Keywords

Introduction

  • The differential diagnosis of chest pain (CP) is broad, with etiologies ranging from life-threatening to those with low morbidity and mortality.

  • CP is one of the most common complaints in the outpatient setting with a prevalence ranging from 20% to 40% depending on criteria, location, and practice [1].

  • The primary care physician (PCP) is often the main point of entry to the healthcare system.

  • Cardiovascular disease, the most life-threatening etiology, must be ruled out in the initial evaluation.

  • Musculoskeletal or “chest wall syndrome” is the most common cause in the primary care setting [2], accounting for 20.4–50% of cases [1,2,3], followed by gastroesophageal reflux disease (GERD).

  • The prevalence of CP due to coronary artery disease (CAD) ranges from 1.5% to 15% [3, 4].

  • A detailed history and physical (H&P) of the patient’s CP can limit unnecessary testing.

Initial Evaluation

  • The “OPQRST” mnemonic provides a helpful framework to approach the history of present illness and narrow the differential diagnosis [5]:

    • Onset of pain

    • Provocation/palliation

    • Quality

    • Radiation

    • Site of pain

    • Timing

  • The pain characteristics (3 P’s) that decrease the likelihood of acute coronary syndrome (ACS) [6] are:

    • Pleuritic pain worsened with inspiration

    • Positional pain worsened with lying down

    • Pain reproduced by palpation

  • The approach to a differential diagnosis of chest pain can be divided into cardiac versus non-cardiac etiologies [7].

Clinical Pearl 1

A negative ECG and troponin do not rule out ACS.

Cardiac Etiologies of Chest Pain

  • Ischemic Heart Disease

    • Ischemic heart disease is an umbrella term that includes stable angina and ACS.

    • Stable angina presents with the following characteristics:

      • Substernal location

      • Onset with exertion

      • Improvement with rest or nitroglycerin [8]

    • If a patient presents with only two out of three characteristics, the chest pain is considered atypical. If a patient has one out of three characteristics, it is considered non-anginal chest pain. The presentation predicts the likelihood that the chest pain is due to CAD (Table 1.1).

    • ACS encompasses unstable angina (UA) and myocardial infarction (MI) [9] and presents with:

      • New onset angina at rest

      • Angina with minimal exertion

      • Crescendo angina

    • Additional symptoms of ACS can include radiation to the arms/shoulder/jaw/neck, shortness of breath, pain similar to prior ACS (if applicable), nausea, and diaphoresis [7, 10].

    • Exam can include Levine’s sign (clenching fist on chest), rales on lung exam, and hypotension [7, 11]. The presence of chest wall tenderness significantly decreases the likelihood of ACS [12, 13].

    • ECG and troponin (if available and risk factors present) can be used for further workup. A normal ECG does not rule out ACS.

    • Risk factors include older age, hypertension, diabetes, hyperlipidemia, and tobacco use [14, 15]. However, up to 12% of patients with acute MI have no risk factors [16].

    • Atherosclerotic cardiovascular disease (ASCVD) risk score can be helpful to determine one’s overall risk of CAD [17, 18].

  • Aortic Dissection

    • Classically presents with abrupt onset sharp/tearing/ripping chest or back pain, though presentation can be subtle [19, 20].

    • Physical exam findings include soft, high-pitched, early diastolic decrescendo murmur heard best at the third intercostal space on the left (consistent with aortic regurgitation) and pulse deficit (blood pressure difference between both arms).

    • Aortic dissection is rare [21,22,23], but should always be considered given its high mortality [19].

  • Pericarditis

    • Classically described as acute onset of sharp, pleuritic (worse with inspiration) chest pain that is positional (worse with laying down, improved with sitting up and leaning forward).

    • May occur in the setting of flu-like symptoms or associated with a history of autoimmune disease.

    • On physical exam, auscultation over the left sternal border reveals a pericardial friction rub that is best heard during expiration with the patient leaning forward [24].

    • Dullness with bronchial breath sounds suggests pericardial effusion (Ewart sign).

    • Assess for cardiac tamponade through inspection of jugular venous pulsations and pulsus paradoxus (decrease in systolic blood pressure greater than 10 mmHg with inspiration) [25].

  • Pulmonary Embolism (PE)

    • Seventy-five percent of cases present with chest pain [26], which is generally lateral or substernal.

    • Pain is of sudden onset, sharp, and pleuritic and commonly occurs with unexplained breathlessness, cough, hemoptysis, or syncope.

    • Clinical suspicion is high according to Wells score [27], including findings suggestive of deep vein thrombosis (DVT) such as calf pain or tenderness, immobilization or surgery, hemoptysis, and previous DVT/PE.

    • PMH, family history (FH), and current medications may reveal prothrombotic risk factors.

    • Physical exam may include elevated jugular venous pulsation and loud S2 over the left upper sternal border.

    • One should always consider PE in any patient with CP, tachycardia, and tachypnea/hypoxemia, especially in patients with risk factors. These patients should be sent to the emergency department for further evaluation.

  • Valvular Heart Disease

    • Aortic stenosis

      • History may include exertional angina, dyspnea, decreased exercise tolerance, syncope, palpitations, or dizziness.

      • Auscultation over the right second intercostal space reveals a harsh crescendo and decrescendo systolic murmur that radiates into the carotid arteries.

      • Palpation of the carotid upstroke during cardiac auscultation may demonstrate a weak pulse that rises slowly to a delayed peak (pulsus parvus et tardus) [28].

      • When grading aortic stenosis, the absence of S2 is specific for stenosis in the severe range.

    • Mitral valve prolapse

      • Most patients are asymptomatic, though some may experience vague chest discomfort.

      • Some cases present with significant mitral regurgitation, leading to fatigue, exertional dyspnea, orthopnea, or palpitations.

      • Auscultation over the apex reveals a late or mid-systolic click with a holosystolic murmur or high-pitched mid-late systolic murmur [29] that radiates to the axilla.

      • The murmur is louder and occurs earlier with a Valsalva maneuver, but is softer and delayed with squatting.

  • Hypertrophic Cardiomyopathy (HCM)

    • HCM with obstruction occurs due to a hypertrophied septum bulging into the left ventricular outflow tract.

    • May present with exercise intolerance, angina, or syncope.

    • HCM has an autosomal dominant pattern of inheritance with 60–70% of HCM patients having an affected family member [30].

    • Auscultation at the left sternal border reveals a systolic murmur that increases with Valsalva and with standing. The murmur decreases with passive leg raising and handgrip maneuvers.

    • To differentiate the murmur of aortic stenosis and HCM:

      • Auscultate the carotid pulse and note murmur severity in response to the Valsalva and handgrip maneuvers.

      • Valsalva maneuver → murmur louder with HCM

      • Handgrip maneuver → murmur softer with HCM

  • A summary of risk factors, history, and physical exam findings associated with cardiac etiologies can be found in Table 1.2.

Table 1.1 Pre-test probability that CP is associated with CAD-based CP characteristic
Full size table
Table 1.2 Risk factors, history, and physical exam for cardiac etiologies of CP
Full size table

Clinical Pearl 2

Most chest pain in primary care is non-cardiac with most common etiologies including chest wall syndrome and GERD.

Non-cardiac Etiologies of Chest Pain

  • Chest Wall Syndrome

    • Chest wall pain due to costochondritis or intercostal muscle spasms are the most frequent causes of CP [31].

    • History and pain to chest wall palpation are clues to the diagnosis.

    • Pain is generally moderate, well localized, continuous or intermittent, and sometimes described as “stinging.”

    • Pain is generally retrosternal and/or on the left side [31] and exacerbated by position and movement.

    • May coexist with CAD [32]. Careful assessment of risk factors and further testing may be needed to rule out cardiac etiology.

  • Gastroesophageal Disorders

    • Amongst the most frequent causes of non-cardiac chest pain [33] are GERD and non-GERD esophageal disorders [34] .

    • GERD

      • A common diagnosis in patients with CP [35, 36].

      • Typically presents with burning retrosternal chest pain, acid regurgitation, and sour/bitter taste in the mouth [37].

      • Usually occurs postprandially, particularly after large fatty meals or spicy foods, and tends to worsen in supine position [38].

      • Risk factors include older age, obesity, and tobacco use [39].

      • An empiric trial of PPI can be used for diagnostic purposes [40, 41].

    • Non-GERD esophageal disorders

      • Present with similar symptoms as GERD, including dysphagia and globus sensation [34, 42].

      • Include nutcracker esophagus (more common) and diffuse esophageal spasm [43].

      • It is important to consider these disorders (and referral to GI) if patient is having symptoms despite trial of PPI.

  • Pneumothorax

    • Potentially life-threatening but rare cause of CP in primary care [44].

    • Presents with sudden-onset pleuritic chest pain and dyspnea.

    • May be tachycardic, tachypneic, and hypoxic [45] on exam.

    • Lung exam may demonstrate focal decreased breath sounds with hyperresonance on percussion.

    • Chest x-ray is the initial diagnostic study and can show air in the pleural space.

  • Psychosocial

    • Anxiety and depression are associated with an increased risk of reporting chest pain [46].

    • Seen as a diagnosis of exclusion and can be discerned through screening questions for anxiety and panic disorders such as the GAD-7 questionnaire [47].

    • Patients report “tightness” sensation of the chest and shortness of breath.

    • Physical exam reveals tachycardia but is otherwise normal.

    • Social history may include drugs of abuse such as cocaine and methamphetamine, which may precipitate cardiac ischemia or vasospasm.

    • Substance abuse may also present with diaphoresis and pupillary dilation.

    • If thought to be the etiology, a urine drug screen should be obtained.

  • Pneumonia

    • Clinical history of fever, productive cough, pleuritic CP, shortness of breath, gastrointestinal symptoms (nausea, vomiting, diarrhea), or history of recent illness.

    • Pertinent exam findings can include decreased and/or bronchial breath sounds, coarse crackles, dullness to percussion, increased tactile fremitus, and egophony.

    • Bronchial breath sounds and dullness to percussion are highly specific findings [48].

  • Herpes Zoster

    • Pain is generally described as “burning,” “throbbing,” or “stabbing” [49] and may develop prior to appearance of rash [50].

    • Exam findings typically include erythematous vesicular rash in a unilateral dermatomal distribution.

    • Thoracic and lumbar dermatomes are the most common sites leading to CP.

  • A summary of risk factors, history, and physical exam findings associated with non-cardiac etiologies can be found in Table 1.3.

Table 1.3 Risk factors, history, and physical for non-cardiac etiologies of CP
Full size table

Clinical Pearl 3

Pleuritic CP differential includes the 5 Ps: pneumonia, pneumothorax, pericarditis, pulmonary embolism, and pleuritis.

Key Learning Points

  • The best approach to chest pain is a thorough history and physical.

  • The 3 P’s pain characteristics that decrease the likelihood of ACS include pleuritic, positional, and reproduced by palpation.

  • Patients without risk factors for CAD can still have ACS.

  • ASCVD score and Wells score can be helpful to assess risk of cardiac or thrombotic etiology, respectively.