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chest pain ddx final C3 (1).pptx
- 1. Chest Pain DDx Hassan H. Al-Homoud #215022811 Abdullah Al-beladi #215019525 Sajjad Al-Khalifah #215009921
- 2. 2/24/2023 By the end of this lecture we should be aware of:-
- 3. Objectives (main) definitions, causes, examination, investigations emergency management
- 5. What is chest pain? Acute chest pain is the recent onset of pain, pressure, or tightness in the anterior thorax between the xiphoid, suprasternal notch, and both mid-axillary lines
- 6. Acute chest pain Somatic pain: Pain from somatic fibers is usually easily described, precisely located, and often experienced as a sharp sensation Visceral pain: Pain from visceral fibers is generally more difficult to describe and imprecisely localized
- 8. Acute Coronary Syndrome ACS is characterized by plaque rupture or erosion with associated thrombosis. Acute coronary syndrome is commonly associated with three clinical manifestations: 1. Unstable angina 2. NSTEMI 3. STEMI (more than 30 minutes)
- 9. Risk Factor Modifiable Non-modifiable hypertension age >40 years old tobacco use male or postmenopausal female hypercholesterolemia family history diabetes History of prior coronary artery disease. truncal obesity sedentary lifestyle. Cocaine use
- 10. symptoms Retrosternal left anterior chest crushing, squeezing, tightness, or heaviness. Radiation of the pain to the arms, neck, or jaw Diaphoresis dyspnea nausea or vomiting. Palpitations Decreased exercise tolerance
- 11. Physical Examination Vital sign abnormalities: hyper- or hypotension. tachycardia, or bradycardia. abnormal heart sounds due to changes in ventricular function or compliance, such as an S3 or S4 gallop diminished S1, or a paradoxically split S2. New murmurs in patients with chest pain may be associated with acute myocardial infarction with chordae tendineae rupture or aortic root dissection. Ischemia-induced congestive heart failure may produce crackles on auscultation of the lungs.
- 12. Physical Examination Vital sign abnormalities: Physical examination findings most strongly associated with acute myocardial infarction in patients presenting with acute chest pain are hypotension, S3 gallop, and diaphoresis Response to medications poorly discriminates between cardiac and noncardiac chest pain. While nitroglycerin reduces anginal pain, it may also relieve the pain from noncardiac conditions such as esophageal spasm.
- 13. Investigation ECG : ST segment depression + T wave inversion Cardiac enzymes: as Troponin, CK-MB elevated Stable angina ECG : normal We can do exercise ECG test (stress test) to check if there is abnormality that doesn’t appear in ECG ECG : ST segment depression + T wave inversion Unstable angina NSTEMI ECG : ST segment elevation & T wave changes Cardiac enzymes elevation. STEMI
- 15. Treatment “ B-MONA” Beta Blocker Morphine Oxygen supply Nitrate Aspirin PCI performed within 90 minutes is the definitive therapy.
- 16. Aortic dissection Aortic dissection occurs after a violation of the intima allows blood to enter the media and dissect between the intimal and adventitial layers. Aortic dissection has a bimodal age distribution. The first peak involves younger patients with specific predisposing conditions such as connective tissue disorders. The second peak includes those aged >50 years with chronic hypertension
- 17. Risk factors Genetics Males < Females Age over 50 years Poorly controlled hypertension Cocaine use. Prior aortic valve replacement.
- 18. symptoms Ripping or tearing sensation radiating to the interscapular area of the back. Sudden in onset, maximal at the time of symptom onset, and may migrate above and below the diaphragm. Secondary symptoms of it: Stroke, acute myocardial infarction, or limb ischemia
- 19. Physical Examination Unilateral pulse deficit. Combination of chest pain and a focal neurologic deficit. • A murmur over the aorta, or other abnormal sound. • A difference in blood pressure between the right and left arms, or between the arms and legs. • Low blood pressure.
- 20. Investigation Elevated cTn Chest radiograp h. D- dimer ECG : ST- segment or T-wave changes. CT aortogram or transesophageal echocardiogram
- 21. Treatment ANTIHYPERTENSIVES: β-Blocker is ideal, and short acting β- blockers such as propranolol, labetalol, or esmolol are preferred VASODILATORS: Vasodilators such as nitroprusside Intravenous access: Hypertension must be managed aggressively in all cases to reduce further damage. The aim is a systolic pressure of between 100 and 120 mm Hg Rapid referral to a surgeon is mandatory.
- 22. Acute pericarditis This refers to inflammation of the pericardium. It is relieved by sitting up and leaning forward Worsens by lying flat and by inspiration. Associated with fever. May radiate to the back, neck, or shoulders. Sharp, severe, constant pain with a substernal location.
- 23. Acute pericarditis A pericar dial friction rub ECG : ST-segment elevation with PR Depression with T inversion. X-ray CT or MRI Treatment : Bed rest and oral NSAIDs (high-dose aspirin indometacin or ibuprofen)
- 24. Cardiac tamponade: It is commonly accompanying an episode of acute pericarditis. When a large volume collects in this space, ventricular filling is compromised leading to embarrassment of the circulation
- 25. symptoms • Fainting and loss of consciousness Restlessness and weakness • Trouble and rapid breathing Chest pain radiating to neck , shoulder or back • Discomfort that's relieved by sitting or leaning forward. Low blood pressure
- 26. Physical Examination Heart sounds are soft and distant Apex beat is commonly obscured A friction rub may be evident due to pericarditis in the early stages, but this becomes quieter as fluid accumulates and pushes the layers of the pericardium apart. As the effusion worsens, signs of cardiac tamponade may become evident: • Raised jugular venous pressure. (Friedreich’s sign) • Kussmaul’s sign (rise in JVP/increased neck vein distension during inspiration). • Pulsus paradoxus (an exaggeration in the normal variation in pulse pressure seen with inspiration such that there is drop in systolic blood pressure of ≥10 mmHg). • Reduced cardiac output. .
- 27. Investigation ECG • Low-voltage QRS complexes with sinus tachycardia. Chest X-ray • Large globular or pear-shaped heart Echocardio graphy • The most useful technique for demonstrating the effusion and looking for evidence of tamponade . Pericardiocentesis is then indicated to relieve the pressure
- 30. DDX ◍ Tension pneumothorax ◍ Pulmonary embolism ◍ Esophageal rupture 30
- 31. Definition ◍ Tension pneumothorax is a life-threatening condition ◍ develops when air is trapped in the pleural cavity under positive pressure ◍ displacing mediastinal structures and compromising cardiopulmonary function.
- 32. Clinical Manifestation ◍ Dyspnea ◍ Hypoxia ◍ Chest pain ◍ Tachycardia ◍ Hypotension ◍ Anxiety ◍ Fatigue
- 33. Physical examination Inspection ◍ Tracheal deviation ◍ jugular venous distention Palpation ◍ Asymmetric lung expansion ◍ Decreased tactile fremitus Percussion ◍ Hyper-resonance percussion ◍ Auscultation Distant or absent breath sounds Unilaterally
- 34. Diagnosis ◍ The diagnosis of a tension pneumothorax should largely be based on the history and physical examination findings. ◍ Ultrasound when there is doubt regarding the diagnosis. ◍ Chest X-ray or CT when the patient is hemodynamically stable
- 36. Pneumothorax
- 37. EMERGENCY Treatment ◍ In patients with unstable vital signs and clinical features suggestive of tension pneumothorax, immediate needle decompression followed by chest tube ◍ X-rays should not be obtained before treatment.
- 38. Needle decompression ◍ Insert a 14-gauge IV needle and catheter into the pleural space in the mid-clavicular line just at the second intercostal space. ◍ The needle is left in place until a chest tube can be inserted.
- 39. Chest Tube ◍ Chest tube is inserted in intercostal space. ◍ Then, attached to underwater seal. All patients should receive supplemental oxygen.
- 41. Pulmonary embolism is the sudden blockage of a major blood vessel (artery) in the lung. Symptoms: Sudden onset of: 1. Shortness of breath 2. Pleuritic chest pain (sharp in character) 3. Cough 4. Agitated, anxious, and confused. Signs: 1. Hypoxemia 2. Tachypnea 3. Tachycardia 4. Hemoptysis 5. Diaphoresis 6. Low grade fever
- 42. 1. Advanced age >50 2. Obesity 3. Pregnancy 4. Malignancy 5. Inherited thrombophilia 6. Recent surgery or major trauma 7. Immobility/bed rest 8. Indwelling central venous catheter 9. Long distance travel 10.Smoking 11.Congestive heart failure 12.Stroke 13.Estrogen use Risk factors
- 43. After history physical examination chest x-ray needs for further diagnostic tests and management depends on Pretest probability assessment. If PE suspected use the two-level PE Wells score. Diagnosis
- 44. Diagnostic criteria of well score
- 45. Two-level PE Wells score PE likely PE unlikely 1. Offer immediate CTPA 1. Offer a D-dimer test 2. If CTPA not immediately available offer short-term parenteral anticoagulant therapy followed by CTPA 2. If D-dimer positive offer immediate CTPA 3. If CTPA negative and DVT suspected consider proximal leg vein ultrasound 3. If CTPA not immediately available offer short-term parenteral anticoagulant therapy followed by CTPA Diagnosis
- 46. If PE suspected in LOW-RISK PATIENT
- 47. stabilization of the patient: maintain the airway, give oxygen, and IV fluids. Hemodynamically stable Anticoagulation is given as SC LMWH or IV UFH Hemodynamically unstable (systolic blood pressure below 100 mm Hg) Thrombolytic therapy if failed, Embolectomy Management in ER Frequent mentoring of cardiac rhythm, blood gases and acidity, blood pressure, and pulse oxygenation
- 49. Etiology of esophageal rupture: • Iatrogenic: following esophageal instrumentation (commonest) • Spontaneous (Boerhaave syndrome) • Trauma: penetrating or blunt trauma • Foreign body • Malignancy Esophageal Rupture
- 50. When to suspect esophageal rupture in trauma cases? Gun shot or stab-wound to the neck, chest or abdomen. Clinical features • Dysphagia/odynophagia or Hypersalivation • Hematemesis • Neck pain or swelling • Retrosternal fullness • Subcutaneous emphysema Traumatic esophageal injury
- 51. Spontaneous (Boerhaave) esophageal injury ◍ Spontaneous rupture of the esophagus that typically occurs after forceful vomiting ◍ Most lethal perforation of the GI tract, with mortality ~35%
- 53. Spontaneous (Boerhaave) esophageal injury History: • Retrosternal chest pain • Severe retching or vomiting, precede onset of pain • Odynophagia, dyspnea, dysphagia or hoarseness Signs: • Crepitus on palpation of chest wall • Hamman’s sign: crunching sound synchronous on auscultation • Signs of Sepsis/fulminant shock
- 54. Spontaneous (Boerhaave) esophageal injury Mackler’s triad: chest pain, vomiting and subcutaneous emphysema
- 55. Diagnosis: contrast (Gastrografin) Esophagram Reveals the location and extent of the perforation by extravasation of the contrast material CT and endoscopy may also be used for diagnosis (controversial)
- 56. Findings in Chest X-ray • Mediastinal or free peritoneal air • Mediastinal widening • Mediastinal air-fluid level • Subcutaneous emphysema • Pleural effusions • Hydropneumothorax However, patients often have non-specific findings; some of these findings may take hours to develop
- 57. Management Supportive • ICU admission • Avoidance of oral intake • NGT to eliminate oral and gastric secretions. • Nutritional support • IV broad spectrum antibiotic • IV PPI
- 58. Management Subsequent management: • Medical management: NPO for 7 days, parenteral nutrition, IV antibiotic fluid drainage. • Endoscopic management • Surgical management
- 59. References
- 60. 2/24/2023
Editor's Notes
- Pain from somatic fibers is usually easily described, precisely located, and often experienced as a sharp sensation. Pain from visceral fibers is generally more difficult to describe and imprecisely localized. Patients with visceral pain are more likely to use terms such as discomfort, heaviness, pressure, tightness, or aching. Visceral pain is often referred to an area of the body corresponding to adjacent somatic nerves.
- Non-classic presentations of acute coronary syndrome occur more frequently in: women Diabetics Elderly patients with psychiatric disease or altered mental status .
- Chest X-ray Echocardiography Cardiac angiography. Most patients with acute coronary syndrome have a normal chest x-ray, but the images are useful to diagnose or exclude other conditions such as pneumonia and pneumothorax. CT help evaluate conditions such as aortic dissection or pulmonary embolism. Cardiac Troponins : is the biomarker of choice for the detection of myocardial injury.
- may decrease cardiac output, and should be used with caution in the presence of hypotension, and in patients with inferior MI.
- . 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, acute myocardial infarction, or limb ischemia
- Physical exam findings for aortic dissection lack sensitivity and specificity. A unilateral pulse deficit of the carotid, radial, or femoral arteries is suggestive of aortic dissection (likelihood ratio 5.7; 95% confidence interval, 1.4–23).42 Focal neurologic deficits are rare, occurring in only 17% of patients with aortic dissection, but the combination of chest pain and a focal neurologic deficit greatly increase the likelihood of aortic dissection.42
- Elevated cardiac enzymes Chest radiography D-dimer ECG : ST-segment or T-wave changes. CT aortogram or transesophageal echocardiogram While a completely normal chest radiograph lowers the likelihood of aortic dissection being present, it does not exclude dissection. A negative d-dimer lowers the probability of aortic dissection (detecting the clotting/declotting expected), but it also cannot exclude the disease. ECG changes are common among patients with aortic dissection, with up to 40% to 50% presenting with ST-segment or T-wave changes. Elevated cTn among patients with aortic dissection is associated with increased mortality. If aortic dissection is suspected, obtain a CT aortogram or transesophageal echocardiogram. Aortic dissection is a life-threatening condition and needs to be treated right away. Dissections that occur in the part of the aorta that is leaving the heart (ascending) are treated with surgery. Dissections that occur in other parts of the aorta (descending) may be managed with surgery or medicines.
- Intravenous access. Adequate analgesia Transfer to an intensive care unit or high dependency unit. Hypertension must be managed aggressively in all cases to reduce further damage. The aim is a systolic pressure of between 100 and 120 mm Hg.
- A pericardial friction rub is the most specific physical exam finding but is not always evident. The classic ECG findings are diffuse ST-segment elevation with PR Depression ECG is diagnostic. There is widespread concave-upwards (saddle-shaped) ST elevation + PR depression + T wave inversion ( in all leads )(Fig. 14.113), reciprocal ST depression in leads aVR and V1, and PR segment depression. These changes evolve over time, with resolution of the ST elevation. Chest X-ray may demonstrate cardiomegaly (in cases with an effusion) which should be confirmed with echocardiography. CT and cardiac MR may be helpful for in cases with thickened (>4 mm) or inflamed (abnormal delayed enhancement) pericardium. Echocardiography: is the procedure of choice for the detection, confirmation, and serial follow-up of patients with acute pericarditis and a pericardial effusion Treatment : Bed rest and oral NSAIDs (high-dose aspirin indometacin or ibuprofen)
- . 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, acute myocardial infarction, or limb ischemia
- ECG reveals low-voltage QRS complexes (<0.5 mV in limb leads) with sinus tachycardia and there may be electric alternans (alteration of QRS amplitude or axis between beats). Chest X-ray (Fig. 14.114) shows large globular or pear-shaped heart with sharp outlines. Typically, the pulmonary veins are not distended. Echocardiography (Fig. 14.115) is the most useful technique for demonstrating the effusion and looking for evidence of tamponade – late diastolic collapse of the right atrium, early diastolic collapse of the right ventricle, ventricular septum displacement into the left ventricle during inspiration, diastolic flow reversal in the hepatic veins during expiration, dilated inferior vena cava with <50% reduction during inspiration. Cardiac CT or MRI should be considered if loculated pericardial effusions are suspected (post-cardiac surgery). Pericardiocentesis is the removal of pericardial fluid with aseptic technique under echocardiographic guidance. It is indicated when a tuberculous, malignant or purulent effusion is suspected. Pericardial biopsy may be needed if tuberculosis is suspected and pericardiocentesis is not diagnostic. Other tests include looking for underlying causes, e.g. blood cultures, autoantibody screen. TREATMENT : Pericardiocentesis is then indicated to relieve the pressure – a drain may be left in temporarily to allow sufficient release of fluid. Pericardial effusions may reaccumulate, most commonly due to malignancy (in the UK). This may require pericardial fenestration, i.e. creation of a window in the pericardium to allow the slow release of fluid into the surrounding tissues.
- It pushes the mediastinum to the opposite hemithorax, and obstructs venous return to the heart
- Hypotension, tracheal deviation, and hyperresonance of the affected side are the hallmarks of tension pneumothorax. Hypoxia results as the collapsed lung on the affected side and the compressed lung on the contralateral side compromise effective gas exchange.
- Hypotension, tracheal deviation, and hyperresonance of the affected side are the hallmarks of tension pneumothorax
- Signs of tension The left lung is completely compressed (arrowheads). The trachea is pushed to the right (arrow) The heart is shifted to the contralateral side - note right heart border is pushed to the right (red line) The left hemidiaphragm is depressed (orange line) Remember If you diagnose a tension pneumothorax clinically - do not request an X-ray - TREAT THE P
- CT is more sensitive and may be useful in patients with bullous changes on x-ray.
- placed in the second intercostal space in the mid- clavicular line to try to reexpand the lung. The tube then con- nects to an underwater seal or to low-pressure suction. If blood is present in the pleural space, a second thoracostomy tube is placed in the fourth, fifth, or sixth intercostal space to drain the blood. The process is repeated until the lung re-expands
- excessive sweating
- There is no need to apply the PERC rule to those patients who are not being evaluated for PE. If the patient is considered low-risk PERC may help avoid further testing. If the patient is moderate or high risk then PERC can not be utilized. Consider d-dimer or imaging based on risk.
- suspicion of the diagnosis before attempting to apply the Wells criteria. using the Wells’ score over clinician gestalt to predict who is low-risk and then applying the PERC rule to stop workup for PE 1- suspicion of the diagnosis 2- then apply the Wells criteria 3-using the Wells’ score to predict who is low-risk THEN applying the PERC rule
- There is no need to apply the PERC rule to those patients who are not being evaluated for PE. If the patient is considered low-risk PERC may help avoid further testing. If the patient is moderate or high risk then PERC can not be utilized. Consider d-dimer or imaging based on risk. - We should do PERC if we suspect PE in low risk patient in ED, and PERC help us to avoid further testing so if all answer NO no further diagnosis
- subcutaneous (SC) low-molecular-weight heparin (LMWH) intravenous (IV) unfractionated heparin (UFH) Embolectomy is the emergency surgical removal of emboli which are blocking blood circulation. It usually involves removal of thrombi (blood clots), and is then referred to as thrombectomy
- The most common cause of esophageal perforation iatrogenic, caused by instrumentation of the esophagus such as endoscopy or nasogastric tube. The most common non-itrogenicc cause is spontaneous The most common cause of non-iatrogenic esophageal perforation is spontaneous rupture, followed by foreign body ingestion (table 2), trauma, and malignancy The majority of the esophageal injuries are penetrating injuries. The incidence of blunt esophageal injuries was one-tenth that of penetrating injuries at one urban Level 1 trauma center [8]. The most common penetrating etiology is gunshot wound (75 percent) in the United States studies, followed by stab wounds, and other mechanisms. Traumatic esopygeal injury may be associated with multiorgan injury. Boerhaave that results from a sudden increase in intraesophageal pressure combined with negative intrathoracic pressure (eg, severe straining or vomiting). Boerhaave syndrome usually occurs in patients with a normal underlying esophagus. However, a subset of patients with Boerhaave syndrome has underlying eosinophilic esophagitis, medication-induced esophagitis, Barrett's or infectious ulcers. Sudden increase in intraesophageal pressure combined with negative intrathoracic pressure such as that associated with severe straining or vomiting, and less frequently with childbirth, seizure, prolonged coughing or laughing, or weightlifting, results in a longitudinal esophageal perforation Rupture of the intrathoracic esophagus results in contamination of the mediastinal cavity with gastric contents. This leads to chemical mediastinitis with mediastinal emphysema and inflammation, and subsequently bacterial infection and mediastinal necrosis. Rupture of the overlying pleura by mediastinal inflammation or by the initial perforation directly contaminates the pleural cavity, and pleural effusion results. Although pericardial tamponade and infected pericardial effusions due to Boerhaave syndrome have been reported, they are rare [6]. If untreated, sepsis and organ failure result In itrogenic perforation, signs and symptoms may not appear until hours after the procedure.
- However, you can reliably diagnose esopygeal rupture based on presence of these features alone
- Boerhaave syndrome is basically esopygeal perforation due to sudden increase in intra-abdominal pressure combined with decrease in intrathoracic pressure. Boerhaave syndrome usually occurs in patients with a normal underlying esophagus. However, a subset of patients with Boerhaave syndrome has underlying eosinophilic esophagitis, medication-induced esophagitis, Barrett's or infectious ulcers. severe straining or vomiting, and less frequently with childbirth, seizure, prolonged coughing or laughing, or weightlifting, results in a longitudinal esophageal perforation However, these signs require at least an hour to develop after an esophageal perforation and even then are present in only a small proportion of patients Mackler’s triad is pathognomonic, however, it is seen in less than 50% of cases.
- Mackler’s triad is pathognomonic, however, it is seen in less than 50% of cases.
- Water-soluble contrast (gastrografin) esophagram shows a distal esophageal perforation (arrow) with extravasation of contrast material into the mediastinum and left pleural space.
- Thoracic and cervical radiography — Findings suggestive of an esophageal perforation on chest radiograph include mediastinal or free peritoneal air or subcutaneous emphysema (image 1A-B) [4]. With cervical esophageal perforations, plain films of the neck may show air in the soft tissues of the prevertebral space. Other findings suggestive of an esophageal perforation include pleural effusions, mediastinal widening, hydrothorax, hydropneumothorax, or subdiaphragmatic air. However, thoracic or cervical radiographs are not sensitive for an esophageal perforation and patients usually have nonspecific findings. In addition, mediastinal emphysema may not become visible radiographically after an hour of perforation and pleural effusion(s) and mediastinal widening take several hours to develop [13]. In one study that included 34 patients with an esophageal perforation, the initial plain chest radiograph was abnormal in approximately 97 percent of patients, but only 27 percent were interpreted as being compatible with an esophageal perforation [4].