Key Clinical Questions
Introduction
According to the 2006 National Hospital Ambulatory Medical Care Survey, 6,392,000 patients presented to emergency departments with a chief complaint of chest pain or related symptoms. Of those, 1,976,000 patients were admitted to the hospital, with a mean length of stay of 3.7 days. Chest pain was the principal admitting diagnosis in 5.4% of all admitted patients.
Because the morbidity and mortality is high if clinicians “miss” a cardiac presentation of chest pain, a significant portion of these admissions are specifically for the purpose of ruling out myocardial infarction. In one study of patients presenting to an emergency department with complaints consistent with cardiac ischemia, 17% ultimately had cardiac ischemia, while 27% had stable angina or other cardiac conditions. Fifty-five percent had noncardiac conditions causing their symptoms. The wide differential diagnosis for this heterogeneous group of patients includes nonischemic life-threatening etiologies as well as more benign causes. Unfortunately, in this study, 2.1% of the patients with acute myocardial infarction were erroneously discharged; this figure plays prominently in the low threshold to admit patients with chest pain.
Chest pain also occurs in patients already admitted to the hospital for other reasons. These patients have already suffered some degree of physical decompensation and the occurrence of chest pain may indicate illness, a complication of hospitalization, or a patient’s response to a very stressful situation. The hospitalist must evaluate the possibility of an immediate life-threatening event, consider the entire differential of possible etiologies, and integrate this information with the patient’s prior clinical diagnoses and course.
Bedside Approach
The initial evaluation of a patient reporting chest pain requires the rapid identification and treatment of any life-threatening conditions. These include the five “do-not-miss” causes of chest pain: (1) aortic dissection, (2) acute myocardial infarction, (3) pulmonary embolism, (4) pneumothorax, and (5) esophageal rupture (Table 77-1) . The electrocardiogram (ECG) is the most important screening intervention for early risk stratification and is often performed at the point of triage as one of the “vital signs.”
Diagnosis | Risk Factors | Characteristic Findings | Diagnostic Testing |
---|---|---|---|
Aortic dissection | Hypertension, connective tissue disease, vasculitis, prior heart or valvular surgery, Turner syndrome, crack cocaine use, cardiac catheterization | New diastolic murmur, upper-extremity pulse deficit, neurologic complications of stroke | Computed tomography, magnetic resonance imaging, transesophageal echocardiography, angiography |
Special considerations: Aortic dissection can be difficult to diagnose, but patients will most commonly present with chest pain; syncope may occur at the time of symptom onset. Dissections can be classified as Stanford type A (involving the ascending aorta) or type B (all others). In one study, 72.7% of patients reported chest pain, 90.6% reported severe or worst pain ever, and 84.8% had abrupt onset. Aortic insufficiency murmur was noted in 31.6% and pulse deficit was noted in 15.1 %. Chest radiograph showed widened mediastinum in 61.6%, and EKGs were less helpful, being normal in 31.3%.* Medical treatment is initially indicated for type B dissections with careful blood pressure control (beta-blockade and nitroprusside). Given the high risk for life-threatening complications such as tamponade, aortic regurgitation, and myocardial infarction, type A dissections are treated as surgical emergencies. | |||
Myocardial infarction | Male sex, age over 55, tobacco use, family history of coronary artery disease, diabetes, hypercholesterolemia, hypertension | S4 or S3 gallop, vomiting, diaphoresis, Levine sign (fist over center chest, low predictive value) | Electrocardiography, cardiac biomarkers |
Special considerations: The diagnosis of ST-segment elevation myocardial infarction should be readily made from a 12-lead EKG and requires urgent intervention to improve survival. These patients will benefit from standard medical therapy as well as reperfusion. According to the 2007 ACC/AHA focused update on the management of patients with ST-elevation myocardial infarction, patients with acute STEMI will benefit from primary percutaneous intervention with a goal door-to-balloon time of 90 minutes or less. Fibrinolytic therapy within 30 minutes is preferred if transfer to a PCI-capable facility will make door-to-balloon time greater than 90 minutes.ch77fn02 These guidelines are directed toward patients presenting to the hospital with STEMI, but may also help to decide when to transfer inpatients who develop STEMI. | |||
Pulmonary Embolism | Immobilization, recent surgery, stroke, paralysis, prior venous thromboembolism, malignancy, recent central venous instrumentation | Dyspnea, pleuritic pain, calf or leg pain or swelling, jugular venous distention | Computed tomography, ventilation-perfusion scan, pulmonary angiography |
Special considerations: Thrombolytic therapy for submassive pulmonary embolism (PE) is a controversial treatment modality. It has been advocated for patients with evidence of right ventricular dilation or hypokinesis on echocardiography, but this indication for use is generally not widely accepted. Thrombolysis for cardiac arrest from PE has been successful in case reports, but does not seem to be helpful in cases of pulseless electrical activity.§ Thrombolytic regimens for PE range from 2–24 hour infusions. For imminent or actual cardiac arrest, a bolus therapy is indicated. One such regimen is tPA, 0.6 mg/kg over 2 minutes. | |||
Pneumothorax | Pneumocystis jirovecii, tuberculosis, chronic obstructive pulmonary disease, Marfans, familial, mechanical ventilation, smoking, cystic fibrosis | Decreased breath sounds, hyperresonant percussion, distended neck veins, tracheal deviation | Chest radiography, computed tomography |
Special considerations: Of all emergency diagnoses, the only one that is immediately reversible is a tension pneumothorax. Needle decompression involves placing a 14-gauge angiocath in the second or third intercostal space in the midclavicular line. In a study of trauma patients with computed tomography scans of the chest, the mean chest wall thickness studied averaged 4.24 cm at this location, and almost a quarter of patients had chest walls thicker than 5 cm.¶ Therefore, one should use the longest catheter possible. Alternatives include using a spinal needle or rapid tube thoracostomy. | |||
Esophageal Rupture | Esophageal instrumentation, forceful emesis, ulcers or esophagitis | “Hammans sign” (mediastinal crunching sound), subcutaneous emphysema, odynophagia, hoarseness (cervical rupture) | Cervical and chest radiography, computed tomography, contrast esophagography |
Special considerations: More than half of all cases of esophageal rupture occur as a complication of medical procedures that involve instrumentation of the esophagus, so knowledge of the inpatient course is paramount.** Spontaneous ruptures classically occur after forceful vomiting, but may also be associated with ingestion of caustic substances or pills, eosinophilic esophagitis, Barretts esophagitis, or ulcers. |
All potentially unstable patients with chest pain should have an intravenous line, supplemental oxygen, and a cardiac monitor placed as soon as possible. This can be accomplished even before the arrival of the physician at the patient’s bedside. The ECG, chest pain characteristics, prior history of coronary artery disease (CAD), and age are independent predictors of acute MI. Although the traditional risk factors for CAD predict long-term risk of disease, they are less helpful in predicting acute MI, and a primary focus on risk factors could be misleading for patients with ACS but with few risk factors. Therefore, an initial risk stratification assessment should include a review of the ECG, analysis of current vital signs, and a targeted history and physical examination. A stat portable chest radiograph should be ordered. With this information, patients can be assigned to one of four classes:
Those with new ST-segment elevations on initial ECG. (These patients should receive immediate consideration for emergent reperfusion therapy.)
Those without ST-segment elevation on initial ECG but who are at high risk on the basis of ECG findings, hemodynamic instability, or history. (These patients should be admitted and consideration should be given for immediate antiplatelet and antithrombotic treatment if no contraindications.)
Those who have no objective evidence of ACS but have symptoms that warrant evaluation. (These patients form the “low risk” chest pain cohort that constitutes the majority of patients undergoing ED evaluation for chest pain.)
Those who have an obvious noncardiac cause for symptoms.
Patients with hemodynamic instability, persistent ECG changes, or ongoing symptoms should be evaluated for emergent coronary angiography. Patients with an obvious noncardiac cause for symptoms would be managed, depending on the alternative diagnosis.
The history remains critically important in initial risk stratification because objective evidence including a diagnostic ECG is only present in a minority of patients. Once emergency conditions have been ruled out or stabilized, a targeted history should be used to identify and prioritize a list of differential possibilities (Table 77-2) . The examiner needs to determine what portions of the history and physical examination are relevant to the clinical questions of whether the patient’s symptoms and signs point to cardiac disease or to other serious causes requiring immediate intervention and, if the evaluation is taking place in the emergency department, whether the patient requires admission to the hospital. Coronary artery disease (CAD) is the leading cause of death for both men and women, and most patients with a prior history of CAD should be admitted to the hospital if they present with chest pain and have a clinical presentation that could be consistent for acute coronary syndrome. For this reason, in patients presenting with chest pain, obtaining a prior history of angina or known CAD is essential to determining if the patient’s current symptoms suggest either an acute coronary syndrome (ACS) or unstable angina (USA).
Cardiac | Pulmonary | Other |
---|---|---|
Aortic dissection | Pneumothorax | Esophageal rupture |
Myocardial infarction | Pulmonary embolism | Mallory-Weiss tear |
Angina | Pleuritis/serositis | Esophageal spasm |
Coronary spasm | Pneumonia | Pancreatitis |
Pericarditis | Cancer | Biliary tract disease |
Myocarditis | Sarcoidosis | Costochondritis |
Valvular disease | Musculoskeletal injury | |
Stress-induced cardiomyopathy | Peptic ulcer disease | |
Gastritis/esophagitis/reflux | ||
Herpes zoster | ||
Mediastinitis | ||
Psychogenic/psychosomatic |
More than 30 years ago, the Coronary Artery Surgery Study (CASS) enrolled 18,844 men and 6,097 women after coronary angiography. Using the reported chest pain characteristics, they classified patients as having definite angina, probable angina, probably not having angina, and definitely not having angina. Combining all patients classed as probably not and definitely not having angina as having nonischemic pain was subsequently shown to discriminate between patients with CAD and those with negative ETT and coronary angiograms. Even today, this scheme is used to facilitate decision making. Classic symptoms of angina include chest heaviness, pressure, tightness, or burning (sometimes with vigorous denial of pain), provocation by physical or emotional stress or cold, relief by rest, radiation to neck, jaw, or shoulder, duration >2 minutes and <20 minutes (unless MI), +/– dyspnea, nausea, and vomiting, diaphoresis, presyncope, and palpitations (Table 77-3).
Age, Year | Asymptomatic | Nonanginal CP | Atypical Angina | Typical Angina | ||||
---|---|---|---|---|---|---|---|---|
Men | Women | Men | Women | Men | Women | Men | Women | |
30–39 | 1.9 | 0.3 | 5.2 | 0.8 | 21.9 | 4.3 | 69.7 | 25.8 |
40–49 | 5.5 | 1.0 | 14.1 | 2.8 | 46.1 | 13.3 | 87.3 | 55.2 |
50–59 | 9.7 | 3.2 | 21.5 | 8.4 | 58.9 | 32.4 | 92.0 | 79.4 |
60–69 | 12.3 | 7.5 | 28.1 | 18.6 | 67.1 | 54.4 | 94.3 | 90.6 |
Patients should be questioned regarding the nature of their “discomfort” (as some patients may not believe that they are experiencing chest pain). Additional questioning should include location, onset, character, severity, radiation, alleviating and exacerbating factors, time course, history of similar episodes, and associated symptoms such as diaphoresis, shortness of breath, and nausea and vomiting. Early questioning about prior experiences of identical symptoms may save considerable time and effort, but one must take care to avoid premature closure in diagnostic decision making, especially when myocardial ischemia is a possibility.
The “PQRST” (provocative/palliative factors, quality, radiation, severity, timing) approach can be used to qualify the different aspects of the patient’s pain and suggest likely etiologies. Physicians should be aware that differences in gender, culture, and underlying pathology may lead to differences in the experience and description of pain. Atypical presentations of ACS are more likely in the elderly and women, especially those over the age of 65, and include symptoms such as dyspnea, epigastric discomfort, and palpitations. In one study of patients with active cardiac ischemia, women reported pain in the neck area while men were more likely to feel pain in the shoulder. Women were more likely to describe their pain as sharp, hot, burning, throbbing, or pressing. In addition, women were more likely to experience various nonpain symptoms, such as trembling, upset stomach, shortness of breath, postprandial pain, palpitations, and neck or throat sensations.Despite anecdotal evidence, most studies have not found a significant increase in the prevalence of unrecognized or atypical presentations in diabetics.
Pain associated with exertion (physical exercise, stress, or sexual intercourse) is often due to cardiac causes. Pain with swallowing suggests an esophageal disorder. Patients with pain that reliably occurs after eating likely have a gastrointestinal etiology; however, some patients with coronary disease have postprandial angina (typically after dinner) in addition to rest angina. One possible mechanism for postprandial angina involves increased myocardial oxygen demand after food intake, but studies suggest that a decrease in coronary blood flow (steal phenomenon) may play a role. In contrast, improvement with food or antacids suggests peptic ulcer disease or gastritis. Pleuritic pain is worst with deep inspiration and suggests pulmonary disease, pericarditis, or a musculoskeletal etiology. In one study, 47% of all patients who were evaluated for and ultimately found to have pulmonary embolism reported pleuritic pain. However, 17% of all patients found to have pulmonary embolism reported chest pain that was nonpleuritic. Pain that is worse with exertion and better with rest is suggestive of cardiac ischemia or pulmonary embolism. More commonly pleuritic but sometimes severe, steady, and retrosternal, the pain of acute pericarditis is classically worst with lying flat and improved with leaning forward. Musculoskeletal pain will be reliably triggered by specific movements. An important consideration is that improvement with nitroglycerin or mucosal anesthesia (“GI cocktail”) is not helpful for distinguishing cardiac from noncardiac causes of pain. Physicians should use these medicines as appropriate to relieve pain but avoid the error of using the patient’s response to guide decision making. Likewise, pain with chest wall palpation should not be used to exclude a cardiac etiology for chest pain.
The patient’s description of the quality of pain should be noted (Table 77-4). In the International Registry of Acute Aortic Dissection (IRAD) study, 50.6% of patients with aortic dissection described a ripping or tearing sensation. In contrast, the pain of myocardial ischemia is classically described as heavy, squeezing, crushing, or pressure. Sharp pain is most typical of pulmonary, musculoskeletal, or gastrointestinal causes; however, beware of the imprecision of the term sharp, which to some patients simply means intense. Burning pain can be seen in cardiac and gastrointestinal disease. Patients suffering from herpes zoster may also report a burning sensation. The nature of the chest pain does not definitely discriminate cardiac from noncardiac chest pain. Keep in mind that “atypical” descriptions of pain are quite common in patients with myocardial ischemia, including sharp, stabbing or, less commonly, pleuritic pain. For example, pain described as pressure-like or squeezing has a Likelihood Ratio (LR) of less than 2 and hence does not reliably distinguish cardiac disease from other causes of chest pain such as esophagitis. Likewise, a pleuritic, stabbing chest pain that has a LR of 0.2 – 0.3 may reduce the likelihood that the chest pain is cardiac in origin but it does not rule it out.
Typical symptoms: pressure, tightness, squeezing, indigestion, or those similar to prior ACS events |
Atypical symptoms: stabbing, pleuritic, pinprick discomfort |
Associated symptoms with increased risk: nausea and vomiting |
Associated symptoms not predictive of increased risk: symptoms relieved by rest or sublingual NTG |