CH 11: CHEST DISCOMFORT

Chest discomfort
! among the most common reasons for which patients present for medical attention at either an
emergency department (ED) or an outpatient clinic
! evaluation of nontraumatic chest discomfort
○ inherently challenging owing to the broad variety of possible causes, a minority of which
are life-threatening conditions that should not be missed
! It is helpful to frame the initial diagnostic assessment and triage of patients with acute chest
discomfort around three categories:
○ myocardial ischemia
○ other cardiopulmonary causes
■ pericardial disease, aortic emergencies, and pulmonary conditions
○ non-cardiopulmonary causes
! Although rapid identification of high-risk conditions is a priority of the initial assessment, strategies
that incorporate routine liberal use of testing carry the potential for adverse effects of unnecessary
investigations.

Epidemiology and Natural History

Chest discomfort
! third most common reason for visits to the ED in the United States, resulting in 6 to 7 million
emergency visits each year.
! More than 60% of patients with this presentation are hospitalized for further testing, and the
remainder undergo additional investigation in the ED.
! As few as 15% of evaluated patients are eventually diagnosed with acute coronary syndrome
(ACS), with rates of 10–20% in most series of unselected populations, and a rate as low as 5% in e
some studies. e
! The most common diagnoses are gastrointestinal causes and fewer than 10% are other life-
threatening cardiopul- monary conditions. p
! In a large proportion of patients with transient acute chest discomfort, ACS or another acute
cardiopulmonary cause is excluded but the cause is not determined. g
! Therefore, the resources and time devoted to the evaluation of chest discomfort in the absence of a
severe cause are substantial.
! Nevertheless, a disconcerting 2% to 6% of patients with chest discomfort of presumed non-ischemic
etiology who are discharged from the ED are later deemed to have had a missed myocardial
infarction (MI).
○ Patients with a missed diagnosis of MI have a 30-day risk of death that is double that of
their counterparts who are hospitalized.
! In a study of >350,000 patients with unspecified presumed non-cardiopulmonary chest discomfort,
the mortality rate 1 year after discharge was <2% and did not differ significantly from age-adjusted
mortality in the general population.
! The estimated rate of major cardiovascular events through 30 days in patients with acute chest pain
who had been stratified as low risk was 2.5% in a large population-based study that excluded
patients with ST-segment elevation or definite noncardiac chest pain. Causes of Chest Discomfort
MYOCARDIAL ISCHEMIA/INJURY
! Angina pectoris
○ Term used chest discomfort caused by MI
! clinical concern in patients presenting with chest symptoms
! Myocardial ischemia
○ precipitated by an imbalance between myocardial oxygen requirements and myocardial
oxygen supply, resulting in insufficient delivery of oxygen to meet the heart’s metabolic
demands
! Myocardial oxygen consumption may be elevated by increases in heart rate, ventricular wall stress,
and myocardial contractilit
! Myocardial oxygen supply is determined by coronary blood flow and coronary arterial oxygen
content.
! When myocardial ischemia is sufficiently severe and prolonged in duration (as little as 20 min),
irreversible cellular injury occurs, resulting in MI.
! Ischemic heart disease
○ most commonly caused by atheromatous plaque that obstructs one or more of the
epicardial coronary arteries
! Stable ischemic heart disease
○ usually results from the gradual atherosclerotic narrowing of the coronary arteries
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 ! Stable angina
○ characterized by ischemic episodes that are typically precipitated by a superimposed
increase in oxygen demand during physical exertion and relieved upon resting
! Ischemic heart disease becomes unstable most commonly when rupture or erosion of one or more
atherosclerotic lesions triggers coronary thrombosis.
! Unstable ischemic heart disease
○ classified clinically by the presence or absence of detectable myocardial injury and the
presence or absence of ST-segment elevation on the patient’s electrocardiogram (ECG)
! When acute coronary atherothrombosis occurs, the intracoronary thrombus may be partially
obstructive, generally leading to myocardial ischemia in the absence of ST-segment elevation.
! Unstable angina
○ Unstable heart disease marked by ischemic symptoms at rest, with minimal activity, or
in an accelerating pattern when there is no detectable myocardial injury
! non–ST elevation MI (NSTEMI)
○ Unstable heart disease marked by ischemic symptoms at rest, with minimal activity, or
in an accelerating pattern when there is evidence of myocardial necrosis
! transmural myocardial ischemia
○ Ensues when the coronary thrombus is acutely and completely occlusive
○ ST-segment elevation on the ECG and myocardial necrosis leads to a diagnosis of ST
elevation MI
! Clinicians should be aware that unstable ischemic symptoms may also occur predominantly because
of increased myocardial oxygen demand (e.g., during intense psychological stress or fever) or
because of decreased oxygen delivery due to anemia, hypoxia, or hypotension
! Acute coronary syndrome
○ encompasses unstable angina, NSTEMI, and STEMI
○ reserved for ischemia precipitated by acute coronary atherothrombosis
! In order to guide therapeutic strategies, a standardized system for classification of MI has been
expanded to discriminate MI resulting from acute coronary thrombosis (type 1) from MI occurring
secondary to other imbalances of myocardial oxygen supply and demand (type 2)
! Other contributors to stable and unstable ischemic heart disease may exist alone or in combination
with coronary atherosclerosis and may be the dominant cause of myocardial ischemia in some
patients
○ endothelial dysfunction
○ microvascular disease
○ vasospasm
! Non-atherosclerotic processes, including congenital abnormalities of the coronary vessels,
myocardial bridging, coronary arteritis, and radiation-induced coronary disease, can lead to coronary
obstruction.
! In addition, conditions associated with extreme myocardial oxygen demand and impaired
endocardial blood flow, such as aortic valve disease, hypertrophic cardiomyopathy, or idiopathic
dilated cardiomyopathy, can precipitate myocardial ischemia in patients with or without underlying
obstructive atherosclerosis.
Characteristics of Ischemic Chest Discomfort
! Chest discomfort characteristic of myocardial ischemia is typically described as aching, heavy,
squeezing, crushing, or constricting.
! The site of the discomfort is usually retrosternal
! Radiation is common and generally occurs down the ulnar surface of the left arm
○ the right arm, both arms, neck, jaw, or shoulders may also be involved
! Stable angina
○ usually begins gradually and reaches its maximal intensity over a period of minutes
before dissipating within several minutes with rest or with nitroglycerin
○ The discomfort typically occurs predictably at a characteristic level of exertion or
psychological stress
! Unstable angina
○ manifest by anginal chest discomfort that occurs with progressively lower intensity of
physical activity or even at rest
! Chest discomfort associated with MI
○ typically more severe, is prolonged (usually lasting ≥30 min), and is not relieved by rest
Mechanisms of Cardiac Pain
! The neural pathways involved in ischemic cardiac pain are poorly understood.
! Ischemic episodes
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○ thought to excite local chemosensitive and mechanoreceptive receptors
■ Stimulate release of adenosine, bradykinin, and other substances that
activate the sensory ends of sympathetic and vagal afferent fibers
○ Afferent fibers traverse the nerves that connect to the upper five thoracic sympathetic
ganglia and upper five distal thoracic roots of the spinal cord
○ From there, impulses are transmitted to the thalamus
○ Within the spinal cord, cardiac sympathetic afferent impulses may converge with
impulses from somatic thoracic structures, and this convergence may be the basis
for referred cardiac pain
! In addition, cardiac vagal afferent fibers synapse in the nucleus tractus solitarius of the medulla
and then descend to the upper cervical spinothalamic tract, and this route may contribute to
anginal pain experienced in the neck and jaw
OTHER CARDIOPULMONARY CAUSES
Pericardial and Other Myocardial Diseases
! Inflammation of the pericardium due to infectious or noninfectious causes can be responsible for
acute or chronic chest discomfort.
! The visceral surface and most of the parietal surface of the pericardium are insensitive to pain.
! Therefore, the pain of pericarditis is thought to arise principally from associated pleural
inflammation.
! Because of this pleural association, the discomfort of pericarditis is usually pleuritic pain that is
exacerbated by breathing, coughing, or changes in position.
! Moreover, owing to the overlapping sensory supply of the central diaphragm via the phrenic nerve
with somatic sensory fibers originating in the third to fifth cervical segments, the pain of pleural
pericarditis is often referred to the shoulder and neck. Involvement of the pleural surface of the lateral
diaphragm can lead to pain in the upper abdomen.
! Acute inflammatory and other non-ischemic myocardial diseases can also produce chest discomfort.
! Takotsubo (stress- related) cardiomyopathy
○ often start abruptly with chest pain and shortness of breath
○ This form of cardiomyopathy, in its most recognizable form, is triggered by an emotionally
or physically stressful event
○ May mimic acute MI because of its commonly associated ECG abnormalities, including
ST-segment elevation, and elevated biomarkers of myocardial injury
○ Observational studies support a predilection for women >50 years of age
! The symptoms of acute myocarditis are highly varied.
○ Chest discomfort may either originate with inflammatory injury of the myocardium or be
due to severe increases in wall stress related to poor ventricular performance
Diseases of the Aorta
! Acute aortic dissection
○ less common cause of chest discomfort
○ important because of the catastrophic natural history of certain subsets of cases when
recognized late or left untreated
! Acute aortic syndromes
○ encompass a spectrum of acute aortic diseases related to disruption of the media of the
aortic wall
○ Aortic dissection
■ involves a tear in the aortic intima, resulting in separation of the media and
creation of a separate “false” lumen
○ Penetrating ulcer
■ ulceration of an aortic atheromatous plaque that extends through the intima
and into the aortic media, with the potential to initiate an intramedial
dissection or rupture into the adventitia.
○ Intramural hematoma
■ aortic wall hematoma with no demonstrable intimal flap, no radiologically
apparent intimal tear, and no false lumen
■ can occur due to either rupture of the vasa vasorum or, less commonly, a
penetrating ulcer
! Each of these subtypes of acute aortic syndrome typically presents with chest discomfort that is
often severe, sudden in onset, and sometimes described as “tearing” in quality.
! Acute aortic syndromes involving the ascending aorta
○ tend to cause pain in the midline of the anterior chest
! Descending aortic syndromes
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 ○ most often present with pain in the back Gastrointestinal Conditions
! Dissections that begin in the ascending aorta and extend to the descending aorta tend to cause pain ! Gastrointestinal disorders
in the front of the chest that extends toward the back, between the shoulder blades ○ most common cause of nontraumatic chest discomfort and often produce symptoms that
! Proximal aortic dissections that involve the ascending aorta (type A in the Stanford nomenclature) are difficult to discern from more serious causes of chest pain, including myocardial
○ at high risk for major complications that may influence the clinical presentation, including: ischemia
■ compromise of the aortic ostia of the coronary arteries, resulting in MI ! Esophageal disorders
■ disruption of the aortic valve, causing acute aortic insufficiency ○ in particular, may simulate angina in the character and location of the pain
■ rupture of the hematoma into the pericardial space, leading to pericardial ○ Gastroesophageal reflux and disorders of esophageal motility are common and should
tamponade be considered in the differential diagnosis of chest pain
! Nontraumatic aortic dissections ○ Acid reflux often causes a burning discomfort.
○ very rare in the absence of hypertension or conditions associated with deterioration of ○ Esophageal spasm
the elastic or muscular components of the aortic media, including pregnancy, bicuspid ■ commonly an intense, squeezing discomfort that is retrosternal in location
aortic disease, or inherited connective tissue diseases, such as Marfan and Ehlers- and, like angina, may be relieved by nitroglycerin or dihydropyridine calcium
Danlos syndromes channel antagonists
! Although aortic aneurysms are most often asymptomatic, thoracic aortic aneurysms can cause ○ Chest pain can also result from injury to the esophagus, such as a Mallory-Weiss tear or
chest pain and other symptoms by compressing adjacent structures even an esophageal rupture (Boerhaave syndrome) caused by severe vomiting
○ This pain tends to be steady, deep, and occasionally severe ! Peptic ulcer disease is most commonly epigastric in location but can radiate into the chest
! Aortitis ! Hepatobiliary disorders
○ whether of noninfectious or infectious etiology, in the absence of aortic dissection is a ○ includes cholecystitis and biliary colic
rare cause of chest or back discomfort ○ may mimic acute cardiopulmonary diseases
○ Usually localizes to the right upper quadrant of the abdomen
Pulmonary Conditions ○ Variable and may be felt in the epigastrium and radiate to the back and lower chest
Pulmonary Embolism ○ Discomfort is sometimes referred to the scapula or may in rare cases be felt in the
! can produce dyspnea and chest discomfort that is sudden in onset shoulder, suggesting diaphragmatic irritation
! Typically pleuritic in pattern, the chest discomfort associated with pulmonary embolism may result ○ Pain is steady, usually lasts several hours, and subsides spontaneously, without
from: symptoms between attacks
○ involvement of the pleural surface of the lung adjacent to a resultant pulmonary infarction ○ Pain resulting from pancreatitis is typically aching epigastric pain that radiates to the
○ distention of the pulmonary artery back
○ possibly, right ventricular wall stress and/or subendocardial ischemia related to acute
pulmonary hypertension Musculoskeletal and Other Causes
! The pain associated with small pulmonary emboli is often lateral and pleuritic and is believed to be ! Chest discomfort can be produced by any musculoskeletal disorder involving the chest wall or the
related to the first of these three possible mechanisms nerves of the chest wall, neck, or upper limbs.
! Massive pulmonary emboli ! Costochondritis causing tenderness of the costochondral junctions (Tietze’s syndrome) is relatively
○ may cause severe substernal pain that may mimic an MI and that is plausibly attributed common.
to the second and third of these potential mecha- nisms ! Cervical radiculitis
○ may also be associated with syncope, hypotension, and signs of right heart failure ○ may manifest as a prolonged or constant aching discomfort in the upper chest and limbs
Pneumothorax ○ pain may be exacerbated by motion of the neck
! Primary spontaneous pneumothorax ! Occasionally, chest pain can be caused by compression of the brachial plexus by the cervical ribs,
○ rare cause of chest discomfort, with an estimated annual incidence in the United States and tendinitis or bursitis involving the left shoulder may mimic the radiation of angina.
of 7 per 100,000 among men and <2 per 100,000 among women ! Pain in a dermatomal distribution can also be caused by cramping of intercostal muscles or by
○ Risk factors include male sex, smoking, family history, and Marfan syndrome herpes zoster
○ The symptoms are usually sudden in onset, and dyspnea may be mild; thus,
presentation to medical attention is sometimes delayed. Emotional and Psychiatric Conditions
! Secondary spontaneous pneumothorax ! As many as 10% of patients who present to EDs with acute chest discomfort have a panic disorder
○ may occur in patients with underlying lung disorders, such as chronic obstructive or related condition
pulmonary disease, asthma, or cystic fibrosis, and usually produces symptoms that are ! The symptoms may include chest tightness or aching that is associated with a sense of anxiety and
more severe difficulty in breathing
! Tension pneumothorax ! The symptoms may be prolonged or fleeting
○ medical emergency caused by trapped intrathoracic air that precipitates hemodynamic
collapse APPROACH TO THE PATIENT
! priorities of the initial clinical encounter include assessment of:
Other Pulmonary Parenchymal, Pleural, or Vascular Disease ○ the patient’s clinical stability
! Most pulmonary diseases that produce chest pain, including pneumonia and malignancy, do so ○ the probability that the patient has an underlying cause of the discomfort that may be
because of involvement of the pleura or surrounding structures. life-threatening
! Pleurisy ! The high-risk conditions of principal concern are acute cardiopulmonary processes, including:
○ typically described as a knifelike pain that is worsened by inspiration or coughing ○ ACS
! Chronic pulmonary hypertension ○ acute aortic syndrome
○ can manifest as chest pain that may be very similar to angina in its characteristics, ○ pulmonary embolism
suggesting right ventricular myocardial ischemia in some cases ○ tension pneumothorax
! Reactive airways diseases ○ pericarditis with tamponade
○ similarly can cause chest tightness associated with breathlessness rather than pleurisy ! Among non-cardiopulmonary causes of chest pain, esophageal rupture likely holds the greatest
urgency for diagnosis.
NON-CARDIOPULMONARY CAUSES ! Patients with these conditions may deteriorate rapidly despite initially appearing well.
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 ! The remaining population with non-cardiopulmonary conditions has a more favorable prognosis ○ condition in which some patients experience relief from angina as they continue at the
during completion of the diagnostic work-up. same or even a greater level of exertion
! A rapid targeted assessment for a serious cardiopulmonary cause is of particular relevance for ! Musculoskeletal etiology
patients with acute ongoing pain who have presented for emergency evaluation. ○ Alterations in the intensity of pain with changes in position or movement of the upper
extremities and neck
History ! The pain of pericarditis
Quality of Pain ○ often is worse in the supine position
! The quality of chest discomfort alone is never sufficient to establish a diagnosis. ○ relieved by sitting upright and leaning forward
! Pressure or tightness ! Gastroesophageal reflux
○ consistent with a typical presentation of myocardial ischemic pain ○ may be exacerbated by alcohol, some foods, or by a reclined position
! It is unusual for angina to be sharp, as in knifelike, stabbing, or pleuritic; however, patients ○ Relief can occur with sitting
sometimes use the word “sharp” to convey the intensity of discomfort rather than the quality ! Exacerbation by eating
! Pleuritic discomfort ○ suggests a gastrointestinal etiology such as peptic ulcer disease, cholecystitis, or
○ suggestive of a process involving the pleura, including pericarditis, pulmonary embolism, pancreatitis
or pulmonary parenchymal processes. ! Peptic ulcer disease
○ Less frequently, the pain of pericarditis or massive pulmonary embolism is a steady ○ tends to become symptomatic 60–90 min after meals
severe pressure or aching that can be difficult to discriminate from myocardial ischemia. ○ However, in the setting of severe coronary atherosclerosis, redistribution of blood flow
! “Tearing” or “ripping” pain to the splanchnic vasculature after eating can trigger postprandial angina.
○ often described by patients with acute aortic dissection ○ The discomfort of acid reflux and peptic ulcer disease is usually diminished promptly by
! Acute aortic emergencies acid-reducing therapies.
○ also present commonly with severe, knifelike pain ○ In contrast with its impact in some patients with angina, physical exertion is very unlikely
! A burning quality to alter symptoms from gastrointestinal causes of chest pain.
○ can suggest acid reflux or peptic ulcer disease ○ Relief of chest discomfort within minutes after administration of nitroglycerin is
○ may also occur with myocardial ischemia suggestive of but not sufficiently sensitive or specific for a definitive diagnosis of
! Esophageal pain, particularly with spasm, can be a severe squeezing discomfort identical to angina. myocardial ischemia.
! Esophageal spasm
Location of Discomfort ○ may also be relieved promptly with nitroglycerin.
! A substernal location with radiation to the neck, jaw, shoulder, or arms ○ A delay of >10 min before relief is obtained after nitroglycerin suggests that the
○ typical of myocardial ischemic discomfort. symptoms either are not caused by ischemia or are caused by severe ischemia, such as
! Radiation to both arms has a particularly high association with MI as the etiology during acute MI.
! Some patients present with aching in sites of radiated pain as their only symptoms of ischemia.
! Pain that is highly localized—for example, that which can be demarcated by the tip of one finger— Associated Symptoms
is highly unusual for angina. ! Symptoms that accompany myocardial ischemia
! Retrosternal location ○ may include diaphoresis, dyspnea, nausea, fatigue, faintness and eructations
○ should prompt consideration of esophageal pain ○ may exist in isolation as anginal equivalents (i.e., symptoms of myocardial ischemia
! Other gastrointestinal conditions usually present with pain that is most intense in the abdomen or other than typical angina), particularly in women and the elderly.
epigastrium, with possible radiation into the chest. ! Dyspnea
! Angina may also occur in an epigastric location. ○ may occur with multiple conditions considered in the differential diagnosis of chest pain
! However, pain that occurs solely above the mandible or below the epigastrium is rarely angina and thus is not discriminative, but the presence of dyspnea is important because it
! Severe pain radiating to the back, particularly between the shoulder blades suggests a cardiopulmonary etiology.
○ should prompt consideration of an acute aortic syndrome ! Sudden onset of significant respiratory distress
! Radiation to the trapezius ridge ○ should lead to consideration of pulmonary embolism and spontaneous pneumothorax.
○ characteristic of pericardial pain and does not usually occur with angina ! Hemoptysis
○ may occur with pulmonary embolism, or as blood-tinged frothy sputum in severe heart
Pattern failure
! Myocardial ischemic discomfort ○ usually points toward a pulmonary parenchymal etiology of chest symptoms
○ usually builds over minutes ! Presentation with syncope or pre-syncope
○ exacerbated by activity and mitigated by rest ○ should prompt consideration of hemodynamically significant pulmonary embolism or
! Aortic dissection, pulmonary embolism, or spontaneous pneumothorax aortic dissection as well as ischemic arrhythmias.
○ pain that reaches its peak intensity immediately ! Although nausea and vomiting suggest a gastrointestinal disorder, these symptoms may occur in
! Pain that is fleeting (lasting only a few seconds) the setting of MI (more commonly inferior MI), presumably because of activation of the vagal reflex
○ rarely ischemic in origin or stimulation of left ventricular receptors as part of the Bezold-Jarisch reflex.
! Pain that is constant in intensity for a prolonged period (many hours to days)
○ unlikely to represent myocardial ischemia if it occurs in the absence of other clinical con- Past Medical History
sequences, such as abnormalities of the ECG, elevation of cardiac biomarkers, or clinical ! useful in assessing the patient for risk factors for coronary atherosclerosis and venous
sequelae (e.g., heart failure or hypotension). thromboembolism as well as for conditions that may predispose the patient to specific disorders
! Both myocardial ischemia and acid reflux may have their onset in the morning. ! a history of connective tissue diseases such as Marfan syndrome should heighten the clinician’s
suspicion of an acute aortic syndrome or spontaneous pneumothorax.
Provoking and Alleviating Factors ! A careful history may elicit clues about depression or prior panic attacks.
! Patients with myocardial ischemic pain
○ usually prefer to rest, sit, or stop walking
! “warm-up angina”

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Physical Examination
General
! Patients with acute MI or other acute cardiopulmonary disorders often appear anxious,
uncomfortable, pale, cyanotic, or diaphoretic.
! Patients who are massaging or clutching their chests may describe their pain with a clenched fist
held against the sternum (Levine’s sign).
! Occasionally, body habitus is helpful—for example, in patients with Marfan syndrome or the
prototypical young, tall, thin man with spontaneous pneumothorax.
Vital Signs
! Significant tachycardia and hypotension
○ indicative of important hemodynamic consequences of the underlying cause of chest
discomfort and should prompt a rapid survey for the most severe conditions, such as
acute MI with cardiogenic shock, massive pulmonary embolism, pericarditis with
tamponade, or tension pneumothorax.
! Acute aortic emergencies
○ usually present with severe hypertension but may be associated with profound
hypotension when there is coronary arterial compromise or dissection into the
pericardium.
! Sinus tachycardia
○ important manifestation of submassive pulmonary embolism
! Tachypnea and hypoxemia point toward a pulmonary cause
! The presence of low-grade fever is non- specific because it may occur with MI and with
thromboembolism in addition to infection
Pulmonary
! Examination of the lungs
○ may localize a primary pulmonary cause of chest discomfort, as in cases of pneumonia,
asthma, or pneumothorax.
! Left ventricular dysfunction from severe ischemia/infarction as well as acute valvular complications
of MI or aortic dissection can lead to pulmonary edema, which is an indicator of high risk
Cardiac
! Often normal in patients with acute myocardial ischemia but may reveal characteristic patterns with
pericardial tamponade or acute right ventricular dysfunction
! Cardiac auscultation
○ may reveal a third or, more commonly, a fourth heart sound, reflecting myocardial
systolic or diastolic dysfunction
! Murmurs of mitral regurgitation or a ventricular-septal defect
○ may indicate mechanical complications of STEMI.
! A murmur of aortic insufficiency may be a complication of proximal aortic dissection. Other murmurs
may reveal underlying cardiac disorders contributory to ischemia (e.g., aortic stenosis or
hypertrophic cardiomyopathy).
! Pericardial friction rubs reflect pericardial inflammation.
Abdominal
! Localizing tenderness on the abdominal examination
○ useful in identifying a gastrointestinal cause of the presenting syndrome
! Abdominal findings
○ infrequent with purely acute cardiopulmonary problems, except in the case of underlying
chronic cardiopulmonary disease or severe right ventricular dysfunction leading to
hepatic congestion.
! Vascular pulse deficits
○ may reflect underlying chronic atherosclerosis, which increases the likelihood of
coronary artery disease
! Evidence of acute limb ischemia with loss of the pulse and pallor, particularly in the upper extremities,
can indicate catastrophic consequences of aortic dissection
! Unilateral lower-extremity swelling should raise suspicion about venous thromboembolism.
Musculoskeletal
! Pain arising from the costochondral and chondrosternal articulations
○ may be associated with localized swelling, redness, or marked localized tenderness
! Pain on palpation of these joints is usually well localized and is a useful clinical sign, though deep
palpation may elicit pain in the absence of costochondritis.
! Although palpation of the chest wall often elicits pain in patients with various musculoskeletal
conditions, it should be appreciated that chest wall tenderness does not exclude myocardial
ischemia
! Sensory deficits in the upper extremities may be indicative of cervical disk disease.
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ELECTROCARDIOGRAPHY
! Crucial in the evaluation of nontraumatic chest discomfort
! Pivotal for identifying patients with ongoing ischemia as the principal reason for their presentation
as well as secondary cardiac complications of other disorders.
! Professional society guidelines recommend that an ECG be obtained within 10 min of
presentation, with the primary goal of identifying patients with ST-segment elevation diagnostic of
MI who are candidates for immediate interventions to restore flow in the occluded coronary artery
! ST-segment depression and symmetric T-wave inversions at least 0.2 mV in depth
○ Useful for detecting myocardial ischemia in the absence of STEMI and are also indicative
of higher risk of death or recurrent ischemia.
! Serial performance of ECGs (every 30–60 min)
○ recommended in the ED evaluation of suspected ACS
! In addition, an ECG with right-sided lead placement should be considered in patients with clinically
suspected ischemia and a nondiagnostic standard 12-lead ECG
! Despite the value of the resting ECG, its sensitivity for ischemia is poor—as low as 20% in some
studies.
! Abnormalities of the ST segment and T wave may occur in a variety of conditions, including:
○ pulmonary embolism
○ ventricular hypertrophy
○ acute and chronic pericarditis
○ myocarditis
○ electrolyte imbalance
○ metabolic disorders
! Notably, hyperventilation associated with panic disorder can also lead to nonspecific ST and T-wave
abnormalities
! Pulmonary embolism
○ most often associated with sinus tachycardia
○ can also lead to rightward shift of the ECG axis, manifesting as an S-wave in lead I, with
a Q-wave and T-wave in lead III
! In patients with ST-segment elevation, the presence of diffuse lead involvement not corresponding
to a specific coronary anatomic distribution and PR-segment depression can aid in distinguishing
pericarditis from acute MI.
CHEST RADIOGRAPHY
! Plain radiography of the chest
○ performed routinely when patients present with acute chest discomfort and selectively
when individuals who are being evaluated as outpatients have subacute or chronic pain
! Chest radiograph
○ most useful for identifying pulmonary processes, such as pneumonia or pneumothorax.
○ Findings are often unremarkable in patients with ACS, but pulmonary edema may be
evident
○ Other specific findings include widening of the mediastinum in some patients with aortic
dissection, Hampton’s hump or Westermark’s sign in patients with pulmonary embolism
or pericardial calcification in chronic pericarditis.
CARDIAC BIOMARKERS
! Laboratory testing in patients with acute chest pain is focused on the detection of myocardial injury.
! Such injury can be detected by the presence of circulating proteins released from damaged
myocardial cells.
! Owing to the time necessary for this release, initial biomarkers of injury may be in the normal range,
even in patients with STEMI.
! cardiac troponin
○ preferred biomarker for the diagnosis of MI and should be measured in all patients with
suspected ACS at presentation and repeated in 3–6 h
○ Testing after 6 h is required only when there is uncertainty regarding the onset of pain
or when stuttering symptoms have occurred.
○ It is not necessary or advisable to measure troponin in patients without suspicion of ACS
unless this test is being used specifically for risk stratification (e.g., in pulmonary
embolism or heart failure).
! Rapid rule-out protocols that use serial testing and changes in troponin concentration over as short
a period as 1–2 h appear promising and have been adopted in some centers where high-sensitivity
assays for troponin are used routinely.
5
 ! In patients presenting >2 h after symptom onset, a concentration of cardiac troponin below the limit
of detection using a high-sensitivity assay may be sufficient to exclude MI with a negative predictive
value >99% at the time of hospital presentation.
! However, with these advantages has come a trade-off: myocardial injury is detected in a larger
proportion of patients who have non-ACS cardiopulmonary conditions than with previous, less
sensitive assays.
! This evolution in testing for myocardial necrosis has rendered other aspects of the clinical evaluation
critical to the practitioner’s determination of the probability that the symptoms represent ACS.
! In addition, observation of a change in cardiac troponin concentration between serial samples is
useful in discriminating acute causes of myocardial injury from chronic elevation due to underlying
structural heart disease, end-stage renal disease, or interfering antibodies.
! The diagnosis of MI is reserved for acute myocardial injury that is marked by a rising and/or falling
pattern—with at least one value exceeding the 99th percentile reference limit—and that is caused
by ischemia.
! Other non-ischemic insults, such as myocarditis, may result in myocardial injury but should not be
labeled MI.
! D-dimer test
○ to aid in exclusion of pulmonary embolism
! B-type natriuretic peptide
○ useful when considered in conjunction with the clinical history and examination for the
diagnosis of heart failure
○ provide prognostic information among patients with ACS and those with pulmonary
embolism
INTEGRATIVE DECISION AIDS
! Multiple clinical algorithms have been developed to aid in decision- making during the evaluation
and disposition of patients with acute nontraumatic chest pain.
! Such decision-aids estimate either of two closely related but not identical probabilities:
○ the probability of a final diagnosis of ACS
○ the probability of major cardiac events during short-term follow-up
! Such decision-aids are used most commonly to identify patients with a low clinical probability of ACS
who are candidates either for early provocative testing for ischemia or for discharge from the ED.
! Goldman and Lee developed one of the first such decision-aids
○ using only the ECG and risk indicators— hypotension, pulmonary rales, and known
ische- mic heart disease—to categorize patients into four risk categories ranging from a
<1% to a >16% probability of a major cardiovascular complication
! Acute Cardiac Ischemia Time-Insensitive Predic- tive Instrument (ACI-TIPI)
○ combines age, sex, chest pain presence, and ST-segment abnormalities to define a
probability of ACS.
! More recently developed decision-aids are shown in Fig. 11-3.
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! Elements common to each of these tools are:
○ symptoms typical for ACS
○ older age
○ risk factors for or known atherosclerosis
○ (4) ischemic ECG abnormalities
○ (5) elevated cardiac troponin levels.
! Although, because of very low specificity, the overall diagnostic performance of such decision-aids
is poor (area under the receiver operating curve, 0.55–0.65), they can help identify patients with a
very low probability of ACS (e.g., <1%).
! Nevertheless, no such decision-aid (or single clinical factor) is sufficiently sensitive and well validated
to use as a sole tool for clinical decision-making.
! Clinicians should differentiate between the algorithms discussed above and risk scores derived for
stratification of prognosis in patients who already have an established diagnosis of ACS.
! The latter risk scores were not designed to be used for diagnostic assessment.
PROVOCATIVE TESTING FOR ISCHEMIA
! Exercise electrocardiography (“stress testing”)
○ commonly employed for completion of risk stratification of patients who have undergone
an initial evaluation that has not revealed a specific cause of chest discomfort and has
identified them as being at low or selectively inter- mediate risk of ACS.
! Early exercise testing
○ safe in patients without high-risk findings after 8–12 h of observation and can assist in
refin- ing their prognostic assessment.
! Patients who are unable to exercise may undergo pharmacological stress testing with either nuclear
perfusion imaging or echocardiography. Notably, some experts have deemed the routine use of
stress testing for low-risk patients unsupported by direct clinical evidence and a potentially
unnecessary source of cost.
! Professional society guidelines identify ongoing chest pain as a contraindication to stress testing.
! In selected patients with persistent pain and nondiagnostic ECG and biomarker data, resting
myocardial perfusion images can be obtained
○ the absence of any perfusion abnormality substantially reduces the likelihood of coronary
artery disease
! In some centers, early myocardial perfusion imaging is performed as part of a routine strategy for
evaluating patients at low or intermediate risk of ACS in parallel with other testing.
! Management of patients with normal perfusion images can be expedited with earlier discharge and
outpatient stress testing, if indicated. Those with abnormal rest perfusion imaging, which cannot
discriminate between old or new myocardial defects, usually warrant additional in-hospital
evaluation.
OTHER NONINVASIVE STUDIES
Echocardiography
! Not necessarily routine in patients with chest discomfort
! However, in patients with an uncertain diagnosis, particularly those with nondiagnostic ST elevation,
ongoing symptoms, or hemodynamic instability, detection of abnormal regional wall motion provides
evidence of possible ischemic dysfunction.
! Diagnostic in patients with mechanical complications of MI or in patients with pericardial tamponade.
! Transthoracic echocardiography is poorly sensitive for aortic dissection, although an intimal flap may
sometimes be detected in the ascending aorta.
CT Angiography
! Emerging as a modality for the evaluation of patients with acute chest discomfort
! Coronary CT angiography
○ sensitive technique for detection of obstructive coronary disease, particularly in the
proximal third of the major epicardial coronary arteries
○ appears to enhance the speed to disposition of patients with a low-intermediate
probability for ACS
○ its major strength being the negative predictive value of a finding of no significant
disease.
! In addition, contrast-enhanced CT can detect focal areas of myocardial injury in the acute setting.
! At the same time, CT angiography can exclude aortic dissection, pericardial effusion, and pulmonary
embolism.
! Balancing factors in the consideration of the emerging role of coronary CT angiography in low-risk
patients are radiation exposure and additional testing prompted by nondiagnostic abnormal results.
6
MRI
! evolving, versatile technique for structural and functional evaluation of the heart and the vasculature
of the chest
! can be performed as a modality for pharmacologic stress perfusion imaging
! Gadolinium-enhanced CMR
○ can provide early detection of MI, defining areas of myocardial necrosis accurately, and
can delineate patterns of myocardial disease that are often useful in discriminating
ischemic from non-ischemic myocardial injury
! Usually not practical for the urgent evaluation of acute chest discomfort
! Can be a useful modality for cardiac structural evaluation of patients with elevated cardiac troponin
levels in the absence of definite coronary artery disease
! Also permits highly accurate assessment for aortic dissection but is infrequently used as the first test
because CT and transesophageal echocardiography are usually more practical.

CRITICAL PATHWAYS FOR ACUTE CHEST DISCOMFORT

! Used to expedite the assessment and management of patients with nontraumatic chest pain, often
in dedicated chest pain units
! Such pathways are generally aimed at:
○ rapid identification, triage, and treatment of high-risk cardiopulmonary conditions (e.g.,
STEMI)
○ accurate identification of low-risk patients who can be safely observed in units with less
intensive monitoring, undergo early exercise testing, or be discharged home
○ through more efficient and systematic accelerated diagnostic protocols, safe reduction
in costs associated with overuse of testing and unnecessary hospitalizations

OUTPATIENT EVALUATION OF CHEST DISCOMFORT

! Chest pain is common in outpatient practice, with a lifetime prevalence of 20–40% in the general
population.
! More than 25% of patients with MI have had a related visit with a primary care physician in the
previous month.
! The diagnostic principles are the same as in the ED.
! However, the pretest probability of an acute cardiopulmonary cause is significantly lower.
! Therefore, testing paradigms are less intense, with an emphasis on the history, physical
examination, and ECG.
! Moreover, decision-aids developed for settings with a high prevalence of significant cardiopulmonary
disease have lower positive predictive value when applied in the practitioner’s office.
! However, in general, if the level of clinical suspicion of ACS is sufficiently high to consider troponin
testing, the patient should be referred to the ED for evaluation

PEACH 2021 7