Chest Pain: Symptoms, Causes, and Diagnosis

Chest Pain Overview

• A common symptom ranging from mild discomfort to severe, life-threatening conditions.
• Requires prompt evaluation and diagnosis.
• Encompasses sensations like pressure, tightness, squeezing, or aching in the chest.
• Pain may radiate to other parts of the upper body.
• Etiology is diverse.
• Includes cardiac, pulmonary, gastrointestinal, and musculoskeletal causes.
• Accurate diagnosis is challenging yet crucial for appropriate management.
• Rapid assessment and risk stratification are essential.
• Key to identifying potentially life-threatening conditions.
• Examples of these conditions: acute coronary syndrome (ACS), pulmonary embolism, and aortic dissection.
• Chest discomfort is a common reason for medical attention at the emergency department (ED) or outpatient clinic.
• Evaluation of nontraumatic chest discomfort is challenging due to a variety of possible causes.
• Chest discomfort can be categorized into: myocardial ischemia, other cardiopulmonary causes, and noncardiopulmonary causes.
• Rapid identification of high-risk conditions is a priority, but routine liberal testing can lead to adverse effects.

Etiology of Chest Pain

• Multifactorial, with cardiac causes being the most critical to rule out due to potential lethality.
• Acute coronary syndrome includes unstable angina and myocardial infarction which results from reduced blood flow to the heart muscle.
• Non-cardiac causes include gastrointestinal disorders like gastroesophageal reflux disease (GERD).
• Pulmonary conditions like pulmonary embolism are also non-cardiac causes.
• Musculoskeletal issues and psychological factors, like panic disorder, can cause chest pain, complicating diagnosis.
• Chest discomfort is one of the three most common reasons for visits to the ED in the United States.
• Results in 6 to 7 million emergency visits each year.
• Over 60% of patients are hospitalized for further testing.
• Most of the remainder undergo additional investigation in the ED.
• Fewer than 15% of evaluated patients are eventually diagnosed with acute coronary syndrome (ACS).
• Rates of ACS vary from 10-20% in unselected populations to as low as 5% in some studies.
• The most common diagnoses are gastrointestinal causes.
• As few as 5% are other life-threatening cardiopulmonary conditions.
• In a large proportion of patients with transient acute chest discomfort, ACS or another acute cardiopulmonary cause is excluded.
• Cause is not determined for a large proportion of patients.
• 2-6% of patients with chest discomfort of presumed nonischemic etiology discharged from the ED were later deemed to have had a missed myocardial infarction (MI).
• Patients with a missed diagnosis of MI have double the 30-day risk of death compared to those hospitalized.
• In a study of more than 350,000 patients with unspecified presumed noncardiopulmonary chest discomfort, the mortality rate 1 year after discharge was under 2%.
• This rate 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.
• The study excluded patients with ST-segment elevation or definite noncardiac chest pain.
• Myocardial ischemia causing chest discomfort, termed angina pectoris, is a primary clinical concern in patients presenting with chest symptoms.
• Ischemia is precipitated by an imbalance between myocardial oxygen requirements and myocardial oxygen supply.
• Results 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 contractility.
• 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 is most commonly caused by atheromatous plaque obstructing one or more of the epicardial coronary arteries.
• Stable ischemic heart disease usually results from the gradual atherosclerotic narrowing of the coronary arteries.
• Stable angina is characterized by ischemic episodes typically precipitated by a superimposed increase in oxygen demand during physical exertion and relieved upon resting.
• Ischemic heart disease becomes unstable.
• Manifests by ischemia at rest or with an escalating pattern, most commonly when rupture or erosion of one or more atherosclerotic lesions triggers coronary thrombosis.
• Unstable ischemic heart disease is further classified clinically by the presence or absence of detectable acute 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 ischemic heart disease is classified as unstable angina when there is no detectable acute myocardial injury and as non-ST elevation MI (NSTEMI) when there is evidence of acute myocardial necrosis.
• When the coronary thrombus is acutely and completely occlusive, transmural myocardial ischemia usually ensues, with ST-segment elevation on the ECG and myocardial necrosis leading to a diagnosis of ST elevation MI (STEMI).
• Clinicians should be aware that unstable ischemic symptoms may also occur predominantly because of increased myocardial oxygen demand or because of decreased oxygen delivery due to anemia, hypoxia, or hypotension.
• Acute coronary syndrome, which encompasses unstable angina, NSTEMI, and STEMI, is typically reserved for ischemia precipitated by acute coronary atherothrombosis.
• A standardized system for classification of MI has been expanded to discriminate MI resulting from acute coronary thrombosis (type 1 MI) from MI occurring secondary to other imbalances of myocardial oxygen supply and demand (type 2 MI).
• Conditions are additionally distinguished from nonischemic causes of acute myocardial injury, such as myocarditis.
• Other contributors to stable and unstable ischemic heart disease include endothelial dysfunction, microvascular disease, and vasospasm, which may exist alone or in combination with coronary atherosclerosis
• Atherosclerosis may be the dominant cause of myocardial ischemia in some patients.
• Nonatherosclerotic processes, can lead to coronary obstruction
• Congenital abnormalities of the coronary vessels, myocardial bridging, coronary arteritis, and radiation-induced coronary disease, fall into this category.
• 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.

Ischemic Chest Discomfort

• Angina pectoris, often referred to simply as “angina,” clinical characteristics are highly similar whether the ischemic discomfort is a manifestation of stable ischemic heart disease, unstable angina, or MI.
• Exceptions are differences in the pattern and duration of symptoms associated with these syndromes.
• Heberden initially described angina as a sense of “strangling and anxiety.”
• Chest discomfort characteristic of myocardial ischemia is typically described as aching, heavy, squeezing, crushing, or constricting.
• In a substantial minority of patients, quality of discomfort is extremely vague.
• May be described as a mild tightness, or merely an uncomfortable feeling, that sometimes is experienced as numbness or a burning sensation.
• Site of discomfort is usually retrosternal, but radiation is common.
• Chest pain 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.
• Discomfort typically occurs predictably at a characteristic level of exertion or psychological stress.
• Unstable angina is manifest by anginal chest discomfort that occurs with progressively lower intensity of physical activity or even at rest.
• Chest discomfort associated with MI is commonly more severe, is prolonged (usually lasting ≥30 min), and is not relieved by rest.
• Neural pathways involved in ischemic cardiac pain are poorly understood.
• Ischemic episodes are thought to excite local chemosensitive and mechanoreceptive receptors.
• Cause 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.
• 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

• 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.
• The discomfort of pericarditis is usually pleuritic pain that is exacerbated by breathing, coughing, or changes in position.
• 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 and pericardial inflammation 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.

Myocardial Diseases

• Acute inflammatory and other nonischemic myocardial diseases can also produce chest discomfort.
• Symptoms of acute myocarditis are highly varied.
• Chest discomfort may originate with inflammatory injury of the myocardium or severe increases in wall stress related to poor ventricular performance.
• Symptoms of Takotsubo (stress-related) cardiomyopathy often start abruptly with chest pain and shortness of breath.
• 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 over 50 years of age.

Diseases of the Aorta

• Acute aortic dissection is a less common cause of chest discomfort.
• Its importance is 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.
• Results in separation of the media and creation of a separate "false" lumen.
• A penetrating ulcer has been described as 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 is an aortic wall hematoma with no demonstrable intimal flap, no radiologically apparent intimal tear, and no false lumen. Intramural hematoma 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.
• Dissections involving the ascending aorta tend to cause pain in the midline of the anterior chest.
• Descending aortic syndromes most often present with pain in the back.
• Dissections that begin in the ascending aorta and extend to the descending aorta tend to cause pain in the front of the chest that extends toward the back, between the shoulder blades.
• Proximal aortic dissections that involve the ascending aorta (type A in the Stanford nomenclature) are at high risk for major complications.
• May influence the clinical presentation, including compromise of the aortic ostia of the coronary arteries, resulting in MI; disruption of the aortic valve, causing acute aortic insufficiency; and rupture of the hematoma into the pericardial space, leading to pericardial tamponade.
• Knowledge of the epidemiology of acute aortic syndromes can be helpful in maintaining awareness of this relatively uncommon group of disorders (estimated annual incidence, 3 cases per 100,000 population).
• Nontraumatic aortic dissections are very rare in the absence of hypertension or conditions associated with deterioration of the elastic or muscular components of the aortic media, including pregnancy, bicuspid aortic disease, or inherited connective tissue diseases, such as Marfan and Ehlers-Danlos syndromes.
• Although aortic aneurysms are most often asymptomatic, thoracic aortic aneurysms can cause chest pain and other symptoms by compressing adjacent structures.
• This pain tends to be steady, deep, and occasionally severe.
• Aortitis, whether of noninfectious or infectious etiology, in the absence of aortic dissection is a rare cause of chest or back discomfort.

Pulmonary Conditions

• Pulmonary and pulmonary-vascular conditions that cause chest discomfort usually do so in conjunction with dyspnea and often produce symptoms that have a pleuritic nature.
• Pulmonary Embolism can produce dyspnea and chest discomfort that is sudden in onset.
• The chest discomfort associated with pulmonary embolism may result from involvement of the pleural surface of the lung adjacent to a resultant pulmonary infarction distention of the pulmonary artery.
• The chest discomfort associated with pulmonary embolism may result from right ventricular wall stress and/or subendocardial ischemia related to acute pulmonary hypertension.
• Pain associated with small pulmonary emboli is often lateral and pleuritic.
• Pain is believed to be related to the first of three possible mechanisms.
• Massive pulmonary emboli may cause severe substernal pain that may mimic an MI.
• The pain is plausibly attributed to the second and third of these potential mechanisms.
• Massive or submassive pulmonary embolism may also be associated with syncope, hypotension, and signs of right heart failure.
• Primary spontaneous pneumothorax is a rare cause of chest discomfort.
• Estimated annual incidence of 7 per 100,000 among men and less than 2 per 100,000 among women.
• Risk factors include male sex, smoking, family history, and Marfan syndrome.
• Symptoms are usually sudden in onset, and dyspnea may be mild thus, presentation to medical attention is sometimes delayed.
• Secondary spontaneous pneumothorax may occur in patients with underlying lung disorders.
• Chronic obstructive pulmonary disease, asthma, or cystic fibrosis are underlying lung disorders.
• Secondary spontaneous pneumothorax usually produces symptoms that are more severe.
• Tension pneumothorax is a medical emergency caused by trapped intrathoracic air that precipitates hemodynamic collapse.
• Most pulmonary diseases that produce chest pain, including pneumonia and malignancy, do so because of involvement of the pleura or surrounding structures.
• Pleurisy is typically described as a knifelike pain that is worsened by inspiration or coughing.
• Chronic pulmonary hypertension can manifest as chest pain that may be very similar to angina in its characteristics.
• Reactive airways diseases similarly can cause chest tightness associated with breathlessness rather than pleurisy.

Noncardiopulmonary causes

• Gastrointestinal disorders are the most common cause of nontraumatic chest discomfort
• Often produce symptoms that are difficult to discern from more serious causes of chest pain, including myocardial ischemia.
• Esophageal disorders, in particular, may simulate angina in the character and location of the pain.
• Gastroesophageal reflux and disorders of esophageal motility are common.
• The pain of esophageal spasm is commonly an intense, squeezing discomfort.
• May be relieved by nitroglycerin or dihydropyridine calcium channel antagonists.
• Chest pain can also result from injury to the esophagus, such as a Mallory-Weiss tear or an esophageal rupture (Boerhaave's syndrome) caused by severe vomiting.
• Peptic ulcer disease is most commonly epigastric in location but can radiate into the chest
• Hepatobiliary disorders, including cholecystitis and biliary colic, may mimic acute cardiopulmonary diseases.
• The pain arising from these disorders usually localizes to the right upper quadrant of the abdomen, but may be felt in the epigastrium and radiate to the back and lower chest.
• May be referred to the scapula or shoulder, suggesting diaphragmatic irritation.
• The pain is steady, usually lasts several hours, and subsides spontaneously.
• Pain from pancreatitis is typically aching epigastric pain that radiates to the back.
• Chest discomfort can be produced by any musculoskeletal disorder.
• Involves the chest wall or the nerves of the chest wall, neck, or upper limbs.
• Costochondritis is relatively common.
• Causes tenderness of the costochondral junctions (Tietze's syndrome).
• Cervical radiculitis presents as a prolonged or constant aching discomfort in the upper chest and limbs, exacerbated by motion of the neck.
• Chest pain can be caused by compression of the brachial plexus by the cervical ribs.
• Tendonitis or bursitis involving the left shoulder may mimic the radiation of angina.
• Pain in a dermatomal distribution can be caused by cramping of intercostal muscles or by herpes zoster.
• Emotional and Psychiatric Conditions such as panic disorder can be a cause.
• Symptoms include chest tightness or aching associated with anxiety and difficulty breathing.
• Symptoms may be prolonged or fleeting.
• Pressure or tightness is consistent with typical myocardial ischemic pain.
• Clinicians need to remember that some patients deny any pain, but dyspnea is an anxiety signal.
• Severity of the discomfort has poor diagnostic accuracy.
• Inquire about the similarity of the discomfort to previous ischemic symptoms.
• Angina is not sharp (knifelike, stabbing, or pleuritic), but patients sometimes use the word sharp to convey the intensity of discomfort.
• Pleuritic discomfort is suggestive of a process involving the pleura.
• Conditions like pericarditis, pulmonary embolism, or pulmonary parenchymal processes fall into this category.
• Pain of pericarditis or massive pulmonary embolism is steady severe pressure or aching.
• Can be difficult to discriminate from myocardial ischemia.
• “Tearing” or "ripping" pain is often described by patients with acute aortic dissection.
• Acute aortic emergencies also present commonly with knifelike pain.
• A burning quality can suggest acid reflux or peptic ulcer disease but may also occur with myocardial ischemia.
• Esophageal pain, particularly with spasm, can be a severe squeezing discomfort identical to angina.
• Substernal location with radiation to neck, jaw, shoulder, or arms is typical of myocardial ischemic discomfort.
• Radiation to both arms has a high association with MI.
• Some patients present with aching in sites of radiated pain exclusively.
• Pain that is highly localized—e.g., demarcated by the tip of one finger—is unusual for angina.
• Retrosternal location suggests esophageal pain.
• Other gastrointestinal conditions usually present with pain in the abdomen or epigastrium, with possible radiation into the chest.
• Angina may also occur in an epigastric location.
• Pain that occurs solely above the mandible or below the epigastrium is rarely angina.
• Severe pain radiating to the back should prompt consideration of acute aortic syndrome.
• Radiation to the trapezius ridge is characteristic of pericardial pain and does not usually occur with angina.
• Myocardial ischemic discomfort builds over minutes.
• It is exacerbated by activity and mitigated by rest.

Additional Factors

• Pain reaching peak intensity immediately suggests aortic dissection, pulmonary embolism, or spontaneous pneumothorax.
• Fleeting pain (lasting only a few seconds) is rarely ischemic.
• Constant pain in intensity for a prolonged period (many hours to days) unlikely to represent myocardial ischemia.
• Clinical consequences such as ECG abnormalities and elevation of cardiac biomarkers, should be present.
• Clinical sequelae (e.g., heart failure or hypotension) contribute.
• Myocardial ischemia and acid reflux may both start in the morning.
• Myocardial ischemic pain patients prefer to rest, sit, or stop walking.
• Clinicians should be aware of “warm-up angina” or angina relief that occurs as patients continue or increase exertion intensity.
• Intensity pain with changes in position or movement of the upper extremities and neck are less likely associated with myocardial ischemia and suggest a musculoskeletal etiology.
• Pain of pericarditis is worse in the supine position and relieved by sitting upright and leaning forward.
• Gastroesophageal reflux may be triggered by alcohol, some foods, or a reclined position; relief can occur with sitting.
• Exacerbation by eating suggests a gastrointestinal etiology: peptic ulcer disease, cholecystitis, or pancreatitis.
• Peptic ulcer disease tends to become symptomatic 60-90 min after meals.
• In severe coronary atherosclerosis, redistribution of blood flow to the splanchnic vasculature after eating can trigger postprandial angina.
• Discomfort of acid reflux and peptic ulcer disease reduces with acid-reducing therapies.
• In contrast with angina, physical exertion is unlikely to alter gastrointestinal symptoms.
• Relief of chest discomfort in minutes after nitroglycerin is suggestive, but not sufficiently sensitive or specific for, myocardial ischemia.
• Esophageal spasm may also be relieved by nitroglycerin.
• A delay of over 10 minutes before relief after nitroglycerin suggests that the symptoms are not caused by ischemia or are caused by severe ischemia, such as during acute MI.

Associated Symptoms

• Myocardial ischemia includes diaphoresis, dyspnea, nausea, fatigue, faintness, and eructations.
• These symptoms may exist in isolation as anginal equivalents, particularly in women and the elderly.
• Dyspnea is not discriminative, its presence suggests a cardiopulmonary etiology.
• Sudden onset of significant respiratory distress indicates pulmonary embolism and spontaneous pneumothorax.
• Hemoptysis indicates pulmonary embolism or severe heart failure and a pulmonary parenchymal etiology of chest symptoms.
• Syncope or presyncope presents when there is hemodynamically significant pulmonary embolism /aortic dissection/ ischemic arrhythmias.
• Nausea and vomiting suggest a gastrointestinal disorder but may occur in MI (inferior MI), due to vagal reflex activation or stimulation of left ventricular receptors.

Diagnosis Considerations

• Past medical history assesses risk factors for coronary atherosclerosis and venous thromboembolism.
• For example, history of connective tissue diseases such as Marfan syndrome should heighten suspicion of an acute aortic syndrome or spontaneous pneumothorax.
• Past history may elicit clues about depression or prior panic attacks.
• Physical exam can provide direct evidence of chest pain etiologies (e.g., unilateral absence of lung sounds).
• It can identify potential precipitants of acute cardiopulmonary causes of chest pain (e.g., uncontrolled hypertension), relevant comorbid conditions (e.g., obstructive pulmonary disease), and complications of the presenting syndrome (e.g., heart failure).
• Findings on physical examination may be normal during unstable ischemic heart disease, an unremarkable physical exam is not definitively reassuring.
• The patient's general appearance is helpful in establishing an initial impression of the severity of illness.
• Patients with acute MI or other acute cardiopulmonary disorders appear anxious, uncomfortable, pale, cyanotic, or diaphoretic.
• Patients massaging or clutching their chests can describe their pain with a clenched fist held against the sternum (Levine's sign).
• Body habitus and physical characteristics give clues.
• The prototypical young, tall, thin man suggest a spontaneous pneumothorax.
• Significant tachycardia and hypotension indicates important hemodynamic consequences of the underlying cause of chest discomfort.
• Prompt rapid survey for conditions like 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 is an important manifestation of submassive pulmonary embolism.
• Tachypnea and hypoxemia point toward a pulmonary cause.
• If a low-grade fever is present this may also occur with a thromboembolism.
• Pulmonary examination localizes the primary cause of chest discomfort, as in cases of pneumonia, asthma, or pneumothorax.
• Left ventricular dysfunction from severe ischemia/infarction and acute valvular complications of MI or aortic dissection can lead to pulmonary edema.
• Jugular venous pulse is often normal with acute myocardial ischemia but may reveal certain patterns of pericardial tamponade or acute right ventricular dysfunction.
• Cardiac auscultation reveals a third heart sound, reflecting myocardial systolic or diastolic dysfunction.
• Murmurs of mitral regurgitation or a ventricular-septal defect may indicate mechanical complications.
• A murmur of aortic insufficiency occurs when there is ascending aortic dissection.
• Reveal underlying cardiac disorders contributory to ischemia (e.g., aortic stenosis or hypertrophic cardiomyopathy).
• Pericardial friction rubs reflect pericardial inflammation.
• Localizing tenderness informs about pain is abdominal-based.

Evaluation Tools

• 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 aortic dissection.
• Unilateral lower-extremity swelling should raise suspicion about venous thromboembolism.
• Musculoskeletal Pain arising is often associated with localized swelling.
• Pain on palpation of these joints is usually well localized and is a useful clinical sign, although deep palpation may elicit pain in the absence of costochondritis.
• Palpation of the chest wall can elicit pain in patients with various musculoskeletal conditions (but this should not exclude myocardial ischemia).
• Sensory deficits in the upper extremities indicates cervical disk disease.
• Electrocardiography is crucial in the evaluation because ECG detects ongoing ischemia and secondary cardiac complications.
• Society guidelines recommend that an ECG be obtained in under 10 minutes.
• Used for patients with ST-segment elevation diagnostic of MI who are candidates for immediate interventions to restore flow in the occluded coronary artery.
• T-wave inversions are useful and indicate a heightened risk.
• Serial performance of ECGs (every 30-60 min) is recommended in the ED evaluation of suspected ACS.
• An ECG with right-sided lead placement should be considered in patients with suspected ischemia.
• Resting ECG’s sensitivity for ischemia is poor.
• Abnormalities of the ST segment may occur in a variety of conditions.
• Pulmonary embolism, ventricular hypertrophy, acute and chronic pericarditis, myocarditis, electrolyte imbalance, and metabolic disorders.
• Hyperventilation with panic disorder leads to nonspecific ST and T-wave abnormalities.
• Pulmonary embolism is most often associated with sinus tachycardia but also leads to rightward shift of the ECG axis.
• ST-segment elevation in patients has diffuse lead involvement not corresponding to a specific coronary anatomic distribution and PR-segment depression.
• Chest radiography is performed routinely with acute chest discomfort.
• Should be selective with patients who have subacute or chronic pain.
• It is useful for identifying pulmonary processes, for example, pneumonia finds pulmonary edema, mediastinum widening, Hampton's hump or Westermark's sign.
• Laboratory testing detects myocardial injury through circulating proteins released from damaged cardiomyocytes.
• Initial biomarkers of injury may be in the normal range, even in patients with STEMI.
• Cardiac troponin is tested in ACS patients- but only to be used for risk stratification.
• High levels of troponin can detect lower blood concentrations of troponin.
• For these test reasons, high-sensitivity assays are generally preferred.
• When a negative troponin result is found, then do serial testing.
• Patients presenting over or under 2-3h may need additional testing.

Additional Info

• Observation of cardiac troponin concentration between serial samples is necessary.
• B-type useful in measurement as well.
• Clinical algorithms help in decision making during evaluation of chest pain patients, Goldman and Lee made one of the first.
• ECGs help in identification of ACS.
• Increasing age is associated with more coronary artery disease.
• Hypertension and smoking also raises the risk of coronary artery disease.
• Eat heart healthy and stay physically active, manage through meditation and avoid smoking.
• Chest can show pressure, radiate to shoulder, back neck and jaw.
• Nausea is a sign.
• Pain can can show GERD
• Cardiovascular is chest pain - palpaltions, dyspnea, respiratory- shortness of heart, cough, pleuritic pain.
• Neurological: Dizziness
• Assessment tools is the HEART Score and TIMI Risk score.
• 3 classifications are those with ECG, no with ECG.
• High risk those with with no object evidence.
• Refer to ER if there is hypotension and trouble breathign
• Coronary arrest and aortic rupture
• Acute and non cardiac pain resolve with management.
• Non pharmalogical interventions: lifestyle, cardiac, patient.
• Pharmalogical : Asprin and nitroglycerin
• Follow up for patients after pain less than 1/2 weeks.