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35 Cards in this Set
- Front
- Back
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Patients with visceral-type chest pain (defined below), significantly abnormal pulse or blood pressure measurements, or with dyspnea should be
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placed directly into a treatment bed, a cardiac monitor initiated, an intravenous line established, oxygen administered, and an ECG ordered. Other less well-defined patients also deserve expeditious evaluation, and experienced triage officers and nurses often have a "gut" feeling about certain patients; that insight should be respected.
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three categories of chest pain are
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(1) chest wall pain, (2) pleuritic or respiratory chest pain, and (3) visceral chest pain.
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In atypical angina, the pain is
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the same as that with exertional angina, but pain occurs at rest. Atypical angina appears to be caused by coronary artery spasm. In about two-thirds of patients with atypical angina, coronary artery lesions are seen, and patients may have exertional as well as rest pain. In both exertional angina and atypical angina, the pattern is stable in terms of frequency of episodes, severity, ease of provocation, and response to rest or nitroglycerin. In UA, the episodic anginal pain has changed its pattern;
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In atypical angina, the pain is
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the same as that with exertional angina, but pain occurs at rest. Atypical angina appears to be caused by coronary artery spasm. In about two-thirds of patients with atypical angina, coronary artery lesions are seen, and patients may have exertional as well as rest pain. In both exertional angina and atypical angina, the pattern is stable in terms of frequency of episodes, severity, ease of provocation, and response to rest or nitroglycerin. In UA, the episodic anginal pain has changed its pattern;
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Using the initial ECG, the incidence of AMI is approximately 80 percent for patients with new ST-segment elevation greater than
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1 mm in two contiguous leads, about 20 percent in patients with new ST-segment depression or T-wave inversion, but less than 4 percent in patients without either of these two patterns.
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The pain associated with a PE occurs when
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inflammation of the parietal pleura overlying the infarction causes chest pain that is generally sharp and related to respiration.
Dyspnea, fever, cough, and/or hemoptysis also may be present, and the chest wall may be tender to palpation. |
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The pain associated with a PE occurs when
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inflammation of the parietal pleura overlying the infarction causes chest pain that is generally sharp and related to respiration.
Dyspnea, fever, cough, and/or hemoptysis also may be present, and the chest wall may be tender to palpation. |
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Esophageal rupture (Boerhaave syndrome) is a rare but potentially life-threatening cause of chest pain. Patients classically present with a history of substernal, sharp chest pain of sudden onset that occurs immediately after an episode of forceful vomiting (see Chap. 75). The patient is usually ill-appearing, dyspneic, and diaphoretic. The physical examination is often normal but may
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reveal evidence of pneumothorax or subcutaneous air. Chest radiography may be normal or may demonstrate pleural effusion (left more common than right), pneumothorax, pneumomediastinum, pneumoperitoneum, and/or subcutaneous air. The diagnosis can be confirmed by a study with water-soluble contrast.
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Esophageal rupture (Boerhaave syndrome) is a rare but potentially life-threatening cause of chest pain. Patients classically present with a history of substernal, sharp chest pain of sudden onset that occurs immediately after an episode of forceful vomiting (see Chap. 75). The patient is usually ill-appearing, dyspneic, and diaphoretic. The physical examination is often normal but may
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reveal evidence of pneumothorax or subcutaneous air. Chest radiography may be normal or may demonstrate pleural effusion (left more common than right), pneumothorax, pneumomediastinum, pneumoperitoneum, and/or subcutaneous air. The diagnosis can be confirmed by a study with water-soluble contrast.
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The pain of acute pericarditis is typically
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acute, sharp, severe, and constant (see Chap. 55). It is usually described as substernal, with radiation to the back, neck, or shoulders, and is exacerbated by lying down and by inspiration. It is classically described as being relieved by leaning forward. A pericardial friction rub is the most important diagnostic finding. The ECG may show diffuse ST-segment elevation and T-wave inversion. In addition, depression of the PR segment is a highly specific ECG finding for pericarditis.
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The pain of acute pericarditis is typically
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acute, sharp, severe, and constant (see Chap. 55). It is usually described as substernal, with radiation to the back, neck, or shoulders, and is exacerbated by lying down and by inspiration. It is classically described as being relieved by leaning forward. A pericardial friction rub is the most important diagnostic finding. The ECG may show diffuse ST-segment elevation and T-wave inversion. In addition, depression of the PR segment is a highly specific ECG finding for pericarditis.
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most frequently diagnosed cardiac valvular abnormality
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Mitral valve prolapse
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most frequently diagnosed cardiac valvular abnormality
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Mitral valve prolapse
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is a particular cause of costochondral pain related to fusiform swelling in one or more upper costal cartilages and has a pain pattern similar to that of other costochondral syndromes
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Tietze syndrome
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is a particular cause of costochondral pain related to fusiform swelling in one or more upper costal cartilages and has a pain pattern similar to that of other costochondral syndromes
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Tietze syndrome
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Peptic ulcer disease is classically characterized as
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postprandial, dull, boring pain in the midepigastric region (see Chap. 77). 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 achieved by antacid medications. Acute pancreatitis and biliary tract disease present with right upper quadrant or epigastric pain and tenderness but also can present with chest pain.
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Peptic ulcer disease is classically characterized as
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postprandial, dull, boring pain in the midepigastric region (see Chap. 77). 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 achieved by antacid medications. Acute pancreatitis and biliary tract disease present with right upper quadrant or epigastric pain and tenderness but also can present with chest pain.
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the American College of Cardiology/ American Heart Association (ACC/AHA) guidelines for management of patients with AMI recommend standing orders that all patients with "ischemic-type pain" have a 12-lead ECG performed within
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10 min of arrival and that the ECG be handed directly to the treating physician for immediate interpretation.
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the American College of Cardiology/ American Heart Association (ACC/AHA) guidelines for management of patients with AMI recommend standing orders that all patients with "ischemic-type pain" have a 12-lead ECG performed within
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10 min of arrival and that the ECG be handed directly to the treating physician for immediate interpretation.
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The normal myocardium depolarizes from
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endocardium to epicardium and repolarizes in the opposite direction.
This creates an electrical potential between normal and ischemic myocardium during depolarization and results in ST-segment elevation in an overlying electrode. Conversely, if the electrode is located over normal myocardium opposite an ischemic region, ST-segment depression will be seen. . If ischemia is limited to the subendocardial area, an overlying electrode will be separated from the ischemic tissue by a layer of normal myo-cardium, resulting in an electrical potential pointed inward from the normal to ischemic tissue, resulting in ST-segment depression |
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The normal myocardium depolarizes from
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endocardium to epicardium and repolarizes in the opposite direction.
This creates an electrical potential between normal and ischemic myocardium during depolarization and results in ST-segment elevation in an overlying electrode. Conversely, if the electrode is located over normal myocardium opposite an ischemic region, ST-segment depression will be seen. . If ischemia is limited to the subendocardial area, an overlying electrode will be separated from the ischemic tissue by a layer of normal myo-cardium, resulting in an electrical potential pointed inward from the normal to ischemic tissue, resulting in ST-segment depression |
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In extensive or transmural ischemia, the direction of repolarization is reversed so that recovery occurs from endocardium to epicardium, resulting
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in T-wave inversions in an overlying electrode. In subendocardial ischemia, the delay does not alter the normal recovery process (epicardium to endocardium), so T waves are not inverted. However, because normal epicardium repolarization is unopposed due to delayed subendocardial repolarization, the T wave in an overlying electrode may be larger than normal (called hyperacute T waves)
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In extensive or transmural ischemia, the direction of repolarization is reversed so that recovery occurs from endocardium to epicardium, resulting
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in T-wave inversions in an overlying electrode. In subendocardial ischemia, the delay does not alter the normal recovery process (epicardium to endocardium), so T waves are not inverted. However, because normal epicardium repolarization is unopposed due to delayed subendocardial repolarization, the T wave in an overlying electrode may be larger than normal (called hyperacute T waves)
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After infarction, the area of necrosis is electrically silent, not able to depolarize. During ventricular depolarization, initial electrical activity will be generated in normal myocardium, away from the infarcted area. This results in
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an electrical potential directed from the infarcted area toward normal myocardium, causing an abnormal initial negative deflection (pathologic Q waves) in the QRS complex of overlying electrodes. Occasionally, small Q waves (called septal Q waves) are seen in the limb or lateral precordial ECG leads. Pathologic Q-waves are distinguished by their duration (greater than 40 ms) and depth (greater than 25 percent of the corresponding R wave).
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After infarction, the area of necrosis is electrically silent, not able to depolarize. During ventricular depolarization, initial electrical activity will be generated in normal myocardium, away from the infarcted area. This results in
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an electrical potential directed from the infarcted area toward normal myocardium, causing an abnormal initial negative deflection (pathologic Q waves) in the QRS complex of overlying electrodes. Occasionally, small Q waves (called septal Q waves) are seen in the limb or lateral precordial ECG leads. Pathologic Q-waves are distinguished by their duration (greater than 40 ms) and depth (greater than 25 percent of the corresponding R wave).
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Pathologic Q-waves are distinguished by
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their duration (greater than 40 ms) and depth (greater than 25 percent of the corresponding R wave).
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Pathologic Q-waves are distinguished by
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their duration (greater than 40 ms) and depth (greater than 25 percent of the corresponding R wave).
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The CK levels usually become abnormally high within
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4 to 8 h after coronary artery occlusion (onset of symptoms), peak between 12 and 24 h, and return to normal between 3 and 4 days
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The CK levels usually become abnormally high within
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4 to 8 h after coronary artery occlusion (onset of symptoms), peak between 12 and 24 h, and return to normal between 3 and 4 days
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The CK levels usually become abnormally high within
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4 to 8 h after coronary artery occlusion (onset of symptoms), peak between 12 and 24 h, and return to normal between 3 and 4 days
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After AMI, serum myoglobin levels begin to rise within
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3 h of onset of symptoms and are abnormally elevated in 80 to 100 percent of patients at 6 to 8 h, peak at 4 to 9 h (see Figure 49-1), and with normal kidney function return to baseline within 24 h from symptom onset.
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After AMI, serum myoglobin levels begin to rise within
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3 h of onset of symptoms and are abnormally elevated in 80 to 100 percent of patients at 6 to 8 h, peak at 4 to 9 h (see Figure 49-1), and with normal kidney function return to baseline within 24 h from symptom onset.
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After AMI, cardiac troponin I (cTnI) and troponin T (cTnT) become elevated after approximately
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6 h, peak at 12 h, and remain elevated for 7 to 10 days.
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After AMI, cardiac troponin I (cTnI) and troponin T (cTnT) become elevated after approximately
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6 h, peak at 12 h, and remain elevated for 7 to 10 days.
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After AMI, cardiac troponin I (cTnI) and troponin T (cTnT) become elevated after approximately
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6 h, peak at 12 h, and remain elevated for 7 to 10 days.
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