Substernal Chest Pain Icd 10


Substernal Chest Pain Icd 10
Precordial pain –

2016 2017 2018 2019 2020 2021 2022 2023 Billable/Specific Code

  • R07.2 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes.
  • The 2023 edition of ICD-10-CM R07.2 became effective on October 1, 2022.
  • This is the American ICD-10-CM version of R07.2 – other international versions of ICD-10 R07.2 may differ.

The following code(s) above R07.2 contain annotation back-references Annotation Back-References In this context, annotation back-references refer to codes that contain:

  • Applicable To annotations, or
  • Code Also annotations, or
  • Code First annotations, or
  • Excludes1 annotations, or
  • Excludes2 annotations, or
  • Includes annotations, or
  • Note annotations, or
  • Use Additional annotations

that may be applicable to R07.2 :

  • R00-R99 2023 ICD-10-CM Range R00-R99

    What is the ICD-10 code for Substernal chest pain?

    ICD-10 code R07.89 for Other chest pain is a medical classification as listed by WHO under the range – Symptoms, signs and abnormal clinical and laboratory findings, not elsewhere classified.

    What is Substernal chest pain?

    Causes of Sternal Pain –

    • Sternum pain is usually caused by problems with the muscles and bones near the sternum and not the sternum itself.
    • Pain felt just behind or below the sternum is called substernal pain and is sometimes caused by gastrointestinal problems,
    • Some of the most common causes of sternum and substernal pain are:
    • For more detail on specific causes, see lists below.

    What is the ICD-10 code for atypical chest pain?

    As there is no explicit definition of ‘atypical’ chest pain, it should be coded to R07.4 Chest pain, unspecified. Assign R07.4 Chest pain, unspecified for documentation of atypical chest pain.

    What is ICD 9 other chest pain?

    VI. CMS Analysis – The NCD includes the narrative Indications and Limitations below. We consider here whether prothrombin testing for chest pain flows from this narrative. Indications

    A PT may be used to assess patients taking warfarin. The prothrombin time is generally not useful in monitoring patients receiving heparin who are not taking warfarin. A PT may be used to assess patients with signs or symptoms of abnormal bleeding or thrombosis. For example: swollen extremity with or without prior trauma; unexplained bruising; abnormal bleeding, hemorrhage or hematoma; petechiae or other signs of thrombocytopenia that could be due to disseminated intravascular coagulation. A PT may be useful in evaluating patients who have a history of a condition known to be associated with the risk of bleeding or thrombosis that is related to the extrinsic coagulation pathway. Such abnormalities may be genetic or acquired. For example: dysfibrinogenemia; afibrinogenemia (complete); acute or chronic liver dysfunction or failure, including Wilson’s disease and hemochromatosis; disseminated intravascular coagulation (DIC); congenital and acquired deficiencies of factors II, V, VII, X; vitamin K deficiency; lupus erythematosus; hypercoagulable state; paraproteinemia; lymphoma; amyloidosis; acute and chronic leukemias; plasma cell dyscrasia; HIV infection; malignant neoplasms; hemorrhagic fever; salicylate poisoning; obstructive jaundice; intestinal fistula; malabsorption syndrome; colitis; chronic diarrhea; presence of peripheral venous or arterial thrombosis or pulmonary emboli or myocardial infarction; patients with bleeding or clotting tendencies; organ transplantation; presence of circulating coagulation inhibitors. A PT may be used to assess the risk of hemorrhage or thrombosis in patients who are going to have a medical intervention known to be associated with increased risk of bleeding or thrombosis. For example: evaluation prior to invasive procedures or operations of patients with personal history of bleeding or a condition associated with coagulopathy prior to the use of thrombolytic medication.


    When an ESRD patient is tested for PT, testing more frequently than weekly requires documentation of medical necessity, e.g., other than chronic renal failure or renal failure, unspecified. The need to repeat this test is determined by changes in the underlying medical condition and/or the dosing of warfarin. In a patient on stable warfarin therapy, it is ordinarily not necessary to repeat testing more than every two to three weeks. When testing is performed to evaluate a patient with signs or symptoms of abnormal bleeding or thrombosis and the initial test result is normal, it is ordinarily not necessary to repeat testing unless there is a change in the patient’s medical status. Since the INR is a calculation, it will not be paid in addition to the PT when expressed in seconds, and is considered part of the conventional prothrombin time. Testing prior to any medical intervention associated with a risk of bleeding and thrombosis (other than thrombolytic therapy) will generally be considered medically necessary only where there are signs or symptoms of a bleeding or thrombotic abnormality or a personal history of bleeding, thrombosis or a condition associated with a coagulopathy. Hospital/clinic-specific policies, protocols, etc., in and of themselves, cannot alone justify coverage.

    We note that ICD-9-CM diagnosis code 786.59, Chest pain, other, is a covered indication in the list, and the list does not specify the other related chest pain diagnoses. We note in addition (as did the requesting party) that 786.50 is included as a covered ICD-9-CM code under Section 190.16 for PTT testing.

    Is angina substernal?

    Causes of Chronic Chest Pain – The leading diagnostic consideration in patients with chronic chest pain is coronary artery disease. The commonest clinical presentation of coronary artery disease is recurrent angina pectoris. A helpful diagnostic feature of coronary artery disease is that the pain usually improves with specific medications.

    • Relief of anginal pain within 3 minutes of taking sublingual nitroglycerin is strong evidence that coronary disease has caused the pain.
    • Decreased frequency of attacks after starting a beta blocker, calcium channel blocker, or long-acting nitrate preparation suggests that coronary artery disease is the cause.

    Esophageal disease is a common cause of recurrent chest pain. Esophagitis, usually secondary to acid reflux from the stomach, frequently causes esophageal pain. The acid causes chemical damage and inflammation of the mucosa, resulting in pain that often has a burning quality.

    Clues to the presence of reflux esophagitis include a history of acid–peptic disease and symptoms of reflux, such as regurgitation or acid taste in the mouth. Chest pain caused by esophageal reflux tends to occur after meals and may be related to body position. Episodes of pain can be induced by bending over at the waist.

    They often occur at night, because the recumbent posture enhances reflux of acid into the esophagus. Relief of pain by antacids, topical lidocaine, or by specific maneuvers to reduce reflux suggests this diagnosis. Esophageal motor disorders also commonly cause chest pain.

    While reflux esophagitis causes pain by irritation of the esophageal mucosa, motor disorders cause pain by contraction and spasm of the muscular wall of the esophagus. Esophageal spasm often occurs as a secondary manifestation of reflux esophagitis. As mucosal irritation and inflammation become more severe, the stimulation of local nerves leads to muscular spasm.

    Chest pain: how to distinguish between cardiac and noncardiac causes

    Such patients will report a pattern of pain similar to that seen in reflux esophagitis, occurring after meals and aggravated by body position. Patients may report varying qualities of pain. With episodes of simple mucosal irritation, the pain may be reported as “heartburn,” while the pain is reported as having a more severe, heavy quality during episodes of muscular spasm.

    Esophageal motor disorders can be independent of acid reflux disease, as in patients with achalasia or diffuse esophageal spasm. These patients show a different pattern of episodes than occurs in patients with acid reflux. The pain usually is unrelated to body position and may occur while eating instead of after meals.

    Dysphagia is frequently a prominent symptom in patients with primary motor disorders. Esophageal motor disorders may be relieved by nitrates and calcium channel blockers, via relaxation of the smooth muscle wall of the esophagus. Because these agents also relieve the chest pain caused by coronary artery disease, the clinician may have difficulty using medication response as a clue to the cause of undiagnosed chest pain.

    1. The clinician must carefully interpret the results of a therapeutic trial, particularly the rapidity of response.
    2. Relief of pain within 3 minutes of a sublingual dose of nitroglycerin is more consistent with coronary artery disease than esophageal motor disorders.
    3. If relief occurs only after 10 to 15 minutes, esophageal disease is more likely.

    Nitrates and calcium channel blockers can relax the lower esophogeal sphincter and aggravate esophageal reflux, thereby increasing symptoms of reflux esophagitis. Myocardial ischemia sometimes occurs in the absence of fixed obstructions of the coronary arteries, resulting in recurrent chest pain.

    Obstructive disease of the intramural small vessels can cause ischemia. Although such lesions occur more frequently in diabetics, small vessel disease is an infrequent cause of chest pain. It should be considered only after more likely etiologies have been excluded. Valvular aortic stenosis, hypertrophic cardiomyopathy, and thyrotoxicosis can also cause myocardial ischemia.

    The quality and pattern of pain in these conditions usually is similar to that of coronary artery disease. These entities nearly always are accompanied by physical examination findings typical of the underlying disease, and so their detection usually is not difficult.

    1. Coronary vasospasm can cause myocardial ischemia in the absence of obstructive coronary disease.
    2. The pain usually has a quality similar to the pain of obstructive coronary disease, but it tends to occur in an unpredictable pattern.
    3. The pain typically is not induced by exertion and may awaken the patient from sleep.

    Some patients report emotional stress as a trigger. The pain frequently responds to sublingual nitroglycerin, and the frequency of episodes decreases after therapy with calcium channel blockers or long-acting nitrates. Approximately 90% of patients with coronary vasospasm have ECG changes during episodes of pain.

    • Thus, the absence of electrocardiographic changes during pain makes coronary vasospasm unlikely.
    • Mitral valve prolapse (MVP) is a controversial etiology of chronic chest pain.
    • Clinical and echocardiographic studies have demonstrated that MVP is a common finding in otherwise healthy adults.
    • Population studies have found the incidence of chest pain to be no higher in individuals with mitral valve prolapse than in those without the disorder.

    Nevertheless, there have been numerous clinical reports of patients in whom mitral valve prolapse was the only identifiable etiology of recurrent chest pain. The patients in these studies have pain with various qualities and patterns, and there is no “typical” chest pain syndrome of MVP.

    • It should be considered as a cause of recurrent chest pain only after more likely causes have been excluded, since there is no specific treatment for the disorder.
    • The major value of diagnosing mitral valve prolapse is to identify those patients at risk of endocarditis and arrhythmias.
    • Prospective studies have shown that patients who develop serious complications have either a late systolic murmur or abnormal electrocardiogram in conjunction with the midsystolic click.

    Thus, it is unnecessary to obtain echocardiography to exclude mitral valve prolapse unless a patient has findings on physical examination and/or electrocardiogram that suggest a risk of complications. The chest wall can cause recurrent chest pain, but the clinical diagnosis of chest wall syndromes has not been described well.

    Where is the Substernal chest?

    Substernal means ‘ below the sternum ‘ and therefore into the chest. Substernal and retosternal ‘behind the sternum’ are often used without differences really considered between either.

    What is Substernal or Retrosternal chest pain?

    Retrosternal chest pain can occur for various reasons, including cardiac or heart-related issues and noncardiac conditions, such as gastroesophageal reflux disease (GERD). Retrosternal chest pain refers to pain that occurs in the space behind the sternum.

    1. It is a more specific way to refer to chest pain.
    2. Chest pain can stem from various conditions that affect the heart, lungs, muscles, skeletal system, or gastrointestinal (GI) tract.
    3. This article reviews several potential causes of retrosternal chest pain and when to consult a doctor.
    4. Issues in the GI tract can lead to chest pain and may include gastritis and GERD,

    Gastritis refers to inflammation of the stomach, with symptoms that include discomfort or pain in the chest. This condition may be acute or chronic, and its underlying causes can include infections and high alcohol intake. GERD is a chronic medical condition where the contents of the stomach flow into the esophagus, or food pipe.

    heartburna burning sensation in the chestindigestiona sour taste in the mouthfrequent belchinga persistent cough

    GERD accounts for 20–60% of chest pain that is not due to cardiac problems. GI-related chest pain can also stem from issues with the muscles in the esophagus, such as :

    an inability of the muscles to contract, resulting in food getting stuck in the chestover contraction of the musclesspasms

    Another possible cause is food pipe sensitivity, where acid or pressure causes discomfort or pain. Learn more about a range of gastrointestinal conditions. Conditions that affect the skeleton, muscles, or tendons of the chest can also lead to chest pain.

    Costochondritis causes inflammation in the cartilage of the chest. It can result in chest pain that feels like a heart attack. Costochondritis is not a medical emergency, but it is best to seek medical attention to rule out a heart attack. Pain behind the sternum can also stem from strains and other injuries that affect the chest.

    A person should speak with a doctor if they do not know the source of the pain. What are some more causes of rib cage pain? Lung problems can lead to retrosternal chest pain in some people. They include:

    Pulmonary embolism: A pulmonary embolism occurs when a blood clot stops blood flow to part of the lung. It can cause chest pain and breathing difficulty, Pneumonia : Pneumonia is a bacterial, viral, or fungal infection in lung tissue. It can cause chest pain, a buildup of fluid in the lungs, breathing difficulty, a cough, and other symptoms. Lung cancer: Lung cancers start in the cells of the bronchi or lungs. As the tumor grows, it can cause symptoms that include chest pain, trouble breathing, and coughing up blood.

    Learn more about lung cancer through our dedicated hub: A deeper look at lung cancer, Problems with the heart can result in chest pain. Examples of these cardiac issues include:

    Heart attack: Also known as myocardial infarction, a heart attack occurs when blood flow and oxygen to one or more areas of the heart stops. Symptoms include pain in the chest that radiates down the arm, fatigue, and nausea. People experiencing a heart attack require immediate medical attention. Heart valve disease: Heart valve disorders are a type of heart disease in which problems with the heart valves stop blood from flowing effectively. Aortic stenosis is one example that often affects older adults. Symptoms include chest pain, fatigue, and other symptoms. Pericarditis: Pericarditis is inflammation of the pericardial sac, which surrounds the heart. Myocarditis: Myocarditis, or inflammation of the heart, often results from an infection. It commonly occurs in younger people but can happen at any age. Symptoms include chest pain and fever.

    A person should seek medical attention if they have chest pain they cannot explain. A doctor can help determine the underlying cause and provide appropriate treatment. Anyone who has symptoms of a heart attack needs immediate medical attention. Signs of a heart attack include :

    feeling faint, weak, or lightheadedchest pain or discomfortdiscomfort or pain in the shoulders or armsshortness of breathjaw, neck, or back pain

    If these signs and symptoms occur, someone should call 911. When is jaw pain a sign of a heart attack? Retrosternal chest pain can occur for several reasons, including heart, lung, muscle, and GI issues. It typically causes pain in the center of the chest.

    What is non cardiac substernal pain?

    What is noncardiac chest pain? – Noncardiac chest pain is defined as recurring pain in your chest — typically, behind your breast bone and near your heart — that is not related to your heart. In most people, noncardiac chest pain is actually related to a problem with their esophagus, most often gastroesophageal reflux disease (GERD),

    What is typical vs atypical chest pain?

    Abstract – Studies indicate that symptoms labeled as “atypical” are more common in women evaluated for myocardial infarction (MI) and may contribute to the lower likelihood of a diagnosis and delayed treatment and result in poorer outcomes compared with men with MI. Atypical pain is frequently defined as epigastric or back pain or pain that is described as burning, stabbing, or characteristic of indigestion. Typical symptoms usually include chest, arm, or jaw pain described as dull, heavy, tight, or crushing. In a recent article published in the Journal of the American Heart Association ( JAHA ), Ferry and colleagues addressed presenting symptoms in men and women diagnosed with MI and reported that typical symptoms in women were more predictive of a diagnosis of MI than for men. A critical question is, are there really typical or atypical symptoms, and if so, who is the reference group? We propose that researchers and clinicians either discontinue using the terms typical and atypical or provide the reference group to which the terms apply (eg, men versus women). We believe it is past time to standardize the symptom assessment for MI so that proper and rapid diagnostic testing can be undertaken; however, we cannot standardize the symptom experience. When we do this, we are at risk of having study results, such as those of Ferry and colleagues, that vary from prior evidence and could lead to what the authors hope to avoid: disadvantaging women in receiving expeditious diagnostic testing and treatment for acute coronary syndrome. Keywords: acute coronary syndrome, clinical presentation, myocardial infarction, sex differences, symptoms Subject Categories: Clinical Studies, Ischemia Symptoms are the trigger that propel individuals with symptoms suspicious of acute coronary syndrome (ACS) to seek emergent care for this potentially life‐threatening condition. After 3 decades of research on sex differences in the symptoms of ACS, ample evidence suggests that although sex differences in symptoms exist, they are modest and do not contribute significantly to risk stratification or provide a rationale for diagnostic testing based on sex. In a large prospective study, we found that only 3 of 13 common symptoms were predictive of a diagnosis of ACS versus non‐ACS. The predictive value of shoulder pain (odds ratio: 2.53 versus 1.11 ) and arm pain (odds ratio: 2.15 versus 1.21 ) for women were nearly twice that of men. Shortness of breath was predictive of a non‐ACS diagnosis for men only.1 Scores of authors have found some sex differences in symptoms of ACS, 2, 3 but small differences were usually based on frequency and distribution of symptoms, not the type of symptom. In many studies, statistical significance was reached when sex differences were as small as a few percentage points. Kahn et al 4 found, for example, that men reported chest pain more frequently than women (86.3% versus 81%; P =0.03). We must distinguish between clinical significance (whether the magnitude of difference is large enough to change clinical care) and statistical significance (which is subject to variability in sampling and measurement) in assessing patients for further intervention. A more critical issue than sex differences in symptoms is likely the magnitude of symptom overlap in individuals ruled in and out for ACS. Approximately 10% to 15% of patients presenting to the emergency department (ED) with symptoms suggestive of ACS are actually experiencing ACS, 5, 6 yet the other 85% of patients look so similar that the same diagnostic testing and resources are required to safely rule them out for ACS. Numerous clinical‐decision aids to assess risk for ACS in the ED have been validated over the years, some with 100% sensitivity.5 Many of these clinical‐decision or prediction rules have facilitated transfer of low‐risk patients to a chest‐pain or clinical‐decision unit or early discharge from the ED.7 In a recent article published in the Journal of the American Heart Association ( JAHA ), Ferry et al 8 addressed presenting symptoms in men and women diagnosed with myocardial infarction (MI) using sex‐specific criteria in a substudy of the High‐STEACS (High‐Sensitivity Troponin in the Evaluation of Patients With Acute Coronary Syndrome) trial. The definition of sex‐specific criteria were troponin levels >99th percentile, which are 16 ng/L for women and 34 ng/L for men.9 The rationale for the study was that sex‐specific thresholds for troponin have identified a population of patients with MI that was previously unrecognized. Therefore, these patients would have been excluded from prior research on sex differences in symptoms. In addition, “atypical” symptom presentations are more common in women than men and may contribute to the lower likelihood of a diagnosis and treatment and result in poorer outcomes compared with men with MI. Atypical pain was defined by Greenslade et al 10 as “epigastric or back pain or pain that was described as burning, stabbing, characteristic of indigestion, or other.” Typical symptoms included “chest, arm, or jaw pain described as dull, heavy, tight, or crushing.” The main study finding was that typical symptoms in women were more predictive of a diagnosis of MI than those in men. We address several limitations to study methods that may mislead researchers, clinicians, and the public. In the High‐STEACS parent study, 16% of men and 12% of women had type 1 MI (myocardial necrosis with troponin levels >99th percentile or myocardial ischemia on the ECG) and the remainder had type 2 (myocardial necrosis caused by increased oxygen demand or decreased supply).8 Importantly, patients with ST‐segment–elevation MI (STEMI) were excluded from the study. The authors stated that patients with STEMI were not included because symptom differences are less important, as the diagnosis is based primarily on the ECG rather than on other features of the clinical presentation. Although ECG criteria for STEMI account for sex and age differences, 11 there are still notable delays in timely reperfusion among women with STEMI compared with men. Jneid et al 12 found that women with STEMI were less likely to receive fibrinolytic therapy alone, primary PCI, or the combination of fibrinolytic therapy and PCI (5.1% versus 6.2%, 47.3% versus 61.1%, and 3.9% versus 5.8%, respectively; P <0.0001). Women presenting with STEMI were also less likely to achieve timely door‐to‐needle time (28.3% versus 35.2%; P0.0005) and timely door‐to‐balloon time (39.0% versus 44.8%; P 13 found that another factor contributing to women's less timely reperfusion was longer prehospital delay compared with men. This finding is concerning because ECGs are frequently not obtained within the recommended 10 minutes of arrival, and in one study, women with ischemic‐type symptoms had a mean time of 53 minutes from presentation to ECG.14 It is vitally important to remember that symptoms are cues for patients that a problem exists. Symptoms trigger clinicians to obtain ECGs, which drive subsequent clinical decision‐making such as activation of the cardiac catheterization laboratory for emergent percutaneous coronary intervention.15 Nearly all patients presenting to the ED are undifferentiated. Neither the patient nor the clinician knows what the diagnosis is until testing is complete. Many emergency medical systems now have the capacity to do prehospital ECGs, Nevertheless, we found in our recent study that only 44.6% of patients with ACS arrived at the ED via emergency medical systems. In addition, a minority of patients (24.6%) experienced STEMI, and only 56.3% of patients with STEMI called emergency medical systems. This leaves a large number of patients presenting to the ED without a diagnosis.13 In addition, individuals presenting to emergency medical systems with chest pain are significantly more likely to receive prehospital ECG compared with those who have nonchest symptoms. Consequently, despite greater availability of prehospital ECG equipment, if the patient does not report chest pain, then they are disadvantaged from even receiving a prehospital ECG.16 Including patients with STEMI is vital to determining true differences or similarities in symptoms between female and male patients, particularly because STEMI is a true emergency requiring time‐dependent reperfusion therapy. In the Clinical Perspective section of their article, Ferry et al 8 state that women with MI are at risk of underdiagnosis and undertreatment if "correct" symptom presentations are not recognized. Researchers, including our team, have spent years attempting to identify sex differences in the symptoms of ACS to provide evidence for clinicians to facilitate expeditious diagnosis and for the public to be able to respond quickly to symptoms. To suggest that there is a "correct" presentation implies there is an "incorrect" symptom presentation, which is not supported by numerous previous studies.1, 17, 18 Assuming a correct presentation can also imply that there is a "standard" symptom presentation, also unsupported by the data to date. The critical question is, are there really typical or atypical symptoms, and if so, who is the reference group? We propose that researchers and clinicians either discontinue using the terms typical and atypical or provide the reference group to which the terms apply (eg, men versus women). Many researchers have reported that upper back pain and fatigue are commonly reported symptoms during ACS, and up to 30% of patients do not experience chest pain.19, 20 This information is important to consider as we try to differentiate patients who will be ruled in compared with those ruled out for ACS. We found that although chest pain is a sensitive symptom for ACS, it is not very specific ( Table ).1 In fact, few other symptoms were sensitive or specific for a diagnosis of ACS. In our multicenter prospective study, we found few symptom differences between patients with and without ACS presenting to the ED.13 Ferry et al 8 defined chest pain as all descriptors of chest symptoms, including pressure or discomfort. Their rationale was that terms other than pain are "functions of sex‐related language rather than symptom differences in symptom presentation." This is an opinion that is counterproductive to science and accurate assessment of symptoms, which are, by definition, subjective and what the patient says they are.

    What kind of chest pain is atypical?

    Main symptoms Quality: Unlike typical chest pain, which is usually a dull pain or pressure sensation, atypical chest pain may be sharp, stabbing, or tearing. Atypical chest pain may get worse when breathing in, may get better with leaning forward, and may be worse when you push on the chest.

    What is the ICD-10 for chest myalgia?

    ICD-10 code M79.1 for Myalgia is a medical classification as listed by WHO under the range – Soft tissue disorders.

    What is the ICD-9 code for 78650?

    ICD-9 code 786.50 for Unspecified chest pain is a medical classification as listed by WHO under the range -SYMPTOMS (780-789).

    Is Substernal the same as Retrosternal?

    Introduction – An enlarged thyroid gland is termed a goiter. The thyroid usually grows anteriorly and/or laterally. The thyroid gland is covered by thin muscles, subcutaneous fat tissue, and skin and does not meet significant resistance while growing. When enlarged, it is typically visible and easily palpable, but may be complicated by body habitus.

    If the thyroid gland grows inferiorly and passes through the thoracic inlet into the thoracic cavity, it is termed a “substernal goiter.” An alternative term is “retrosternal goiter”. Substernal goiter may involve one or both the lobes of the thyroid gland and may cause deviation and/or compression of the trachea, and less commonly esophagus or venous structures.

    Tracheal compression has been reported in 35% to 73% of substernal goiters. Up to 10% of substernal goiters are located in the posterior mediastinum, and 90% of that 10% posterior mediastinal goiters are right-sided, as left-sided subclavian arteries and the aortic arch do not allow for left-sided expansion.

    What are the 3 P’s of chest pain?

    Table 1. Specific Details of the Chest Pain History* Table 2. Value of Specific Components of the Chest Pain History for the Diagnosis of Acute Myocardial Infarction (AMI) Clinical Review Clinician’s Corner November 23/30, 2005 JAMA.2005;294(20):2623-2629. doi:10.1001/jama.294.20.2623 Context The chest pain history, physical examination, determination of coronary artery disease (CAD) risk factors, and the initial electrocardiogram compose the information immediately available to clinicians to help determine the probability of acute myocardial infarction (AMI) or acute coronary syndrome (ACS) in patients with chest pain.

    • However, conflicting data exist about the usefulness of the chest pain history and which components are most useful.
    • Objective To identify the elements of the chest pain history that may be most helpful to the clinician in identifying ACS in patients presenting with chest pain.
    • Evidence Acquisition MEDLINE and Ovid were searched from 1970 to September 2005 by using specific key words and Medical Subject Heading terms.

    Reference lists of these articles and current cardiology textbooks were also consulted. Evidence Synthesis Certain chest pain characteristics decrease the likelihood of ACS or AMI, namely, pain that is stabbing, pleuritic, positional, or reproducible by palpation (likelihood ratios 0.2-0.3).

    Conversely, chest pain that radiates to one shoulder or both shoulders or arms or is precipitated by exertion is associated with LRs (2.3-4.7) that increase the likelihood of ACS. The chest pain history itself has not proven to be a powerful enough predictive tool to obviate the need for at least some diagnostic testing.

    Combinations of elements of the chest pain history with other initially available information, such as a history of CAD, have identified certain groups that may be safe for discharge without further evaluation, but further study is needed before such a recommendation can be considered reasonable.

    Conclusion Although certain elements of the chest pain history are associated with increased or decreased likelihoods of a diagnosis of ACS or AMI, none of them alone or in combination identify a group of patients that can be safely discharged without further diagnostic testing. Differentiating acute coronary syndromes (ACS) from benign causes of chest pain is critical because of the consequences of misdiagnosis in either direction.

    Despite diagnostic advances, missed acute myocardial infarction (AMI) and ACS remain problematic, with estimates ranging between 2% and 10%.1 – 5 Conversely, a large proportion of patients with chest pain who are admitted do not turn out to have ACS.6 This overtriage has enormous economic implications for the US health care system, estimated at $8 billion in annual costs.7, 8 Distinguishing whether a patient presenting with chest pain has ACS or a non-ACS problem is at best difficult.

    The differential diagnosis of chest pain is broad and includes many systems, such as pulmonary, musculoskeletal, gastrointestinal, dermatologic, psychiatric, and cardiovascular (including ACS and non-ACS).9, 10 In addition to ACS, this differential includes other immediately life-threatening diseases such as pulmonary embolism, tension pneumothorax, and aortic dissection, necessitating rapid diagnosis and treatments that are markedly different than those for ACS.

    The tools most readily available to guide disposition of the patient with chest pain are the patient’s age and sex, history of coronary artery disease (CAD) or its risk factors, and the chest pain history. Usually, an initial 12-lead electrocardiogram (ECG) is added as well.

    In patients without significant ECG changes, risk factors for CAD have been shown to be poor predictors of AMI or ACS.4, 11, 12 The initial 12-lead ECG has a sensitivity of only 20% to 60% for AMI, 13 – 15 and a single set of biochemical markers also has poor sensitivity.14 – 16 Because none of these tools used alone is a reliable predictor of ACS, the chest pain characteristics are usually used in conjunction with them to help determine disposition.

    Although this article discusses the chest pain history, AMI and ACS may also present with nonpain equivalent symptoms or be truly silent.17, 18 Typical and atypical chest pain Although a consensus exists about what represents a typical chest pain description, the equivalent definition for atypical chest pain is less clear.

    Heberden 19 provided the first description of typical ischemic chest pain in 1768: a painful sensation in the breast accompanied by a strangling sensation, anxiety, and occasional radiation of pain to the left arm. He also observed an association with exertion and relief with rest.20 Chest pain symptoms that do not fall into this typical category have been termed atypical,

    However, authors and clinicians using this term often fail to define it or disagree on its definition, making its use potentially confusing. We have reviewed the literature to identify the elements of the chest pain history that may be most helpful to the clinician and to identify its limitations.

    We performed a MEDLINE search of articles written between 1970 and 2005 by using the following search terms: chest pain, atypical, myocardial infarction, acute coronary syndrome, clinical characteristics, esophageal, location, quality, severity, duration, pleuritic, positional, chest wall tenderness, exercise, rest, emotion, nitroglycerin, GI cocktail, diabetic, elderly, and gender,

    In addition, the following Medical Subject Heading terms were used: myocardial infarction (subheading diagnosis ), chest pain (alone and with subheading classification ), angina pectoris, and medical history taking, An Ovid search was performed with the aid of a professional librarian, and the following terms were used: chest pain and atypical,

    1. Criteria used for study selection were controlled study design and English language.
    2. We present data from prospective and retrospective observational investigations, as well as systematic reviews.
    3. We required that observational studies include at least 80 patients.
    4. Studies were included if at least 1 chest pain characteristic was described and if diagnosis of either ACS or AMI was made with appropriate diagnostic testing.

    We also reviewed the most recent editions of commonly used textbooks.21 – 23 Some articles addressed the predictors of AMI; others, ACS. We have attempted to maintain that distinction. We have quoted positive likelihood ratios (and 95% confidence intervals) from published meta-analyses when they exist and otherwise calculated them from published raw numbers.

    1. If published likelihood ratios differed, we presented the one with the narrowest 95% confidence interval.
    2. We included the number of subjects included in these analyses.
    3. For areas of controversy, such as those in which likelihood ratios did not achieve statistical significance or study results conflicted, we commented in text but did not tabulate.

    A Review of Chest Pain Characteristics Table 1 identifies standard questions and suggests some considerations. Table 2 guides the interpretation of the patient’s chest pain history and summarizes the results of our literature review. Quality. Typical chest pain qualities, such as pressure or aching, are generally thought to be indicative of cardiac ischemia.

    However, formal investigations have yielded conflicting findings and have demonstrated that these descriptors predict AMI weakly or not at all.2, 3, 24 – 28 Extensive meta-analyses by Chun and Magee 29 and Panju et al 24 determined that typical predictors of pain such as pressurelike were associated with positive likelihood ratios of 1 to 2, which are values that are not robust enough to be independently useful in establishing a myocardial infarction (MI) diagnosis.

    On the other hand, studies have shown that certain descriptors such as sharp and stabbing more powerfully differentiate nonischemic from ischemic pain. Both Lee et al 2 and Panju et al 24 found that pain described as sharp or stabbing significantly decreased the likelihood of chest pain representing an AMI.

    1. Cultural differences may play a role in the connotation of these descriptive adjectives, particularly the word sharp,30 Finally, an additional helpful historical item in identifying ACS is chest pain that is worse than previous angina or similar to previous MI.25, 29 Location.
    2. Classic ischemic chest pain is often described as occurring in the substernal or left chest area, but few studies have examined whether specific chest pain locations predict AMI or ACS.

    Everts et al 31 concluded that a pain location of central or midchest has little value for predicting AMI. The physiologic explanation for this may be that esophageal pathology typically induces retrosternal pain as well.9 The same authors also found that pain in the middle-left chest (inframammary region) was more common in patients without AMI, although differences may be too small to be useful.31, 32 Many studies have shown that the region of infarction (inferior/posterior vs anterior) is not associated with differences in pain location, 33 – 35 although patients with inferior AMI more often have abdominal pain or other gastrointestinal symptoms than those with anterior infarctions.33 Radiation.

    The term radiation of chest pain usually refers to pain that originates in the chest but travels to nonchest areas, such as the jaw, back, or arm. Ischemic chest pain is classically described as radiating from the chest to one arm or both arms, a teaching supported by several studies.3, 14, 24, 25, 27, 29 In the study by Goodacre et al 14 of 893 chest pain patients with nondiagnostic ECGs, likelihood ratios were determined independently through the use of multiple logistic regression.

    For pain radiating to the shoulders or both arms, the adjusted positive likelihood ratio for AMI was 4.07 (2.53-6.54). Size of the Area of Chest Pain. In addition to the location and radiation of chest pain, the size of the area involved deserves consideration.

    One study examined the traditional teaching that localized pain suggests a musculoskeletal or psychiatric (DaCosta’s syndrome) origin.31, 36 In this study, 27 of 403 AMI patients (7%) vs 46 of 419 non-AMI patients (11%) localized their pain to a small area (a point or the size of a coin), 31 which yielded a likelihood ratio of 0.6, but the 95% confidence interval was 0.3 to 1.0.

    Severity. Eriksson et al 35 conducted a study of consecutive patients admitted to a cardiac care unit to compare the severity of chest pain in ACS vs nonischemic groups and found no statistically significant difference. Others have conducted similar studies and also found no differences.37 Time Variables.

    1. Chest pain indicative of ACS is typically described as having a crescendo pattern, reaching maximal intensity only after several minutes.
    2. In a review article, Constant 32 states that pain that is maximal in intensity at onset is unlikely to represent cardiac ischemia.
    3. In contradistinction, pain from aortic dissection is described by patients as “severe” or “the worst pain ever” in 91% of cases and of abrupt onset in 85%.38 Traditional teaching states that the classic duration of angina pectoris is 2 to 10 minutes, with 10 to 30 minutes suggesting unstable angina.23, 32 Pain lasting more than 30 minutes is considered indicative of either an AMI or a nonischemic etiology.32 Experts consider recurrent pain that lasts for many hours or days with each episode unlikely to be cardiac.32 Unfortunately, the data to support these timing distinctions are limited.27, 39 For chest pain lasting longer than 30 minutes, the diagnosis most often confused with AMI is gastroesophageal disease.9, 40 At the other extreme, consensus among experts is that pain that lasts only seconds is rarely indicative of ischemic chest pain, although this has not been demonstrated in formal studies.32 Precipitating and Aggravating Factors An easy-to-remember construct for possible precipitating factors is the 3 p ‘s, which are chest pain that is pleuritic, positional, or reproducible with chest wall palpation.

    Pleuritic Chest Pain. Chest pain that is reproduced on deep inspiration or with coughing is often associated with non-ACS diseases such as pulmonary embolism or costochondritis and has been shown by several studies to be suggestive of non-AMI.2, 3, 25 In the study by Lee et al, 2 chest pain that was only partially pleuritic (deep breathing reproduces the pain only sometimes) was a less valid discriminant than pain that was fully pleuritic.

    • Positional Chest Pain.
    • Chest pain that is exacerbated by changes in position is thought to be more indicative of nonischemic causes.
    • For example, pericarditis is often alleviated by leaning forward, whereas musculoskeletal chest pain can typically be reproduced by arm or neck movement.32, 41 Several studies have confirmed that a positional component of chest pain represents a non-ACS etiology.2, 25 Palpable Chest Pain.

    Although chest-wall tenderness is technically part of the physical examination, not the medical history, several studies have demonstrated that it suggests a non-ACS etiology.2, 3, 14, 25 Exercise. The association between exercise and angina is well established in the literature.23, 39, 42 However, the relationship between exercise and AMI is less clearly elucidated.

    Mittleman et al 43 established that, among AMI patients, heavy exertion in the hour preceding their event was common, confirming a correlation between exercise and AMI. In addition, Goodacre et al 14 found that exertional pain is associated with AMI. Furthermore, when exertional pain is lacking, the likelihood of AMI decreases.

    Emotion and Stress. Although several studies have suggested linkages between emotional stress and AMI, attributing this relationship to high sympathetic activity, data to support using this as a discriminant to identify ACS have not been established.44 – 46 Of note, a syndrome of reversible cardiomyopathy triggered by emotionally stressful events and occurring primarily in women may mimic evolving ACS.47 Nitroglycerin.

    • Previous thought held that rapid relief of chest pain with sublingual nitroglycerin strongly supports the diagnosis of angina.48, 49 In addition to relaxing coronary smooth muscle, nitroglycerin causes relaxation of esophageal muscle and thus can alleviate esophageal causes of chest pain as well.
    • Conventional teaching states that relief of cardiac pain is rapid (less than 5 minutes), whereas esophageal pain takes more than 10 minutes to subside.9 However, recent studies indicate that there is no association between AMI and relief of chest pain with nitroglycerin.50, 51 “GI Cocktail.” The GI cocktail is commonly used in emergency departments to treat dyspepsia.

    Compositions vary, but it is usually a mixture of viscous lidocaine, a liquid antacid, and Donnatal (composed of several anticholinergics and a barbiturate). It has been common practice to use the GI cocktail to differentiate cardiac from esophageal chest pain according to a study from the 1970s.52 However, more recent studies and case series have contradicted these findings.53, 54 Rest.

    Rest characteristically relieves the pain associated with stable angina within 1 to 5 minutes.23 If pain continues for longer than 10 minutes after rest, the patient has traditionally been considered to be experiencing unstable angina, an AMI, or noncardiac pain. In a comparison of cardiac and esophageal patients, 32 of 52 (62%) with cardiac and 9 of 18 (50%) with esophageal pathology experienced relief of pain by rest ( P =,39).9 This lack of significance from this small study makes it unclear whether relief of chest pain with rest is helpful in differentiating ACS from noncardiac pathology.

    Several studies have examined the ability of associated symptoms such as nausea, vomiting, and diaphoresis to predict AMI.3, 14, 25 – 27 Two meta-analyses discovered that nausea and diaphoresis predict AMI.24, 29 However, in the study by Goodacre et al, 14 the association between nausea, vomiting, diaphoresis, and AMI disappeared on multivariable testing.

    1. Combinations of Characteristics of the Chest Pain History to Formulate Low-Risk Groups No single element of the chest pain history is a powerful enough predictor of non-ACS or non-AMI to allow the clinician to make decisions according to it alone.
    2. However, some authors have made efforts to combine elements.2, 28, 55 – 64 Several simply combined atypical features into a decision rule or a scale, 2, 55 – 57 whereas others used computer-aided algorithms.58 – 64 Although several of these studies have demonstrated an ability to improve triage decisions within an experimental framework, these protocols have either not been validated or have demonstrated mixed results when implemented in clinical settings.2, 58 – 64 Recently, a semiquantitative chest pain score was used to improve risk stratification as compared with the Thrombolysis In Myocardial Infarction risk score.56 In a patient population with negative troponin and ECG test results without ST-segment deviation, this chest pain score was used to assist with risk stratification.

    In this study, no patients in the lowest-risk category (n = 111) met the end point of mortality or MI at 1 year.56 Among the efforts to combine elements of the chest pain history with other available data is the work by Lee et al 2 that identified 3 variables that defined a very low-risk group for AMI.

    • When chest pain was sharp or stabbing; was positional, pleuritic, or reproducible with palpation; and occurred in patients with no history of angina or MI, none of 48 patients were diagnosed with an AMI at hospital discharge.
    • Unfortunately, only 8% of their overall study population (596 patients) were in this category.

    Chest Pain Characteristics Associated With High or Low Probabilities for ACS and AMI: Typical and Atypical Chest Pain Although Heberden’s 19 description of typical chest pain contains many features that have been substantiated by formal studies, the concept of atypical chest pain is more elusive.

    There is no standard, uniformly agreed-on definition of atypical chest pain. One broadly used definition is any chest pain that does not meet Heberden’s 19 classic description.20 The other is one that indicates a decreased likelihood of cardiac etiology.41, 49 For example, Diamond 49 classified chest pain into typical angina and atypical angina according to the number of criteria it met when substernal location, precipitation by exertion, and relief by nitroglycerin were considered.

    However, distinctions between these terminologies have become blurred. Furthermore, evidence correlating chest pain characteristics with ACS or AMI likelihood is either sparse or, in many cases, conflicting. According to this literature review, we can categorize characteristics of chest pain into groups by quality and amount of evidence.

    For pain that is stabbing, pleuritic, positional, or reproduced by palpation, likelihood ratios of 0.2 to 0.3 suggest that this pain more likely represents a non-ACS syndrome. For other chest pain characteristics, such as pain limited to the inframammary region or that is nonexertional, there is weaker evidence.

    Although chest pain that lasts only seconds or is constant over days may also fall into this category, data are limited. Conversely, for chest pain that radiates to one or both arms or shoulders or is precipitated by exertion, likelihood ratios of 2.3 to 4.7 suggest that this pain more likely represents an ACS syndrome.

    There is weaker evidence that other features of the chest pain history suggest an ACS etiology, including chest pain that is associated with nausea, vomiting, or diaphoresis; is worse than previous angina or similar to previous MI pain; or is described as “pressure.” Limitations of the Chest Pain History Likelihood ratios for various elements of the chest pain history that are bracketed by the values 0.2 and 4.7 make it a helpful but imperfect tool.

    In addition, because many of the likelihood ratios published treat elements of the chest pain history as independent rather than interdependent variables, they most likely overestimate their strength as predictors. The quality component of the chest pain history lends itself to a high degree of subjectivity.

    • For example, in certain cultures the term sharp actually denotes pain that is severe, rather than knifelike.30 Beyond cultural and linguistic differences, certain subpopulations may present with chest pain symptoms that differ from those in a general population.
    • Women, patients with diabetes mellitus, and elderly persons represent particular groups that have been the subjects of research in this area.65 – 74 In these populations, the predictive power of the chest pain history may be even further weakened.

    Finally, variability in physician history-taking adds to subjectivity because of poor interphysician reliability and problems with medical record entry.75 Determining Patient Risk and Disposition: The Chest Pain History in Context When treating a patient with chest pain, the goal of the clinician is to determine the likelihood of ACS or non-ACS, as well as that of other life-threatening conditions.

    In general, the chest pain history has been used to predict the likelihood of AMI and ACS, not final outcomes such as mortality. For these final outcomes, it represents a less powerful risk stratification tool than biomarkers or even the initial ECG.76 – 80 In particular, no single element of the chest pain history conveys a powerful enough likelihood ratio to safely allow the clinician to discharge a patient without some additional testing.

    Despite this limitation, the chest pain history is of value and conveys useful information. At the initial encounter, it represents one of the few data points available to establish formal or informal path probabilities for ACS ( Box ). In this context, it is used in conjunction with other information available initially, including the patient’s age, sex, and history of coronary disease and, to a lesser degree, findings on physical examination.

    1. Although risk factors for CAD are often considered as well, their appropriate use as applied to individual patients has been subject to debate.12, 81 – 83 The initial ECG is easy to obtain and immediately available and thus is also included in this set of initially available information. Box.
    2. Risk Stratification for Acute Myocardial Infarction and Acute Coronary Syndrome According to Components of the Chest Pain History Low Risk Pain that is pleuritic, positional, or reproducible with palpation or is described as stabbing 2, 3, 24, 25, 29 Probable Low Risk Pain not related to exertion or that occurs in a small inframammary area of the chest wall 14, 31, 42 Probable High Risk Pain described as pressure, is similar to that of prior myocardial infarction or worse than prior anginal pain, or is accompanied by nausea, vomiting, or diaphoresis 3, 14, 24, 25, 27 – 29 High Risk Pain that radiates to one or both shoulders or arms or is related to exertion 3, 14, 24, 25, 27, 29 By virtue of this integration into other initially available information, the chest pain history is potentially useful in 3 ways.

    The first is the yet-unachieved goal of identifying patients who can be sent home safely without further immediate evaluation. Although confirmatory studies need to be undertaken, existing literature suggests that certain features of the chest pain history, in conjunction with other initially available information, may be able to achieve this goal.2, 56, 57 Second, because the chest pain history helps to establish previous probabilities of the likelihood of ACS or AMI, it is an integral part of determining the need for and intensity of additional testing and the necessary period of observation.

    • Finally, the chest pain history may point the clinician to other diagnostic possibilities.
    • Although some of these possibilities, such as gastroesophageal reflux disease, can be evaluated on outpatients, others such as pulmonary embolus or aortic dissection require immediate evaluation.
    • The chest pain history joins demographic information, the history of CAD and its risk factors, and the physical examination as information immediately available to the clinician to determine the likelihood of AMI and ACS when a patient is first evaluated with chest pain.

    Although certain chest pain characteristics decrease or increase the likelihood of ACS or AMI, with likelihood ratios that range from 0.2 to 4.7, none of them are powerful enough to support discharging patients according to the chest pain history alone.

    Certain combinations of components of the chest pain history, in conjunction with other information available immediately to the clinician, have been associated with low risk of AMI.56 – 64, 78, 79 However, combination protocols have yet to prove successful when implemented in the clinical setting.6, 79 The identification of a group at low risk for short-term mortality and morbidity and reproducible identification of that group within a nonexperimental framework remains an important area of future research.

    Despite this limitation, the chest pain history, when interpreted in light of existing literature, allows the clinician to establish approximate probabilities for acute cardiac ischemia. In combination with other initially available data, it helps the clinician determine how intensive a diagnostic and monitoring strategy for AMI or ACS to pursue and whether to consider other life-threatening illnesses requiring immediate evaluation.

    1. Despite its shortcomings, the chest pain history represents a diagnostic tool that is commonly used, relatively inexpensive, and universally available.
    2. Corresponding Author: John T.
    3. Nagurney, MD, MPH, Massachusetts General Hospital, 55 Fruit St, Clinics 115, Boston, MA 02114 ( [email protected] ).

    Financial Disclosures: None reported. Acknowledgment: We thank the faculty, nursing, and administrative staff of our emergency department for their dedication in caring for patients with chest pain and the residents of the Harvard Affiliated Emergency Medicine Residency for asking thought-provoking questions.1.

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    What is the difference between angina pain and chest pain?

    Overview – Angina (an-JIE-nuh or AN-juh-nuh) is a type of chest pain caused by reduced blood flow to the heart. Angina is a symptom of coronary artery disease. Angina is also called angina pectoris. Angina pain is often described as squeezing, pressure, heaviness, tightness or pain in the chest.

    1. It may feel like a heavy weight lying on the chest.
    2. Angina may be a new pain that needs to be checked by a health care provider, or recurring pain that goes away with treatment.
    3. Although angina is relatively common, it can still be hard to distinguish from other types of chest pain, such as the discomfort of indigestion.

    If you have unexplained chest pain, seek medical help right away.

    What is the code for acute chest pain?

    R072 Precordial pain
    R0782 Intercostal pain
    R0789 Other chest pain
    R079 Chest pain, unspecified

    What is the ICD-10 for chest pain with SOB?

    ICD-10-CM Code for Chest pain on breathing R07.1.

    What is the ICD-10 code for chest pain in setting of CAD?

    1. ICD-10-CM Codes
    2. I00-I99
    3. I20-I25
    4. I25-
    5. 2023 ICD-10-CM Diagnosis Code I25.119

    What is the ICD-10 for intercostal chest pain?

    R072 Precordial pain
    R0782 Intercostal pain
    R0789 Other chest pain
    R079 Chest pain, unspecified

    What is the ICD-10 code for R02 07?

    ICD-10 code: R02.07 Necrosis of skin and subcutaneous tissue, not elsewhere classified: Ankle, foot and toes ICD-Code The skin is supplied with oxygen and nutrients through the blood. If, for example, the skin is not supplied with enough blood or any at all, this area of the skin can die.

    G: Confirmed diagnosis V: Tentative diagnosis Z: Condition after A: Excluded diagnosis L: Left R: Right B: Both sides

    This information is not intended for self-diagnosis and does not replace professional medical advice from a doctor. If you find an ICD code on a personal medical document, please also note the additional indicator used for diagnostic confidence.Your doctor will assist you with any health-related questions and explain the ICD diagnosis code to you in a direct consultation if necessary.

    G: Confirmed diagnosis V: Tentative diagnosis Z: Condition after A: Excluded diagnosis L: Left R: Right B: Both sides

    : ICD-10 code: R02.07 Necrosis of skin and subcutaneous tissue, not elsewhere classified: Ankle, foot and toes

    What does precordial chest pain mean?

    What causes precordial catch syndrome? – “Precordial” means “in front of the heart,” which identifies where the pain occurs rather than the source or cause of it. Experts believe that precordial catch syndrome occurs when nerves in the inner lining of the chest wall are pinched or irritated, possibly the ribs, cartilage or the lining of the lung, called the pleura.