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Chest pain cardiac or not Dr Yasser Diab


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Chest pain cardiac or not with common pitfalls in diagnosis focusing into life threatening causes and quick glance at emergency management. auditorium at Farwaniya hospital ED ,State Of Kuwait.

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Chest pain cardiac or not Dr Yasser Diab

  1. 1. By Yasser Diab Farwanyia hospital Emergency department
  2. 2. INTRODUCTION  Emergency department clinicians have a difficult task, identifying which patients to admit and which patients to discharge home.  Chest pain is one of the most common causes for referral to emergency departments (ED), accounting for several million visits annually. (S.Goodacre et al 2005)  Cardiac disease accounts for only 8-18% of all cases of chest pain and the majority of chest pain seen in primary care is due to more benign conditions - e.g. gastrooesophageal reflux disease (GORD), muscle sprains, panic disorder or shingles. (Ruigomez et al 2006)  GORD is the most common cause of non-cardiac chest pain.(Flooket al 2007) The evaluation of patients with acute chest pain in emergency rooms is time consuming and expensive, and it often results in uncertain diagnosis (Hamm et al 1997)
  3. 3. Aetiologies of patients over 35 years of age, admitted to hospital from the emergency department with a chief complaint of non-traumatic chest pain: Kohn MA et al 2005 acute myocardial infarction (10.7%) angina/coronary artery disease (22.5%) atypical chest pain (29.4%) aortic dissection (0.3%) other cardiac causes, primarily CHF and atrial fibrillation, (13.8%) pulmonary embolus (0.4%) non-PE pulmonary causes, primarily bacterial pneumonia, (11.2%) but also spontaneous pneumothoraces (0.6%) abdominal causes (1.6%) other (10.2%).
  4. 4. Percentage of patients presenting to the emergency department with acute chest pain (Nawar et al 2007)
  5. 5. In one insurance industry—based study, the physician group most likely to be sued for missed myocardial infarction (MI) was Family practitioners (32%), followed by General internists (22%) and ED physicians (15%). (Rockville 1996) Meanwhile, an increase in overcrowding in emergency departments was associated with a substantial increase in the system response interval and the ambulance transport interval for patients with chest pain. (Michael et al 2003) Some Statics In the US, an estimated 5 million patients per year present to the Emergency Department with chest pain, but accurate diagnosis remains a challenge (Rosamond et al 2008). More than 50% of patients presenting to emergency facilities with unexplained chest pain will have coronary disease ruled out. About 1.5 million patients/ year are admitted for workup of acute coronary syndrome (ACS). Approximately 8 billion dollars/year are spent to evaluate complaints related to chest pain.
  6. 6. Chest pain means pain at the anterior thorax, between xiphoid and suprasternal notch and between the right and left midaxillary lines. It is classified into 1. Visceral chest pain: Originates from deep thoracic structures (heart, blood vessels, oesophagus) and is often (but not always) described as dull, heavy or aching in nature. It is transmitted via the autonomic system (so usually associated with anorexia,sweating, nausea, vomiting, palpitations, dizziness, and syncope) but may be referred via an adjacent somatic nerve - e.g. referred cardiac pain felt in the jaw or left arm. 2. Somatic chest pain: arises in the chest wall, pericardium and parietal pleura and is characteristically sharp in nature and more easily localised (usually dermatomal).
  7. 7. Differential diagnosis of chest pain Potentially life-threatening causes Common non-life-threatening causes 1. Acute coronary syndromes • Acute myocardial infarction  ST segment elevation MI  Non-ST segment elevation MI • Unstable angina 2. Pulmonary embolism 3. Aortic dissection 4. Myocarditis (most common cause of sudden death in theyoung) 5. Tension pneumothorax 6. Acute chest syndrome (in sickle cell disease) 7. Pericarditis 8. Boerhaave’s syndrome (perforated esophagus) 1. Gastrointestinal • Biliary colic • Gastroesophageal reflux • Peptic ulcer disease 2. Pulmonary • Pneumonia • Pleurisy 3. Chest wall syndromes • Musculoskeletal pain • Costochondritis • Thoracic radiculopathy • Texidor’s twinge (precordial catch syndrome) 4. Psychiatric • Anxiety 5. Shingles
  8. 8. Step-by-step diagnostic approach History ECG Chest pain Examination Differential diagnosis & exclusion of lifethreatening causes Management Investigation
  9. 9. History • A rapid and accurate history is the first step in the ED diagnosis of chest pain and is the key to right diagnosis. • The pain should be analyzed into its usual characteristics: site and radiation, quality, intensity, duration, onset and offset, precipitating and relieving factors, and associated symptoms. • The character of chest pain should be determined, as this can help differentiate between cardiac, respiratory, musculoskeletal, and other causes. • Association with serious medical problems such as diabetes, Marfan syndrome, thyroid illness, anemia and SLE should be kept in mind. • The ability to take a detailed history will obviously be limited with severe acute pain. • Associated symptoms may include: Syncope: Consider myocardial infarction, pulmonary embolus and dissecting aneurysm. Pain on inspiration: Consider pleurisy, pericarditis, pneumothorax and musculoskeletal (chest wall pain). Thoracic back pain: Consider spinal dysfunction, myocardial infarction, angina, aortic dissection, pericarditis and gastrointestinal disorders such as a peptic ulcer, cholecystitis and oesophageal spasm. • Patient age is helpful in evaluating chest pain. Chest pain in children and young adults (< 30 yr) is less likely to result from myocardial ischemia, although MI can occur in people in their 20s. Musculoskeletal and pulmonary disorders are more common causes in these age groups.
  10. 10. Duration of pain : can provide clues to the severity of the disorder. Long-standing pain (ie, for weeks or months) is not a manifestation of a disorder that is immediately life threatening. Such pain is often musculoskeletal in origin. Similarly, brief (< 5 sec), sharp, intermittent pains rarely result from serious disorders. Serious disorders typically manifest pain lasting minutes to hours, although episodes may be recurrent (eg, unstable angina may cause several bouts of pain over 1 or more days). Exacerbation and relief like exercise and rest, emotional stress, movement and respiration, or specific posture can point to the cause. Nitroglycerin may relieve pain of both myocardial ischemia and noncardiac smooth muscle spasm (eg, esophageal or biliary disorders); its efficacy or lack thereof should not be used for diagnosis. Associated findings may also suggest a cause, the presence or absence of specific risk factors can point to etiology of the pain. Fever is nonspecific but, if accompanied by cough, suggests a pulmonary cause.Patients with Raynaud syndrome or migraine headaches sometimes have coronary spasm.
  11. 11. Clinical Classification of Chest Pain Typical Meets three of the following characteristics 1.Substernal chest discomfort of CHARACTERISTIC quality and duration. 2.Provoked by exertion or emotional stress. 3.Relieved by rest and/or GTN spray. Atypical Meets two of these characteristics Non-cardiac Meets one or none of these characteristics
  12. 12. • The history is often influenced by the patient’s own reluctance to seek care for chest pain. In fact, the average patient waits 2 hours before seeking care for chest pain. (Welsh et al 2003). • According to the Rapid Early Action for Coronary Treatment (REACT) study, patients with chest pain do not seek timely care for the following reasons: • A lack of knowledge about symptoms, especially atypical or minor symptoms. • A wait-and-see attitude that assumes the pain is self-limiting and will go away. • A false assessment of personal risk factors. • A lack of knowledge about the importance of rapid and timely interventions. • The fear of causing a false alarm. (Finnegan et al 2000). • Description of chest pain alone cannot be used to rule out a cardiac event, however. In a landmark study, Lee et al evaluated the symptoms and ECG results of 596 patients presenting with chest pain to the ED and found that patients with characteristics of chest pain usually thought to indicate a noncardiac cause may indeed be suffering from cardiac ischemia. For instance, o approximately 7% of patients with an MI or UA had pleuritic chest pain, o up to 20% of patients with an MI or UA had pain reproduced by chest wall palpation o 13% had positional chest pain. • Additionally, they determined that no single clinical factor could be used to eliminate cardiac ischemia from the differential diagnosis. (Lee et al 1985).
  13. 13. Cardiac pain Non-cardiac causes of chest pain  Often heavy, pressing and tight. Symptoms that may indicate ACS include: (NICE Guidelines 2010) • Pain in the chest and/or other areas (eg, the arms, back or jaw) lasting longer than 15 minutes. • Chest pain with nausea and vomiting, marked sweating and/or breathlessness, or haemodynamic instability. • New-onset chest pain, or abrupt deterioration in stable angina, with recurrent pain occurring frequently with little or no exertion and often lasting longer than 15 minutes.  However, clinical features are not completely reliable in the diagnosis of acute, undifferentiated chest pain:  The site and nature of pain, the presence of nausea and vomiting and diaphoresis were not found to be predictive of ACS in one study.(Goodacre et al 2002) • ACS is often atypical (without chest pain). There is some evidence to suggest that this occurs more frequently in women, particularly premenopausal women (Methot et al 2004) • ACS pain can be intermittent and appear to 'settle', providing false reassurance.  Response to nitrates or antacids does not prove the diagnosis as angina and GORD may appear to be relieved by both.  Consider it when recent trauma, past medical history, and current medications.  Pleuritic pain (pain is aggravated during inspiration and when coughing) may indicate a respiratory or musculoskeletal cause of pain.  Musculoskeletal pain is usually associated with tenderness of the chest wall.  Gastrointestinal chest pain may be very difficult to distinguish from cardiac chest pain, especially in patients with oesophageal spasm.  Screen for Panic disorder: A positive screen ('yes' to either question) is highly sensitive for panic disorder but should not preclude cardiac testing in patients with risk factors: (Cayley et al 2012) • 'In the past six months, did you ever have a spell or an attack when you suddenly felt anxious or frightened or very uneasy?' • 'In the past six months, did you ever have a spell or an attack when for no apparent reason your heart suddenly began to race, you felt faint or couldn't catch your breath?'
  14. 14. Key questions: 1) Where exactly do you get the pain? 2) Does the pain travel anywhere? 3) Can you give me a careful description of the pain? 4) How long did the pain last and could you do anything to relieve it? 5) Is the pain brought on by exertion and relieved by rest? 6) Do cold conditions bring it on? 7) Do you have any other symptoms, such as breathlessness, faintness, sweating or back pain? 8) Is the pain made worse by breathing or coughing, or by movement or pressing on that area? 9) Is there any blood in any sputum you bring up? 10) Is your pain associated with what you eat and drink? Or with a bitter taste in your mouth? 11) Do you get the pain on stooping over and after lying in bed at night? 12) Do antacids relieve your pain? 13) Have you noticed a rash where you get the pain? 14) Have you had a blow to your chest or an injury to your back?
  15. 15. Assessment using OLD CARTS framework: Seidel et al 2003
  16. 16. Discription Location Radiation Associations Acute coronary syndromes crushing, tightening, squeezing, or a Pressure like Retrosternal left anterior chest or Epigastric. R or L shoulder, R or L arm/hand, jaw Dyspnea, diaphoresis, nausea Pulmonary embolism Heaviness, tightness Whole chest (massive) or Focal chest (segmental) none Dyspnea, unstable vital signs, feeling of impending doom if massive or just Tachycardia, Tachypnea if segmental Aortic dissection Ripping, tearing Midline, Substernal Intrascapular area of back Secondary arterial branch occlusion Pneumothorax Sudden, sharp, lancinating, pleuritic One side of chest Shoulder, back Dyspnea Pericarditis /temponade Sharp, constant or pleuritic Substernal none Fever, pericardial friction rub perforated esophagus Sudden, sharp, after forceful vomiting Substernal back Dyspnea, diaphoresis, signs of sepsis
  17. 17. Physical examination The examination should focus on the following areas: 1. General appearance: evidence of atherosclerosis (senile arcus, thickened vessels), pale and sweating (myocardial infarction, dissecting aneurysm or pulmonary embolus), hemiparesis(? aortic dissection) 2. Pulses: both radial and femoral, check for nature of pulse and absence of femoral pulses 3. Blood pressure: hypotension or shock in MI, pneumothorax ,PE or dissection, hypertension in Aortic dissection 4. Temperature: high in pneumonia , low in shock. 5. Palpation:  Of chest wall, lower cervical spine and thoracic spine, look for evidence of localized tenderness, pathological fracture, spinal dysfunction, herpes zoster  Palpation of legs: check for evidence of deep venous thrombosis. 6. Examination of chest: check for evidence of pneumothorax.  Reduced breath sounds, hyper-resonant percussion note and vocal fremitus → pneumothorax.  Friction rub → pericarditis or pleurisy.  Basal crackles → cardiac failure.  Apical systole murmur → mitral valve prolapse.  Aortic diastolic murmur → proximal dissection (aortic regurgitation). 7. Upper abdominal palpation: check for tenderness suggestive of gall bladder disease or peptic ulceration. In Myocardial infarction, the examination may be normal but the patient, apart from being cold, clammy or shocked, may have muffled heart sounds, a gallop rhythm, a systolic murmur. With a Aortic dissection the patient may also appear cold, clammy and shocked, but may show absent femoral pulses, hemiparesis and a diastolic murmur of aortic regurgitation.
  18. 18. Red flags Certain findings raise suspicion of a more serious etiology of chest pain: 1. Abnormal vital signs (tachycardia, bradycardia, tachypnea, hypotension) 2. Signs of hypoperfusion (e.g., confusion, ashen color, diaphoresis) 3. Shortness of breath 4. Hypoxemia on pulse oximetry 5. Asymmetric breath sounds or pulses 6. New heart murmurs 7. Pulsus paradoxus > 10 mm Hg
  19. 19. ELECTROCARDIOGRAPHY • The initial ECG is the easiest, simplest, most important tool for early diagnosis and risk stratification. • Current recommendations indicate that it should be performed within 10 minutes of ED presentation for all patients with chest discomfort or other symptoms suggestive of ACS (ACC/AHA 2007), and may best be considered one of the “vital signs” for patients with chest pain. (Anderson et al 2007) • This may be diagnostic for ischemia and myocardial infarction, although it is important to bear in mind that it may be normal with both, including the early minutes to hours of an acute infarction. • The presence of ST-segment elevation or new LBBB should prompt consideration for immediate reperfusion therapy. ST-segment depression is associated with a marked increase in risk of MI and ischemic complications. • As little as 0.5 mm of ST-segment depression predicts increased risk; the greater the extent of depression, the higher the likelihood of MI and death. (Kaul et al 2003) • T-wave inversion and Q waves are markers of ischemia but less predictive than ST-segment depression (Savonitto et al 1999). • It can be helpful to differentiate between myocardial infarction, pulmonary embolism and pericarditis. • The ECG in pulmonary embolism may show right axis deviation. Pericarditis is characterised by low voltages and saddle-shaped ST segment elevation.
  20. 20. Typical ECG pattern for specific possible causes of acute chest pain: (a) Acute pulmonary embolism (B) Acute pericarditis (C) Acute inferolateral myocardial infarction
  21. 21. Other tests: • Radiological: Chest X-ray, CT scan, Echocardiography… • Lab tests: Cardiac biomarkers, D-dimer…
  22. 22. Pitfalls To Avoid 1. “But the ECG was normal.” While a normal or near normal ECG reduces the likelihood of MI and the likelihood of a complication should an MI develop, it does not exclude this diagnosis. (Howell et al 1994), Rouan et al. found that 3% of MI patients had completely normal presenting ECG and another 7% of MI patients had non-specific ECG. 2. “Normal cardiac enzymes exclude an Ml diagnosis” : Cardiac enzymes have a characteristic time-related release, so all patients with suspected ACS should undergo serial cardiac biomarker sampling. 3. I know the troponin was elevated, but the patient has renal failure.” Recent data show that the troponin T level retains its prognostic value in all degrees of renal dysfunction. 4. “I know that he had persistent tearing back pain, but the chest x-ray was negative.” This is a difficult diagnosis to make and may be fatal when treated inappropriately.
  23. 23. 5. “He had ECG changes and severe chest pain; why did I need a chest film?” Because he had an aortic dissection. Nearly half of all patients with dissection have some ECG changes. Almost 10% have dissection involving the coronary arteries, in which the ECG may show an AMI. 6. “I only did one set of enzymes because his pain was atypical.” If your suspicion is high enough to get enzymes in the first place, it should be high enough to do them right—serial levels over a six- or eight-hour period (or delta levels over a shorter period). One negative set drawn more than six hours after pain onset accompanied by a normal ECG may be an exception to this rule. 7. “The pain wasn’t ripping or tearing; it didn’t even radiate to the back.” Aortic Dissection may not fit the “classic” description. Perform a detailed physical examination looking for a pulse deficit or neurologic abnormalities, CXR for mediastinal changes, and order CT angiography when the diagnosis remains in doubt.
  24. 24. 8. “But the left bundle branch block was old—I even got a prior ECG to prove it.” It is very difficult (almost impossible) to diagnose AMI in the presence of a left bundle— and individuals with a left bundle branch block have underlying cardiac disease in the first place. Use cardiac markers and be liberal in admission or observation in such patients with chest pain. 9. We must be careful not to place words in the patient's mouth: Rephrasing of the patient's description may help clarify misunderstandings, try not to ask leading questions. 10. “Young patients cannot have an Ml”: Studies found that patients with missed MIs were generally younger than those correctly diagnosed as having an MI at the same hospital. (Rusnak et al 1989). 11. Indigestion symptoms exclude an Ml diagnosis: indigestion-like symptoms occurred in 10% of MI patients (Lee et al 1985).While the administration of antacids with or without topical anaesthetic agents may soothe oesophageal or gastric irritation, pain relief does not prove the absence of cardiac ischaemia.
  25. 25. 12.Sharp pain or chest wall tenderness excludes the diagnosis of Ml: 8% of MI patients complained of a 'sharp or stabbing' pain 19% pleuritic' discomfort, 8% chest wall tenderness, 11% of MI patients had pain that was positional in nature (Tierney et al 1986). 13.Do not assess symptoms of an ACS differently in ethnic groups.(NICE 2010) There are no major differences in symptoms of an ACS among different ethnic groups. 14.Do not routinely administer oxygen, (NICE 2010) only offer supplemental oxygen if: • oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94–98%. • chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88–92% until blood gas analysis is available. 15.Do not use people's response to (GTN) to make a diagnosis. (NICE 2010)
  26. 26. 16.Referred pain from spinal disorders, especially of the lower cervical spine— one of the great pitfalls in medical practice 17.Over-Labelling chest pain as psychological in an anxious patient presenting with acute chest pain. 18.Being unaware that up to 20% of myocardial infarctions are silent, especially in elderly patients, and that pulmonary embolism is often painless.
  27. 27. Acute coronary syndrome
  28. 28. The diagnosis of NSTE-ACS may be easy to confirm but is often hard to be excluded (Hollander et al 2003)  Of the patients presenting to the emergency department for chest pain, 55 to 85 percent do not have a cardiac cause for their symptoms. (Hollander et al 2007)  Of those admitted for chest pain, more than 60 percent do not have acute coronary syndromes. (Hoffmann et al 2006) and unnecessary admissions for chest pain in the U.S. alone cost billions of dollars annually. (Hoffmann et al 2006) But ACS still the most important and the most mistaken cause of chest pain
  29. 29. Clinical presentation: (Canto et al 2002,ESC 2011) • Angina can be felt anywhere between the ear and the umbilicus. • The typical clinical presentation of angina is retrosternal pressure or heaviness radiating to the left arm, neck, or jaw, which may be intermittent (usually lasting for several minutes) or persistent. • These complaints may be accompanied by other symptoms such as diaphoresis, nausea, abdominal pain, dyspnoea, and syncope. • However, atypical presentations are not uncommon. These include epigastric pain, indigestion, stabbing chest pain, chest pain with some pleuritic features, or increasing dyspnoea. • Atypical complaints are more often observed in older (>75 years) patients, in women, and in patients with diabetes, chronic renal failure, or dementia. • Anginal equivalents: Anginal equivalents are exertional pain in the jaw, neck, ear, arm, shoulder, back, or epigastric area; exertional dyspnea; nausea and vomiting; diaphoresis; and fatigue.
  30. 30. Features that Suggest ACS: (Guidelines And Protocols Advisory Committee, ACC/AHA 2011) 1) Cardiac chest “pain” is usually described as an unpleasant sensation in the chest: “pressing”, “squeezing”, “constricting”, “bursting”, “burning”, “a band around the chest”, “a weight in the centre of the chest” or a “vise tightening around the chest”. Clenching the fist in front of the sternum (Levine’s sign) is a strong indication of an ischemic origin of the pain. 2) Acute coronary syndrome may present with acute shortness of breath with or without evidence of chest pain 3) May radiate or be completely isolated to: the neck, jaw, teeth, epigastrium, shoulder or arms (most commonly the left). It is frequently associated with shortness of breath, diaphoresis, weakness, nausea and vomiting, and occasionally associated with gas, belching or “indigestion”. 4) The discomfort may be partially or fully relieved by nitroglycerine but may not respond to nitroglycerine at all. There may or may not be a prodrome of the discomfort precipitated by exercise, cold weather or emotional stress relieved by rest or nitro-glycerine. 5) Chest discomfort that lasts for more than 10 minutes or occurs at rest suggests unstable angina; but chest discomfort that lasts for more than 20 minutes suggests acute myocardial infarction..
  31. 31. Features of Chest Pain that do not Suggest ACS: 1) Pleuritic pain (i.e., sharp or knifelike pain brought on by respiratory movements or cough). 2) Pain or discomfort that is localised to the skin or chest wall and can be reproduced by localised pressure. Pain that is localised to a small area of the chest (< 3 cm in diameter), or pain that radiates to the right lower chest. 3) Pain that is sharp, stabbing or knifelike and aggravated by deep breathing or rotating the chest. 4) Pain that lasts for less than 15 seconds is rarely ischemic in origin. 5) Pain that radiates into the lower extremities. 6) Pain that is worse in the supine position and relieved by sitting up or leaning forward is suggestive of pericarditis. 7) Dissection of the aorta often causes pain in the back in addition to the front of the chest.
  32. 32. Historical Factors that Increase the Likelihood of Acute Myocardial Infarction Historical and Exam Factors that Decrease the Likelihood of Acute Myocardial Infarction  Radiation to right arm or shoulder.  Radiation to both arms or shoulders.  Associated with exertion.  Radiation to left arm.  Associated with diaphoresis.  Associated with nausea or vomiting.  Worse than previous angina or similar to previous myocardial infarction.  Described as pressure.  Described as pleuritic.  Described as positional.  Described as sharp.  Reproducible with palpation.  Inframammary location.  Not associated with Exertion.
  33. 33. Risk factors that increases the probability of CAD Identify potential precipitating causes of myocardial ischemia  Age >40 years old.  Male sex.  Postmenopausal female.  A positive family history.  Known atherosclerosis in non-coronary territories, such as peripheral or carotid artery disease.  Past medical history of CAD: the most predictive risk factor for cardiac ischemia  Hypertension.  Hyperlipidemia.  Diabetes mellitus.  Sedentary lifestyle  Truncal obesity such as uncontrolled hypertension, thyrotoxicosis, anemia, or gastrointestinal bleeding.
  34. 34. Physical examination • Aim (Anderson et al 2011, ACC/AHA 2011) 1. To exclude non-cardiac causes of chest pain and non-ischaemic cardiac disorders (e.g. Pulmonary embolism, aortic dissection, pericarditis, valvular heart disease) or potentially extracardiac causes such as acute pulmonary diseases (e.g. Pneumothorax, pneumonia, or pleural effusion). 2. Comorbid conditions that could impact therapeutic risk and decision making, such as pulmonary disease and malignancies. 3. Assess the hemodynamic impact of the ischemic event. • Patients with evidence of LV dysfunction on examination (rales, S3 gallop) or with acute mitral regurgitation have a higher likelihood of severe underlying CAD and are at a high risk of a poor outcome. • Examination of the peripheral vessels can also provide important prognostic information. The presence of bruits or pulse deficits that suggest extracardiac vascular disease identifies patients with a higher likelihood of significant CAD
  35. 35. ECG changes Electrocardiogram:  should be obtained within 10 min after first medical contact (ESC 2011, ACC/AHA 2007)  ST elevation Patients whose current ECG suggests ischemia can be Other assessed with greater diagnostic accuracy or LBBB if a prior ECG is available for comparison changes STEMI  ST-segment elevation : occurs within minutes and may last for up to 2 weeks. ST elevation of ≥2 mm in adjacent chest leads and ≥1 mm in adjacent limb leads.  New LBBB: denotes LAD , if no old baseline ECG, Sgarbosa crieteria can be used with >90% specifity Sgarbossa's criteria: identify acute myocardial infarction in the presence of a left bundle branch block (LBBB) or a paced rhythm (Sgarbossa et al 1996) ≥3 points = 90% specificity of STEMI (sensitivity of 36%)
  36. 36. Posterior extension is suggested by: Horizontal ST depression in V1-3 Tall, broad R waves (> 30ms) in V2-3 Dominant R wave (R/S ratio > 1) in V2 Upright T waves in V2-3
  37. 37. Right ventricular infarction is suggested by: ST elevation in V1 ST elevation in lead III > lead II
  38. 38. NSTEMI/UA: • Changes can be transient and/or fixed, especially if a diagnosis of NSTEMI is made. • ST-segment depression of ≥0.05 mV is highly specific of myocardial ischemia (unless isolated in V1–V3, suggesting a posterior STEMI). • T-wave inversion is sensitive but nonspecific for acute ischemia unless very deep (≥0.3 mV). • Rarely, Q waves may evolve or there may be transient or new LBBB.
  39. 39. Electrocardiograms Demonstrating Normalization Of Prior Negative T-Wave In Patient With NSTE-ACS:
  40. 40. Limitations of ECG as a diagnostic tool of ACS: 1. Relatively low diagnostic sensitivity for ACS, especially for unstable angina; ischemic changes are apparent at the time of presentation in only 20% to 30% of patients who have an acute MI (kontos et al 2009). 2. Conversely, 5% to 10% of patients with MI have normal findings on ECG at presentation. 3. The sensitivity of ECG is affected by the anatomic location of the culprit vessel and is less likely to be diagnostic in patients with left circumflex lesions. (Huey et al 1988 ). How to overcome these limitations: 1. Serial assessment (every 15-30 minutes) should be performed routinely in patients with ongoing symptoms or ECG findings that are suggestive but not diagnostic of ischemia. (Anserson et al 2008) 2. Addition of posterior leads and multilead ECG devices. Results have been mixed for routine use of posterior leads however, the cost-effectiveness of routine use is unclear. (Zalenski et al 1993)
  41. 41. BIOMARKERS • Current recommendations advise that all patients with suspected ACS should undergo serial cardiac biomarker sampling. (Morrow et al 2007). • If baseline data are negative, further sampling should be obtained 6 to 8 hours later depending on symptom onset. • Current recommendations indicate troponin as the preferred biomarker, and considered as the “GOLD STANDARD” for diagnosis of AMI. (ACC/ESC) • Troponin is a complex of three regulatory proteins (troponin c, troponin i, and troponin t) that is integral to muscle contraction in skeletal muscle and cardiac muscle, but not smooth muscle. • Cardiac troponins T and I are the preferred markers for myocardial injury as they have the highest sensitivities and specificities for the diagnosis of acute myocardial infarction (nice guidelines March 2010) • Elevation is defined as >10% of 99th percentile or CV upper reference limit in the appropriate clinical setting. (ACC/ESC guidelines 2011) 1. 99th percentile is the the upper limit of what can be expected in a normal. 2. CV is coefficient of variation: is the percent variation in assay results that can be expected when the same sample is repeatedly analyzed.
  42. 42. Timing of Release of Various Biomarkers After Acute Myocardial Infarction. Anderson J L et al. Circulation. 2011;123:e426-e579 Copyright © American Heart Association, Inc. All rights reserved.
  43. 43. TEST Advantages Disadvantages Comment Cardiac troponins 1. Powerful tool for risk stratification. 2. Greater sensitivity and specificity than CK-MB. 3. Detection of recent MI up to 2 weeks after onset. 4. Useful for selection of therapy. 5. Detection of reperfusion. 1. Low sensitivity in very early phase of MI (less than 6 h after symptom onset) and requires repeat measurement at 8 to 12 h, if negative 2. Limited ability to detect late minor Re-infarction. Useful as a single test to efficiently diagnose NSTEMI (including minor myocardial damage),with serial measurements. Clinicians should familiarize themselves with diagnostic “cutoffs” used in their local hospital laboratory CK-MB 1. Rapid, cost-efficient, accurate assays 2. Ability to detect early reinfarction. 1.Loss of specificity in setting of skeletal muscle disease or injury, including surgery. 2. Low sensitivity during very early MI (less than 6 h after symptom onset) or later after symptom onset (more than 36 h) and for minor myocardial damage (detectable with troponins). Prior standard and still acceptable diagnostic test in most clinical circumstance Myoglobin 1. High sensitivity 2. Useful in early detection of MI 3. Detection of reperfusion 4. Most useful in ruling out MI 1. Very low specificity in setting of skeletal muscle injury or disease 2. Rapid return to normal range limits sensitivity for later presentations. More convenient early marker than CK-MB isoforms because of greater availability of assays for Myoglobin.
  44. 44. Non-MI-Related important Causes Of Elevated Troponin • Renal impairment or failure. • Trauma to chest. • Congestive heart failure. • Aortic valve disease. • Pulmonary embolism. • Pneumonia. • Septic shock.
  45. 45. • In the literature, several risk scores for NSTE-ACS have been published. The most reputed are the TIMI, PURSUIT, GRACE and HEART risk scores. • They are a good predictive indicators for death or MI at 1 year and enabled the identification of high-risk subsets of patients who will benefit most from myocardial revascularization performed during initial hospital stay (De Araújo et al 2005).
  46. 46. Advantages of the HEART score as a stratification tool in ED (A.J. Six et al 2008)  The HEART score is an easy, quick and reliable predictor of outcome in chest pain patients and can therefore be used for Triage.  Facilitates communication between doctors with figures: 1. A score of 0-3 points holds a risk of 1.6% and therefore supports a policy of early discharge. 2. A score of 4-6 points, indicates a risk of 13%, immediate discharge is not an option and should be admitted for clinical observation, treated as an ACS awaiting final diagnosis and subjected to noninvasive investigations, such as repeated troponin, exercise testing and possibly advanced ischemia detection. 3. A score ≥7 points, with a risk of 50%, implies early aggressive treatment including invasive strategies.
  47. 47. Guidelines for the Identification of ACS Patients by ED Registration Clerks or Triage Nurses (ACC/AHA 2011) Chest pain can be triaged into traumatic and atraumatic etiologies. The evaluation of atraumatic chest pain requires an algorithmic approach that first excludes potentially life threatening conditions before working through the various aetiologies of chest pain. 1-Registration/clerical staff Patients with the following chief complaints require immediate assessment by the triage nurse and should be referred for further evaluation: o Chest pain, pressure, tightness, or heaviness; pain that radiates to neck, jaw, shoulders, back, or 1 or both arms o Indigestion or “heartburn” nausea and/or vomiting associated with chest discomfort o Persistent shortness of breath. o Weakness, dizziness, lightheadedness, loss of consciousness
  48. 48. 2-Triage nurse Patients with the following symptoms and signs require immediate assessment by the triage nurse for the initiation of the ACS protocol: • Chest pain or severe epigastric pain, non-traumatic in origin, with components typical of myocardial ischemia or MI. • Central / substernal compression or crushing chest pain. • Pressure, tightness, heaviness, cramping, burning, aching sensation. • Unexplained indigestion, belching, epigastric pain. • Radiating pain in neck, jaw, shoulders, back, or 1 or both arms. • Associated dyspnea. • Associated nausea and/or vomiting. • Associated diaphoresis. If these symptoms are present, obtain immediate ECG.
  49. 49. 3-Medical history The triage nurse should take a brief, targeted, initial history with an assessment of current or past history of: • CABG, PCI, CAD, angina on effort, or MI. • GTN use to relieve chest discomfort. • Risk factors, including smoking, hyperlipidemia, hypertension, diabetes mellitus, family history, and cocaine or methamphetamine use. • Regular and recent medication use. The brief history must not delay entry into the ACS protocol.
  50. 50. 4-Special considerations o Women may present more frequently than men with atypical chest pain and symptoms. o Diabetic patients may have atypical presentations due to autonomic dysfunction. o Elderly patients may have atypical symptoms such as generalized weakness, stroke, syncope, or a change in mental status.
  51. 51. Acute Coronary Syndromes Algorithm (ACLS guidelines):
  52. 52. Pulmonary Embolism History (Runyon MS vol6) Examination Investigation o Classic presentatioin: The PIOPED study :Worsley et al 1995  Dyspnea (73%)  Pleuritic chest pain (66%)  Cough (37%)  Hemoptysis (13%)  Symptoms may vary from sudden catastrophic hemodynamic collapse to gradually progressive dyspnea.  Suspected in patients with respiratory symptoms unexplained by an alternative diagnosis. o Atypical: Syncope, Abdominal pain, Fever, Productive cough, Hemoptysis Wheezing, Decreasing level of consciousness, New onset of atrial fibrillation,, Flank pain, Delirium (in elderly patients). o Tachypnea (respiratory rate >16/min) - 96% o Crepitations- 58% o Accentuated second heart sound - 53% o Tachycardia (heart rate >100/min) - 44% o Fever (temperature >37.8°C) - 43% o Diaphoresis - 36% o S3 or S4 gallop - 34% o Clinical signs and symptoms suggesting thrombophlebitis - 32% o Lower extremity edema - 24% o Cardiac murmur - 23% o Cyanosis - 19% o ECG: • Tachycardia • Nonspecific ST-T wave abnormalities • S1 Q3 T3 pattern • P pulmonale • Af o CXR: may normal or Westermark sign. o Angiography: The gold standard for diagnosis of segmental and sub segmental emboli. o ECHO: • RV condition (strain, dilatation). • Pulmonary artery pressure. • Pericardial effusion • May show the emboli if central. o D-Dimer: useful in low or moderate pretest probability patients. (Wells score of ≤4 with a negative qualitative D-dimer test exclude pulmonary embolism Geersing et al 2012) o Troponin: high in 50% (Konstantinides 2008).
  53. 53. Modified Wells Score for Pretest Probability of Pulmonary Embolism Clinical Characteristic Score Previous pulmonary embolism or deep vein thrombosis + 1.5 Heart rate >100 beats per minute + 1.5 Recent surgery or immobilization (within the last 30 d) + 1.5 Clinical signs of deep vein thrombosis + 3 Alternative diagnosis less likely than pulmonary embolism + 3 Hemoptysis + 1 Cancer (treated within the last 6 months) + 1 Clinical Probability of Pulmonary Embolism Score Low 0-1 Intermediate 2-6 High ≥6
  54. 54. Massive PE Submassive PE Low-risk PE Acute PE with sustained hypotension: (systolic blood pressure [SBP] < 90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE such as arrhythmia, hypovolemia, sepsis, or left ventricular [LV] dysfunction), pulselessness, or persistent profound bradycardia (heart rate < 40 beats per minute with signs or symptoms of shock). Acute PE without systemic hypotension (SBP ≥ 90 mm Hg) but with either RV dysfunction or myocardial necrosis. RV dysfunction means the presence of at least 1 of the following: • RV dilation or RV systolic dysfunction on echocardiography • RV dilation on CT • Elevation of BNP (> 90 pg/mL) • Elevation of N-terminal pro-BNP (> 500 pg/mL) or • Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion) Myocardial necrosis: Defined as either of the following: • Elevation of troponin I (> 0.4 ng/mL) or • Elevation of troponin T (> 0.1 ng/mL) Acute PE and the absence of the clinical markers of adverse prognosis that define massive or submassive PE. American Heart Association Proposed Definitions
  55. 55. Shock Index = HR/SBP
  56. 56. Pericarditis History Findings Investigations Character sharp or stabbing precordial Fever. or retrosternal chest pain, pain become Tachycardia dull with dyspnea and orthopnea in Pericardial friction rub: A triphasic tamponade (systole, diastole and atrial systole) best Onset is sudden or gradual onset and heard with the diaphragm of the Radiates to the back, neck, left stethoscope at the lower left sternal shoulder, or arm. border or apex when the patient is sitting Referral of pain to the left trapezial and leaning forward. ridge (due to inflammation of the joining Signs of tamponade: diaphragmatic pleura) is a particular Beck’s triad: hypotension, distinguishing feature. raised JVP, and quiet heart sounds Aggravated by inspiration or Pulsus paradoxus >10mmhg drop during movement. Typically, chest pain is most inspiration. severe when the patient is supine and is relieved when the patient sits up and leans forward. Associated symptoms include fever, dyspnea due to accentuated pain with inspiration, and dysphagia from irritation of the esophagus by the posterior pericardium. ECG: diagnostic in most cases: Sinus tachycardia: from pain or effusion. Widespread concave ST elevation, especially in I, V5, and V6 ST amplitude: T wave amplitude: • A ratio of > 0.25 suggests pericarditis • A ratio of < 0.25 suggests BER PR segment depression throughout most of the limb leads. Chest X ray: for tamponade. Lab investigations: for diagnosis of the cause i.e. CBC, kidney functions, ESR, serologic studies, bacterial work up and thyroid functions.
  57. 57. Features suggesting pericarditis in ECG: 1. Generalised ST elevation of concave manner. 2. Presence of PR depression, elevation in aVR. 3. Normal T wave amplitude. 4. ST segment / T wave ratio > 0.25 5. Absence of “fish hook” appearance in V4 6. ECG changes evolve slowly over time Benign Early Repolarisation •ST segment height = 1 mm •T wave height = 6 mm •ST / T wave ratio = 0.16 •The ST / T wave ratio < 0.25 Pericarditis •ST segment height = 2 mm •T wave height = 4 mm •ST / T wave ratio = 0.5 •The ST / T wave ratio > 0.25
  58. 58. Myocarditis History Examination Invstigations • Recent history (≤1-2 wk) of flulike symptoms of fevers, arthralgias, and malaise or pharyngitis, tonsillitis, or upper respiratory tract infection (viral myocarditis) • Mild symptoms of chest pain (in concurrent pericarditis), fever, sweats, chills, dyspnea. • Palpitations, syncope, or sudden cardiac death due to underlying ventricular arrhythmias or AV block especially in giant cell myocarditis (in young adults, myocarditis causes up to 20% of all cases of sudden death). Signs of acute decompensation of heart failure like tachycardia, gallop, mitral regurgitation, edema) and, in those with concomitant pericarditis, with pericardial friction rub. Specific conditions: •Sarcoid myocarditis: lymphadenopathy, also with arrhythmias, sarcoid involvement in other organs (up to 70%) •Acute rheumatic fever - usually affects heart in 50-90%; associated signs, such as erythema marginatum, polyarthralgia, chorea, subcutaneous nodules (jones criteria) •Hypersensitive/eosinophilic myocarditis pruritic maculopapular rash and history of using offending drug •Giant cell myocarditis - sustained ventricular tachycardia in rapidly progressive heart failure. •Peripartum cardiomyopathy - heart failure developing in the last month of pregnancy or within 5 months following delivery. • ECG: often nonspecific eg, sinus tachycardia, nonspecific ST- or T-wave changes. Occasionally, heart block (AV block or intraventricular conduction delay), ventricular arrhythmia, or injury patterns. • CBC: Leukocytosis(eosinophilia) • Elevated ESR and CRP • Rheumatologic screening - To rule out systemic inflammatory diseases • Elevated cardiac enzymes – CK or cardiac troponins • Serum viral antibody titers - For viral myocarditis
  59. 59. Aortic dissection • When to suspect? History Spittell et al 1993 Findings investigation Risk factors: atherosclerosis, uncontrolled hypertension, coarctation of the aorta, bicuspid aortic valves, aortic stenosis, Marfan syndrome, Ehlers- Danlos syndrome, and pregnancy Sudden onset of severe chest pain of tearing or ripping quality (classic symptom) pain also may be: • Anterior: anterior arch or aortic root • Intrascapular: descending aorta • Abdominal: with abdominal and renal br. Pain migrates with propagation of the dissection. Associations: CVS accident, acute MI, altered mental status ,syncope, hemoptysis, dyspnea, fever. High-risk examination features: • Pulse deficit.(don’t rely on this) • Systolic blood pressure limb differential greater than 20mm Hg. • Focal neurologic deficit: hemiparesis, hemiplegia, hemihypothesia, horner’s.. • Murmur of aortic regurgitation (new). EM Practice Guidelines Update © 2010 • ECG: to rule out STEMI. • CXR: widened mediastinum, pleural effusion,tracheal deviation (Mammen et al 2008). • CT & MRI : 98% sensitivity.
  60. 60. Emergency management: 1. Rate / Pressure Control: Titrate to heart rate < 60 IV beta blockade Labetalol (If contraindication, substitute diltiazem or verapamil). BP Control if high by IV vasodilator to titrate to BP< 120 mmHg 2. Pain Control: I.V. opiates & titrate to pain control. 3.If hypotensive or shocked: IV fluid bolus Titrate to MAP of 70 mm Hg Or Euvolemia. 4. Urgent surgical consultation.
  61. 61. Pneumothorax History Examination Investigation Classic presentation: Sudden acute or subacute one-sided, sharp, lancinating, pleuritic chest pain and sudden onset dyspnea. exacerbated by deep respiration and coughing, alleviated by shallow breathing and immobilization sometimes with irritative cough Tension pneumothorax: Associated with Hypotension, hypoxia, chest pain, dyspnea Spontaneous pneumothorax: No clinical signs or symptoms If a bleb ruptures results in classic picture Iatrogenic pneumothorax: similar to those of spontaneous pneumothorax, depending on patient’s age, presence of underlying lung disease, and extent of pneumothorax Catamenial pneumothorax: (Korom et al 2004) Women aged 30-40 years with onset of symptoms within 48 hours of menstruation. Pneumomediastinum: Respiratory findings: Tachypnea and Respiratory distress. Tracheal shift to the contralateral side with a large tension pneumothorax. Unilateral distant or absent breath sounds. Hyperresonance on percussion Decreased TVF. Ipsilateral crackles or wheezes Cardiovascular findings: Tachycardia: if more than 135 bpm, tension pneumothorax is likely. Pulsus paradoxus and Hypotension Jugular venous distention: seen in tension pneumothorax, may be absent if hypotension is severe. Cardiac apical displacement. chest x-ray: Pleural line (D.D. scapular line) no lung parenchyma beyond, usually upper lobe. CT scanning: recommended for uncertain or complex cases.
  62. 62. Emergency treatment: Needle Thoracostomy Classical management of tension pneumothorax is emergent chest decompression with needle thoracostomy. A 14-16G intravenous cannula is inserted into the second rib space in the mid-clavicular line. The needle is advanced until air can be aspirated into a syringe connected to the needle. The needle is withdrawn and the cannula is left open to air. An immediate rush of air out of the chest indicates the presence of a tension pneumothorax. The manoeuver essentially converts a tension pneumothorax into a simple pneumothorax.
  63. 63. Esophageal rupture: Boerhaave syndrome means spontaneous rupture usually results from transient increase in intraesophageal pressure (coughing, straining, seizures, and childbirth have been reported as causing perforations), common in alcoholic males. The pain is acute, severe, unrelenting, and diffuse, in the chest, neck, and abdomen. Pain can radiate to the back and shoulders, exacerbated by swallowing, associated with dysphagia, dyspnea, hematemesis, and cyanosis can be present as well Examination may be normal or ill-appearing, dyspneic, and diaphoretic patient and may reveal evidence of pneumothorax or subcutaneous air. Fever, hemodynamic instability, septic complication occure lately. CXR findings includes: unilateral effusion, usually on the left. pneumothorax, pneumomediastinum, pneumoperitoneum, and/or subcutaneous air. Diagnosed by: Esophagram or CT scan. Mainstays of therapy include the following: 1. Intravenous volume resuscitation. 2. Administration of broad-spectrum antibiotics. 3. Prompt surgical intervention.
  64. 64. Musculoskeletal “chest wall pain syndromes” • It is important to rule out visceral causes of chest pain, including cardiac, esophageal,or pulmonary causes, such as angina, myocardial infarction, malignancies, or pulmonary embolism, before definitively diagnosing musculoskeletal chest pain. (Proulx & Zryd 2009) • Pain is characterized by highly localized, sharp, positional chest pain and completely reproducible by light to moderate palpation of a discrete area of the chest wall, although chest wall tenderness occurs in some patients with pulmonary embolism and myocardial ischemia as mentioned.
  65. 65. Pain related to bony and cartilaginous structures of the chest wall •Costochondritis •Tietze syndrome •Rib pain: -Fractures related to trauma -Stress fractures •Slipping rib syndrome •Painful xiphoid syndrome Pain related to muscles •Muscle strains: 1)Pectoralis muscle strains 2)Injuries to internal oblique/external oblique muscles 3)Serratus anterior muscle injury •Myofascial pain •Fibromyalgia •Precordial catch syndrome •Epidemic myalgia Pain related to thoracic spine •Thoracic disc herniation Miscellaneous causes of chest wall pain •Skin-related conditions -Herpes zoster -Neoplasms •SAPHO syndrome: Causes of musculoskeletal chest pain
  66. 66. Peptic ulcer disease History and presentation: “Classic" history, including epigastric burning pain; relief of pain with ingestion of milk, food, or antacids; and night pain, also history of upper endoscopy, NSAIDS intake, or H.pylori infection. Pain is characterized as a postprandial, dull, boring pain in the midepigastric region. Patients often describe being awakened from sleep by discomfort. Duodenal ulcer pain is usually relieved after eating food, in contrast to gastric ulcer Symptoms, which are often exacerbated by eating. Symptomatic relief is usually provided by antacid medications. Acute pancreatitis and biliary tract disease present with right upper quadrant or epigastric pain and tenderness but also can cause chest pain. Examination: Epigastric tenderness (neither sensitive nor specific for the diagnosis). Findings indicative of complications: a rigid abdomen consistent with peritonitis in perforation; abdominal distention or a succussion splash due to obstruction; occult or gross rectal blood or blood in the nasogastric aspirate signaling ulcer bleeding.
  67. 67. Acute chest syndrome The acute chest syndrome (ACS) is an acute pulmonary illness that occurs in patients with sickle cell disease. ACS is currently defined as a new infiltrate on chest radiograph in conjunction with 1 other new symptom or sign: chest pain, cough, wheezing, tachypnea, and/or fever (> 38.5°C). 1. Serial chest radiographs 2. Consider ventilation and perfusion imaging 3. Serial hematologic testing • Complete blood count • Reticulocyte count 4. Secretory phospholipase A2 measurement, if available 5. Arterial blood gas with co-oximetry 6. Blood cultures 7. Consider bronchoscopy
  68. 68. Panic disorders
  69. 69.  The patient's age, presenting symptoms, time course of symptom development and resolution, and lack of other identifiable medical causes are often helpful in considering the differential diagnosis of a panic attack.(Zauble et al 1998)  One screening question that has been shown to rapidly identify patients who are suffering from panic attacks is: "Have you experienced brief periods for seconds or minutes of an overwhelming panic or terror which was accompanied by racing heart, shortness of breath, or dizziness? (Ballenger et al 1998) Treatment: 1. Cognitive Behavioral Therapy (CBT). 2. Pharmacotherapy: selective serotonin reuptake inhibitors (SSRIs), serotonin/norepinephrine reuptake inhibitors (SNRIs), TCAs, monoamine oxidase inhibitors (MAOIs), and Benzodiazepines.
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