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Chest pain

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Madinah Munawarah KSA
Meeqat General Hospital Medical Complex

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Chest pain

  1. 1. By DR.SALAH ELDOKANY M.D.CARDIOLOGY CARDILOGY CONSULTANT Madinah Munawarah KSA Meeqat General Hospital Medical Complex
  2. 2. EPIDEMIOLOGY IN PRIMARY CARE POPULATIONS 60 percent not "organic" in origin ( 36 percent Musculoskeletal chest pain out of which 13% reflux eosophigitis 11 percent Stable angina pectoris 1.5 percent unstable angina or myocardial infarction
  3. 3. The correct diagnosis is most often derived from a vigilantly obtained, detailed history:  pain description;  associated symptoms;  and in some cases disease risk factors supported by specific physical findings, an electrocardiogram, and/or chest x-ray
  4. 4. EMERGENCY RESPONSE TO CHEST PAIN IN THE OFFICE – potentially unstable based upon 1. history, 2. appearance, 3. or vital signs, – should be transported immediately to an emergency department in an ambulance equipped with a defibrillator.
  5. 5. Primary approach – Stabilization of such patients should begin in the prehospital setting 1. intravenous access, 2. placement of a cardiac monitor, 3. and supplemental oxygen if breathlessness, hypoxemia, or signs of heart failure or shock are present – Noninvasive monitoring of oxygen saturation may be used to decide on the need for oxygen administration. – A 12-lead electrocardiogram and a blood sample for cardiac enzyme measurement should be obtained if possible.
  6. 6. Prehospital management – Patients who are thought to be experiencing an acute coronary syndrome (ACS) should chew a 325 mg aspirin tablet. – Sublingual nitroglycerin should be given for chest pain unless the patient has relatively low blood pressure without intravenous access or has recently taken a phosphodiesterase inhibitor such as sildenafil (Viagra™).
  7. 7. In the emergency department (ED) – patients presenting with chest pain should be rapidly evaluated to determine if their symptoms are suggestive of acute ischemia, – or some other potentially life-threatening illness.
  8. 8. Chest pain suggestive of acute coronary syndrome Triage for rapid care Focused history and examination Asperin 160-325 mg SL nitroglycerin 0.4 mg every 5 min for 3 doses Morphine sulphate 2-4 mg iv initially then 2-8 mg every 5-15 min as needed GOAL is 10 min Intravenous access Initial lab including serum biomarkers Continuous ECG monitoring (with emergency defibrillator and airway equipment) Initial supplementation of O2 > 90 %
  9. 9. Initial 12 leads ECG ; if not diagnostic repeat ever 5- 10 min ST elevation / new LBBB Strong suspicion of ischemia but no persistent ST elevation Normal/ non diagnostic ECG with negative biomarkers Anticoagulation Betablockers if no contraindication Intravenous nitroglycerin unless contraindicated Anticoagulation Beta-blockers if no contraindication Intravenous nitroglycerin unless contraindicated Continue evaluation and monitoring in ED / moitored bed ECG /cardiac enzymes every 6- 12 hr Perimary PCI goal less thann 90 min OR Thrombolysis with goal of 30 min ST depression Elevated cardiac biomarkers Persistent chest pain HD instability TIMI Score ≥ 3 Look for high risk features: Cathetrization for high risk and medical therapy for low risk Evidence of ischemia or infarction Treat for non ST elevation ACS Stress test or Imaging study yesNo
  10. 10. HINTS
  11. 11. history and focused physical examination – presenting symptoms, characteristics of the pain and important associated symptoms, past history of or risk factors for cardiovascular disease, and potential contraindications to thrombolytic therapy – potentially emergent noncardiac causes of chest pain, such as acute aortic dissection, pulmonary embolism, tension pneumothorax, perforating peptic ulcer, and esophageal rupture – Examination should address hemodynamic status and a screening neurologic examination, especially if thrombolysis is entertained as a potential therapy.
  12. 12. Deferential diagnosis for ischemic cardiac pain
  13. 13. EKG who is in need ?? – Any patient over 30 with chest pain – Any patient over 50 with any of the following: dyspnea, altered mental status, upper extremity pain, syncope, or weakness – Any patient over 80 with abdominal pain, nausea, or vomiting This proposed rule should not replace clinical judgement Glickman SW, Shofer FS, Wu MC, et al. Development and validation of a prioritization rule for obtaining an immediate 12-lead electrocardiogram in the emergency department to identify ST- elevation myocardial infarction. Am Heart J 2012; 163:372.
  14. 14. EKG – When present, ECG abnormalities are an early sign of myocardial ischemia. Criteria for the two major categories of electrocardiographic manifestations of acute myocardial ischemia are listed here: – Findings consistent with ST elevation myocardial infarction (STEMI): New ST elevation at the J point in two anatomically contiguous leads using the following diagnostic thresholds: ≥0.1 mV (1 mm) in all leads other than V2-V3, where the following diagnostic thresholds apply: ≥0.2 mV (2 mm) in men 40 years; ≥0.25 mV (2.5 mm) in men <40 years, or ≥0.15 mV (1.5 mm) in women. – Findings consistent with Non ST elevation myocardial infarction or unstable angina: New horizontal or down-sloping ST depression ≥0.05 mV (0.5 mm) in two anatomically contiguous leads and/or T inversion ≥0.1 mV (1 mm) in two anatomically contiguous leads with prominent R wave or R/S ratio >1. Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Circulation 2012; 126.
  15. 15. Localization of the lesion – Anterior wall ischemia – Two or more of the precordial leads (V1-V6) – Anteroseptal ischemia – Leads V1 to V3 – Apical or lateral ischemia – Leads aVL and I, and leads V4 to V6 – Inferior wall ischemia – Leads II, III, and aVF – Right ventricular ischemia – Right-sided precordial leads – Posterior wall ischemia – Posterior precordial leads – The right-sided leads V4R, V5R, and V6R should be obtained if there is evidence of inferior wall ischemia, demonstrated by ST elevation in leads II, III, and aVF. – The posterior leads V7, V8, and V9 may also be helpful if there is evidence of posterior wall ischemia, as suggested by prominent R waves and ST depressions in leads V1 and V2.
  16. 16. – The initial ECG is often NOT diagnostic in patients with ACS. – In two series, the initial ECG was nondiagnostic in 45 percent and normal in 20 percent of patients subsequently shown to have an acute MI. – In the early hours of infarction, peaked, hyperacute T waves may be the only abnormality. In addition to evolution of the ECG, an uncommon source of error is pseudonormalization of baseline T wave inversion Pope JH, Ruthazer R, Beshansky JR, et al. Clinical Features of Emergency Department Patients Presenting with Symptoms Suggestive of Acute Cardiac Ischemia: A Multicenter Study. J Thromb Thrombolysis 1998; 6:63. Fesmire FM, Percy RF, Bardoner JB, et al. Usefulness of automated serial 12-lead ECG monitoring during the initial emergency department evaluation of patients with chest pain. Ann Emerg Med 1998; 31:3.
  18. 18. CLINICAL PRESENTATION – characteristics of the patient's chest discomfort and associated symptoms increase the likelihood of ACS, while others make the diagnosis unlikely. – Of note, older patients, diabetics, and women are more likely to present with symptoms such as dyspnea, weakness, nausea and vomiting, palpitations, and syncope, and may not manifest chest discomfort.
  19. 19. Ischemic chest pain
  20. 20. Onset – Ischemic pain is typically gradual in onset, although the intensity of the discomfort may wax and wane.
  21. 21. Provocation and palliation – provoked by an activity, such as exercise, which increases cardiac oxygen demand – does not change with respiration or position. – It may or may not respond to nitroglycerin and, if there is improvement, this may only be temporary.
  22. 22. Quality often characterized more as a discomfort than pain, and it may be difficult for the patient to describe. – squeezing, – tightness, – pressure, – constriction, – crushing, – strangling, – burning, – heartburn, – fullness in the chest, – band-like sensation, – knot in the center of the chest, – lump in throat, – ache, – heavy weight on chest (elephant sitting on chest), like a bra too tight, – and toothache (when there is radiation to the lower jaw). It is generally not described as sharp, fleeting, knife-like, stabbing, or pins and needles-like Increased pain severity does not appear to correlate with an increased likelihood of acute MI In some cases, the patient cannot qualify the nature of the discomfort but places his or her clenched fist in the center of the chest, known as the "Levine sign."
  23. 23. Radiation – Ischemic pain often radiates to other parts of the body including the upper abdomen (epigastrium), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw), – and not infrequently to the back (specifically the interscapular region) – Pain radiating to the upper extremities is highly suggestive of ischemic pain
  24. 24. Site – Ischemic pain is not felt in one specific spot, but rather it is a diffuse discomfort that may be difficult to localize. – The patient often indicates the entire chest, rather than localizing it to a specific area by pointing a single finger.
  25. 25. Time course – Angina is usually brief (two to five minutes) and is relieved by rest or with nitroglycerin. – In comparison, patients with an acute coronary syndrome (ACS) may have chest pain at rest, and the duration is variable but generally lasts longer than 30 minutes. – Classic anginal pain lasting more than 20 minutes suggests ACS.
  26. 26. Historical features increasing likelihood of ACS – prior history of ACS – other vascular disease – Risk factors for ACS, particularly age, male sex, diabetes, hypertension, hyperlipidemia, and cigarette smoking – Recent cocaine use
  27. 27. –Associated symptoms The most common is shortness of breath, – which may reflect mild pulmonary congestion resulting from ischemia-mediated diastolic dysfunction. – Other symptoms may include belching, – nausea, – indigestion, – vomiting, – diaphoresis, – dizziness, – lightheadedness, – clamminess, – and fatigue.
  28. 28. NONischemic chest discomfort – Pleuritic pain, sharp or knife-like pain related to respiratory movements or cough – Primary or sole location in the mid or lower abdominal region – Any discomfort localized with one finger – Any discomfort reproduced by movement or palpation – Constant pain lasting for days – Fleeting pains lasting for a few seconds or less – Pain radiating into the lower extremities or above the mandible Panju AA, Hemmelgarn BR, Guyatt GH, Simel DL. The rational clinical examination. Is this patient having a myocardial infarction? JAMA 1998; 280:1256. Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA 2005; 294:2623.
  29. 29. – In a review of over 430,000 patients with confirmed acute myocardial infarction (MI) from the National Registry of Myocardial Infarction II, one-third had no chest pain on presentation to the hospital – These patients often present with symptoms such as dyspnea alone, weakness, nausea and/or vomiting, palpitations, syncope, or cardiac arrest. They are more likely to be older, diabetic, and women Canto JG, Shlipak MG, Rogers WJ, et al. Prevalence, clinical characteristics, and mortality among patients with myocardial infarction presenting without chest pain. JAMA 2000; 283:3223.
  31. 31. PHYSICAL EXAMINATION – Responsiveness, airway, breathing and circulation according to guidelines of ACLS
  32. 32. CPR: cardiopulmonary resuscitation; ET: endotracheal tube; EtCO2: end tidal carbon dioxide; IO: intraosseous; IV: intravenous; PEA: pulseless electrical activity; VF: ventricular fibrillation; VT: ventricular tachycardia. Reprinted with permission. Adult Advanced Cardiovascular Life Support: 2010. American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. © 2010 American Heart Association, Inc.
  33. 33. Cardiac enzymes – Troponin as a predictive value for mortality
  34. 34. Plasma troponin T Mortality rates at 30 days related to the plasma level of cardiac troponin T measured at baseline in 801 patients presenting with symptoms and ECG changes of acute ischemia. There is a progressive increase in mortality with higher troponin levels. Data from Ohman EM, Armstrong PW, Christenson RH, et al. N Engl J Med 1996; 335:1333.
  35. 35. Kaplan-Meier estimates of survival show that a positive serum troponin, obtained any time during the first 24 hours after admission for an acute coronary syndrome, predicts a higher mortality at 30 days and one year. Data from Newby LK, Christenson RH, Ohman M, et al. for the GUSTO IIa Investigators, Circulation
  36. 36. Trponin I Mortality rate at 42 days according to the level of cardiac troponin I measured at baseline in 1404 patients with unstable angina or non-Q wave myocardial infarction. There was a progressive increase in risk with higher troponin levels. Data from Antman EM, Tanasijevic MJ, Thompson B, et al. N Engl J Med 1996; 335:1342.
  37. 37. EARLY RISK STRATIFICATION – TIMI risk score – TIMI risk index – ACCF/AHA classification – GRACE risk models – CHADS2 score – Patients at low risk – Individual risk factors
  38. 38. LATE RISK STRATIFICATION – Left ventricular function – Right ventricular function – Stress testing – Candidates for testing – Timing – Stress protocol – Stress testing in women – Continuous electrocardiography
  39. 39. LATE RISK STRATIFICATION – Left ventricular function – Right ventricular function – Stress testing – Candidates for testing – Timing – Stress protocol – Stress testing in women – Continuous electrocardiography
  40. 40. TIMI score – To calculate the score, a value of one is assigned when each variable was present and 0 when it was absent 1. Age ≥65 years 2. Presence of at least three risk factors for CHD 3. Prior coronary stenosis of ≥50 percent 4. Presence of ST segment deviation on admission ECG 5. At least two anginal episodes in prior 24 hours 6. Elevated serum cardiac biomarkers 7. Use of aspirin in prior seven days
  41. 41. A higher TIMI risk score correlated significantly with increased numbers of events (all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring revascularization) at 14 days – Score of 0/1 — 4.7 percent – Score of 2 — 8.3 percent – Score of 3 — 13.2 percent – Score of 4 — 19.9 percent – Score of 5 — 26.2 percent – Score of 6/7 — 40.9 percent A similar predictive value has been noted for postdischarge events at six weeks and for major cardiac events at 30 days in patients who have undergone PCI, which is now performed in most patients with a non-ST ACS
  42. 42. ACCF/AHA classification
  43. 43. LATE RISK STRATIFICATION – Left ventricular function – Right ventricular function – Stress testing – Candidates for testing – Timing – Stress protocol – Stress testing in women – Continuous electrocardiography
  44. 44. MANAGEMENT
  45. 45. MANAGEMENT ST elevation – Selection and implementation of the optimal reperfusion strategy is the most important step in the management of STEMI – Reperfusion therapy, whether percutaneous coronary intervention (PCI) or thrombolytics, should NOT await the result of cardiac biomarker measurement. – Rapid implementation of primary PCI is more likely to be achieved if the hospital protocol involves immediate activation of the PCI team by the emergency clinician and immediate transfer of the patient to the catheterization laboratory
  46. 46. MANAGEMENT Non-ST elevation
  47. 47. ACS with no evidence of ischemia or infarction
  48. 48. Stress testing – Stress testing, usually with exercise, can be used to detect residual ischemia and to assess the exercise capacity needed for the cardiac rehabilitation exercise prescription
  49. 49. Candidates for testing – Predischarge stress testing to detect residual ischemia is generally not performed in patients who have undergone PCI or CABG and have been fully revascularized – Such patients often undergo exercise testing a few weeks or more after discharge as part of a cardiac rehabilitation program or for activity counseling.
  50. 50. Candidates for testing – In contrast, patients who have undergone partial revascularization or no revascularization are candidates for predischarge testing, but should be properly screened.
  51. 51. Exercise testing appears to be safe if – he patient has undergone in-hospital cardiac rehabilitation – There have not been symptoms of heart failure or recurrent angina for 12 to 24 hours – The electrocardiogram has been stable for 12 to 24 hours
  52. 52. Timing – before or after soon after discharge. – While the high-risk patient will often undergo an invasive study, lower-risk patients may undergo stress testing after being symptom free and stable for 12 to 24 hours.
  53. 53. Stress protocol – varies with physician preferences, – patient characteristics, – and local laboratory expertise.
  54. 54. – Exercise ECG testing, which is most often performed, relies on both symptoms and objective changes on the ECG. – In selected low risk patients (ie, without heart failure, arrhythmias, or angina), an early full Bruce (symptom limited) protocol has been safely completed as early as 24 hours or before discharge
  55. 55. Other consideration – Cocaine-related ACS: Give benzodiazepines (eg, Lorazepam 2 to 4 mg IV every 15 minutes or so) as needed to alleviate symptoms; do NOT give beta blockers – Stop NSAID therapy if possible – Correct any electrolyte abnormalities, especially hypokalemia and hypomagnesemia
  56. 56. Cardiac arrhythmias during ACS – Sustained ventricular tachyarrhythmias in the peri-infarction period must be treated immediately as previously noted in ACLS guidelines – supraventricular tachyarrhythmias in the peri-infarction period may pose less immediate risk of cardiac arrest
  57. 57. Cardiac arrhythmias during ACS – Sustained ventricular tachyarrhythmias in the peri-infarction period must be treated immediately as previously noted in ACLS guidelines – supraventricular tachyarrhythmias in the peri-infarction period may pose less immediate risk of cardiac arrest – Bradyarrhythmias occurring early in the setting of an inferior wall MI (within the first 24 hours) may respond to treatment with atropine – Later bradyarrhythmias, wide QRS-complex bradyarrhythmias, and those occurring in the setting of an anterior wall MI may require temporary pacemaker placement
  58. 58. Disposition of patient without STEMI – For patients without STEMI, the ECG remains a critical component in determining risk for adverse outcomes in ACS. The patient's hemodynamic status, serum biomarkers, and historical risk factors, as well as available hospital resources, should also be used to determine appropriate disposition.
  59. 59. High-risk patient – The patient has a high-risk ACS if ST segment depression (≥0.05 mV [0.5 mm]) is present in two or more contiguous leads, – elevated serum biomarkers, – and/or the TIMI risk score is ≥5.
  60. 60. High-risk patient 1. This patient is typically admitted to an intensive care unit, coronary care unit, or monitored cardiac unit depending upon the persistence of symptoms and evidence of hemodynamic compromise. 2. Those with persistent pain or hemodynamic compromise generally undergo urgent angiography and revascularization. 3. Others with resolution of symptoms and stable hemodynamics are typically referred for early elective angiography and revascularization if appropriate.
  61. 61. High-risk patient – If there is no ST segment elevation or depression or new LBBB, regardless of the presence or absence of Q waves, the patient with definite or probable ACS should still be admitted to a monitored care unit for further evaluation. – Those patients manifesting high-risk features either on presentation or during their emergency department course should be admitted and considered for early PCI.
  62. 62. Low and moderate risk patient – Make an initial determination of the likelihood of ACS after the history, physical examination and serial (two or three) electrocardiograms have been performed – As shown in next table
  63. 63. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 2002 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation).
  64. 64. Low and moderate risk patient – Make an initial determination of the likelihood of ACS after the history, physical examination and serial (two or three) electrocardiograms have been performed – Consider alternative life-threatening diagnoses. – Reassess the likelihood of ACS and assess the short-term risk of an adverse event after return of the first and second biomarkers. – If after reassessment, the patient is felt to be at low or intermediate risk of an adverse event, noninvasive diagnostic testing is generally performed. – If after reassessment, the patient is felt to be at low or intermediate risk of an adverse event, noninvasive diagnostic testing is generally performed.
  65. 65. FINAL DISPOSITION — – The final disposition decision in most patients will occur after clinical observation, serial cardiac markers, serial ECGs, and cardiac stress testing or imaging: 1. Patients with indeterminate stress testing or imaging results may benefit from cardiology consultation if not already obtained. Many such patients will be admitted. 2. Patients with positive stress testing or imaging results should be evaluated by a cardiologist and admitted to the hospital. 3. If the results of this testing are negative for a cardiac cause, and other life threatening components of the differential diagnosis have been ruled out, discharge home is appropriate for stable patients. These patients are labeled as having noncardiac chest pain.
  • DrKasimFisayoMDMBBSC

    Feb. 15, 2021
  • IdrisAlnoor1

    Mar. 28, 2020

By DR.SALAH ELDOKANY M.D.CARDIOLOGY CARDILOGY CONSULTANT Madinah Munawarah KSA Meeqat General Hospital Medical Complex


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