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GOALS  Determine clinical stability; assess need for transfer to emergency department (ED) for timely intervention  Identify patients with acute coronary syndrome (ACS) and other life-threatening emergencies  Identify and manage stable patients with non-cardiac chest pain precipitants  Coordinate with cardiology to appropriately evaluate and manage patients diagnosed with chronic coronary disease (CCD), especially those presenting to Triage and Treatment Area (TTA) with recurrent chest pain ALERTS • Women with chest pain are at risk for underdiagnosis, so history should emphasize accompanying symptoms • Transfer clinical unstable patients directly to ED by EMS (i.e., do not delay transfer for electrocardiogram [ECG] or other evaluation) • Emergent transfer for reperfusion therapy if evidence of ST-segment elevation myocardial infarction (STEMI) • Patients with ACS symptoms, stable vital signs, and no evidence of STEMI should be transferred to ED for monitoring and serial cardiac troponin evaluation This Acute Chest Pain Care Guide is based on the 2021 American Heart Association (AHA)/American College of Cardiology (ACC) Guideline for the Evaluation and Diagnosis of Chest Pain, which relies on cardiac troponin (cTn) as part of the assessment of patients with acute chest pain and suspected ACS. High-sensitivity cTn (hs-cTn) is preferred for a biomarker diagnosis. Acute troponin testing, which is typically done in the ED, cannot be done in our setting, so adaption of all AHA/ACC guideline recommendations is not possible. INTRODUCTION Approximately 1% of all ambulatory visits in primary care and approximately 4% of all emergency department visits were for acute chest pain. Within the United States, heart disease remains the leading cause of death since the early 1900s, yet only 2-4% of patients presenting to a primary care provider with chest pain will have ACS. National guidelines and cardiovascular societies increasingly recognize health disparities that exist among diverse patient populations and the need for cultural competency training to improve provider awareness of non-ACS causes of chest pain as well as anginal equivalent symptoms that may indicate ACS.1,2,3 Chest pain is broadly defined as pressure, tightness, squeezing, heaviness, or burning that can occur in the chest, shoulder, arms, jaw, neck, and upper abdomen. Chest pain should be described as “cardiac”, “possible cardiac”, or “noncardiac” to determine the cause of chest pain. Furthermore, cardiac chest pain can be “ischemic” or “nonischemic” in etiology.1 EVALUATION The most common causes of chest pain in the primary care setting are chest wall pain, reflux esophagitis, and costochondritis.2 However, acute chest pain can be caused by many life-threatening conditions, such as ACS, pulmonary embolism (PE), and acute chest syndrome, among others. Detailed evaluation of a patient’s chest pain history (characteristics), cardiac risk factors, focused physical exam, and ECG findings can help differentiate acute chest pain etiologies, but the presence or absence of ACS can only be confirmed by cTn/hs-cTn results, which is not available at CCHCS for acute chest pain.1 The classic symptoms of ACS are substernal chest pain, often described as pressure or crushing, with radiation to the jaw and/or left arm. However, this classic presentation is not described by many groups, including elderly patients, patients with diabetes, and women, in whom cardiac ischemia may present as shortness of breath, nausea or vomiting, lightheadedness, confusion, presyncope or syncope, as well as vague abdominal symptoms. See Health Equity Alert Box.1,4 Furthermore, there may be differences in the description and perception of chest pain and associated symptoms among various diverse patient groups, so consider sociocultural differences in the evaluation and management of patients presenting with HEALTH EQUITY ALERT Ischemic heart disease represents the leading cause of death in women, who experience relatively worse outcomes compared to men. This is due to sex-specific differences from biological factors, as well as gender specific differences from broader social, environmental, and community factors. There exists a knowledge gap regarding these differences in presentation, risk factors, pathophysiology, and response to treatment, which contributes to cardiovascular outcome disparities. In addition to traditional risk factors, sex-specific risk factors include autoimmune disease, pregnancy, menopause, and depression.4 acute chest pain.1 Remember that some populations present with ACS differently, so consider these differences during rapid assessment (see Appendix 1).1,2,3,4 CCHCS Care Guide: Acute Chest Pain | 3 CCHCS Care Guide: Acute Chest Pain December 2024 Evaluation, cont’d STEP 1: CLINICAL STABILITY When a patient presents with acute chest pain, a rapid assessment is needed, starting by determining clinical stability. • Assess the patient’s vital signs and level of consciousness. If the patient is clinically unstable or has altered level of consciousness, initiate EMS transfer to higher-level of care (HLOC). • Unless a noncardiac cause is evident, obtain and review ECG within 10 minutes of arrival for all patients who present with acute chest pain, irrespective of setting. As per AHA/ACC national guidelines, target initial medical decision making within 10 minutes of obtaining ECG and interpretation, which includes machine automatic interpretation ECG +/- provider review) in a clinically stable patient. If ECG shows ST elevation or new left bundle branch block (LBBB), assume STEMI ACS and initiate EMS transfer for STEMI. Notify EMS of STEMI so patient is directed to appropriate ED. Compare ECG to prior baseline ECG, if available. See Appendix 2 for ECG Interpretation. o A normal ECG markedly reduces the probability that chest pain is due to acute myocardial infarction (MI), but it does not exclude another serious, life-threatening cardiac etiology. • Emergently transfer the following patients to HLOC. While awaiting EMS transfer to HLOC, continue to monitor level of consciousness, vital signs, cardiac rhythm, and oxygen saturation: o Patient with unstable vital signs, such as heart rate (HR) ≤50 or ≥100, respiratory rate (RR) ≤12 or >20, systolic blood pressure (SBP) ≤90 mmHg, and SpO2 <95% on ambient air. o Patient with ECG showing ST elevation or new LBBB. Notify EMS of STEMI so patient is directed to appropriate ED. o Patient with ECG showing high-grade heart block or unstable arrhythmia/bradycardia/tachycardia. o Patient with serious life-threatening conditions, such as STEMI/ACS, PE, acute chest syndrome, tension pneumothorax, cardiac tamponade, and esophageal rupture. • For stable patients, continue monitoring and proceed to next steps in evaluation of chest pain.1,2 CCHCS Care Guide: Acute Chest Pain | 4 CCHCS Care Guide: Acute Chest Pain December 2024 Evaluation, cont'd STEP 2: STABLE PATIENT WITH ABNORMAL ECG • ECG abnormalities other than STEMI or new LBBB: Compare ECG to prior baseline ECG, if available. These non STEMI/non-LBBB ECG abnormalities include ST depression, T-wave flattening, T-wave inversion, heart block, arrhythmia, or other changes from ECG baseline. Left ventricular hypertrophy (LVH), bundle branch blocks, and ventricular pacing may mask signs of ischemia. • Continue evaluation with cardiac risk factor assessment, acute chest pain history, and focused physical examination, as detailed below. Consider other serious life-threatening conditions, such as non-ST elevation ACS (NSTE-ACS), PE, acute chest syndrome, tension pneumothorax, cardiac tamponade, and esophageal rupture. • Utilize the patient's cumulative burden of traditional and nontraditional cardiac risk factors, acute chest pain history and descriptors, and ECG findings to determine ACS risk. • Identify prior cardiac testing, if available. • Unless clear non-serious, non-life-threatening cause of acute chest pain is identified, consider transfer to HLOC for cTn/hs-cTn and further evaluation.1,2 • Emergently transfer the following patients to HLOC: o Patient becomes clinically unstable during the course of their evaluation with unstable vital signs, defined as new or deteriorating HR ≤50 or ≥100, RR ≤12 or >20, SBP ≤90 mmHg, and SpO2 <95% on ambient air. o Patient with ECG that evolves to showing ST elevation or new LBBB. Notify EMS of STEMI so patient is directed to appropriate ED. o Patient with ECG showing high-grade heart block or unstable arrhythmia/bradycardia/tachycardia. o Patient with suspected ACS and high-risk features, such as continuing chest pain, severe dyspnea, presyncope/syncope, palpitations, and/or evolving ECG findings. o Increased clinical suspicion for serious life-threatening conditions, such as ACS, PE, acute chest syndrome, tension pneumothorax, cardiac tamponade, and esophageal rupture.1,2,3 • Consider using clinical decision tools to stratify a patient's risk that acute chest pain is due to coronary artery disease (CAD), like INTERCHEST Score (see Table 1) or Marburg Heart Score, which are validated for patients seen in a primary care setting.2,5,6 There are many clinical decision pathways used to aid in medical decision-making for disposition from ED that are mentioned. However, these clinical decision pathways necessitate cTn/hs-cTn results and are only validated for patients that present to ED with acute chest pain. Therefore, these clinical decision pathways cannot be used for CCHCS patient population.1,2,5,6 • In general, patients who have "not low" CAD risk by the INTERCHEST Score (2-5) may need to be sent to HLOC for cTn/hs-cTn and further evaluation. • Consider repeating ECGs at 15-30 minute intervals for patients with baseline abnormal ECG (e.g. LVH, bundle branch block, ventricular pacing) or with new T-wave abnormalities in patients without ongoing chest pain and lower clinical suspicion for ACS (i.e. low INTERCHEST Score of ≤1). o NSTE-ACS may demonstrate progressive or evolving ST deviation on ECG, as well as other ECG abnormalities such as T-wave flattening or inversion. At initial presentation of NSTE-ACS, it may be difficult to distinguish between unstable angina and non-ST elevation myocardial infarction (NSTEMI). The distinction between these two types of NSTE-ACS is based on cTn/hs-cTn. 2BTable 1: INTERCHEST Score This clinical prediction tool is used for acute chest pain in primary care settings to determine if diagnostic workup can be done non-urgently in a stable "low" risk patient or if further testing for ischemia should be done more urgently in a "not low" risk patient. The INTERCHEST Score should not be used in patients with a readily apparent cause of chest pain (e.g. trauma, infection), clear anginal equivalent symptoms (e.g. jaw pain, dyspnea on exertion, arm pain), or if other testing (e.g. ECG) has suggested a clear cardiac etiology. INTERCHEST Score Variable Points History of CAD 1 Female ≥65 yo or male ≥55 yo 1 Chest pain related to effort 1 Pain reproducible by palpation -1 Provider initially suspected a serious condition 1 Chest discomfort feels like "pressure" 1 Score CAD Risk Probability of CAD ≤1 Low 2.1% 2-5 Not low 43.0% CCHCS Care Guide: Acute Chest Pain | 5 December 2024 Evaluation, cont'd CCHCS Care Guide: Acute Chest Pain • Consider chest x-ray for further evaluation. Also consider urine drug screen for further evaluation of chest pain etiology, since stimulant use is common in our clinical setting, and patients younger than expected can present with ACS due to recent cocaine or methamphetamine use.1,2 • In addition to evaluating for NSTE-ACS, consider that patients with acute chest pain who are found to have PE may present with nonspecific ECG abnormalities. Consider assessing a patient's pretest probability of PE using the Wells Score for PE (see Table 2). o If a patient has a low probability of PE (Wells Score <2), check PE Rule-out Criteria (PERC) Rule (see Table 3) to determine if patient warrants further testing. o If a patient has an increased probability of PE (Wells Score ≥2) or PERC Rule is not fulfilled, then consider transfer to HLOC for further workup of PE.1,2,3 Table 2: Wells Score The Wells Score risk stratifies patients for PE and provides an estimated pre-test probability. Wells Score for Pulmonary Embolism (PE) Variable Points Clinical signs and symptoms of deep vein thrombosis (DVT) 3 PE is top diagnosis OR equally likely 3 Heart rate > 100 1.5 Immobilization for at least 3 days OR surgery in the previous 4 weeks 1.5 Previous, objectively diagnosed DVT or PE 1.5 Hemoptysis 1 Malignancy 1 Score Risk of PE Probability of PE <2 Low 1.3% 2-6 Moderate 16.2% >6 High 37.5% Table 3: PERC Rule The Pulmonary Embolism Rule-out Criteria (PERC) Rule was designed to identify patients with low pre-test probability of PE (by Wells Score <2) in whom the risk of unnecessary testing outweighs the risk of PE. Pulmonary Embolism Rule-Out Criteria Variable Age <50 Heart rate <100 Oxygen saturation on room air ≥95% No hemoptysis No estrogen use No prior DVT or PE No unilateral leg swelling No surgery/trauma requiring hospitalization within the previous 4 weeks CCHCS Care Guide: Acute Chest Pain | 6 CCHCS Care Guide: Acute Chest Pain December 2024 Evaluation, cont'd STEP 3: STABLE PATIENT WITH NORMAL ECG • Continue evaluation with cardiac risk factor assessment, acute chest pain history, and focused physical examination. Consider other serious life-threatening conditions, such as NSTE-ACS, PE, acute chest syndrome, tension pneumothorax, cardiac tamponade, and esophageal rupture. • Utilize the patient's cumulative burden of traditional and nontraditional cardiac risk factors, acute chest pain history and descriptors, and ECG findings to determine ACS risk. • Identify prior cardiac testing, if available. The warranty period of prior cardiac testing should be considered when symptoms are unchanged in quality, severity, and frequency from prior episodes of chest pain (see Table 4). In patients with recent cardiac testing and normal findings 3BTable 4: Warranty Period for Prior Normal Cardiac Testing In patients with recent cardiac testing with normal findings, who do not have evidence of ACS, provided there are no changes in symptom frequency or severity. Test Modality Result Warranty Period Anatomic Normal coronary angiogram Coronary computed tomographic angiography 2 years Stress testing Normal stress test (given adequate stress levels) 1 year who do not have evidence of ACS, further testing is of limited value, provided that adequate exercise levels were achieved, or pharmacologic testing was performed, imaging was of sufficient quality, and there are no changes in symptom frequency or severity. • Consider using clinical decision tools to stratify a patient's risk that acute chest pain is due to CAD, like INTERCHEST Score (see Table 1 on page 5) or Marburg Heart Score, which are validated for patients seen in a primary care setting.2,5,6 There are many clinical decision pathways used to aid in medical decision-making for disposition from ED that are mentioned. However, these clinical decision pathways necessitate cTn/hs-cTn results and are only validated for patients that present to ED with acute chest pain. Therefore, these clinical decision pathways cannot be used in our patient population.1,2,5,6 • In general, patients who have "not low" CAD risk by the INTERCHEST Score (2-5) may need to be sent to HLOC for cTn/hs cTn and further evaluation. For patients with "low" CAD risk by the INTERCHEST SCORE (0-1), who have a normal ECG and a normal physical examination, consider close follow up at the institution with referral to specialists if they have remained symptom free throughout evaluation and monitoring.3,4,5 • If symptoms recur or evolve during a patient's evaluation and monitoring, consider repeating another ECG even if initial ECG was normal.1,2,3 Compare ECGs to prior baseline ECG, if available. Left ventricular hypertrophy, bundle branch blocks, and ventricular pacing may mask signs of ischemia. On a repeat ECG, NSTE-ACS may demonstrate new ST deviation, as well as other ECG abnormalities such as T-wave flattening or inversion. Consider transfer to HLOC for cTn/hs-cTn and further evaluation for patient with suspected ACS and high-risk features, such as recurring/evolving chest pain, severe dyspnea, presyncope/syncope, palpitations, and/or new/evolving ECG findings. • Consider chest x-ray for further evaluation. Also consider urine drug screen for further evaluation of chest pain etiology, since stimulant use is common in our clinical setting, and patients younger than expected can present with ACS due to recent cocaine or methamphetamine use.1,2as • Consider assessing for PE using the Wells Score for PE (see Table 2 on page 6), followed by (PERC) Rule (see Table 3 on page 6) if Wells Score <2. If a patient has an increased probability of PE (Wells Score ≥2) or PERC Rule is not fulfilled, then consider transfer to HLOC for further workup of PE. Proceed with further evaluation and management if there is a clear diagnosis of noncardiac chest pain or if the patient is no longer symptomatic and can be safely managed at the institution with appropriate follow up chest pain.1,2,3 CCHCS Care Guide: Acute Chest Pain | 7 CCHCS Care Guide: Acute Chest Pain December 2024 Evaluation, cont'd HISTORY Conduct a history including both personal and family, paying particular attention to the following: • Cardiac risk factors: Identify both traditional risk factors (male, age >45 yo, diabetes mellitus (DM), dyslipidemia, hypertension (HTN), smoking, family history of CAD, prior cardiac history, and/or known CAD, and nontraditional risk factors (see Table 5). Also identify prior cardiac testing, such as prior coronary angiogram or stress testing. In our clinical setting, stimulant use is common, and patients younger than expected can present with ACS due to recent cocaine or methamphetamine use.1,2 Table 5: Cardiac Risk Factor Assessment These are common traditional and non-traditional cardiac risk factors for CAD. In our setting, consider stimulant use as a cause of chest pain, especially among younger patients without traditional risk factors present with ACS. Patients with known CAD, especially those who had recent cardiac revascularization procedures are high risk for recurrent ischemia.1,2,4,8 Traditional Risk Factors for Coronary Artery Disease Male Age >45 yo Diabetes Hypertension Dyslipidemia Overweight and obesity Family history of premature CAD History of stroke/Transient ischemic attack (TIA) Known CAD History of myocardial infarction (MI) Smoking history Poor diet Sedentary lifestyle Known peripheral artery disease (PAD) Prior PCI and/or CABG Nontraditional Risk Factors for Coronary Artery Disease CKD Premature menopause (before age 40 yo) Coronary artery spasm History of chest radiation Estrogen or oral contraceptive pill use HIV NAFLD/MASLD Thyroid disease Cardiomyopathy Sickle cell disease (SCD) Chronic inflammatory conditions (e.g. lupus, rheumatoid arthritis) Stimulant use, e.g. cocaine, methamphetamine History of pregnancy associated conditions, e.g. preeclampsia Elevated biomarkers, e.g. hs CRP, Lp(a), apoB, ABI History of COVID-19 Percutaneous coronary intervention (PCI), coronary artery bypass graft (CABG), chronic kidney disease (CKD), human immunodeficiency virus (HIV), non-alcoholic fatty liver disease (NAFLD), metabolic dysfunction-associated steatotic liver disease (MASLD), high-sensitivity C-reactive protein (hs-CRP), lipoprotein (a) (Lp[a]), apolipoprotein B (apoB), ankle-brachial index (ABI), coronavirus disease 2019 (COVID-19) • Chest pain history and descriptors: Obtain details on the following information that can help better identify potential chest pain etiology (see Figure 1 and Table 6 on page 9).1 Remember that some populations present with ACS differently, so consider these differences during rapid assessment (see Appendix 1).1,2,3,4 CCHCS Care Guide: Acute Chest Pain | 8 December 2024 Evaluation, cont’d Figure 1: Probability of Ischemia Like most visceral discomfort, the sensation produced by cardiac ischemia is characteristically deep, difficult to localize, and usually diffuse. Point tenderness renders cardiac ischemia less likely. Reported symptoms lie somewhere on a continuum of higher or lower probability of cardiac ischemia based on the presence or absence of specific characteristics.1 Table 6: Chest Pain Characteristics1 CCHCS Care Guide: Acute Chest Pain Characteristic Common Corresponding Causes Nature and Quality • Anginal symptoms are perceived as retrosternal chest discomfort (e.g. pain, discomfort, heaviness, tightness, pressure, construction, squeezing). • Sharp chest pain that increases with inspiration and lying supine is unlikely related to cardiac ischemia (i.e. these symptoms usually occur with acute pericarditis). Onset and Duration • Anginal symptoms gradually build in intensity over a few minutes. • Sudden onset of ripping chest pain with radiation to the upper or lower back is unlikely to be anginal but is suspicious for an acute aortic syndrome, which is a serious life-threatening condition. • Fleeting chest pain, which lasts a few seconds in duration, is unlikely to be related to cardiac ischemia. Location and Radiation • Pain that can be localized to a very limited area and pain radiating to below the umbilicus or hip are unlikely related to cardiac ischemia. Severity • Ripping chest pain, often described as “the worst chest pain of my life”, especially when sudden in onset and occurring in a patient with uncontrolled hypertension or a patient with a known bicuspid aortic valve or aortic dilation, is suspicious for an acute aortic syndrome, which is a serious life-threatening condition. Precipitating Factors • Physical exercise or emotion stress are common triggers for anginal symptoms. • Occurrence at rest or with minimal exertion associated with anginal symptoms, usually indicates cardiac ischemia. • Positional chest pain is usually nonischemic. Relieving Factors • Relief with nitroglycerin is not necessarily diagnostic of myocardial ischemia and should not be used as a diagnostic criterion. Associated Symptoms • Common symptoms associated with cardiac ischemia include, but are not limited to, dyspnea, palpitations, diaphoresis, lightheadedness, presyncope or syncope, jaw and/or neck pain, and upper abdominal pain with heartburn unrelated to meals or nausea/vomiting. • Symptoms on the left or right side of the chest, stabbing chest pain, sharp chest pain, or discomfort in the throat or abdomen may occur in patients with diabetes, women, and elderly patients. Special Populations • Some populations of patients are less likely to have a “classic” presentation of ACS. For example, patient ≥75 yo may present with shortness of breath, syncope, mental impairment, abdominal pain, or an unexpected fall. See Appendix 1. CCHCS Care Guide: Acute Chest Pain | 9 CCHCS Care Guide: Acute Chest Pain December 2024 Evaluation, cont’d PHYSICAL EXAMINATION In patients with acute chest pain, a focused cardiovascular and pulmonary examination should be performed to aid in the diagnosis of ACS or other serious life-threatening causes of chest pain. These focused examinations also help to identify complications and to facilitate rapid implementation of appropriate treatment of serious life-threatening conditions. A normal physical examination does not exclude ACS or other serious life-threatening conditions. Specific findings may be useful in establishing the correct diagnosis (see Table 7 on page 11-13 and Table 8 on page 13). • Vital Signs • Jugular venous pressure elevation • Cardiac examination, such as auscultating for S3 gallop, new murmurs, friction rub, etc. • Chest wall examination, such as looking for new rash over area of pain, point tenderness to palpation, etc. • Pulmonary examination, such as increased work of breathing, crackles, absent breath sounds, etc.1,2,3,9 CHEST X-RAY In patients presenting with acute chest pain, a chest radiograph is useful to evaluate for other potential cardiac, pulmonary, and thoracic causes. Do not delay transfer to HLOC to obtain chest x ray. Typically, chest x-ray is normal in ACS, unless heart failure is present. This can be done to identify other serious life-threatening causes of chest pain, such as acute chest syndrome in patients with SCD.3,8 See Health Equity Alert Box. MEDICAL DECISION-MAKING Transfer to HLOC for patients who are clinically unstable, patients who have altered level of consciousness, patients with ECG showing STEMI, patients with ECG showing new LBBB, and patients in whom there is a high clinical suspicion for a serious life threatening cause of chest pain. Also consider transfer to HLOC for patients with chest pain of uncertain etiology who may benefit from cTn/hs-cTn and further urgent evaluation. The following table summarizes many of the important identifiers and findings of various causes of serious life threatening acute chest pain (see Table 8 on page 13). HEALTH EQUITY ALERT SCD affects 1 out of 365 Black Americans and 1 out of 16,300 Latinos in the United States (US). As these populations are overrepresented in US carceral settings, it is essential that providers in these setting understand SCD and its complications. An acute complication of SCD is acute chest syndrome, which is the leading cause of mortality among patients with SCD and accounts for a quarter of deaths. It can be caused by vaso-occlusion, ischemic, and endothelial injury within the pulmonary microvasculature. A diagnosis of acute chest syndrome in a patient with SCD is made with the following criteria: • New pulmonary infiltrates on chest x-ray involving at least one lung segment and one of the following symptoms: • Chest pain • Temperature more than 38.5°C • Tachypnea, wheezing, rales, coughing, evidence of increased work of breathing • Hypoxemia relative to baseline, which is more than 2% decrease in oxygen saturation at room air8 Clinically stable patients who have acute chest pain who are determined to have a “low” risk of CAD may not require immediate transfer to HLOC, and further outpatient evaluation is generally safe and appropriate. Outpatient evaluation for CAD for these “low” risk patients may be done with an exercise or pharmacology stress test. Consider outpatient evaluation for other non-ischemic and non-cardiac etiologies, as clinically indicated. If there is a readily apparent cause of chest pain, further evaluation, treatment, and management should be directed to these causes as clinically appropriate. Shared decision-making is crucial, and patients should be actively involved in treatment decisions based on their individual needs, preferences, and understanding of the benefits, risks, and alternatives of various treatment options.1,2,3,9 See patient education attachments PE-1 through PE-2 for details. CCHCS Care Guide: Acute Chest Pain | 10 December 2024 CCHCS Care Guide: Acute Chest Pain Evaluation, cont’d Table 7: Characteristics of Serious Life-Threatening Chest Pain1 Differentiation of Serious Life-Threatening Cause of Acute Chest Pain Diagnosis Chest Pain Descriptors Physical Examination Findings Electrocardiogram Chest X-ray ACS • Substernal/left sided chest pressure or tightness • Onset often gradual • Pain radiating to shoulders or pain with exertion increases relative risk • “Nonclassic” symptoms (e.g., dyspnea, weakness) more common in elderly, women, diabetics • Assume symptoms of ACS or mechanical complication of MI within days or a few weeks of PCI or CABG is from an occluded artery or graft • Diaphoresis • Tachypnea • Tachycardia, hypotension, crackles, S3, mitral regurgitation murmur • Examination may be normal in uncomplicated cases • ST segment elevations in ≥2 contiguous leads, Q waves, new LBBB are evidence of acute MI • Single ECG is not sensitive for ACS and does NOT exclude ACS if initially normal • Prominent R waves with ST segment depressions in V1 and V2 strongly suggest posterior MI • Nonspecific • May show evidence of heart failure Mechanical complications of MI • Complications of MI declined with advances in reperfusion, but mortality remains high between 10-40% • Ventricular septal rupture can occur 24 hours to 2 weeks after MI; free wall rupture can occur 5 days to 2 weeks after MI; and papillary muscle rupture can occur 2-7 days after MI • Presentation ranges from acute or recurrent chest pain with dyspnea on exertion to severe cardiogenic shock • Assume symptoms of ACS or mechanical complication of MI within days or a few weeks of PCI or CABG is from an occluded artery or graft • Ventricular septal rupture can present as hypotension, tachycardia, with new murmur that is harsh, loud, and holosystolic • Free wall rupture can present as sudden profound right heart failure and shock causing death, but subacute rupture can present as hypotension, tachycardia • Papillary muscle rupture can present as acute onset hypotension, severe pulmonary edema, and new mitral regurgitation murmur • Ventricular septal rupture may show heart block, ST segment elevation • Free wall rupture may range from features of pericarditis to sudden bradycardia then pulseless electrical activity from tamponade • Papillary muscle rupture may show ST segment elevation • Ventricular septal rupture may reveal left ventricular enlargement and pulmonary edema • Free wall rupture may show cardiomegaly with clear lung fields • Papillary muscle rupture may reveal pulmonary edema Cardiac tamponade • Pain from pericarditis often sharp anterior chest pain made worse by inspiration or lying supine, leaning forward • Pain relieved by sitting forward • Dyspnea, fatigue common • Presyncope or syncope • Pericardial effusion and pericarditis in renal failure and dialysis patients • Tamponade creates obstructive shock and hemodynamic instability with findings of tachycardia, hypotension, elevated jugular venous pressure, pulsus paradoxus • Muffled heart sounds • Pericardial effusion can cause friction rub • Decreased QRS amplitude and electrical alternans can appear with significant effusions • Diffuse PR segment depressions with or without ST segment elevations in pericarditis • May reveal enlarged cardiac silhouette CCHCS Care Guide: Acute Chest Pain | 11 Decem

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