Acute Coronary Syndromes: Myocardial Infarction and Unstable Angina PDF

C h a p ter 18 Acute Coronary Syndromes: Myocardial Infarction and Unstable Angina Maame Yaa A. B. Yiadom Acute coronary syndromes (ACS) encompass a spectrum of cardiac disorders with myocardial ischemia and/or injury. These include ST-elevation myocardial infarction (STEMI), non-STEMI (NSTEMI),...

C h a p ter 18 Acute Coronary Syndromes: Myocardial Infarction and Unstable Angina Maame Yaa A. B. Yiadom Acute coronary syndromes (ACS) encompass a spectrum of cardiac disorders with myocardial ischemia and/or injury. These include ST-elevation myocardial infarction (STEMI), non-STEMI (NSTEMI), and unstable angina. ■■ CLINICAL FEATURES Chest pain is the most common symptom for patients with ACS. Important elements of the history include the timing of symptom onset, location, quality, severity, and duration. Also important is whether the pain is intermittent, constant, or waxing and waning. Twenty percent to 30% of all patients diagnosed with ACS report atypical symptoms, and their chief complaint may not include chest pain. These atypical symptoms can include shortness of breath, nausea, diaphoresis, back pain, abdominal pain, dizziness, or palpitations. Clinical features associated with chest pain that is diagnosed as ACS include substernal or left-sided chest pain, radiation of pain to one or both arms, and chest pain accompanied with nausea, vomiting, or diaphoresis. Discuss risk factors for coronary artery disease (CAD) with patients to stratify the risk of ACS. These risk factors include older age, male gender, family history, smoking, hypertension, hypercholesterolemia, and diabetes. Patients with a long history of cocaine use may be at risk for accelerated CAD development, and recent use can cause acute ischemia from coronary vasospasm. The presence or absence of risk factors alone are poorly predictive of the likelihood of myocardial infarction in a patient presenting with acute symptoms. Physical examination can help identify signs of hemodynamic dysfunction from cardiac strain or acute heart failure such as pallor, diaphoresis, altered mental status, elevated jugular venous distension, peripheral edema, or rales on pulmonary exam. ■■ DIAGNOSIS AND DIFFERENTIAL Consider alternative diagnoses for patient symptoms based on clinical assessment, which may include diseases such as pulmonary embolism, congestive heart failure, gastroesophageal reflux disease, symptomatic hiatal hernia, chronic obstructive pulmonary disease, asthma, pneumonia, pneumothorax, pericarditis, myocarditis, aortic dissection, chest trauma, chest wall disorders, or mediastinal disorders. Promptly obtain an ECG to assess for signs of cardiac ischemia. Findings diagnostic for STEMI include at least one of the four criteria listed in Table 18-1. In the setting of symptoms suggestive of ischemia, ECG findings consistent with STEMI should be acted upon promptly to initiate appropriate 131 18_Cydulka_Ch18.indd 131 15/03/17 12:31 PM 132 SECTION 4: Cardiovascular Diseases Table 18-1 Electrocardiographic ST-Segment-Based Criteria for Acute Myocardial Infarction Location Electrocardiographic Findings Anteroseptal ST-segment elevations in V1, V2, and possibly, V3 Anterior ST-segment elevations in V1, V2, V3, and V4 Anterolateral ST-segment elevations in V1–V6, I, and aVL Lateral ST-segment elevations in I and aVL Inferior ST-segment elevations in II, III, and aVF Inferolateral ST-segment elevations in II, III, aVF, and V5 and V6 True posterior* Initial R waves in V1 and V2 > 0.04 s and R/S ratio ≥1 Right ventricular ST-segment elevations in II, III, and aVF and ST elevation in right-side V4 *Posterior wall infarction does not produce Q-wave abnormalities in conventional leads and is diagnosed in the presence of tall R waves in V1 and V2. therapy. ECG findings that do not meet criteria for STEMI but raise concerns for NSTEMI or unstable angina may include ST or T wave changes in a coronary artery distribution (see Table 18-2). For patients with suspected ACS, obtain serum troponin, chest radiograph, CBC, electrolytes, and PT/PTT. NSTEMI is diagnosed when an elevated serum troponin is identified in a patient with symptoms consistent with myocardial ischemia. Consider repeating troponin levels within 3 hours when diagnostic uncertainty remains. Over time, a patient may progress in disease severity, prompting consideration for serial ECGs to identify any dynamic ischemic changes, bedside echocardiography to assess for cardiac wall motion abnormalities, and/or additional serum troponin testing. Consult with cardiology to determine whether early cardiac catheterization may be appropriate for patients with NSTEMI who continue to have concerning symptoms or dynamic changes. Table 18-2 Anatomic Distribution of Ischemic ECG Changes Location Location of ST or T Wave Changes Coronary Artery Involvement Inferior II, III, AVF* RCA in 80%; RCX in 20% Lateral I, AVL, V5-6 LCX Septal V1-3* LAD septal branches Anterior V1-4, loss of Q wave in V5-6* LAD Right ventricular V1, right-sided V4 RCA Posterior V7-9 (left-sided leads), R waves in V1, LCX Atrial V1-6 RCA *Can be accompanied with signs of dysrhythmia. Abbreviations: RCA, right coronary artery; RCX, right circumflex artery; LCX, left circumflex artery; LAD, left anterior descending artery. 18_Cydulka_Ch18.indd 132 15/03/17 12:31 PM CHAPTER 18: Acute Coronary Syndromes 133 Unstable angina is a clinical diagnosis based on history, physical examination findings, and diagnostic testing that does not reveal a STEMI or NSTEMI. This may precede STEMI or NSTEMI or may be the presenting diagnosis that leads to a new diagnosis of CAD. Unstable angina characteristically presents with chest pain (or atypical ACS symptoms) associated with evidence of obstructive coronary artery disease and has one of the following three characteristics: (1) began within the past 2 months; (2) has increasing frequency, intensity, or duration of existing angina symptoms; or (3) existing angina begins to occur at rest. Additional diagnostic testing that may be helpful when unstable angina is considered includes coronary CT angiogram, exercise treadmill testing, cardiac nuclear perfusion imaging, or cardiac MRI. ■■ EMERGENCY DEPARTMENT CARE AND DISPOSITION 1. STEMI treatment begins immediately upon recognition of diagnostic ECG findings. Goals include reperfusion by reducing thrombus, limiting thrombus extension, and relieving obstructive CAD. The effectiveness of interventions is time sensitive. Options include administering systemic thrombolytic therapy within 30 minutes of arrival or initiating percutaneous coronary intervention (PCI) within 90 minutes. PCI is the preferred therapy, when possible, based on greater benefits and fewer risks in patients without contraindications to thrombolysis (Table 18-3) who can achieve PCI within 120 minutes. See Table 18-3 for medications used in the treatment of STEMI. 2. For patients with a suspected ACS, begin cardiac monitoring, place an intravenous line, and provide supplemental oxygen if oxygen saturation is less than 95%. Administer aspirin 160 to 325 mg orally chewed. Consider oral, transdermal, or intravenous nitroglycerin to treat any ongoing angina. Morphine sulfate may be used as an adjunct if pain continues despite treatment with nitroglycerin. 3. Clopidogrel is recommended for use along with aspirin for patients with moderate to high-risk NSTEMI and STEMI, and in patients in whom PCI is planned. Use as an alternative to aspirin in patients allergic to aspirin. Clopidogrel increases risk of bleeding, and should be held at least 5 days before coronary artery bypass grafting (CABG). 4. Begin anticoagulation for patients with unstable angina or NSTEMI using unfractionated heparin or low-molecular-weight heparins (LMWH). These are also options for patients undergoing PCI revascularization, in consultation with your cardiology consultant. Unfractionated heparin is preferred for patients in whom CABG is planned. 5. Factor Xa inhibitors such as fondaparinux have similar efficacy to unfractionated heparin in patients with unstable angina or NSTEMI, and current guidelines consider it an option as an antithrombin. In STEMI patients lacking renal impairment, fondaparinux may be considered for those patients treated with thrombolytics that are not fibrin specific such as streptokinase. 6. Direct thrombin inhibitors, such as bivalirudin, bind directly to thrombin in clot and are resistant to agents that degrade heparin. Comparison of bivalirudin with unfractionated heparin found no outcomes benefit 18_Cydulka_Ch18.indd 133 15/03/17 12:31 PM 134 SECTION 4: Cardiovascular Diseases Table 18-3 Drugs Used in the Emergency Treatment of STEMI Antiplatelet Agents Aspirin Clopidogrel Prasugrel Ticagrelor Antithrombins Unfractionated heparin Enoxaparin Fondaparinux Fibrinolytic Agents Streptokinase Anistreplase Alteplase Reteplase Tenecteplase Glycoprotein IIb/IIIa Inhibitors† Abciximab Eptifibatide Tirofiban Other Anti-Ischemic Therapies Nitroglycerin Morphine 162–325 mg Loading dose of 600 mg PO followed by 75 mg/d. No loading dose is administered in patients > 75 years old receiving fibrinolytics Loading dose of 60 mg promptly and no more than 1 h after PCI once coronary anatomy is defined and a decision is made to proceed with PCI Loading dose is 180 mg PO followed by 90 mg twice a day Bolus of 60 U/kg (maximum, 4000 U) followed by infusion of 12 U/kg/h (maximum, 1000 U/h) titrated to a partial thromboplastin time 1.5-2.5 × control 30 mg IV bolus followed by 1 mg/kg SC every 12 h 2.5 mg SC* 1.5 MU over 60 min 30 U IV over 2–5 min Body weight > 67 kg: 15 mg initial IV bolus; 50 mg infused over next 30 min; 35 mg infused over next 60 min Body weight < 67 kg: 15 mg initial IV bolus; 0.75 mg/kg infused over next 30 min; 0.5 mg/kg infused over next 60 min 10 U IV over 2 min followed by 10 U IV bolus 30 min later Weight Dose (total dose not to exceed 50 mg) 30 mg <60 kg 35 mg ≥60 but <70 kg 40 mg ≥70 but <80 kg 45 mg ≥80 but <90 50 mg ≥90 0.25 mg/kg bolus followed by infusion of 0.125 µg/ kg/min (maximum, 10 µg/min) for 12–24 h 180 µg/kg bolus followed by infusion of 2.0 µg/kg/ min for 72–96 h 0.4 µg/kg/min for 30 min followed by infusion of 0.1 µg/kg/min for 48–96 h Sublingual: 0.4 mg every 5 min × 3 PRN pain IV: Start at 10 µg/min, titrate to 10% reduction in MAP if normotensive, 30% reduction in MAP if hypertensive 2–5 mg IV every 5–15 min PRN pain (Continued) 18_Cydulka_Ch18.indd 134 15/03/17 12:31 PM CHAPTER 18: Acute Coronary Syndromes 135 Table 18-3 Drugs Used in the Emergency Treatment of STEMI (Continued) Metoprolol 50 mg PO every 12 h on first day, unless significant hypertension, may consider 5 mg IV over 2 min every 5 min up to 15 mg; withhold β-blockers initially if the patient is at risk for cardiogenic shock/adverse effects‡ Atenolol 25–50 mg PO, unless significant hypertension, may consider 5 mg IV over 5 min, repeat once 10 min later; withhold β-blockers initially if the patient is at risk for cardiogenic shock/adverse effects‡ *Fondaparinux should not be used as monotherapy for PCI; if used, addition of unfractionated heparin or bivalirudin is recommended before PCI. †American College of Cardiology/American Heart Association 2009 focused update for STEMI patients recommended glycoprotein IIB/IIa inhibitors be given at the time of PCI; benefit prior to arrival in the cardiac catheterization laboratory is uncertain. ‡Risk factors for cardiogenic shock/adverse effects: (1) signs of heart failure; (2) evidence of a low cardiac output state; (3) increased risk for cardiogenic shock (cumulatively: age >70 years old, systolic blood pressure <120 mm Hg, sinus tachycardia >110 beats/min or bradycardia <60 beats/min, and longer duration of STEMI symptoms before diagnosis and treatment); or (4) standard relative contraindications to β-blockade (PR interval >0.24 s, second- or third-degree heart block, active asthma, or reactive airway disease). Abbreviations: MAP, mean arterial pressure; PCI, percutaneous coronary intervention; PRN, as needed; STEMI, ST-segment elevation myocardial infarction. 7. 8. 9. 10. in NSTEMI patients, but less bleeding occurred and no dosage adjustment is required in renal impairment. For patients with STEMI, bivalirudin may be considered as an alternative to unfractionated heparin and GP IIb/IIIa inhibitors. In treatment settings without timely access to PCI, fibrinolytics are indicated for patients with STEMI if time to treatment is <6 to 12 hours from symptom onset, and the ECG has at least 1-mm ST-segment elevation in two or more contiguous leads. The dosages of individual fibrinolytic agents are listed in Table 18-3. STEMI patients who have received fibrinolytics should receive fulldose anticoagulation started in the ED and maintained for a minimum of 48 hours. Similar efficacy and safety profiles have been demonstrated for tPA, rtPA, and TNK. Contraindications for fibrinolytics are listed in Table 18-4. Before administering thrombolytics, obtain informed consent. Arterial puncture should be avoided, as should venipuncture or central line placement in areas which are not readily compressible. Tissue plasminogen activator (tPA) is a naturally occurring human protein and is not antigenic. tPA is fibrin-specific and has a half-life of 5 minutes. When compared with traditional dosing, front-loaded tPA has been shown to have superior 90-minute patency rates and reocclusion rates, with no increase in bleeding risk. Reteplase (rPA) is a non-fibrin-specific deletion mutant of tPA with a prolonged half-life of 18 minutes and its use may have a faster time to perfusion. The main advantage of reteplase is that it is given as a double bolus rather than continuous infusion. 18_Cydulka_Ch18.indd 135 15/03/17 12:31 PM 136 SECTION 4: Cardiovascular Diseases Table 18-4 Contraindications to Fibrinolytic Therapy in ST-Segment Elevation Myocardial Infarction Absolute contraindications Any prior intracranial hemorrhage Known structural cerebral vascular lesion (e.g., arteriovenous malformation) Known intracranial neoplasm Ischemic stroke within 3 months Active internal bleeding (excluding menses) Suspected aortic dissection or pericarditis Relative contraindications Severe uncontrolled blood pressure (>180/100 mm Hg) History of chronic, severe, poorly controlled hypertension History of prior ischemic stroke >3 months or known intracranial pathology not covered in contraindications Current use of anticoagulants with known INR >2–3 Known bleeding diathesis Recent trauma (past 2 weeks) Prolonged CPR (>10 min) Major surgery (<3 weeks) Noncompressible vascular punctures (including subclavian and internal jugular central lines) Recent internal bleeding (within 2–4 weeks) Patients treated previously with streptokinase should not receive streptokinase a second time Pregnancy Active peptic ulcer disease Other medical conditions likely to increase risk of bleeding (e.g., diabetic retinopathy) 11. Tenecteplase (TNK) is a fibrin-specific substitution mutant of tPA that is given as a single weight-based bolus. 12. Streptokinase (SK) activates circulating plasminogen, is not fibrinspecific, and is capable of generating an allergic reaction (minor: 5% to 5.7%, anaphylaxis: <0.2% to 0.7%). Hypotension occurs in up to 15% of patients and is usually responsive to fluids and slowing of SK infusion. Contraindications include hypotension, prior SK administration within 6 months, and streptococcal infection within a year. SK’s half-life is 23 minutes, but systemic fibrinolysis persists for 24 hours. Administer heparin within 4 hours of starting SK. 13. The most significant complication of systemic thrombolytics is bleeding, particularly intracranial hemorrhage. If significant bleeding occurs, discontinue thrombolytics, heparin, and aspirin. Crystalloid and red blood cell infusion may be necessary. Cryoprecipitate and fresh frozen plasma (FFP) may be used to reverse fibrinolysis by replenishing thrombotic factors. Begin with 10 units of cryoprecipitate and obtain fibrinogen levels. If the fibrinogen level is <1 g/L, administer a second 10 U of cryoprecipitate. If bleeding continues despite a fibrinogen >1 g/L, or if the fibrinogen level is <1 g/L after 20 U of cryoprecipitate, administer 2 U of FFP. If hemorrhage continues, administer platelets or antifibrinolytic agents such as aminocaproic acid or tranexamic acid. 18_Cydulka_Ch18.indd 136 15/03/17 12:31 PM CHAPTER 18: Acute Coronary Syndromes 137 14. Recent evidence shows no benefit to early IV administration of β-blockers on cardiac rhythm, infarct size, reinfarction, or mortality. Oral β-blocker therapy does not need to be initiated emergently unless there is a specific indication such as significant tachycardia or hypertension. β-blockers should be initiated within the first 24 hours of hospitalization for patients lacking contraindications. 15. Glycoprotein IIb/IIIa (GP IIb/IIIa) antagonists bind to platelets and inhibit their aggregation. Abciximab, eptifibatide, and tirofiban are currently available. There is no current evidence supporting the routine use of GP IIb/IIIa inhibitor therapy prior to angiography in patients with STEMI, and the use of these agents upstream is uncertain. Use of GP IIb/IIIa inhibitors should be guided by local interdisciplinary review of ongoing clinical trials, guidelines, and recommendations. 16. The disposition of ACS patients depends on their specific ischemic diagnosis and hemodynamic status. STEMI patients often are taken immediately to the catheterization laboratory for definitive treatment. Patients treated with thrombolytics who have continued hemodynamic instability and pain or have not reperfused may be candidates for rescue angioplasty. Emergent CABG may also be indicated for some patients. Patients in refractory cardiogenic shock should undergo emergent angioplasty. Intraaortic balloon pump or other LV-assisting devices may also be indicated for these patients. Admission to a critical care unit is appropriate. 17. NSTEMI or unstable angina patients who have ongoing chest pain, ECG changes, dysrhythmias, or hemodynamic compromise are also admitted for further care in a cardiac intensive care unit. Patients with symptoms of unstable angina but resolved chest pain, normal or nonspecific ECG changes, and no complications may often be admitted to a monitored inpatient bed. ■■ FURTHER READING For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8th ed., see Chapter 49, “Acute Coronary Syndromes” by Judd E. Hollander and Deborah B. Diercks. 18_Cydulka_Ch18.indd 137 15/03/17 12:31 PM