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Home , Mediastinitis, Strain pattern

Chapter 18 Chest Pain James E. Brown and Glenn C. Hamilton

■ PERSPECTIVE ation of pain is caused by somatic afferent fibers synapsing in the same dorsal root ganglia as the thoracic viscera. This stimu- Nearly 6 million patients present to the emergency depart- lation can “confuse” the patient’s central nervous system ment (ED) each year with complaints of chest pain, constitut- into misperceiving that the pain originates in the arms or ing 5% of all patients seen in EDs in the United States.1 Chest shoulders. pain is a symptom caused by several life-threatening diseases and has a broad differential diagnosis. It is complicated by a frequent disassociation between intensity of symptoms and ■ DIAGNOSTIC APPROACH signs and seriousness of underlying pathology. Differential Considerations Epidemiology Due to the indistinct nature of visceral pain, the differential diagnosis of chest pain is broad and includes many of the most The epidemiology of the critical diagnoses causing chest pain critical diagnoses in medicine and many nonemergent condi- varies widely. coronary syndromes (ACS), aortic dissec- tions (Table 18-1). tion, (PE), , with tamponade, and are potentially cata- Rapid Stabilization and Assessment strophic causes of chest pain. Due to its high incidence and potential lethality, ACS is the most significant potential diag- The initial questions are, “Must I intervene immediately?”, nosis in the ED. Of all deaths in the United States, 36% are and “What are the life-threatening possibilities in this patient?” attributed to cardiovascular diseases; these account for approx- The answers are usually apparent within the first few minutes imately 870,000 deaths per year.2 Historically, emergency phy- after assessing the patient’s appearance and vital signs. One of sicians misdiagnose 3 to 5% of myocardial infarctions (MIs), the critical diagnoses is tension pneumothorax. If a patient accounting for 25% of malpractice losses in emergency medi- presents with chest pain, respiratory distress, shock, and uni- cine.3,4 Thoracic aortic dissection has an incidence of 0.5 to 1 lateral reduction or absence of breath sounds, immediate per 100,000 population with a mortality rate exceeding 90% if intervention with needle or tube thoracostomy is required. misdiagnosed. The true incidence of PE is unclear, with esti- Additionally, patients with severe derangements in vital signs mates of 70 per 100,000. This equates to approximately 100,000 require stabilizing treatment during a search for the precipitat- PE cases per year in the United States.5 Although the inci- ing cause. Patients who present with respiratory distress dence of tension pneumothorax is also unclear, the incidence require immediate intervention and lead the emergency phy- of spontaneous pneumothorax ranges from 2.5 to 18 per sician to consider a more serious cause of the pain (Fig. 18-1; 100,000 total patients. The total incidence of esophageal also see Chapter 17). rupture is 12.5 cases per 100,000 persons. The true incidence All patients, except those with obvious benign causes of of pericarditis is unknown, but is diagnosed in 1 of every 1000 chest pain, must have an electrocardiogram (ECG) within hospital admissions.6 Up to 5% of ED chest pain patients minutes of reporting their pain. This ECG should be read for without acute ST elevation MI may have pericarditis.7 acute MI by the emergency physician as soon as it is com- pleted. Patients with positive ECG findings and those consid- Pathophysiology ered at high risk are triaged directly to the treatment area and monitored. Symptomatic derangements in vital signs are Afferent fibers from the heart, lungs, great vessels, and esopha- addressed. If vital signs are stable, a focused history and physi- gus enter the same thoracic dorsal ganglia. Through these cal examination are performed. Most patients also require a visceral fibers, each organ produces the same indistinct quality chest radiograph to evaluate the chest pain. If a cardiac cause and location of pain. The quality of visceral chest pain varies is suggested and vital signs are stable, pain relief with nitro- widely and is described as “burning,” “aching,” “stabbing,” or glycerin (0.4 mg sublingual every 3–5 minutes) may be appro- “pressure.” Since dorsal segments overlap three segments priate. Aspirin (81–325 mg) is a consideration for patients above and below a level, disease of a thoracic origin can without hemorrhagic disorders, known allergies, or vascular produce pain anywhere from the jaw to the epigastrium. Radi- dissections. Clopidogrel (loading dose 300 mg) or other anti-

132 Chapter 18 / Chest Pain

133 - - - ­ DIAGNOSES

NONEMERGENT Valvular prolapse Hypertrophic Pleuritis Tumor Esophageal spasm Esophageal reflux Peptic ulcer Biliary colic Muscle strain Rib fracture Arthritis Tumor Costochondritis Nonspecific chest wall pain Spinal root compression Thoracic outlet Herpes zoster Postherpetic neuralgia Psychologic Hyperventilation about the patient’s about activity the at patient’s the onset DIAGNOSES

10 pain scale. Alterations in pain severity are documented at times of onset, peak, present, and after intervention. versus somatic be to likely more is area small a to localized visceral in origin. Pain localized at the periphery of the can also be characterized comfort, such by as nonspecific “bloating” or dis “indigestion.” pain “Tearing” that may migrate from the front to back “Sharp” dissection. aortic in or description classic the is front back to or “stabbing” pain is seen more in pulmonary and muscu of pain may be helpful. progres whereas syndrome, Pain coronary ischemic an suggests occurring during exertion loskeletal diagnoses. Patients complaining of a “burning” or “indigestion” type of pain may initially be thought to have a gastrointestinal etiology, but due to nature of chest the pain, all visceral causes of pain may present with any of the preceding descriptions. Of may vary among ethnic groups, and, for example, “sharp” note, descriptors may mean “severe.” sudden of Pain MI. acute suggests rest at pain of onset sive onset is more typical with aortic dissection, PE, or pneu mothorax. Pain after meals is more indicative of a gastro- intestinal cause. The severity of pain is commonly quantified using a 1-to- The location of the discomfort is described. Pain that is The patient is asked to describe the character of the Additional history pain or discomfort. Descriptions “crushing,” such or “pressure” as lead the “squeezing,” emergency physician to suspect a cardiac ischemic syndrome, although cardiac

3. 4. 1. 2. are key to diagnosis. Information pertinent to the differential and examination, physical history, the by obtained is diagnosis ECG in 80 to 90% of patients. History Unstable Coronary spasm angina Prinzmetal’s Cocaine-induced pericarditis or Pneumothorax Mediastinitis Esophageal tear (Mallory-Weiss) Cholecystitis Pancreatitis EMERGENT ECGϮ embolus RV strain RV Tension Pulmonary CXRϮ Pain

pneumothorax and signs of shock 8 Chest

of

ECGϪ CXRϩ: air/fluid rupture mediastinal Esophageal DIAGNOSES

ECG/CXR Diagnosis

Acute Pulmonary embolus Esophageal rupture (Boerhaave) Acute coronary ischemia Aortic dissection pneumothorax Tension CRITICAL Absent breath sounds w/shock Initial assessment aortic ECGϮ CXRϩ: widened Thoracic aneurysm Differential Initial assessment of chest critical CXR, x-ray; diagnoses.

Findings SYSTEM

Acute ECGϩ edema CXRϮ: coronary syndrome pulmonary ORGAN Cardiovascular Pulmonary Gastrointestinal Musculoskeletal Neurologic Other Table Table 18-1 should undergo prompt bedside cardiac ultrasound. Pivotal application defies pain chest of nature complex and broad The with patient a to approach organized An algorithm. simple a of chest pain is essential, however, to ensure that all causes are examination physical and history The appropriately. evaluated platelet agents may also be an alternative. Patients with low voltage on the ECG, diffuse ST segment elevation, elevated jugular venous pressure on examination, Figure 18-1. right ventricular. RV, electrocardiogram; ECG, 134 chest is more likely with a pulmonary rather than cardiac Significant Symptoms of Chest Pain etiology. Lower chest or upper abdominal pain may be of Table 18-2 cardiac or gastrointestinal origin. SYMPTOM FINDING DIAGNOSIS 5. Any description of radiation of pain should be noted. Transthoracic pain through to the back should suggest Pain Severe, crushing, Acute MI aortic dissection or gastrointestinal causes, especially pan- pressure, Coronary ischemia creatitis or posterior ulcer. Inferioposterior myocardial substernal, ischemia may also present primarily as thoracic back pain. exertional, Coronary spasm Radiation to the arms, , or jaw increases the likeli- radiation to jaw, hood of cardiac ischemia.9,10 Pain located primarily in the neck, shoulder,

• Cardinal Presentations arm

back, especially interscapular back pain that migrates to Tearing, severe, Aortic dissection wo 11

T the base of the neck, suggests aortic dissection. radiating to or 6. Duration of pain is another important historical factor. located in back, 12 e c tion Pain that lasts a few seconds is rarely of cardiac origin. maximum at S

/ Pain that is exertional but lasts for only a few minutes after onset, may rest may be a manifestation of cardiac ischemia.9 Pain that migrate to upper is maximal at onset may be due to aortic dissection.11 Pain back or neck that is not severe and persists over the course of days is Pleuritic Esophageal rupture less likely to be of serious origin than pain that is severe Pneumothorax or has a stuttering or fluctuating course. Cholecystitis Pericarditis 7. The clinician should consider aggravating or alleviating Myocarditis factors. Pain that worsens with exertion and improves with 9 Indigestion or Acute MI rest is more likely related to coronary ischemia. Pain burning Coronary ischemia related to meals is more suggestive of a gastrointestinal Esophageal rupture cause. Pain that worsens with respiration is seen more Unstable angina Fundamental Clinical Concepts

often with pulmonary, pericardial, and musculoskeletal Coronary spasm ■

Esophageal tear I causes. 8. Other associated symptoms may suggest the visceral Cholecystitis

PART nature of the pain (Table 18-2). Diaphoresis should lead Associated Aortic dissection to an increased clinical suspicion for a serious or visceral syncope/ PE cause. Hemoptysis, a classic PE sign, is rarely seen.13 Near- near-syncope Acute MI syncope and syncope lead to higher likelihood of a cardio- Pericarditis vascular cause or PE. Dyspnea is seen in cardiovascular Myocarditis and pulmonary disease. Nausea and vomiting may be seen Associated Acute MI in cardiovascular and gastrointestinal complaints. dyspnea Coronary ischemia PE 9. A history of prior pain and the diagnosis of that episode (SOB, DOE, PND, Tension pneumothorax can facilitate the diagnostic process, but the physician orthopnea) Pneumothorax must be wary of prior presumptive diagnoses that may be Unstable angina misleading. A prior history of cardiac testing, such as stress Pericarditis testing, echocardiography, or angiography, may be useful Associated PE in determining if the current episode is suggestive of hemoptysis cardiac disease. Similarly, patients with previous sponta- Associated 14 Esophageal rupture neous pneumothorax or PE are at increased risk of nausea/ Acute MI recurrence. vomiting Coronary ischemia 10. The presence of risk factors for a particular disease is pri- Unstable angina marily of value as an epidemiologic marker for large popu- Coronary spasm lation studies (Box 18-1). In the ED, presence of risk Esophageal tear factors in an individual patient without established disease Cholecystitis has minimal or no effect on the clinical likelihood (pretest DOE, dyspnea on exertion; MI, myocardial infarction; PE, Pulmonary embolism; probability) of a specific disease process. PND, paroxysmal nocturnal dyspnea; SOB, shortness of breath.

Physical Examination and expedites the National Heart, Lung, and Blood Institute’s Specific findings may be found in a variety of causes (Table recommended “door to treatment” times from arrival to per- 18-3). cutaneous coronary intervention (PCI) or thrombolytic therapy in acute MI. Patients with a new injury pattern on ECG (Table Ancillary Studies 18-5) or new ischemic ECG changes should have appropriate therapy instituted at this point (Fig. 18-2; see also Chapter 77). The two most commonly performed studies in patients with An ECG showing right ventricular strain pattern, in the chest pain are the chest radiograph and 12-lead ECG (Table appropriate setting, should raise the clinical suspicion for PE. 18-4). An ECG should be performed within 10 minutes of Diffuse ST segment elevation helps make the diagnosis of arrival in all patients with chest pain in whom myocardial pericarditis. ischemia is a possibility.15,16 This generally includes all male A chest radiograph is performed for patients with a possibly patients 33 years old and older and female patients over the serious cause of chest pain. Pneumothorax is definitively diag- age of 39 who complain of pain from the umbilicus to the nosed at this point. A wide mediastinum or ill-defined aortic mandible unless a noncardiac cause is readily apparent. Rapid knob increases the clinical suspicion for acute aortic dissection. acquisition of the ECG facilitates the diagnosis of acute MI , subcutaneous air, or mediastinal air-fluid Chapter 18 / Chest Pain 135 pneumothorax pneumothorax pneumothorax effusion) DIAGNOSES Acute MI Coronary ischemia Pericarditis Esophageal rupture Mediastinitis Acute MI Coronary ischemia Tension PE Pericarditis Tension Pneumothorax PE Tension Esophageal rupture Pneumothorax Mediastinitis Acute MI Coronary ischemia Unstable angina Esophageal rupture Esophageal tear Cholecystitis Pancreatitis Pancreatitis Cholecystitis PE Aortic dissection Acute MI Coronary ischemia Aortic dissection Coronary spasm Aortic dissection Pericarditis (with Acute MI Aortic dissection Coronary ischemia gallop 4 “crunch” on cardiac auscultation sign) (Hamman’s diminished/ absent breath sounds emphysema tenderness quadrant tenderness quadrant tenderness swelling, warmth, pain, tenderness, or erythema difference difference in upper extremity blood pressures pressure /S 3 FINDING Pericardial rub Audible systolic JVD Unilateral Pleural rub Subcutaneous Rales Epigastric Left upper Right upper Unilateral leg Focal findings Stroke Significant Significant Narrow pulse New murmur S examination examination examination examination examination Pulmonary Abdominal Extremity Neurologic SIGN Cardiovascular tion pneumothorax ulcer pneumothorax pneumothorax (Mallory-Weiss) (early) pneumothorax Examina

DIAGNOSES PE Tension Acute MI Pneumothorax Acute MI Aortic dissection Coronary ischemia PE Esophageal rupture Unstable angina Cholecystitis Perforated peptic Tension PE Acute MI Aortic dissection (late) Coronary ischemia Esophageal rupture Pericarditis Myocarditis Acute MI PE Aortic dissection Coronary ischemia Tension Esophageal rupture Coronary spasm Pericarditis Myocarditis Mediastinitis Cholecystitis Esophageal tear Acute MI Coronary ischemia Unstable angina Acute MI Coronary ischemia Aortic dissection PE Esophageal rupture Pericarditis Myocarditis Mediastinitis Cholecystitis PE Tension Pneumothorax ysical Ph

in

distress Findings

FINDING Acute respiratory Diaphoresis Hypotension Hypertension Fever Hypoxemia Pivotal

SIGN Appearance Vital Vital signs Table Table 18-3 JVD, jugular venous distention; MI, myocardial infarction; PE, pulmonary jugular myocardial PE, infarction; venous MI, embolism. JVD, distention; 136

BOX 18-1 Risk Factors Associated with Potentially Catastrophic Causes of Chest Pain

Acute coronary syndromes Aortic dissection Past or family history of Hypertension Age Congenital disease of the aorta or Men >33 years Inflammatory aortic disease Women >40 years Connective tissue disease Diabetes mellitus Pregnancy Hypertension Arteriosclerosis

• Cardinal Presentations Cigarette use/possible passive exposure Cigarette use Elevated cholesterol (LDL)/triglycerides Pericarditis or myocarditis wo T Sedentary lifestyle Obesity Autoimmune disease (e.g., systemic lupus erythematosus) e c tion

S Postmenopausal Acute / Left Recent myocardial infarction or Cocaine abuse Malignancy Pulmonary embolism Radiation therapy to mediastinum Prolonged immobilization Uremia Surgery >30 minutes in last 3 mo Drugs Prior deep vein thrombosis or pulmonary embolus Prior pericarditis Pregnancy or recent pregnancy Pneumothorax Pelvic or lower extremity trauma Prior pneumothorax Oral contraceptives with cigarette smoking Valsalva’s maneuver Congestive Chronic lung disease

Fundamental Clinical Concepts Chronic obstructive pulmonary disease Cigarette use

■ Obesity

I Past medical or family history of hypercoagulability PART

Table 18-4 Ancillary Testing of Patients with Chest Pain Table 18-5 Electrocardiogram Findings in Ischemic Chest Pain TEST FINDING DIAGNOSIS Classic myocardial ST segment elevation (>1 mm) in ECG New injury Acute MI infarction contiguous leads; new LBBB; Aortic dissection Q waves ≥0.04 sec duration New ischemia Coronary ischemia Subendocardial infarction inversion or ST segment Coronary spasm depression in concordant leads RV strain PE Diffuse ST segment Pericarditis Unstable angina Most often normal or nonspecific elevation changes; may see T wave inversion CXR Pneumothorax with Tension mediastinal shift pneumothorax Pericarditis Diffuse ST segment elevation; Wide mediastinum Aortic dissection PR segment depression Pneumothorax Esophageal LBBB, left bundle-branch block. rupture Pneumothorax Effusion Esophageal probability of PE effectively excludes the diagnosis.13,17,18 rupture (see Chapter 87.) Increased cardiac silhouette Pericarditis Patients at high pretest probability for PE should undergo Pneumomediastinum Esophageal diagnostic imaging (multidetector computed tomography rupture [CT], or, less commonly, pulmonary angiography or a Mediastinitis ventilation-perfusion lung scan).19 High pretest probability ABG Hypoxemia, A-a gradient PE warrants initiation of anticoagulation (heparin or low- VQ scan or High probability or any PE molecular-weight heparin) therapy in the ED before the spiral CT positive in patient with imaging study, in the absence of a contraindication. high clinical suspicion Patients with suspected thoracic aortic dissection may be ABG, arterial blood gas; CT, computed tomography; ECG, electrocardiogram; evaluated by CT angiography, transesophageal echocardiog­ MI, myocardial infarction; RV, right ventricular. raphy, or magnetic resonance imaging. Selection of imaging modality depends on patient status and availability of the testing equipment.20 level may be seen in esophageal rupture. Increased cardiac CT with a 64 or higher detector scanner has the potential silhouette may indicate pericarditis or cardiomyopathy. to rule out all of the life-threatening causes of chest pain. Pneumomediastinum is seen with esophageal rupture and Although the “triple rule out” of ACS, PE, and thoracic dis- mediastinitis. A serum D-dimer assay may help discriminate section are the causes most commonly discussed, pneumotho- patients with PE from those with a possible gastrointestinal rax, mediastinitis, and pericardial effusions are also diagnosed cause. A low serum D-dimer in a patient without a high pretest with CT.21,22 Chapter 18 / Chest Pain 137 High Risk Heparin or LMWH IV nitroglycerin Beta-blocker Revascularization: Fibrinolysis or llb-llla inhibitor GP + PCl Elevated troponin ↓ 0.5 mm New ST Recurrent ischemia Heart failure with ischemia function Depressed LV Hemodynamic instability PCI in last 6 months Prior CABG Practical Practical implementation of the guidelines al: al:

Yes Early Invasive Treatment Heparin or LMWH IV nitroglycerin Beta-blocker llb-llla inhibitor GP Diagnostic catheterization in 12–48 hr

Yes No

Risk ACS? Possible evaluation New LBBB stratification Acute STEMI: ST ↑ > 1 mm or ST Completed initial Completed Initiate emergency care Initiate emergency Cardiac monitor Oxygen therapy Aspirin Nitroglycerin IV access Laboratory tests Yes No >10 minutes rest pain - resolved inversion >2 mm T-wave Intermediate troponin elevation >0.01 ng/mL, < 0.1 ng/mL) (TnT Discharge Intermediate Risk Intermediate

No resolved Discharge testing Stable angina — Low Risk ischemia Evidence of ongoing Provocative

No intermediate or high risk features Nondiagnostic ECG and cardiac markers Age < 70

Early Conservative Treatment Observation bed Heparin or LMWH IV nitroglycerin Beta-blocker Continuous ECG monitoring Repeat ECGs at regular intervals Cardiac markers

testing Center Discharge Provocative ED Chest Pain Clinical Clinical guidelines for emergency department management of chest pain of acute myocardial ischemic coronaryACS, origin. syndrome;

evaluation myocardial infarction; TnT, troponin T. (Adapted from Gibler WB, Cannon CP, Blonikalns et AL, (Adapted from Cannon GiblerCP, WB, T. troponin TnT, evaluation myocardial infarction; for unstable angina/non-ST-segment elevation myocardial infarction in the emergency A department: scientific statement from theAmerican Heart Association Council on Clinical Cardiology (Subcommittee on Acute Council Cardiac and on Care), QualityCardiovascular Nursing, of Care and Outcomes Research in Interdisciplinary Working Collaboration Group, with the Society of Circulation 2005.) Chest 111:2699, Pain Centers. Figure 18-2. left LBBB, low-molecular- bundle-branch LMWH, block; intravenous; IV, glycoprotein; coronary CABG, artery GP, electrocardiogram; bypass ECG, graft; ST echocardiographic STEMI, percutaneous segment peak; leftmyocardial PCI, coronaryinfarction; MI, ST, ventricular; intervention; weight LV, heparin; 138

ADDITIONAL

OR

presentation. Full history is essential. Fewer than 15% of patients hospitalized for unstable angina go on to acute MI. May respond to NTG. May manifest similarly to non–Q wave infarction “indigestion” or “unable to describe.” Other atypical presentations include altered mental status, stroke, angina pattern without extended pain, severe fatigue, syncope. Elderly may present with weakness, congestive heart failure, or chest tightness. 25% of nonfatal MIs are unrecognized by patient. The pain may have resolved by the time of evaluation May be pain-free at Pain may present as ATYPICAL ASPECTS • Cardinal Presentations wo T e c tion S / TESTS

enzyme changes. angina Variant has (Prinzmetal’s) episodic pain, at rest, often severe, with prominent ST segment elevation Q waves or ST segment–T wave changes) occur in 80% of patients. CK-MB and troponins are helpful if elevated, but may be normal Often no ECG or ECG changes (new USEFUL omfort

4 TION Disc

or

and S 3 EXAMINA Pain

Fundamental Clinical Concepts

■

I

Chest uncomfortable. Blood pressure usually is elevated, but normotension and hypotension are seen. The heart rate is usually mildly increased, but bradycardia can be seen. Patients may be diaphoretic and show peripheral poor perfusion. There are no diagnostic examination findings for MI, although S transient nature, may have similar cardiac findings as in MI, especially intermittent diaphoresis heart sounds and new murmur are supportive

Patients are anxious and Nonspecific findings of a PHYSICAL PART tral

IN Cen

with

Common Common PREVALENCE EMERGENCY DEPARTMENT esenting Pr

> 40

Illness

by emotional stress or exertion. Often comes on at rest. May come on in early awakening period. Prodromal pain pattern often elicited. Previous history of MI or angina. Age years, positive risk factors, and male sex increase possibility precipitating factors. May be a decrease in amount of physical activity that initiates pain. Previous history of MI or angina. Over 40 years old, presence of risk factors, and male sex increase probability May be precipitated Not clearly related to SUPPORTING HISTORY tastrophic Ca

entially Pot

of nausea, vomiting, dyspnea May have mild diaphoresis, nausea, dyspnea with pain. Increasing pattern of dyspnea on exertion

Diaphoresis, Often minimal. ASSOCIATED SYMPTOMS

mo)

2

< erentiation min and is min or

Diff

min. Angina

HISTORY

10 and of preexisting angina with more severe, prolonged, or frequent pain (crescendo angina). Pain usually lasts > usually moderately severe to severe and rapid in onset. May be more “pressure” than pain. Usually retrosternal, may radiate to neck, both jaw, arms, upper back, epigastrium, and sides of chest (left more than right). Lasts more than 15–30 unrelieved by NTG at rest lasting 15–20 new-onset angina (duration with minimal exertion. Pattern of pain change important in gauging risk for AMI. Unpredictable responses to NTG and rest

Changes in pattern Discomfort is PAIN Causes

Angina Infarction Unstable Myocardial Table 18-6 Chapter 18 / Chest Pain

139

negative

rules out, if truly truly if out, rules

occur in 5% in occur

perfusion scan scan perfusion

like pain may may pain like

infarction. Lung Lung infarction.

< 20%. Angina- 20%. in

less common less due to pulmonary pulmonary to due

Hemoptysis occurs occurs Hemoptysis

peripheral cyanosis are are cyanosis peripheral of consolidation consolidation of

intermittent Wheezes and and Wheezes exacerbation patients oligemia, or signs signs or oligemia, greatest risk factor risk greatest

be episodic or or episodic be 30–40% of patients. patients. of 30–40% cause of COPD COPD of cause complex complex volume loss, loss, volume DVT or PE is the the is PE or DVT

beginning. May May beginning. diaphoresis are seen in in seen are diaphoresis heart. May be subtle subtle be May heart. medically medically 40% show some some show 40% factors. Previous Previous factors.

cases maximal at at maximal phlebitis, and and phlebitis, venous plexus, right right plexus, venous elderly or or elderly normal, although although normal, cancer are all risk risk all are cancer

about half the the half about in onset and and onset in are common. Fever, Fever, common. are knee, prostate/pelvis prostate/pelvis knee, volumes of of volumes film is usually usually is film heart disease, and and disease, heart

accompanies accompanies embolus. Abrupt Abrupt embolus. pulmonic second sound sound second pulmonic lower extremities above above extremities lower with high high with helpful. Chest Chest helpful. contraceptives, contraceptives,

than pain. Cough Cough pain. than with massive massive with rales, and an increased increased an and rales, Emboli usually from from usually Emboli departments departments A-a gradient is is gradient A-a oral oral Pregnancy,

postoperative. role, often more more often role, more consistent consistent more Tachycardia, inspiratory inspiratory Tachycardia, mortality rate is 10%. 10%. is rate mortality common in in common Widened 90%.

> < has occurred, e.g., e.g., occurred, has play a prominent prominent a play Central pain is is pain Central 16/min. 16/min. rate bronchospasm. Acute Acute bronchospasm. patients, but but patients, Hg in in Hg mm 80

2 o of immobilization immobilization of apprehension apprehension lateral-pleuritic. lateral-pleuritic. Embolism gases show P show gases often have a respiratory respiratory a have often dyspnea with or without without or with dyspnea ambulatory ambulatory

Often some period period some Often Dyspnea and and Dyspnea Pain is more often often more is Pain Pulmonary blood Arterial Patients are anxious and and anxious are Patients Patients may present with with present may Patients Uncommon in in Uncommon

diagnosis

murmur supportive of of supportive murmur screening

or insufficiency aortic or useful in in useful

pericardial friction rub rub friction pericardial CT, MRI most most MRI CT,

medically cord. New-onset New-onset cord. may migrate may echocardiogram, echocardiogram,

are generally managed managed generally are mesentery, renal, spinal spinal renal, mesentery, sensation, and and sensation, Transesophageal Transesophageal incidence

surgically. Descending Descending surgically. coronary (1–2%), (1–2%), coronary a “tearing” “tearing” a 95–99%. 95–99%. increased increased

often approached approached often vascular occlusions: occlusions: vascular has often Pain of accuracy valves have have valves

aneurysms are more more are aneurysms insufficiency. Other Other insufficiency. or into abdomen. abdomen. into or has diagnostic diagnostic has bicuspid aortic aortic bicuspid

ischemia possible ischemia Ascending aortic aortic Ascending dissections cause aortic aortic cause dissections interscapular area area interscapular Aortic angiography angiography Aortic congenital congenital

arteries can mimic MI mimic can arteries silhouette (90%). silhouette extremity extremity 50% of proximal proximal of 50% chest to the back back the to chest syndrome and and syndrome

Dissection into coronary coronary into Dissection abnormal aortic aortic abnormal abdominal and and abdominal of peripheral pulses. pulses. peripheral of anteriorly in in anteriorly Marfan’s Marfan’s

may be minimal. minimal. be may film shows shows film paraplegia, paraplegia, absence or decrease Radiates Radiates males to females. females. to males

examination findings findings examination changes. Chest Chest changes. paresis or or paresis is asymmetrical asymmetrical is at beginning. beginning. at 1 ratio ratio 1 : 3 patients.

complications. Physical Physical complications. nonspecific nonspecific 70–90% of of 70–90% neuropathy, neuropathy, 50–60% of cases, there there cases, of 50–60% that is maximal maximal is that

with neurologic neurologic with hypertrophy, hypertrophy, hypertension in in hypertension stroke, peripheral peripheral stroke, In BP. elevated severe chest pain pain chest severe

pain-free. May present present May pain-free. left ventricular ventricular left History of of History complications of of complications peripherally but with with but peripherally Dissection have rapid-onset rapid-onset have

Rare for patient to present present to patient for Rare ECG usually shows shows usually ECG Median age 59 years. years. 59 age Median Neurologic Neurologic Often poorly perfused perfused poorly Often Rare Aortic Aortic 90% of patients patients of 90%

SYMPTOMS HISTORY PAIN DEPARTMENT HISTORY TION EXAMINA PHYSICAL ASPECTS TESTS USEFUL

SUPPORTING ASSOCIATED EMERGENCY ATYPICAL ADDITIONAL OR

PREVALENCE IN 140

ADDITIONAL

OR

shock state. This entity often considered late in differential diagnostic process , cystic . Can be complicated by pneumomediastinum 50-year-olds. 50-year-olds. May have associated , ventricular dysrhythmias. Idiopathic most common (80%). with aspirin, Treated NSAID Patient may present in May be subtle in COPD, ATYPICAL ASPECTS More common in 20- to • Cardinal Presentations wo T

e c tion S / TESTS

< 6.0. Diagnosis for ST segment has mediastinal air, a left-sided pleural effusion, pneumothorax, or a widened mediastinum. pH of pleural effusion is supported by water-soluble contrast esophagram or esophagoscopy Inspiratory and expiratory films may enhance contrast between air and lung parenchyma. Tension pneumothorax should be diagnosed on physical examination elevation across the precordial leads. Erythrocyte sedimentation rate may be elevated ECG pattern typical Chest film usually Chest film definitive. USEFUL omfort—cont’d TION Disc

or

EXAMINA Pain

Fundamental Clinical Concepts

■

I

Chest heard, often fleeting, position-dependent (50% of patients). consolidation, subcutaneous emphysema may be present increased resonance on percussion. Elevated pressure in neck veins occurs in tension pneumothorax

Friction rub may be Signs of lung Decreased breath sounds, PHYSICAL PART tral

IN Cen

with

even more rare complication Rare Rare Infrequent PREVALENCE EMERGENCY DEPARTMENT Tamponade Tamponade esenting Pr

Illness

when supine, but improves sitting up. Often preceded by viral illness or underlying disease (SLE or uremia) with known gastrointestinal problems. History of violent emesis, foreign body, caustic ingestion, blunt trauma, alcoholism, esophageal disease previous episode, or asthenic body type Pain is often worse Older individual Chest trauma, SUPPORTING HISTORY tastrophic Ca

entially Pot

of diaphoresis dyspnea (late), shock prominent role. Hypotension and altered mental states occur in tension pneumothorax

Dyspnea, Diaphoresis, Dyspnea has a ASSOCIATED SYMPTOMS erentiation Diff

HISTORY

and recurrent pain unrelated to exercises or meals. Or it may be a sharp, stabbing, pleuritic-type pain that does not change with chest wall motion. May be severe. Not relieved by NTG preceded by vomiting and is abrupt in onset. Pain is persistent and unrelieved, localized along the esophagus, and increased by swallowing and neck flexion acute and maximal at onset. Most often lateral-pleuritic, but central pain can occur in large pneumothorax

Dull, aching Pain usually is Pain is usually PAIN Causes

Rupture NSAID, nonsteroidal anti-inflammatory drug; NTG, nitroglycerin; PE, pulmonary systemic PE, lupus SLE, nonsteroidal embolus; nitroglycerin; erythematosus. anti-inflammatory NTG, NSAID, drug; Pericarditis Esophageal Pneumothorax Table 18-6 AMI, acute myocardial infarction; CK-MB, an isoform of creatine kinase; COPD, chronic obstructive pulmonary disease; CT, computed tomography; DVT, deep vein thrombosis; ECG, electrocardiogram; MRI, magnetic MRI, an acute resonance electrocardiogram; deep AMI, imaging; myocardial isoform CK-MB, infarction; vein chronic ECG, of thrombosis; computed obstructive DVT, creatine tomography; pulmonary COPD, kinase; CT, disease; Chapter 18 / Chest Pain

141 - Figure

Pericarditis • U/S for risk effusion/tamponade • NSAIDs • Corticosteroids • Cardiology consultation DISPOSITION

AND

rupture Esophageal • IV fluid resuscitation Analgesia • • IV antibiotics • Early surgical consultation Frequently, Frequently, no definitive diagnosis is established. Any MANAGEMENT a rapid review of the pivotal findings and the potential diag- ). 18-6 noses (Table ■ The management of ACS is discussed in Chapter 76. The references for this chapter can be found online by accessing the accompanying Expert Consult website. 18-3 outlines the approach to treatment of critical noncardiac diagnoses. Patients with admitted to the critical intensive care unit. diagnoses Patients with diagnoses emergent typically generally are admitted to are the hospital, on most often telemetry units. Patients are most frequently with treated as outpatients. Hospitalization nonemergent is diagnoses required in certain circumstances, particularly when patients have other comorbid conditions. coro having be may pain chest of type any almost with patient nary ischemia, PE, or aortic dissection. When a clear pattern an make to physician emergency the allow to emerge not does continued evaluation,alternative hospi- diagnosis confidently, talization, or observation admission may be the best course.

- - ­ Tension 23,24 pneumothorax • Cardiac monitor access • Intravenous • Oxygen therapy • Needle decompression thoracostomy Tube • Complete initial evaluation Complete Differential diagnosis based Differential Specific tests per Table 18-6 Table Specific tests per on history, physical, and ECG on history, embolism Pulmonary • IV heparin or SQ LMWH Thrombolysis if severe • cardiovascular instability 23 TABLE

Elevated troponin in the correct clinical setting clinical correct the in troponin Elevated Aortic 25,26 Clinical Clinical guidelines for emergency department management of chest pain from potentially catastrophic nonmyocardial origins. dissection

• Beta-blockade • IV antihypertensive therapy • Decrease contractility • Immediate surgical consult/transfer Troponins (I and Troponins T), when elevated, identify patients with Laboratory testing is useful in the evaluation of ACS. DIAGNOSTIC ■ After the patient is stabilized and assessment has been com ACS who have the highest risk for an adverse outcome. pleted, the findings are matched chest causing diseases to critical potentially seven the of patterns the classic and atypical pain. This matching process is continual while evaluating the patient and monitoring the Any response inconsis- to therapy. tency in findings with the primary working diagnoses requires CK-MB, an isoform of CK, is more specific for cardiac ische mia. Evaluating this enzyme produces results, and peak fewer sensitivity approaches 98%. false-positive Sensitivity at 4 hours is, however, only about 60%. CK-MB isoforms improve The hours. 6 at 93% approaching 80%, to hours 4 at sensitivity current universal definition ofMI places CK and CK-MB in a secondary role to troponins. ECG, electrocardiogram; IV, intravenous; NSAIDs, nonsteroidal anti-inflammatory drugs; SQ, subcutaneous; LMWH, low-molecular-weight heparin; low-molecular-weight nonsteroidal heparin; LMWH, anti-inflammatory subcutaneous; NSAIDs, SQ, drugs; intravenous; IV, electrocardiogram; ECG, false-positive multiple with associated is (CK) kinase Creatine results and has no use in the evaluation of unstable angina. U/S, ultrasound. U/S, is synonymous with acute MI and is embedded in the univer sal definition of MI. Figure 18-3. Sensitivity for acute MI at 4 hours is 60%, rising to nearly 100% nearly to rising 60%, is hours 4 at MI acute for Sensitivity hours. 12 by