Approach to Chest Pain PDF

Approach to chest pain Dr Ali Husam Hadi Emergency medicine specialist  Introduction ❖ Chest pain ranges between life-threatening & non–life-threatening diseases. ❖ It may be complicated by disassociation between intensity of symptoms and...

Approach to chest pain Dr Ali Husam Hadi Emergency medicine specialist  Introduction ❖ Chest pain ranges between life-threatening & non–life-threatening diseases. ❖ It may be complicated by disassociation between intensity of symptoms and signs and seriousness of underlying pathology. ❖ Acute coronary syndrome (ACS), aortic dissection, pulmonary embolism (PE), pneumothorax, pericarditis with tamponade, and esophageal rupture are potentially catastrophic causes of chest pain. ❖ Chest pain that is atypical or of unclear cause is a daily presentation in virtually every ED.  Pathophysiology ❖ Afferent bers from the heart, lungs, great vessels, and esophagus enter the same thoracic dorsal ganglia. ❖ These visceral bers produce the same indistinct quality and location of pain from each organ. ❖ Dorsal segments overlap three segments above and below a level, so thoracic origin disease can produce pain anywhere from the jaw to the epigastrium. fi fi  Initial assessment and rapid stabilization ❖ All patients, except those with obvious benign causes of chest pain, undergo electrocardiography (ECG) as soon as possible after reporting their pain. ❖ In clinical evaluation we should ask ourselves these questions: “Should I intervene now?” and “What are the life-threatening possibilities in this patient?”; the answer will depend on the assessment of the patient’s appearance, ECG, and vital signs. ❖ Patients with abnormal vital signs, ECG ndings of ischemia or injury, a history of prior coronary artery disease, multiple atherosclerotic risk factors, or any abrupt, new, or severe chest pain or dyspnea should be quickly placed into a treatment bed. ❖ The ECG should be obtained ideally within 10 minutes of arrival and should be read for acute myocardial infarction (MI) by the emergency clinician promptly after it is completed. fi  Initial assessment and rapid stabilization ❖ Initiate cardiac monitoring and IV access. ❖ Identify and treat immediate life needs such as supporting the airway, breathing, and circulation. ❖ Measure vital signs promptly and at regular intervals. ❖ Administer oxygen if ambient saturation is 50 years old or those with known coronary artery disease. ❖ Consider ACS in patients presenting with new palpitations, as myocardial ischemia may enhance automaticity and irritability, potentially leading to dysrhythmias. Moreover, tachycardia can elevate myocardial oxygen demand, triggering myocardial ischemia. fi ❖ Major risk factors for coronary artery disease include age >40 years old, male or postmenopausal female, hypertension, tobacco use, hypercholesterolemia, diabetes, truncal obesity, family history, and a sedentary lifestyle. ❖ Cocaine use is associated with AMI even in young people with minimal or no coronary artery disease, and chronic cocaine use may accelerate atherosclerosis and severe coronary artery disease. ❖ While cardiac risk factors are useful in predicting coronary artery disease risk within a given population, they are less useful for diagnosing the presence or absence of ACS in an individual patient. ❖ Patients with known coronary artery disease and prior ACS are at risk for another ACS event; therefore, identify previous episodes of chest pain; prior echocardiography, stress testing, or coronary angiography; or prior revascularization (stent placement or coronary artery bypass graft surgery). ❖ The examination of patients with ACS is often normal, and there are no exam ndings that diagnose or exclude ACS. Use the exam in conjunction with history to search for other causes and guide therapy. ❖ Vital sign abnormalities from ACS may include hyper- or hypotension, tachycardia, or bradycardia. ❖ Patients with acute myocardial ischemia or infarction may have abnormal heart sounds due to changes in ventricular function or compliance. ❖ New murmurs in patients with chest pain may be associated with AMI with chordae tendineae rupture or aortic root dissection. ❖ Ischemia-induced congestive heart failure may produce crackles on auscultation of the lungs. ❖ Reproducible chest wall tenderness suggests a musculoskeletal etiology, but is reported in up to 15% of patients with con rmed AMI and cannot exclude the diagnosis of ACS. fi fi ❖ ECG: Guidelines recommend a screening ECG within 10 minutes of ED arrival in patients with chest pain or other symptoms concerning for ACS. ❖ Rapid ECG screening limits delays in identifying STEMI, allows more rapid time to reperfusion, and improves patient outcomes. ❖ New ST-segment elevation of ≥1 mm in at least two contiguous leads represents an AMI that will bene t from rapid reperfusion interventions. ❖ Because there are several conditions that represent occlusion of the coronary arteries other than STEMI, a new paradigm has emerged in which there is occlusive myocardial infarction (OMI) and non-occlusive myocardial infarction (NOMI). ❖ OMI may involve: STEMI, hyperacute T waves, De Winter’s T waves, posterior MI, Sgarbossa criteria in LBBB, Wellen’s syndrome, ST depression in aVR and new onset bundle branch block. fi ❖ ST-segment elevation also occurs in patients with pericarditis, myocarditis, early repolarization, left ventricular hypertrophy, ventricular aneurysms and LBBB, so not every ST elevation is a candidate for reperfusion. ❖ NOMI may involve: ST depression, T wave attening or inversions and non speci c T wave changes. ❖ A normal ECG lacks the sensitivity to exclude ACS, notably unstable angina or NSTEMI. ❖ Misinterpretation of ECGs or failure to detect ischemic changes that are present occurs in up to 40% of missed AMI cases. ❖ Furthermore, the initial ECG represents only a single time point in a dynamic pathophysiologic process. Thus, if there is a high concern for ACS, the ECG should be repeated at 15- to 30-minute intervals and compared to prior ECGs. fl fi  Location of MI ECG ndings Anteroseptal or ST-segment elevations in V1, V2, V3, and V4 anterior Anterolateral ST-segment elevations in V1–V6, I, and aVL Lateral ST-segment elevations in I, aVL, V5 and V6 Inferior ST-segment elevations in II, III, and aVF Inferolateral ST-segment elevations in II, III, aVF, and V5 and V6 Initial R waves in V1 and V2 >0.04 s and R/S ratio ≥1; Posterior posterior ECG shows 0.5-mm ST elevation in V7–V9 (may be associated with inferior) Inferior MI with ST-elevation in lead III > lead II and ST-elevation in V1; Right ventricular ST segment elevation in RV leads V3R–V6R fi ❖ Cardiac Troponins Cardiac troponins (cTn) are proteins essential to cardiac muscle contraction that are present within cardiac myocyte cytoplasm. ❖ Myocardial injury resulting in the disruption of myocyte cell membrane integrity results in extracellular cTn leak, which can be detected in the patient’s peripheral blood and used to identify and quantify myocardial damage. ❖ Due to its high sensitivity and nearly complete cardiac speci city, cTn is the biomarker of choice for the detection of myocardial injury. ❖ Although cTn elevation is speci c for myocardial injury, elevation does not indicate the mechanism of injury. There are numerous non-ischemic causes of cTn elevations. ❖ AMI can be differentiated from non-ischemic cTn elevations based on the pattern of cTn elevation and the clinical context. ❖ The diagnostic criteria for AMI includes a gradual rise of cTn combined with any of the following: symptoms consistent with ischemia, characteristic acute ECG changes (ST-segment and T-wave changes, new left bundle branch block, or new Q waves), or imaging evidence of a new regional wall motion abnormality or new loss of viable myocardium. ❖ cTn testing has made older cardiac biomarkers, such as myoglobin and creatine kinase-MB, obsolete in ACS care. fi fi  ❖ Recently developed fth-generation assays, commonly referred to as high-sensitivity troponin assays, have much higher sensitivity compared to previous assays. ❖ Among patients presenting within 3 hours of chest pain onset, high-sensitivity cTn assays are 92% to 94% sensitive for AMI compared to 76% for the previous assay. ❖ Obtain cardiac cTn levels in all patients with suspected ACS. ❖ A single fourth-generation cTn assay will identify most patients (approximately 80%) with AMI within 2 to 3 hours of ED arrival, and the sensitivity of two high-sensitivity cTn samples drawn 1 hour apart within 3 hours of presentation approaches 100% for AMI. ❖ Thus, serial measurements of cTn are generally needed to safely exclude AMI in most patients presenting with chest pain. ❖ AMI may safely be excluded with a single cTn in select, low-risk patients with constant symptoms for >6 to 12 hours. ❖ Patients with diagnostic ST-segment elevation on their initial ECG do not require serum marker measurement to make treatment and disposition decisions. ❖ Conversely, serum markers are useful in patients with non-diagnostic ECGs for diagnosis of NSTEMI and risk strati cation of patients with STEMI, NSTEMI, and unstable angina. fi fi  ACS management ❖ ST-Elevation (STEMI): Immediate reperfusion therapy is crucial. ❖ This can be achieved through percutaneous coronary intervention (PCI) or thrombolysis within 90 minutes of the rst medical contact. ❖ Additionally, antiplatelets, anticoagulants, and nitrates should be administered as soon as possible. ❖ The same treatment is applied for STEMI equivalents (OMI). ❖ ST-Depression or T-wave Inversion (NSTEMI/Unstable Angina): In such cases, medical therapy is initiated. ❖ This includes antiplatelets, anticoagulants, nitrates, beta-blockers, and statins. ❖ If the patient is in shock, nitroglycerin should be avoided. Instead, 250 ml of isotonic uid should be administered, and inotropes may be considered. ❖ Rales or Jugular Venous Distension (JVD): Excessive uid intake should be avoided, and diuretics should be used cautiously. ❖ In all cases, the patient should be admitted to the hospital, preferably to cardiac care unit (CCU) or the intensive care unit (ICU) if respiratory support needed, for close monitoring and appropriate treatment. fl fl fi  PULMONARY EMBOLISM ❖ Symptoms of PE include sharp chest pain (may worsen with inspiration, called “pleuritic”), dyspnea, hypoxemia, syncope, or shock. ❖ There may be associated cough or hemoptysis. Patients with PE may be febrile (fever often not very high if present) or have leg swelling or pain, and some patients will report chest wall tenderness. ❖ Common physical examination ndings include tachypnea, tachycardia, and hypoxemia. ❖ PE risk factors include recent surgery, trauma, prolonged immobility, active cancer, estrogens from birth control pills or hormone replacement therapy (particularly when combined with smoking), procoagulant syndromes, or a history of prior PE or deep venous thrombosis. ❖ Clinical decision aids, such as the Wells and Revised Geneva Scores, can risk-stratify patients with possible PE. ❖ The Pulmonary Embolism Rule Out Criteria exclude PE in patients with a low pretest probability without further diagnostic testing. fi ❖ Normal d-dimer testing in a hemodynamically stable, low- to intermediate-risk patient effectively excludes PE; in those with higher risk assessment, a negative d-dimer has limited value. ❖ In patients with PE, elevated cardiac troponin indicates ventricular dysfunction and identi es patients with an elevated risk of death and complications. ❖ In PE, ECG ndings are nonspeci c, with the most common nding being sinus tachycardia, other changes can be seen like the classic S1Q3T3, right ventricular strain, RBBB or right axis deviation. ❖ Chest radiographs often have nonspeci c changes, but in rare cases, they may show signs of pulmonary infarction. CT pulmonary angiography is the test of choice and is highly sensitive for the detection of large to medium-sized PEs. ❖ Treatment is tailored to the severity of the condition and involves administering anticoagulants such as intravenous heparin or subcutaneous low molecular weight heparin, oral anticoagulants, providing oxygen, and, if the patient’s condition is unstable, administering thrombolytics. fi fi fi fi fi  AORTIC DISSECTION ❖ Pain from aortic dissection is classically described as a ripping or tearing sensation radiating to the interscapular area of the back. The pain is often sudden in onset, maximal at the time of symptom onset, and may migrate or be noted above and below the diaphragm. ❖ Secondary symptoms of aortic dissection result from arterial branch occlusions and include stroke ndings (lateralizing weakness or sensory changes), AMI, or limb ischemia. ❖ Risk factors include male sex, age over 50 years, poorly controlled hypertension, cocaine or amphetamine use, a bicuspid aortic valve or prior aortic valve replacement, certain connective tissue disorders (Marfan’s syndrome and Ehlers-Danlos syndrome), and pregnancy. ❖ Physical exam ndings for aortic dissection lack sensitivity and speci city. A unilateral pulse de cit of the carotid, radial, or femoral arteries may suggests aortic dissection in the setting of acute chest pain. ❖ Focal neurologic de cits are rare, occurring in only 16% of patients with aortic dissection, but the combination of chest pain and a focal neurologic de cit increases the likelihood of aortic dissection. ❖ A chest radiograph may reveal a wide mediastinum, but while a completely normal chest radiograph reduces the probability, it does not de nitively rule out dissection. ❖ When aortic dissection is suspected, obtain a CT aortogram or transesophageal echocardiogram. ❖ Treatment involves intravenous antihypertensives, beta-blockers, and an urgent surgical consultation. fi fi fi fi fi fi fi  Pneumonia ❖ Pneumonia is potentially life threatening in the elderly, immunocompromised, or patients with multiple comorbid conditions. ❖ Chest pain from pneumonia is usually described as sharp or pleuritic and associated with fever, cough, sputum production, dyspnea and possibly hypoxemia. ❖ Auscultation may reveal decreased breath sounds, rales, or bronchial breath sounds over the affected areas of consolidation. ❖ A chest radiograph usually con rms the diagnosis. ❖ Treatment for pneumonia depends on its severity and type, and may include antibiotics, oxygen, corticosteroids, bronchodilators, analgesia, and antipyretics. fi  ESOPHAGEAL RUPTURE (BOERHAAVE’S SYNDROME) ❖ Patients classically present with a history of sudden-onset sharp substernal chest pain following forceful vomiting. ❖ Patients with esophageal rupture are usually ill-appearing and may be tachycardic, febrile, dyspneic, or diaphoretic. ❖ Physical examination may reveal crepitus in the neck or chest from subcutaneous emphysema. ❖ Hamman’s crunch, audible crepitus that varies with the heartbeat on auscultation of the precordium, is a rare nding associated with pneumomediastinum. ❖ Chest radiography could show a pleural effusion (left more common than right), pneumothorax, pneumomediastinum, pneumoperitoneum, or subcutaneous air, although a normal radiograph cannot exclude esophageal rupture. ❖ When suspecting esophageal rupture, obtain a CT with oral water soluble contrast. ❖ Treatment include: IV uid resuscitation, Analgesia, IV antibiotics, Early surgical consultation, IV antifungal coverage in immunocompromised patients or those on PPIs. fi fl  SPONTANEOUS PNEUMOTHORAX ❖ The symptoms of spontaneous pneumothorax are sudden-onset, sharp, pleuritic chest pain with dyspnea. ❖ Classically, spontaneous pneumothorax occurs in tall, slender males. ❖ Risk factors for spontaneous pneumothorax include smoking and chronic lung diseases such as asthma and chronic obstructive pulmonary disease. ❖ Approximately 1% to 3% of patients with a spontaneous pneumothorax may develop a tension pneumothorax. ❖ Auscultation may reveal decreased breath sounds and hyperresonance to percussion on the ipsilateral side. ❖ However, the physical exam ndings of a simple pneumothorax are inconsistent and cannot be used to rule out its presence, as the diagnosis is made through chest radiography. fi ❖ Tension pneumothorax is a clinical diagnosis characterized by the patient’s vital instability, accompanied by decreased air entry on the side of the pneumothorax. ❖ In such cases, chest radiographs are contraindicated. However, if the diagnosis is uncertain, bedside ultrasound can be used as an alternative diagnostic tool. ❖ Treatment is based on the cause and size of the pneumothorax. ❖ It may include oxygen therapy, analgesia, and a tube thoracostomy. ❖ For tension pneumothorax, rapid decompression can be achieved using a needle, nger, or tube thoracostomy, whichever method is the fastest. fi  ACUTE PERICARDITIS ❖ Pain from acute pericarditis is classically described as a sharp, severe, constant pain with a substernal location. ❖ The pain may radiate to the back, neck, or shoulders; is worsened by lying at and by inspiration; and is relieved by sitting up and leaning forward. ❖ A pericardial friction rub is the most speci c physical exam nding, but is not always evident. ❖ The classic ECG ndings are diffuse ST-segment elevation with PR depression. ❖ Treatment for pericarditis varies depending on its underlying cause and may include the use of nonsteroidal anti-in ammatory drugs (NSAIDs), corticosteroids, colchicine, and assessing for the presence of pericardial effusion or tamponade. fi fl fi fi fl  CARDIAC TAMPONADE ❖ Non-Traumatic Cardiac Tamponade is the accumulation of pericardial uid, causing compression of the heart, leading to decreased cardiac output. ❖ Causes include: Malignancy (most common non-traumatic cause), Uremia (renal failure), Pericarditis (viral, bacterial, TB), Autoimmune diseases (e.g., lupus), Aortic dissection (extension into pericardium), Post-cardiac surgery or myocardial infarction (late complication) ❖ Clinical Presentation: ❖ Beck’s Triad: Hypotension, Jugular venous distension, Muf ed heart sounds. ❖ Tachycardia, Pulsus paradoxus (decrease in systolic BP >10 mmHg during inspiration). ❖ Dyspnea, Chest pain, Fatigue. fl fl ❖ Diagnosis: ❖ ECG: Low voltage QRS, Electrical alternans. ❖ CXR: Enlarged, globular ("water bottle") cardiac silhouette. ❖ Echocardiography: Key diagnostic tool; shows pericardial effusion, diastolic collapse of right ventricle. ❖ Emergency Treatment: ❖ Pericardiocentesis: Immediate drainage of pericardial uid. ❖ Fluid resuscitation while preparing for pericardiocentesis (to maintain preload). ❖ Cardiology cosultation. ❖ Consider de nitive treatment for the underlying cause (e.g., malignancy, infection). fi fl  CHEST WALL PAIN ❖ Musculoskeletal or chest wall pain is characterized by sharp, highly localized, and positional pain. ❖ The pain should be completely reproducible by light to moderate palpation or by speci c movements and may be increased by inspiration or coughing. ❖ However, chest wall tenderness is also reported by some patients with ACS and PE. ❖ Costochondritis is an in ammation of the costal cartilages or their sternal articulations and causes chest pain that is variably sharp, dull, and often increased with respirations. ❖ Xiphodynia is in ammation of the xiphoid process that causes sharp, pleuritic chest pain reproduced by light palpation. ❖ Pleurisy is in ammation of the parietal pleura resulting in sharp pleuritic chest pain. ❖ Treatment is with analgesia. fl fl fl fi  GI PAIN ❖ GI disorders often cannot be reliably differentiated from ACS by history and physical examination alone. ❖ Gastritis and esophageal re ux usually cause a burning or gnawing sensation in the lower chest, accompanied by a metallic or sour taste in the back of the mouth. The pain may be alleviated by antacids but worsens when lying down. ❖ Peptic ulcer disease is classically described as a postprandial, dull, boring pain in the epigastric region and may be awakened from sleep by discomfort. ❖ Duodenal ulcer pain may be relieved after eating food, whereas gastric ulcer pain is often exacerbated by eating. ❖ Acute pancreatitis and biliary disease typically present with right upper quadrant or epigastric pain and tenderness, but can also cause chest pain. ❖ Esophageal spasm is often associated with re ux disease and is characterized by a sudden onset of dull or tight substernal chest pain. ❖ The pain is frequently precipitated by consumption of hot or cold liquids or a large food bolus and may be relieved by nitroglycerin. ❖ Treatment should be directed toward the underlying cause and may include antacids, PPIs, opioid analgesics, lifestyle modi cations, and consultation or referral to a gastrointestinal specialist. fl fl fi  PANIC DISORDER ❖ Panic disorder is characterized by recurrent, unexpected, and discrete periods of intense fear or discomfort (panic attacks) with at least four of the following symptoms: chest pain, dyspnea, palpitations, diaphoresis, nausea, tremor, choking, dizziness, fear of losing control or dying, paresthesias, chills, or hot ashes. ❖ In one study, 25% of ED patients with chest pain met diagnostic criteria for panic disorder. ❖ Conversely, 9% of the patients identi ed as having panic disorder were ultimately diagnosed with ACS on hospital discharge. ❖ This means panic disorder is best a diagnosis of exclusion or a co-diagnosis with ACS (or another cause). ❖ Do not assume panic disorder in a patient with chest pain in the ED until further testing allows better risk strati cation. fi fl fi Thank you