Analgesic therapy in ACS relieves the patient’s “chest pain.” Morphine may be used to treat chest pain that persists after three sublingual nitroglycerin tablets have been taken. Morphine is a vasodilator, which lowers myocardial oxygen demands while increasing myocardial oxygen supply.

Patient E reported that morphine had relieved his chest pain. His blood pressure and heart rate had returned to “normal.” His initial troponin tests came back negative for cardiac damage. The doctor decided to admit the patient to the telemetry/stepdown floor for additional observation and monitoring. His admitting diagnosis was UA/possible ACS, and he had orders for serial troponin monitoring, continuous ECG monitoring, and an immediate 12-lead ECG with chest pain.

Comments and justification: Patient E’s increasingly severe and frequent chest pain episodes, as well as the presence of nonspecific changes on 12-lead ECG and his prior history of CHD, CABG, and stent placements, indicate that the patient is at increased risk for MI. Serial troponins can provide valuable diagnostic information and can be used to confirm or rule out NSTEMI. Continuous ECG monitoring detects ST-segment changes that indicate ischemia and infarction. A 12-lead ECG recorded during chest pain can also reveal whether there is ischemia/infarction and which part of the heart is at risk.

The second set of cardiac biomarkers for Patient E revealed elevated troponin levels. A repeat ECG revealed no signs of ischemia or infarction. Eight hours later, the third set of cardiac biomarkers revealed that troponin T was positive for myocardial damage. NSTEMI was confirmed as a diagnosis. Another ECG taken immediately after the laboratory work was returned revealed no evidence of ischemia; however, Patient E developed chest pain minutes later. Continuous ECG monitoring revealed ST-segment depression in the inferior leads.

Comments and justification: ECG changes and cardiac biomarker elevation suggestive of myocardial ischemia and infarction can occur over a few minutes to several hours. Serial measurements are recommended in patients with persistent chest pain, initial negative ECG findings, and cardiac biomarker levels. As with Patient E, biomarker changes suggestive of an infarct can appear several hours after the initial episode of chest pain. In the absence of ST-segment elevation, elevated cardiac troponin levels are diagnostic for NSTEMI.

The doctor prescribed continuous heparin infusions and a bolus dose of eptifibatide followed by a continuous infusion. Patient E had been given aspirin in the emergency room; on the floor, he was given 600 mg of clopidogrel and a low dose of a beta-blocker. Patient E experienced another bout of chest pain that was not alleviated by sublingual nitroglycerin or intravenous morphine. As a result, the doctor prescribed a continuous nitroglycerin drip.

Comments and justification: The immediate goal of NSTEMI treatment is to relieve ischemia and prevent further infarction. Key management components include aspirin (chewed) and clopidogrel to reduce platelet formation and aggregation, as well as nitroglycerin and morphine for ischemic pain relief via reduced myocardial workload and decreased myocardial oxygen demand. If sublingual nitroglycerin fails to relieve chest pain, a continuous nitroglycerin infusion titrated to relieve chest pain while keeping blood pressure within a prescribed range may be used. Anticoagulation is a crucial component in the treatment of acute NSTEMI. A continuous heparin infusion is one anticoagulation option; heparin can be combined with a glycoprotein IIb/IIIa inhibitor. A glycoprotein IIb/IIIa inhibitor, such as eptifibatide, may be used in the early stages of NSTEMI. Eptifibatide can be started before cardiac catheterization and continued for a set period after catheterization and stent placement.

Patient E was transported to the cardiac catheterization laboratory for diagnostic coronary angiography and potential PCI. Cardiac catheterization revealed that he had blocked a section of his right coronary artery. The patient’s previous stent remained patent, as did the other vein grafts from previous surgery. A PCI with bare-metal stent placement was performed.

Comments and rationale: During PCI, intracoronary stents are used to help keep the lumen of the affected vessel open. The interventional cardiologist performing the procedure decides whether to use a bare-metal or drug-eluting stent.

Patient E was returned to his room after recovering in the cardiac catheterization area. The post-catheterization orders called for 4 hours of bed rest, the continuation of the eptifibatide drip for 18 hours after the PCI procedure, and serial monitoring of cardiac biomarkers and complete blood count. Continuous ECG monitoring, frequent vital sign checks, frequent monitoring of the arterial puncture site for evidence of bleeding or hematoma, and assessment for signs of recurrent chest pain (indicating occlusion of the infarct-related vessel) or severe left flank pain were all part of the nursing care (indicative of retroperitoneal bleed). Patient E’s urine output was monitored and recorded, and he was encouraged to drink fluids.

Comments and Rationale: Monitoring for bleeding, maintaining the eptifibatide drip as ordered to reduce the risk of stent occlusion, and monitoring the patient for changes in vital signs, heart rhythm, or the development of chest pain are key elements of care during the immediate post-PCI period. During this time, potential complications include bleeding from the puncture site and occlusion of the coronary artery.

Patient E’s initial blood work after the PCI revealed a drop in platelet count from high normal to borderline low. Six hours later, the second blood work set revealed a dramatic drop in his platelet count. The physician was notified, and the eptifibatide infusion was terminated. Closely monitoring the patient for any signs of bleeding was an appropriate nursing intervention.

Comments and rationale: Using glycoprotein IIb/IIIa inhibitors can result in a dangerous drop in platelet counts in some people. Careful monitoring of platelet levels at specified intervals during the infusion is recommended to identify this complication and intervene on time.

QUESTION

Acute Coronary Syndrome Case Study

Please provide complete, thorough, and detailed answers to all questions in the case study. Multiple choice answers should include the correct choice and RATIONALE for that choice and/or rationale why other choices are incorrect.