Differential Diagnosis of Chest Pain:
Skin: Laceration, Burns, Herpes
Suba: Cellulitis, Abscess
MSK: Chostochondritis, sprains, strains, myositis
Pleural Space: Pleurisy, Pulmonary embolism, Pulmonary Tumor, Pneumothorax, Pneumonia
Heart: Acute coronary syndrome, MI, myositis
Esophagus: Esophageal rupture, GERD, Esophagitis, Boerhaves
Trachea: Tracheitis, Tracheal Tear
Aorta: Aortic dissection, Aortic stenosis
Acute coronary syndrome: UA, NSTEMI, STEMI
Hx: Frequent but not always exertional chest pain that is often not sharp or positional and radiates to both arms. Pain not easily reproducible.
Women and patients with diabetes are more likely to have atypical angina symptoms, such as fatigue, dyspnea, and nausea.
Px: An S3 is occasionally present.
Dx: ECG changes or elevated cardiac enzymes in initial workup followed by stress testing or catheterization.
Telemetry monitoring w/ ongoing ECG assesments and troponin measurements.
Coronary angiography allows direct evaluation of the coronary anatomy, with possible percutaneous coronary intervention or surgical revascularization if indicated.
Although patients with unstable angina may have similar electrocardiographic findings to those with NSTEMI, they can be differentiated by the lack of elevation in serum cardiac biomarkers.
Tx: Patients with ischemic chest pain and STEMI benefit from reperfusion therapy, either thrombolytic therapy or primary angioplasty (primary percutaneous coronary intervention = PCI)[The goal of therapy in patients STEMI is to perform PCI within 90 minutes of presentation to a PCI-capable facility or within 120 minutes if the patient requires transfer from a non–PCI-capable hospital. However, patients may benefit from treatment up to 12 hours after the onset of symptoms and possibly even after this time, depending on clinical circumstances].
Thrombolytic therapy has not shown a clear benefit for patients with STEMI who present more than 12 hours after the onset of symptoms. It remains second-line treatment when PCI is not possible or is contraindicated.
β-Blockers reduce mortality and should be given to all patients with acute coronary syndrome except those with heart failure, systolic blood pressure of less than 90 mm Hg, bradycardia (<50/min), or second-degree atrioventricular block.
Complete β-blockade typically results in a resting pulse rate of approximately 55 to 60/min.
Clopidogel (antiplatelet) - DES - 1 yr; Bare Metal - 1 mo; angioploasty - none
Hx: Acute-onset chest pain
Dx: Normal cardiac biomarkers, and T-wave inversions on electrocardiogram.
Tx: MONA BASH C (attempt to minimize ischemia by addressing both the supply and demand of oxygen within myocardial cells).
Chronic stable Angina
Dx: Exercise ECG testing is the standard stress test for the diagnosis of CAD in patients with normal baseline ECG findings.
Stress testing is most useful in patients with an intermediate pretest probability of CAD. For patients with a low pretest probability of CAD, stress testing is not useful because an abnormal test result is likely a false-positive finding and a normal test result only confirms the low pretest probability of CAD. For patients with a high pretest probability of CAD, stress testing is not useful to diagnose CAD and empiric medical therapy should be initiated.
If abnormalities that limit ST-segment analysis are present (left bundle branch block, left ventricular hypertrophy, paced rhythm, Wolff-Parkinson-White pattern), imaging (echocardiography or nuclear) increases diagnostic accuracy and ability to determine the site and extent of ischemia.
Tx: Coronary revascularization has been shown to be beneficial in patients with chronic stable angina and the following conditions: angina pectoris that is refractory to medical therapy; a large area of ischemic myocardium and high-risk criteria on stress testing; high-risk coronary anatomy, including left main coronary artery stenosis or three-vessel disease; and significant coronary artery disease with reduced left ventricular systolic function. In appropriately selected patients, revascularization, with either percutaneous coronary intervention or coronary artery bypass grafting (CABG) surgery, has been shown to reduce angina, increase longevity, and improve left ventricular performance.
Used in patients with a history of MI and in stable heart failure.
Dihydropyridine calcium channel blockers (eg, amlodipine, felodipine, nifedipine)
Second-line agents. Reduce blood pressure; do not affect heart rate and can be used with β-blockers. Avoid short-acting agents (such as nifedipine).
Nondihydropyridine calcium channel blockers (verapamil, diltiazem)
Mostly used in patients who cannot take β-blockers. Avoid in patients with heart failure; use with caution in patients taking β-blockers (bradycardia).
Reduce blood pressure and afterload by a reduction in peripheral vascular resistance. Reduce ventricular remodeling and fibrosis after infarction. Improve long-term survival in patients with LVEF ≤40% and, possibly, in patients with high cardiovascular risk (eg, diabetes mellitus, PVD).
Can be used with β-blockers and calcium channel blockers. Tachyphylaxis occurs with continued use; requires nitrate-free period (8-12 h/d). Side effects include headache. Avoid in patients taking PDE-5 inhibitors.
Dilate coronary arteries and reduce preload. Indicated for all patients with chronic stable angina for use on an as-needed basis.
Indicated as add-on therapy for patients not responding to standard therapy; used in combination with a nitrate, β-blocker, or calcium channel blocker. Avoid using with verapamil or diltiazem (prolongs QT interval).
Indicated for all patients with stable angina, barring contraindications; reduces major cardiovascular events by 33%.
Thienopyridine derivatives (eg, clopidogrel, ticlopidine, prasugrel)
Aspirin alternatives, but significantly more expensive. Improve outcomes in patients with recent ACS or stent placement. In patients with stable CAD, thienopyridine derivatives do not improve outcomes.
In patients with mild to moderate elevations in total and LDL cholesterol and a history of MI, statins are associated with a 24% risk reduction for fatal and nonfatal MI.
Pulmonary embolism (PE)
Sudden-onset dyspnea, nonproductive cough, tachycardia, and mild hypoxia is highly suggestive of acute pulmonary embolism (PE).
Modified Wells score
Clinical signs of DVT
Alternate diagnosis less likely than PE
Previous PE or DVT
Heart rate >100
Recent surgery or immobilization
Total score for clinical probability
≤4 = PE unlikely
>4 = PE likely
Dx: Given clinically stablity (normotensive, mild hypoxemia) with no evidence of distress, the diagnosis of PE can be confirmed with CT angiography (CTA). If CTA confirms PE, clinical judgment can dictate whether anticoagulation is initiated or other options are pursued (eg, inferior vena cava filter placement) based on the estimated risk of bleeding from the peptic ulcer.
In low-probability patients, a normal D-dimer can exclude the diagnosis. If intermediate or high probability, ventilation-perfusion scan or spiral CT is indicated.
A ventilation-perfusion scan is the most appropriate study to confirm the suspected diagnosis of pulmonary embolism in this patient with kidney failure. Ventilation-perfusion scans detect abnormalities of blood flow in comparison to the pattern of ventilation, with areas of mismatch between perfusion and ventilation being evidence of vascular occlusion due to a pulmonary embolus.
Tx: Early, effective anticoagulation decreases the mortality risk of acute PE and should be considered in patients without absolute contraindications (eg, hemorrhagic stroke, massive gastrointestinal bleed).
In the absence of contraindications, the patient should be treated initially with intravenous or subcutaneous unfractionated heparin, low-molecular-weight heparin, or fondaparinux. Most patients with pulmonary embolism are treated in the hospital, although carefully selected, stable patients may be candidates for outpatient treatment. Following initial therapy, patients are usually transitioned to warfarin for long-term therapy, with factor Xa and direct thrombin inhibitors being increasingly-available options for this purpose.
Ddx: Viral or idiopathic
Autoimmune disease (eg, SLE)
Uremia (acute or chronic renal failure)
Early: Peri-infarction pericarditis
Late: Dressler syndrome
Hx: Substernal chest discomfort that can be sharp, dull, or pressure-like in nature, often relieved with sitting forward; usually pleuritic.
Dx: ECG changes may include ST-segment elevation (usually diffuse) or more specifically (but less commonly) PR-segment depression.
Unlike other etiologies of pericarditis, uremic pericarditis does not typically cause diffuse ST elevation (or PR depression) on ECG as the inflammation does not affect the myocardium.
Pulsus paradoxus greater than 10 mm Hg is a typical finding in cardiac tamponade.
Tx: Anti-inflammatory therapy with nonsteroidal anti-inflammatory drugs (NSAIDs) is the mainstay of treatment.
Initiation of dialysis is indicated for uremic pericarditis (symptomatic uremia) and typically leads to resolution of symptoms.
Sudden onset of pleuritic chest pain and dyspnea in a smoker or COPD patient. Other findings include sudden, sharp, nonradiating pleuritic chest pain and shortness of breath with hyperresonance, decreased breath sounds, and decreased chest wall expansion on the side of the pneumothorax in a patient with underlying lung disease.
Dx: Chest radiograph (initial test of choice) or CT scan confirms the diagnosis.
Pneumothorax occurring in patients without known lung disease or a clear precipitating cause is termed primary spontaneous pneumothorax (PSP). PSP tends to occur more often in men, smokers, and those with a family history of PSP.
The incidence of AAA is higher in men than in women and in whites versus blacks, and it increases with age.
Substernal chest pain with radiation to the back or midscapular region; often described as “tearing” or “ripping” pain.
Severe abdominal or back pain with syncope, followed by vague discomfort is typical for a ruptured abdominal aortic aneurysm (AAA) that has been locally contained, preventing immediate death. The sentinel event of sudden, severe back pain associated with loss of consciousness marks the occurrence of rupture. Symptoms after that time are likely caused by either local irritation and inflammation related to the rupture and hemorrhage or expansion of the aneurysm against adjacent structures. Leukocytosis and anemia are common. Contained rupture of AAA, when misdiagnosed, is most often mistaken for renal colic, acute myocardial infarction, or diverticulitis.
Pulse or blood pressure differential useful but uncommonly present.
Chest radiograph may show a widened mediastinal silhouette, pleural effusion, or both.
Intense retrosternal pain after vomiting; often associated with ethanol use. Pneumomediastinum on CXR can be seen.
Chest pain with exertion, heart failure, syncope. Typical systolic murmur at the base of the heart radiating to the neck. Panic attack May be indistinguishable from angina. Often diagnosed after a negative evaluation for ischemic heart disease. Often associated with palpitations, sweating, and anxiety.
Typically more reproducible chest pain. Includes muscle strain, costochondritis, and fracture. Should be a diagnosis of exclusion.
Burning-type chest discomfort usually precipitated by meals and not related to exertion. It is often worse upon lying down and improved with sitting.
May be indistinguishable from angina. Often diagnosed after a negative evaluation for ischemic heart disease. Often associated with palpitations, sweating, and anxiety.
Tx: Treatment options for panic disorder include medication and psychotherapy. Cognitive behavioral therapy (CBT) has been shown to be the most effective psychotherapeutic intervention in controlled trials. Selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors have been shown to be effective.
Cocaine raises blood pressure, heart rate, and myocardial oxygen requirements. It can also induce spasm of the coronary circulation even if there is no preexisting coronary artery stenosis.
Dx: Narrow complex tachycardia with T-wave inversion and ST-segment depression in the lateral leads consistent with ischemia; U tox.
Tx: Patients with chest pain in the setting of cocaine use should be evaluated and managed as any other patient with chest pain except for the use of β-blockers. The use of β-blockers in patients with cocaine-induced chest pain is controversial because of the pharmacologic concern that they may leave the patient with unopposed α-mediated vasoconstriction, leading to increased blood pressure and myocardial ischemia. Instead, calcium channel blockers and benzodiazepines are safe in this setting and are effective in lowering the heart rate, blood pressure, and myocardial oxygen demand that occur primarily because of the sympathetic stimulation due to cocaine.