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In 2008 about 6.4 million persons over age 15 presented to emergency departments with complaints of chest pain. That represented about 6.3% of all visits for persons in this age group in the United States.1
Because of its high incidence and potential mortality, EMTs and paramedics spend considerable time learning to identify and treat acute coronary syndrome (ACS). Although they occur less frequently, there are also non-ACS etiologies of chest pain that are potentially life-threatening and with which prehospital providers should be familiar. These include pulmonary embolism, pneumothorax, pericarditis with tamponade and esophageal rupture. In addition, there are numerous etiologies of non-ACS chest pain that are less lethal but still require transport to an ED.
This month’s article uses a case-based approach to highlight two of the more frequent non-ACS causes of chest pain, as well as one of the more lethal. It walks through differential diagnoses to show how to evaluate and weigh the evidence for and against the various etiologies of non-cardiac chest pain and arrive at a best guess for a diagnosis. For each of the cases, we suggest and discuss a list of possible diagnoses. These lists are not meant to be inclusive, but to serve as a starting point for discussion.
Pathophysiology of Chest Pain
Understanding the pathophysiology of chest pain is an important component of understanding how chest pain from any etiology is perceived by the patient.
In the nervous system, efferent nerves (motor neurons) carry signals away from the central nervous system (CNS) to effectors such as glands or muscles. Afferent neurons (sensory or receptor neurons) carry nerve impulses from sense organs and receptors back toward the CNS. Stimulation of somatic or visceral afferent pain fibers results in two distinctly different perceptions of pain. Somatic nerve fibers innervate the skin and parietal pleura in the lungs, and enter the spinal cord at specific levels along its length. This specificity allows for the creation of dermatomes, areas of skin primarily innervated by single nerves. As a result, pain from somatic nerve fibers is typically perceived by the patient as sharp and can be precisely located and easily described. Think of a patient with a fractured rib—she can easily describe the pain and point to exactly where it hurts.
Visceral afferent nerve fibers innervate the internal organs, including the heart, visceral pleura, lungs, aorta and esophagus. These nerves from the various thoracic organs enter the spinal cord at multiple levels, rather than single specific levels, as with somatic nerves. This nonspecific relationship with the spinal cord results in the imprecise nature of visceral pain, which is often described as a heaviness, aching or discomfort. As a result, the origin of visceral pain is often difficult to determine and can be perceived anywhere from the epigastrium to the jaw.
In addition, the sensation of radiation is created when a visceral afferent nerve fiber enters the spinal cord at the same level as a somatic afferent nerve fiber. As a result, the visceral pain is often attributed to an area of the body innervated by the somatic nerve fiber. This is why the patient with irritation of the diaphragm will experience shoulder pain, and the patient with myocardial ischemia may experience neck, jaw or arm pain.2Table 1 lists the etiologies of non-cardiac chest pain that will be discussed in this article. This list is not inclusive, but meant to fall within a realistic spectrum of illness about which prehospital providers learn and may see regularly.
• Shortness of breath, chest pain and malaise in a 64-year-old male.
A 64-year-old male presents conscious, alert and oriented in moderate distress complaining of shortness of breath. A resident of Sunnyside Nursing Home, a minimum-care facility, he describes a three-day history of increasing shortness of breath, chest pain and malaise. He says the shortness of breath came first, about three days ago, followed by chest discomfort the next day. He describes the chest pain as sharp, non-radiating, located under his left breast and reproducible with inspiration. A nursing home staffer reports the patient “did not sleep well last night,” and he says he suffered from insomnia due to a combination of his difficulty breathing and chest pain. He’s also had a nonproductive cough over the past two days and has a low-grade fever.
The patient has a history significant for type 2 diabetes, hypertension, coronary artery disease, atrial fibrillation and two myocardial infarctions. His medications include aspirin, lisinopril, Coumadin and metformin. He has no known drug allergies. Vital signs are heart rate 98 and irregular; blood pressure 132/88; respiratory rate 20/min. and deep; pulse oximetry 91% on room air; and a temperature of 100.1ºF (37.8ºC) via tympanic thermometer.
The physical exam reveals decreased breath sounds, rhonchi and rales to the left base, capillary refill of 4 seconds, dry mucous membranes and poor skin turgor. The patient’s skin is warm, dry and slightly pale. His blood glucose is 92 mg/dL, and he shows atrial fibrillation on the cardiac monitor. A 12-lead ECG is nondiagnostic for acute myocardial infarction.
The initial presentation of an elderly male in a nursing home with difficulty breathing, cough and fever seems like a strong candidate for pneumonia. Pneumonia typically produces chest pain that is pleuritic in nature (reproducible with inspiration) and sharp. It is also associated with fever, productive or nonproductive cough, and hypoxia, if ventilation is impaired enough. Auscultation of the lung fields may reveal decreased breath sounds as well as rales or rhonchi over the affected lobes, and diffuse wheezing from airway passage irritation. In addition, this patient exhibited signs of a common complication of pneumonia, dehydration (poor skin turgor, dry skin).
Prehospital BLS management of this patient would include oxygen administration via nasal cannula or nonrebreather mask, placing the patient in a position of comfort, and rapid transport to an ED. The patient is ventilating adequately, so assisting ventilations with a bag mask is not necessary at this time. ALS treatment of the patient with pneumonia would include assuring adequate ventilation and oxygenation and treating for dehydration and shock, if present. This could include nebulized bronchodilators for wheezing and IV fluids for volume repletion.
A 12-lead ECG that is nondiagnostic for AMI does not rule out AMI as an etiology of chest pain (Photo 1). Table 2 lists the ECG findings characteristic of specific etiologies of chest pain. In fact, this patient should be considered a high risk for AMI, as he has a medical history of diabetes and hypertension and a cardiac history significant for two heart attacks. It may be worth diving deeper into this patient’s complaint of insomnia. Did he experience worse difficulty breathing when lying flat (orthopnea)? If so, that could be a sign of left heart failure and pulmonary edema secondary to AMI. However, we’ve already noted rhonchi and rales to the lower left lung, which is inconsistent with what we’d expect with pulmonary edema (rales bilaterally at the bases). The patient’s description of his pain helps make AMI a less likely etiology, as the pain associated with AMI tends to be visceral in nature, not pleural, though this is not always the case.
The patient’s description of his pain (sharp, reproducible with inspiration, under the left breast) is also consistent with the pain characteristic of pulmonary embolism, which tends to be pleuritic in nature—the somatic pain fibers in the parietal pleura overlying a pulmonary infarction are activated as the pleura becomes inflamed and irritated. In addition, his decreased SpO2 (especially in the absence of any chronic lung disease), tachycardia, cough, rales over the affected area and presence of a fever are all consistent with PE. Some arguments against PE as a diagnosis in this patient include the lack of hemoptysis with his cough, the history of fever and malaise, and the fact that he’s on Coumadin. Assuming the patient’s Coumadin levels are therapeutic, formation of a pulmonary embolism is less likely. In addition, the patient lacks any significant risk factors for PE such as a history of immobility, deep vein thrombosis, cancer, recent trauma or a history of hypercoagulability.
Pleural effusion is another consideration with this patient. A pleural effusion is an accumulation of fluid in the pleural space resulting from increased fluid production or decreased fluid absorption. Infection, malignancy, increased capillary hydrostatic pressure and reduced vascular oncotic pressure are among possible etiologies. Chest pain in pleural effusion occurs from irritation of the pleura and is commonly described as sharp, stabbing and worse with deep inspiration. The pain can be localized or refer to the shoulder if the diaphragm is irritated as well. Other symptoms of pleural effusion include dyspnea with exertion, fever if the etiology is infectious in nature, cough, and decreased lung sounds as the effusion accumulates and takes up space in the thoracic cavity. The finding of lower lung rales and rhonchi doesn’t necessarily point away from this diagnosis, and a chest x-ray in the ED will help reveal the answer.
Spontaneous pneumothorax should be high on the differential for any patient with a unilateral decrease in breath sounds. The pain associated with pneumothorax also tends to be sharp and pleuritic, and a decrease in SpO2 ranging from mild to hypoxic can occur depending on the total decrease in lung volume. In this patient, however, we not only have a decrease in lung sounds, but also associated rales and rhonchi over the same area, which is not characteristic of pneumothorax. In addition, the patient is 64, far outside the normal range of 20–30 years old for spontaneous pneumothorax. Patients with COPD also have increased risk of spontaneous pneumothorax secondary to bleb rupture, but this patient does not have a history of COPD.
Chest wall (musculoskeletal) chest pain can occur from a number of etiologies, including costrochondritis, an inflammation of the costal cartilages and/or their articulations with the sternum. The pain associated with costrochondritis is typically sharp and reproducible with palpation or deep inspiration due to its somatic innervation. Consider this and other less serious diagnoses only after the ones previously discussed have been ruled out.
• Chest discomfort and vomiting in a 36-year-old male.
A 36-year-old male presents conscious, alert and oriented complaining of dyspnea and chest discomfort. He describes an acute onset of epigastric pain 10 hours prior after an episode of severe vomiting. The pain is described as a 7/10, diffuse, radiating to his back and worse with swallowing. The patient says he was heavily intoxicated at the time of onset. His dyspnea has worsened gradually since the event.
The patient reports a history of GERD, for which he takes Zantac. He also says this pain “is nothing like my heartburn pain,” and has been unrelieved with over-the-counter antacids. He has no allergies to medications and says cardiac disease does not run in his family. Your clinical exam reveals diminished lung sounds on the left, subcutaneous emphysema in the neck and left axillary region, and warm, pale, slightly diaphoretic skin. A crunching sound can be auscultated over the precordium with each heartbeat.
Vital signs are heart rate 104 and regular; blood pressure 90/60; respiratory rate 22 with adequate tidal volume; oral temperature 102.5ºF (39.2ºC); and pulse oximetry 92% on room air. His blood glucose is 136 mg/dL, and he shows sinus tachycardia on the cardiac monitor. A 12-lead ECG is nondiagnostic for AMI.
Spontaneous esophageal rupture, also known as Boerhaave’s syndrome, occurs secondary to a sudden increase in esophageal intraluminal pressure, usually due to violent vomiting or retching, and often follows heavy food and alcohol intake (Photo 3). The tear in the esophagus allows gastric contents and air to enter the mediastinal space, resulting in pneumomediastinum. The dyspnea associated with pleural irritation from gastric contents is one way of differentiating esophageal rupture from other gastrointestinal etiologies of chest pain. In addition, this patient said that not only did over-the-counter antacids not relieve his pain, but that the pain was different from his normal GERD-related pain.
The pain associated with perforated esophagus is often described as severe, diffuse and radiating to the shoulders and/or back. It can be worse with swallowing. The crunching heard over the precordium, known as Hamman’s sign, occurs secondary to mediastinal emphysema, the result of air escaping from the esophagus. Much like how you can feel subcutaneous air beneath the skin, you can hear the crunching sound produced with each heartbeat when air is in the mediastinum. In this patient’s case, the air tracked through the mediastinum, up and out to his neck and left chest, where it was palpable. Boerhaave’s syndrome is responsible for 10%–15% of all esophageal perforations; the vast majority are iatrogenic (secondary to a medical procedure).3
Untreated, an esophageal perforation can lead to pleural effusion, empyema, mediastinitis, pneumonitis or pericarditis, all of which can lead to sepsis. The mortality rate associated with esophageal perforation is high, about 30%, and it is the most lethal type of perforation of the gastrointestinal tract.4 As such, it is important for the prehospital care provider to have a high index of suspicion for esophageal rupture and encourage transport to the ED to prevent any delays in treatment.
Prehospital BLS management of this patient would include oxygen administration via a nasal cannula or nonrebreather mask, placing the patient in a position of comfort, and rapid transport to an ED. ALS treatment includes establishing large-bore IV access and administering an isotonic crystalloid to treat the developing shock. Antiemetics are useful to treat nausea and prevent further episodes of vomiting. An IV analgesic can be considered if the patient is experiencing pain. Providers must be vigilant in protecting the airway if vomiting continues and level of consciousness decreases, as this greatly increases the risk for aspiration and airway compromise.
It can be difficult to differentiate between a perforated esophagus, AMI, pulmonary embolism, PUD and GERD based on pain alone, as the esophagus, stomach and heart share some of the same visceral afferent nerve roots. However, the combination of no risk factors for AMI, young age, no significant cardiac history, no family history, a nondiagnostic 12-lead and physical exam findings consistent with esophageal perforation make AMI less likely.
GERD occurs when gastric secretions and/or bile and pancreatic secretions from the duodenum and stomach move retrograde into the esophagus, causing irritation and erosion of the esophageal mucosa. This results in the classic symptom of heartburn, often described as a retrosternal burning that occurs most often after eating, drinking or lying supine. GERD is the most common cause of noncardiac chest pain or discomfort, accounting for about 50% of all cases.4 Although this patient has a history of GERD, it is an unlikely cause of his pain. We would not expect GERD pain to be so severe or worse with swallowing. In addition, the patient says the pain he is experiencing is not his typical GERD-related pain. Further, Hamman’s sign, decreased lung sounds and subcutaneous emphysema are not characteristic of GERD.
PUD, ulcers located in the stomach and duodenum, is characterized by burning epigastric pain and may also be described as dull, aching or sharp. Patients will often feel relief with the ingestion of milk, antacids or after eating a meal, presumably because the food will prevent gastric acids from coming into contact with the ulcer. Pain tends to recur after gastric emptying, and patients will often report being woken at night by their pain, after their stomachs have emptied. Patients with PUD may have abdominal pain with palpation, but abdominal tenderness is neither specific nor sensitive for diagnosis.5 PUD is an unlikely cause of this patient’s chest pain, as he has no history of the disease, the onset of his pain was sudden and severe, the description is not characteristic of PUD, and the pain is reproducible with swallowing.
Gastritis is an acute or chronic inflammation of the gastric mucosa and can occur as a result of numerous etiologies. The signs and symptoms associated with gastritis can vary widely and include gnawing or burning epigastric pain, abdominal pain, nausea, vomiting and gastrointestinal bleeding. Gastritis is not likely in this patient because he does not describe his pain as gnawing or burning, and we would not expect such an acute, severe onset without a predisposing factor such as ingestion of a potentially questionable food source. He also does not take any medications that would increase his risk of gastritis, such as NSAIDs or corticosteroids. And the associated signs found in this patient (Hamman’s sign, subcutaneous emphysema) are not consistent with gastritis.
A 62-year-old male presents conscious and alert though disoriented and in noticeable distress complaining of chest pain. Family members say the patient, who is normally oriented to person, place and time, was “absolutely fine today” and suffered an acute onset of chest pain described as severe, tearing and radiating to his back. At no point did he have any complaints previously.
The man has a medical history significant for hypertension and coronary artery disease, for which he takes aspirin and Procardia. He is allergic to opiates. The physical exam reveals a left-sided facial droop, slurred speech and left-sided weakness. His skin is cool, pale and diaphoretic. Vital signs are heart rate 104 and regular; blood pressure 180/100; respiratory rate 20 with adequate tidal volume; and pulse oximetry 89% on room air. His blood glucose is 122 mg/dL, and he shows sinus tachycardia on the cardiac monitor. A 12-lead ECG is nondiagnostic for AMI.
This patient has suffered an acute event that led to almost-immediate hemodynamic instability. Aortic dissection, AMI and pulmonary embolism (the “big three”6) should be considered.
Based on his presentation and the history of the event, aortic dissection should be at the top of this patient’s differential diagnosis. Aortic dissection occurs when a tear in the tunica intima of the aorta allows blood to enter the tunica media and dissect between the intima and adventitia. It is characterized by an acute onset of severe chest pain that radiates to the back. As the dissection progresses down the aorta, it can involve arteries branching off, resulting in decreased perfusion to the organs they supply. Involvement of the root of the aorta can lead to coronary artery involvement and acute coronary syndrome. In such cases, the normal evidence of myocardial ischemia may be present on 12-lead ECG. Table 2 lists the ECG changes associated with non-cardiac etiologies of chest pain. Involvement of the brachiocephalic artery (which gives rise to the right common carotid artery) or left common carotid artery (which branches directly off the aortic arch) can lead to stroke syndromes. If the renal artery, a branch of the abdominal aorta, is involved, then acute renal failure can occur. This patient most likely has involvement of the brachiocephalic and right common carotid arteries, as evidenced by signs of stroke. Risk factors for aortic dissection include connective tissue disorders and hypertension, which this patient not only has a history of but is experiencing right now.
Prehospital BLS management of this patient would include oxygen administration via nonrebreather mask and assuring adequate ventilation, position of comfort and rapid transport to an ED. ALS treatment would entail establishing large-bore IV access and administering an isotonic crystalloid to treat shock, should it develop. In the ED, treatment for this patient will most likely include immediate lowering of his blood pressure with labetalol or nitrates. The use of a nitrate, such as nitroprusside, must be accompanied by administration of a beta blocker to prevent compensatory tachycardia.7
AMI is less likely in this patient because of the abrupt onset of his chest pain. The pain or discomfort of AMI is more likely to build over time, not occur immediately and so severely. In addition, the presence of signs characteristic of stroke is not consistent with AMI.
Consider PE in any patient with acute-onset hemodynamic instability, tachycardia and hypoxia (Photo 2). In such cases, signs of obstructive shock such as jugular venous distention may also be present. In addition, a large PE may result in S1Q3T3 pattern on the ECG, a sign of right ventricular strain as blood and pressure back up into the right side of the heart. On a 12-lead, this appears as a large S wave in lead I, a large Q wave and an inverted T wave in lead III. This patient’s pain is not consistent with PE, nor is his hypertension.
Pericarditis is an infection of the pericardium. The pain associated with pericarditis is typically described as sharp, severe, substernal and constant, but comes on gradually, not immediately. It may radiate to the neck or back and is often relieved by leaning forward. Patients with pericarditis may exhibit a pleural friction rub upon auscultation and ECG findings including diffuse ST segment elevation, T-wave inversion and PR depression across multiple leads, which is not present in this case. In addition, pericarditis will not result in hemodynamic instability like we see in this patient unless there is an accompanying pericardial tamponade. Tamponade as a result of a medical etiology such as pericarditis typically develops slowly, and hemodynamic instability does not occur abruptly, as happened with this patient. In addition, hypotension, narrowed pulse pressure and JVD may be present if pericardial tamponade results in obstructive shock.
There are many etiologies of non-cardiac chest pain, a small sample of which were discussed in this article. While the exact etiology can sometimes be difficult to determine in the prehospital environment, the list can often be narrowed by understanding the pathophysiology of chest pain, obtaining a good history, performing a detailed physical exam, and comparing your findings against your understanding of disease.
Scott R. Snyder, BS, NREMT-P, is EMT program director for the San Francisco Paramedic Association. Contact him at email@example.com.
Sean M. Kivlehan, MD, MPH, NREMT-P, is an emergency medicine resident at the University of California, San Francisco and a former New York City paramedic. Contact him at firstname.lastname@example.org.
Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is performance improvement coordinator for Vitalink/Airlink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. Contact him at email@example.com.