1. IN THE NAME OF GOD

2. Approach to the Patient with Chest Pain
M.ROUZBAHANI MD
INTERVENTIONAL CARDOLOGIST
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3. Acute chest pain is one of the most common reasons for seeking care in the emergency department (ED), and it accounts for approximately 8 million ED visits annually in the United States.

4. The diagnosis of ACS is missed in approximately 2% of patients, which can lead to substantial consequences—for example, the short-term mortality in patients with acute myocardial infarction (MI) who are mistakenly discharged from the ED increases twofold over that expected for patients who are admitted to the hospital.

5. CAUSES OF ACUTE CHEST PAIN
In a typical population of patients undergoing evaluation for acute chest pain in EDs, about 15% to 25% have acute MI or unstable angina. A small percentage has other life-threatening problems, such as PE or acute aortic dissection, but most leave the ED without a diagnosis or with a diagnosis of a non–cardiac-related condition. Such noncardiac conditions include musculoskeletal syndromes, disorders of the abdominal viscera (including gastroesophageal reflux disease), and psychological conditions.

6. Myocardial Ischemia or Infarction
The most common serious cause of acute chest discomfort is myocardial ischemia or infarction
Which occurs when the supply of myocardial oxygen is inadequate for the demand.
Coronary spasm can occur in normal coronary arteries or, in patients with coronary disease, near atherosclerotic plaque and in smaller coronary arteries

7. The classic manifestation of ischemia is angina, which is usually described as a heavy chest pressure or squeezing, a burning feeling, or difficulty breathing.
The discomfort often radiates to the left shoulder, neck, or arm. It typically builds in intensity over a period of a few minutes.

8. The pain may begin with exercise or psychological stress, but ACS most commonly occurs without obvious precipitating factors.

9. Pain reproduced with movement or palpation of the chest wall or arms
ACC/AHA guidelines list the following as pain descriptions uncharacteristic of myocardial ischemia
Pleuritic pain
Primary or sole location of the discomfort in the middle or lower abdominal region
Pain that may be localized by the tip of one finger, particularly over the left ventricular apex
Pain reproduced with movement or palpation of the chest wall or arms

10. Constant pain that persists for many hours
ACC/AHA guidelines list the following as pain descriptions uncharacteristic of myocardial ischemia
Constant pain that persists for many hours
Very brief episodes of pain that last a few seconds or less
Pain that radiates into the lower extremities

11. no single factor suffices to exclude the diagnosis of acute ischemic heart disease
Clinicians should be mindful of “angina equivalents” such as jaw or shoulder pain in the absence of chest pain or dyspnea, nausea or vomiting, and diaphoresis
patients without chest pain had higher in-hospital mortality

12. In particular, women, older persons, and individuals with diabetes may be more likely to report atypical symptoms of myocardial ischemia or infarction
among patients hospitalized with MI, women—particularly young women—are significantly less likely than men to manifest chest pain

13. Pericardial Disease
The visceral surface of the pericardium is insensitive to pain, as is most of the parietal surface.
Therefore, noninfectious causes of pericarditis (e.g., uremia) usually cause little or no pain.
In contrast, infectious pericarditis almost always involves the surrounding pleura, so patients typically experience pleuritic pain withbreathing, coughing, and changes in position.

14. pain from infectious pericarditis is frequently felt in the shoulders and neck.
Pericarditis occasionally causes a steady, crushing substernal pain resembling that of acute MI.

15. Vascular Disease
Acute aortic dissection usually causes a sudden onset of excruciating ripping pain, the location of which reflects the site and progression of the dissection.
Ascending aortic dissection tends to be manifested as pain in the midline of the anterior aspect of the chest, and posterior descending aortic dissection tends to cause pain in the back of the chest.

16. Aortic dissections are rare, with an estimated annual incidence of 3 per 100,000, and usually occur in the presence of risk factors, including Marfan and Ehlers-Danlos syndromes, bicuspid aortic valve, pregnancy (for proximal dissections), and hypertension (for distal dissections).

17. Pulmonary emboli often cause a sudden onset of dyspnea and pleuritic chest pain, although they may be asymptomatic.
Massive pulmonary emboli tend to cause severe and persistent substernal pain, which is attributed to distention of the pulmonary artery.

18. Smaller emboli that lead to pulmonary infarction can cause lateral pleuritic chest pain.
Hemodynamically significant pulmonary emboli may cause hypotension,syncope, and signs of right-sided heart failure.
Pulmonary hypertension can result in chest pain similar to that of angina pectoris, presumably because of right-heart hypertrophy and ischemia

19. Pulmonary Conditions
Tracheobronchitis
pneumonia
Pneumothorax
Asthma

20. Gastrointestinal Conditions
esophageal reflux
Esophageal spasm
Mallory-Weiss tears
Boerhaave syndrome
peptic ulcer disease
Cholecystitis
Pancreatitis

21. Musculoskeletal and Other Causes
Costochondritis
Cervical disc disease
Trauma or strain
Herpes zoster
Panic disorder

22. Initial Assessment
that patients with symptoms consistent with ACS should not be evaluated solely over the telephone but should be referred to facilities that allow evaluation by a physician and recording of a 12-lead electrocardiogram (ECG).
immediate referral to an ED for patients with suspected ACS who experience chest discomfort at rest for longer than 20 minutes, hemodynamic instability, or recent syncope or near-syncope.

24. Persistent shortness of breath
Guidelines recommend that patients with the following chief complaints undergo immediate assessment by triage nurses and be referred for further evaluation
Chest pain, pressure, tightness, or heaviness; pain that radiates to the neck, jaw, shoulders, back, or one or both arms
Indigestion or heartburn; nausea and/or vomiting associated with chest discomfort
Persistent shortness of breath
Weakness, dizziness, lightheadedness, loss of consciousness

25. For such patients, initial assessment involves taking a history, performing a physical examination, obtaining an ECG and chest radiograph, and measuring biomarkers of myocardial injury.

26. History
Cocaine used
Hx o mi
Risk factors(male,DM,oldage)

27. Physical Examination
identify potential precipitating causes of myocardial ischemia (e.g., uncontrolled hypertension), important comorbid conditions (e.g., chronic obstructive pulmonary disease), and evidence of hemodynamic complications (e.g., congestive heart failure, new mitral regurgitation, hypotension)
In addition to vital signs, examination of peripheral vessels should include assessment for the presence of bruits or absent pulses, which suggest extracardiac vascular disease

28. For patients whose clinical findings do not suggest myocardial ischemia, the search for noncoronary causes of chest pain should focus first on potentially life-threatening issues (e.g., aortic dissection, PE)
Aortic dissection is suggested by blood pressure or pulse disparities or by a new murmur of aortic regurgitation accompanied by back or midline anterior chest pain

29. A friction rub may accompany pericarditis
A friction rub may accompany pericarditis. Differences in breath sounds in the presence of acute dyspnea and pleuritic chest pain raise the possibility of pneumothorax. Tachycardia, tachypnea, and an accentuated pulmonic component of the second heart sound (P2) may be the major manifestations of PE on physical examination.

30. Electrocardiography should be obtained within 10 minutes
The ECG aids in both diagnosis and prognosis.
New persistent or transient ST-segment abnormalities (≥0.05 mV)
lesser amounts of ST-segment deviation orT wave inversion of 0.2 mV or less and are not as helpful for risk stratification

32. Completely normal findings on an ECG do not exclude the possibility of ACS; the risk for acute MI is approximately 4% in patients with a history of CAD and 2% in those with no such history.
Patients with normal or nearly normal findings on an ECG, however, have a better prognosis than do those with clearly abnormal ECGs at initial evaluation.

33. Diffuse ST-segment elevation and PR-segment depression suggest pericarditis. Right-axis deviation, right bundle branch block, T wave inversions in leads V1 to V4, and an S wave in lead I and Q wave and T wave inversions in lead III suggest PE.
Serial electrocardiographic tracings improve the clinician’s ability to diagnose acute MI, particularly if combined with serial measurement of cardiac biomarkers
Posterior leads

34. Chest Radiography
A chest radiograph is typically obtained for all patients with chest pain.
It is usually nondiagnostic in patients with ACS but can show pulmonary edema secondary to ischemia-induced diastolic or systolic dysfunction.
It is more useful for diagnosing or suggesting other disorders; for example, it may show a widened mediastinum or aortic knob in patients with aortic dissection.

35. The chest radiograph can reveal pneumonia or pneumothorax.
The chest radiograph generally has normal findings in PE but can show atelectasis, an elevated hemidiaphragm, a pleural effusion, or more rarely, a Hampton hump or Westermark sign.

36. Biomarkers
Patients with chest discomfort possibly consistent with ACS should undergo measurement of biomarkers of myocardial injury . The preferred biomarker is cardiac troponin (T or I; cTnT or cTnI); creatine kinase MB isoenzyme (CK-MB) is less sensitive.

37. TROPONINS.
With serial sampling for up to 12 hours after arrival at the hospital, cardiac troponins offer a sensitivity higher than 95% and a specificity of 90%. Using only a single sample at initial evaluation results in substantially worse performance, with a sensitivity of just 70% to 75%.
Elevated cardiac troponin levels can also occur in patients with severe sepsis;
Elevated levels of cardiac troponins have been reported in patients with renal disease.

38. TROPONINS
Such damage may occur with other forms of myocardial injury, such as in the setting of myocarditis, myocardial contusion, or cardioversion or defibrillation; left ventricular strain from congestive heart failure,hypertensive crisis, or extreme exercise; right ventricular strain from PE; or other causes of acute pulmonary hypertension

39. CREATINE KINASE MB
It can be found in skeletal muscle, tongue, diaphragm, small intestine, uterus, and prostate.
muscular dystrophy; patients who participate in high-performance athletics, such as marathon running; and in patients with rhabdomyolysis
alcohol abuse or trauma.

40. CREATINE KINASE MB
One advantage of CK-MB is a shorter half-life in the circulation, which makes it useful for gauging the timing of an MI (a normal CK-MB with an elevated troponin level could represent a small MI or an MI that occurred several days ago)
for diagnosing reinfarction in a patient who has experienced an MI in the past week.

41. OTHER MARKERS. Serum myoglobin Ischemia modified albumin (IMA) D-dimer
BNP and N-terminal pro-BNP

42. PROGNOSTIC IMPLICATIONS OF TEST RESULTS.
Abnormal levels of CK-MB, cTnI, and cTnT predict an increased risk for complications
patients with a very low probability of ACS should not undergo measurement of biomarkers because false-positive results could lead to unnecessary hospitalizations
The ACC, AHA, and NACB guidelines recommend cTnI or cTnT as the preferred first-line markers, but CK-MB (by mass assay) is an acceptable alternative.

43. If the initial set of markers is negative, another sample should be drawn 3 to 6 hours later.

44. According to the ACC and AHA recommendations, patients with a low risk for ACS or associated complications can be observed for 6 to 12 hours while undergoing electrocardiographic monitoring and serial measurement of cardiac markers.
Patients in whom evidence of ischemia or other indicators of increased risk develop should be admitted to the coronary care unit for further management.

45. Patients in whom recurrent pain or other predictors of increased risk do not develop can be triaged for early noninvasive testing before or after discharge. Outpatient stress testing is a reasonable option if the patient is at low risk for ACS and if the testing can be accomplished within 72 hours; such a strategy has been shown to be safe. In such patients it is prudent to prescribe aspirin and possibly beta-adrenergic blocking agents (beta blockers) and to provide them with sublingual nitroglycerin.

46. Early Noninvasive Testing
Treadmill Electrocardiography
Treadmill exercise electrocardiography is inexpensive and available at many hospitals every day,
Patients with low clinical risk for complications can safely undergo exercise testing after 6 to 8 hours of an evaluation that reveals no evidence of myocardial ischemia.

48. For low-risk patients with no evidence of myocardial ischemia after serial ECGs and biomarkers, outpatient stress testing ideally within 24 hours, and no later than 72 hours, has proved safe.

49. Imaging Tests
Stress echocardiography and radionuclide scans are the preferred noninvasive testing modalities for patients who cannot undergo treadmill electrocardiographic testing because of physical disability or who have resting ECGs that confound interpretation.
Echocardiography can also be used, with and without stress, to detect wall motion abnormalities consistent with myocardial ischemia.

50. Cardiac magnetic resonance imaging (MRI) is also being explored for the assessment of patients with suspected ACS.
In contrast to the functional imaging data from stress testing, coronary computed tomographic angiography (CTA) offers noninvasive anatomic data.

52. THANK YOU