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Chest Pain Diagnosis: Coronary Syndromes, Aortic Dissection, Pulmonary Embolism, and More, Lecture notes of History

An in-depth analysis of various causes of chest pain, focusing on acute coronary syndromes (ACS), aortic dissection, pulmonary embolism (PE), pneumothorax, pericarditis with tamponade, and esophageal rupture. It discusses the symptoms, diagnosis, and prevalence of these conditions, as well as the importance of prompt diagnosis and treatment. The document also includes tables and charts to help differentiate between the various causes of chest pain.

What you will learn

  • What are the symptoms and risk factors for pulmonary embolism?
  • How is aortic dissection diagnosed and treated?
  • What are the symptoms and causes of acute coronary syndromes?

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PERSPECTIVE
Nearly 6 million patients present to the emergency depart-
ment (ED) each year with complaints of chest pain, constitut-
ing 5% of all patients seen in EDs in the United States.1 Chest
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
signs and seriousness of underlying pathology.
Epidemiology
The epidemiology of the critical diagnoses causing chest pain
varies widely. Acute coronary syndromes (ACS), aortic dissec-
tion, pulmonary embolism (PE), pneumothorax, pericarditis
with tamponade, and esophageal rupture are potentially cata-
strophic causes of chest pain. Due to its high incidence and
potential lethality, ACS is the most significant potential diag-
nosis in the ED. Of all deaths in the United States, 36% are
attributed to cardiovascular diseases; these account for approx-
imately 870,000 deaths per year.2 Historically, emergency phy-
sicians misdiagnose 3 to 5% of myocardial infarctions (MIs),
accounting for 25% of malpractice losses in emergency medi-
cine.3,4 Thoracic aortic dissection has an incidence of 0.5 to 1
per 100,000 population with a mortality rate exceeding 90% if
misdiagnosed. The true incidence of PE is unclear, with esti-
mates of 70 per 100,000. This equates to approximately 100,000
PE cases per year in the United States.5 Although the inci-
dence of tension pneumothorax is also unclear, the incidence
of spontaneous pneumothorax ranges from 2.5 to 18 per
100,000 total patients. The total incidence of esophageal
rupture is 12.5 cases per 100,000 persons. The true incidence
of pericarditis is unknown, but is diagnosed in 1 of every 1000
hospital admissions.6 Up to 5% of ED chest pain patients
without acute ST elevation MI may have pericarditis.7
Pathophysiology
Afferent fibers from the heart, lungs, great vessels, and esopha-
gus enter the same thoracic dorsal ganglia. Through these
visceral fibers, each organ produces the same indistinct quality
and location of pain. The quality of visceral chest pain varies
widely and is described as “burning,” “aching,” “stabbing,” or
“pressure.” Since dorsal segments overlap three segments
above and below a level, disease of a thoracic origin can
produce pain anywhere from the jaw to the epigastrium. Radi-
ation of pain is caused by somatic afferent fibers synapsing in
the same dorsal root ganglia as the thoracic viscera. This stimu-
lation can “confuse” the patient’s central nervous system
into misperceiving that the pain originates in the arms or
shoulders.
DIAGNOSTIC APPROACH
Differential Considerations
Due to the indistinct nature of visceral pain, the differential
diagnosis of chest pain is broad and includes many of the most
critical diagnoses in medicine and many nonemergent condi-
tions (Table 18-1).
Rapid Stabilization and Assessment
The initial questions are, “Must I intervene immediately?”,
and “What are the life-threatening possibilities in this patient?”
The answers are usually apparent within the first few minutes
after assessing the patient’s appearance and vital signs. One of
the critical diagnoses is tension pneumothorax. If a patient
presents with chest pain, respiratory distress, shock, and uni-
lateral reduction or absence of breath sounds, immediate
intervention with needle or tube thoracostomy is required.
Additionally, patients with severe derangements in vital signs
require stabilizing treatment during a search for the precipitat-
ing cause. Patients who present with respiratory distress
require immediate intervention and lead the emergency phy-
sician to consider a more serious cause of the pain (Fig. 18-1;
also see Chapter 17).
All patients, except those with obvious benign causes of
chest pain, must have an electrocardiogram (ECG) within
minutes of reporting their pain. This ECG should be read for
acute MI by the emergency physician as soon as it is com-
pleted. Patients with positive ECG findings and those consid-
ered at high risk are triaged directly to the treatment area and
monitored. Symptomatic derangements in vital signs are
addressed. If vital signs are stable, a focused history and physi-
cal examination are performed. Most patients also require a
chest radiograph to evaluate the chest pain. If a cardiac cause
is suggested and vital signs are stable, pain relief with nitro-
glycerin (0.4 mg sublingual every 3–5 minutes) may be appro-
priate. Aspirin (81–325 mg) is a consideration for patients
without hemorrhagic disorders, known allergies, or vascular
dissections. Clopidogrel (loading dose 300 mg) or other anti-
132
Chapter 18 Chest Pain
James E. Brown and Glenn C. Hamilton
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■ PERSPECTIVE

Nearly 6 million patients present to the emergency depart-

ment (ED) each year with complaints of chest pain, constitut-

ing 5% of all patients seen in EDs in the United States.^1 Chest

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

signs and seriousness of underlying pathology.

Epidemiology

The epidemiology of the critical diagnoses causing chest pain

varies widely. Acute coronary syndromes (ACS), aortic dissec-

tion, pulmonary embolism (PE), pneumothorax, pericarditis

with tamponade, and esophageal rupture are potentially cata-

strophic causes of chest pain. Due to its high incidence and

potential lethality, ACS is the most significant potential diag-

nosis in the ED. Of all deaths in the United States, 36% are

attributed to cardiovascular diseases; these account for approx-

imately 870,000 deaths per year.^2 Historically, emergency phy-

sicians misdiagnose 3 to 5% of myocardial infarctions (MIs),

accounting for 25% of malpractice losses in emergency medi-

cine.3,4^ Thoracic aortic dissection has an incidence of 0.5 to 1

per 100,000 population with a mortality rate exceeding 90% if

misdiagnosed. The true incidence of PE is unclear, with esti-

mates of 70 per 100,000. This equates to approximately 100,

PE cases per year in the United States.^5 Although the inci-

dence of tension pneumothorax is also unclear, the incidence

of spontaneous pneumothorax ranges from 2.5 to 18 per

100,000 total patients. The total incidence of esophageal

rupture is 12.5 cases per 100,000 persons. The true incidence

of pericarditis is unknown, but is diagnosed in 1 of every 1000

hospital admissions.^6 Up to 5% of ED chest pain patients

without acute ST elevation MI may have pericarditis.^7

Pathophysiology

Afferent fibers from the heart, lungs, great vessels, and esopha-

gus enter the same thoracic dorsal ganglia. Through these

visceral fibers, each organ produces the same indistinct quality

and location of pain. The quality of visceral chest pain varies

widely and is described as “burning,” “aching,” “stabbing,” or

“pressure.” Since dorsal segments overlap three segments

above and below a level, disease of a thoracic origin can

produce pain anywhere from the jaw to the epigastrium. Radi-

ation of pain is caused by somatic afferent fibers synapsing in

the same dorsal root ganglia as the thoracic viscera. This stimu-

lation can “confuse” the patient’s central nervous system

into misperceiving that the pain originates in the arms or

shoulders.

■ DIAGNOSTIC APPROACH

Differential Considerations

Due to the indistinct nature of visceral pain, the differential

diagnosis of chest pain is broad and includes many of the most

critical diagnoses in medicine and many nonemergent condi-

tions (Table 18-1).

Rapid Stabilization and Assessment

The initial questions are, “Must I intervene immediately?”,

and “What are the life-threatening possibilities in this patient?”

The answers are usually apparent within the first few minutes

after assessing the patient’s appearance and vital signs. One of

the critical diagnoses is tension pneumothorax. If a patient

presents with chest pain, respiratory distress, shock, and uni-

lateral reduction or absence of breath sounds, immediate

intervention with needle or tube thoracostomy is required.

Additionally, patients with severe derangements in vital signs

require stabilizing treatment during a search for the precipitat-

ing cause. Patients who present with respiratory distress

require immediate intervention and lead the emergency phy-

sician to consider a more serious cause of the pain (Fig. 18-1;

also see Chapter 17).

All patients, except those with obvious benign causes of

chest pain, must have an electrocardiogram (ECG) within

minutes of reporting their pain. This ECG should be read for

acute MI by the emergency physician as soon as it is com-

pleted. Patients with positive ECG findings and those consid-

ered at high risk are triaged directly to the treatment area and

monitored. Symptomatic derangements in vital signs are

addressed. If vital signs are stable, a focused history and physi-

cal examination are performed. Most patients also require a

chest radiograph to evaluate the chest pain. If a cardiac cause

is suggested and vital signs are stable, pain relief with nitro-

glycerin (0.4 mg sublingual every 3–5 minutes) may be appro-

priate. Aspirin (81–325 mg) is a consideration for patients

without hemorrhagic disorders, known allergies, or vascular

dissections. Clopidogrel (loading dose 300 mg) or other anti-

Chapter 18 Chest Pain

James E. Brown and Glenn C. Hamilton

Chapter 18 (^) / Chest Pain

are key to diagnosis. Information pertinent to the differential

diagnosis is obtained by the history, physical examination, and

ECG in 80 to 90% of patients.

History

1. The patient is asked to describe the character of the

pain or discomfort. Descriptions such as “squeezing,”

“crushing,” or “pressure” lead the emergency physician

to suspect a cardiac ischemic syndrome, although cardiac

ischemia can also be characterized by nonspecific dis-

comfort, such as “bloating” or “indigestion.” “Tearing”

pain that may migrate from the front to back or back to

front is the classic description in aortic dissection. “Sharp”

or “stabbing” pain is seen more in pulmonary and muscu-

loskeletal diagnoses. Patients complaining of a “burning”

or “indigestion” type of pain may initially be thought to

have a gastrointestinal etiology, but due to the visceral

nature of chest pain, all causes of pain may present with

any of the preceding descriptions. Of note, descriptors

may vary among ethnic groups, and, for example, “sharp”

may mean “severe.”

2. Additional history about the patient’s activity at the onset

of pain may be helpful. Pain occurring during exertion

suggests an ischemic coronary syndrome, whereas progres-

sive onset of pain at rest suggests acute MI. Pain of sudden

onset is more typical with aortic dissection, PE, or pneu-

mothorax. Pain after meals is more indicative of a gastro-

intestinal cause.

3. The severity of pain is commonly quantified using a 1-to-

10 pain scale. Alterations in pain severity are documented

at times of onset, peak, present, and after intervention.

4. The location of the discomfort is described. Pain that is

localized to a small area is more likely to be somatic versus

visceral in origin. Pain localized at the periphery of the

Table 18-1 Differential^ Diagnosis^ of^ Chest^ Pain

ORGAN SYSTEM CRITICAL DIAGNOSES EMERGENT DIAGNOSES NONEMERGENT DIAGNOSES Cardiovascular Acute myocardial infarction Unstable angina Valvular heart disease Acute coronary ischemia Coronary spasm Aortic stenosis Aortic dissection Prinzmetal’s angina Mitral valve prolapse Cardiac tamponade Cocaine-induced pericarditis or myocarditis Hypertrophic cardiomyopathy Pulmonary Pulmonary embolus Pneumothorax Pneumonia Tension pneumothorax Mediastinitis Pleuritis Tumor Pneumomediastinum Gastrointestinal Esophageal rupture (Boerhaave) Esophageal tear (Mallory-Weiss) Esophageal spasm Cholecystitis Esophageal reflux Pancreatitis Peptic ulcer Biliary colic Musculoskeletal Muscle strain Rib fracture Arthritis Tumor Costochondritis Nonspecific chest wall pain Neurologic Spinal root compression Thoracic outlet Herpes zoster Postherpetic neuralgia Other (^) Psychologic Hyperventilation

Figure 18-1. Initial assessment of critical diagnoses. CXR, chest x-ray;

ECG, electrocardiogram; RV, right ventricular. Initial assessment Absent breath sounds w/shock ECG/CXR ECG CXR: pulmonary edema Acute coronary syndrome Thoracic aortic aneurysm Esophageal rupture Pulmonary embolus Tension pneumothorax ECG CXR: mediastinal air/fluid ECG RV strain CXR ECG CXR: widened mediastinum

platelet agents may also be an alternative. Patients with low

voltage on the ECG, diffuse ST segment elevation, elevated

jugular venous pressure on examination,^8 and signs of shock

should undergo prompt bedside cardiac ultrasound.

Pivotal Findings

The broad and complex nature of chest pain defies application

of a simple algorithm. An organized approach to a patient with

chest pain is essential, however, to ensure that all causes are

evaluated appropriately. The history and physical examination

Chapter 18 (^) / Chest Pain

Table 18-3 Pivotal^ Findings^ in^ Physical^ Examination

SIGN FINDING DIAGNOSES Appearance Acute respiratory distress

PE

Tension pneumothorax Acute MI Pneumothorax Diaphoresis Acute MI Aortic dissection Coronary ischemia PE Esophageal rupture Unstable angina Cholecystitis Perforated peptic ulcer Vital signs Hypotension Tension pneumothorax PE Acute MI Aortic dissection (late) Coronary ischemia Esophageal rupture Pericarditis Myocarditis Tachycardia Acute MI PE Aortic dissection Coronary ischemia Tension pneumothorax Esophageal rupture Coronary spasm Pericarditis Myocarditis Mediastinitis Cholecystitis Esophageal tear (Mallory-Weiss) Bradycardia Acute MI Coronary ischemia Unstable angina Hypertension Acute MI Coronary ischemia Aortic dissection (early) Fever PE Esophageal rupture Pericarditis Myocarditis Mediastinitis Cholecystitis Hypoxemia PE Tension pneumothorax Pneumothorax SIGN FINDING DIAGNOSES Cardiovascular examination Significant difference in upper extremity blood pressures Aortic dissection Narrow pulse pressure Pericarditis (with effusion) New murmur Acute MI Aortic dissection Coronary ischemia S 3 /S 4 gallop Acute MI Coronary ischemia Pericardial rub Pericarditis Audible systolic “crunch” on cardiac auscultation (Hamman’s sign) Esophageal rupture Mediastinitis JVD Acute MI Coronary ischemia Tension pneumothorax PE Pericarditis Pulmonary examination Unilateral diminished/ absent breath sounds Tension pneumothorax Pneumothorax Pleural rub PE Subcutaneous emphysema Tension pneumothorax Esophageal rupture Pneumothorax Mediastinitis Rales Acute MI Coronary ischemia Unstable angina Abdominal examination Epigastric tenderness Esophageal rupture Esophageal tear Cholecystitis Pancreatitis Left upper quadrant tenderness Pancreatitis Right upper quadrant tenderness Cholecystitis Extremity examination Unilateral leg swelling, warmth, pain, tenderness, or erythema

PE

Neurologic examination Focal findings Aortic dissection Stroke Acute MI Coronary ischemia Aortic dissection Coronary spasm JVD, jugular venous distention; MI, myocardial infarction; PE, pulmonary embolism.

PART I^ ■ Fundamental Clinical Concepts / Se Ction two

Cardinal Presentations

Table 18-4 Ancillary^ Testing^ of^ Patients^ with^ Chest^ Pain

TEST FINDING DIAGNOSIS ECG New injury Acute MI Aortic dissection New ischemia Coronary ischemia Coronary spasm RV strain PE Diffuse ST segment elevation Pericarditis CXR Pneumothorax with mediastinal shift Tension pneumothorax Wide mediastinum Aortic dissection Pneumothorax Esophageal rupture Pneumothorax Effusion Esophageal rupture Increased cardiac silhouette Pericarditis Pneumomediastinum Esophageal rupture Mediastinitis ABG Hypoxemia, A-a gradient PE V Q^ ^  scan or spiral CT High probability or any positive in patient with high clinical suspicion

PE

ABG, arterial blood gas; CT, computed tomography; ECG, electrocardiogram; MI, myocardial infarction; RV, right ventricular.

Acute coronary syndromes

Past or family history of coronary artery disease

Age

Men >33 years

Women >40 years

Diabetes mellitus

Hypertension

Cigarette use/possible passive exposure

Elevated cholesterol (LDL)/triglycerides

Sedentary lifestyle

Obesity

Postmenopausal

Left ventricular hypertrophy

Cocaine abuse

Pulmonary embolism

Prolonged immobilization

Surgery >30 minutes in last 3 mo

Prior deep vein thrombosis or pulmonary embolus

Pregnancy or recent pregnancy

Pelvic or lower extremity trauma

Oral contraceptives with cigarette smoking

Congestive heart failure

Chronic obstructive pulmonary disease

Obesity

Past medical or family history of hypercoagulability

Aortic dissection

Hypertension

Congenital disease of the aorta or aortic valve

Inflammatory aortic disease

Connective tissue disease

Pregnancy

Arteriosclerosis

Cigarette use

Pericarditis or myocarditis

Infection

Autoimmune disease (e.g., systemic lupus erythematosus)

Acute rheumatic fever

Recent myocardial infarction or cardiac surgery

Malignancy

Radiation therapy to mediastinum

Uremia

Drugs

Prior pericarditis

Pneumothorax

Prior pneumothorax

Valsalva’s maneuver

Chronic lung disease

Cigarette use

BOX 18-1 Risk F actoRs associated with P otentially catastRoPhic causes oF chest P ain

Table 18-5 Electrocardiogram Chest Pain^ Findings^ in^ Ischemic

Classic myocardial infarction ST segment elevation (> 1 mm) in contiguous leads; new LBBB; Q waves ≥0.04 sec duration Subendocardial infarction T wave inversion or ST segment depression in concordant leads Unstable angina Most often normal or nonspecific changes; may see T wave inversion Pericarditis Diffuse ST segment elevation; PR segment depression LBBB, left bundle-branch block.

level may be seen in esophageal rupture. Increased cardiac

silhouette may indicate pericarditis or cardiomyopathy.

Pneumomediastinum is seen with esophageal rupture and

mediastinitis. A serum D-dimer assay may help discriminate

patients with PE from those with a possible gastrointestinal

cause. A low serum D-dimer in a patient without a high pretest

probability of PE effectively excludes the diagnosis.13,17,

(see Chapter 87.)

Patients at high pretest probability for PE should undergo

diagnostic imaging (multidetector computed tomography

[CT], or, less commonly, pulmonary angiography or a

ventilation-perfusion lung scan).^19 High pretest probability

warrants initiation of anticoagulation (heparin or low-

molecular-weight heparin) therapy in the ED before the

imaging study, in the absence of a contraindication.

Patients with suspected thoracic aortic dissection may be

evaluated by CT angiography, transesophageal echocardiog-

raphy, or magnetic resonance imaging. Selection of imaging

modality depends on patient status and availability of the

testing equipment.^20

CT with a 64 or higher detector scanner has the potential

to rule out all of the life-threatening causes of chest pain.

Although the “triple rule out” of ACS, PE, and thoracic dis-

section are the causes most commonly discussed, pneumotho-

rax, mediastinitis, and pericardial effusions are also diagnosed

with CT.21,

PART I^ ■ Fundamental Clinical Concepts / Se Ction two

Cardinal Presentations

Table 18-

Causes

and

Differentiation

of

Potentially

Catastrophic

Illness

Presenting

with

Central

Chest

Pain

or

Discomfort

PAIN HISTORY ASSOCIATED SYMPTOMS SUPPORTING HISTORY PREVALENCE IN EMERGENCY DEPARTMENT PHYSICAL EXAMINATION USEFUL TESTS ATYPICAL OR ADDITIONAL ASPECTS Myocardial Infarction Discomfort is usually moderately severe to severe and rapid in onset. May be more “pressure” than pain. Usually retrosternal, may radiate to neck, jaw, both arms, upper back, epigastrium, and sides of chest (left more than right). Lasts more than 15– min and is unrelieved by NTG Diaphoresis, nausea, vomiting, dyspnea May be precipitated 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 Common Patients are anxious and 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 and S 3 4 heart sounds and new murmur are supportive ECG changes (new 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 Pain may present as “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 Unstable Angina Changes in pattern of preexisting angina with more severe, prolonged, or frequent pain (crescendo angina). Pain usually lasts >^10 min. Angina at rest lasting 15– min or new-onset angina (duration

mo) with minimal exertion. Pattern of pain change important in gauging risk for AMI. Unpredictable responses to NTG and rest Often minimal. May have mild diaphoresis, nausea, dyspnea with pain. Increasing pattern of dyspnea on exertion Not clearly related to 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 Common Nonspecific findings of a transient nature, may have similar cardiac findings as in MI, especially intermittent diaphoresis Often no ECG or enzyme changes. Variant angina (Prinzmetal’s) has episodic pain, at rest, often severe, with prominent ST segment elevation May be pain-free at 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

Chapter 18 (^) / Chest Pain PAIN HISTORY ASSOCIATED SYMPTOMS SUPPORTING HISTORY PREVALENCE IN EMERGENCY DEPARTMENT PHYSICAL EXAMINATION USEFUL TESTS ATYPICAL OR ADDITIONAL ASPECTS Aortic Dissection 90% of patients have rapid-onset severe chest pain that is maximal at beginning. Radiates anteriorly in chest to the back interscapular area or into abdomen. Pain often has a “tearing” sensation, and may migrate Neurologic complications of stroke, peripheral neuropathy, paresis or paraplegia, abdominal and extremity ischemia possible Median age 59 years. History of hypertension in 70–90% of patients. 3 :^ 1 ratio males to females. Marfan’s syndrome and congenital bicuspid aortic valves have increased incidence Rare Often poorly perfused peripherally but with elevated BP. In 50–60% of cases, there is asymmetrical decrease or absence of peripheral pulses. 50% of proximal dissections cause aortic insufficiency. Other vascular occlusions: coronary (1–2%), mesentery, renal, spinal cord. New-onset pericardial friction rub or aortic insufficiency murmur supportive of diagnosis ECG usually shows left ventricular hypertrophy, nonspecific changes. Chest film shows abnormal aortic silhouette (90%). Rare for patient to present pain-free. May present with neurologic complications. Physical examination findings may be minimal. Dissection into coronary arteries can mimic MI Aortic angiography has diagnostic accuracy of 95–99%. Transesophageal echocardiogram, CT, MRI most useful in screening Ascending aortic aneurysms are more often approached surgically. Descending are generally managed medically Pulmonary Embolism Pain is more often lateral-pleuritic. Central pain is more consistent with massive embolus. Abrupt in onset and maximal at beginning. May be episodic or intermittent Dyspnea and apprehension play a prominent role, often more than pain. Cough accompanies about half the cases Often some period of immobilization has occurred, e.g., postoperative. Pregnancy, oral contraceptives, heart disease, and cancer are all risk factors. Previous DVT or PE is the greatest risk factor Uncommon in ambulatory patients, but common in departments with high volumes of elderly or medically complex patients Patients are anxious and often have a respiratory rate

16/min. Tachycardia, inspiratory rales, and an increased pulmonic second sound are common. Fever, phlebitis, and diaphoresis are seen in 30–40% of patients. Wheezes and peripheral cyanosis are less common Arterial blood gases show P o^2 <^

mm Hg in 90%. Widened A-a gradient is helpful. Chest film is usually normal, although 40% show some volume loss, oligemia, or signs of consolidation due to pulmonary infarction. Lung perfusion scan rules out, if truly negative Patients may present with dyspnea with or without bronchospasm. Acute mortality rate is 10%. Emboli usually from lower extremities above knee, prostate/pelvis venous plexus, right heart. May be subtle cause of COPD exacerbation Hemoptysis occurs in

20%. Angina- like pain may occur in 5%

Chapter 18 (^) / Chest Pain

Laboratory testing is useful in the evaluation of ACS.

Creatine kinase (CK) is associated with multiple false-positive

results and has no use in the evaluation of unstable angina.

CK-MB, an isoform of CK, is more specific for cardiac ische-

mia. Evaluating this enzyme produces fewer false-positive

results, and peak sensitivity approaches 98%. Sensitivity at 4

hours is, however, only about 60%. CK-MB isoforms improve

sensitivity at 4 hours to 80%, approaching 93% at 6 hours. The

current universal definition of MI places CK and CK-MB in a

secondary role to troponins.^23

Troponins (I and T), when elevated, identify patients with

ACS who have the highest risk for an adverse outcome.23,

Sensitivity for acute MI at 4 hours is 60%, rising to nearly 100%

by 12 hours.25,26^ Elevated troponin in the correct clinical setting

is synonymous with acute MI and is embedded in the univer-

sal definition of MI.

■ DIAGNOSTIC TABLE

After the patient is stabilized and assessment has been com-

pleted, the findings are matched to the classic and atypical

patterns of the seven potentially critical diseases causing chest

pain. This matching process is continual while evaluating the

patient and monitoring the response to therapy. Any inconsis-

tency in findings with the primary working diagnoses requires

a rapid review of the pivotal findings and the potential diag-

noses (Table 18-6).

■ MANAGEMENT AND DISPOSITION

The management of ACS is discussed in Chapter 76. Figure

18-3 outlines the approach to treatment of critical noncardiac

diagnoses. Patients with critical diagnoses generally are

admitted to the intensive care unit. Patients with emergent

diagnoses typically are admitted to the hospital, most often

on telemetry units. Patients with nonemergent diagnoses

are most frequently treated as outpatients. Hospitalization is

required in certain circumstances, particularly when patients

have other comorbid conditions.

Frequently, no definitive diagnosis is established. Any

patient with almost any type of chest pain may be having coro-

nary ischemia, PE, or aortic dissection. When a clear pattern

does not emerge to allow the emergency physician to make an

alternative diagnosis confidently, continued evaluation, hospi-

talization, or observation admission may be the best course.

Figure 18-3. Clinical guidelines for emergency department management of chest pain from potentially catastrophic nonmyocardial origins.

ECG, electrocardiogram; IV, intravenous; NSAIDs, nonsteroidal anti-inflammatory drugs; SQ, subcutaneous; LMWH, low-molecular-weight heparin; U/S, ultrasound. Complete initial evaluation

  • Cardiac monitor
  • Intravenous access
  • Oxygen therapy Tension pneumothorax Esophageal rupture Pulmonary Pericarditis embolism Aortic dissection
  • IV heparin or SQ LMWH
  • Thrombolysis if severe cardiovascular instability
  • U/S for effusion/tamponade risk
  • NSAIDs
  • Corticosteroids
  • Cardiology consultation
  • IV fluid resuscitation
  • Analgesia
  • IV antibiotics
  • Early surgical consultation
  • Needle decompression
  • Tube thoracostomy Differential diagnosis based on history, physical, and ECG Specific tests per Table 18-
  • Beta-blockade
  • IV antihypertensive therapy
  • Decrease contractility
  • Immediate surgical consult/transfer

The references for this chapter can be found online by accessing the

accompanying Expert Consult website.