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A detailed case study of a 49-year-old female patient experiencing intermittent squeezing chest pain. The case study includes a comprehensive history, physical examination, and diagnostic workup. It provides valuable insights into the assessment and management of chest pain, particularly in patients with a history of myocardial infarction. The document also includes exercises and questions designed to enhance understanding and critical thinking skills.
Typology: Exams
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Reason for Encounter Chest pain
History of present illness A 57 - year-old female 10 days status post inferolateral STEMI with stent placement, presents to the ED with a 2.5-hour history of progressively worsening chest pain. The pain is sharp and stabbing, gets to pierce through her back with inspiration. Pain is partially relieved by sitting up and leaning forward. She reports mild nausea without vomiting, denies fever/chills, palpitations, lightheadedness/syncope, SOB, cough, URI, or extremity/catheterization site pain or swelling. She reports compliance with her antiplatelet medications (ASA and clopidogrel), pantoprazole, and aspirin since discharge. On exam, patient is febrile, shallow respirations at normal rate, low-normal oxygen saturation, and has pericardial friction rub. PMH is significant for hypertension, hyperlipidemia, tobacco abuse, obesity, and family history of heart attack and type- 2 diabetes.
Past Medical History Hypertension Hyperlipidemia Hospitalizations / Surgeries Acute inferolateral wall ST-elevation myocardial infarctionwith PCI/stenting of the right coronary artery (RCA). Balloon angioplasty of the left circumflex artery.
Medications Clopidogrel 75 mg QD Atorvastatin 80 mg QD at bedtime Pantoprazole 40 mg QD Aspirin 81 mg QD
Allergies Bactrim (rash)
Preventive health Up to date immunization including flu shots annually. Reports gynecology exam was normal.
Family History Father - Heart attack, 59 years old Mother - Type 2 Diabetes Sister - Type 2 Diabetes
HEENT / Neck Head: Normocephalic, atraumatic, no deformities, facial features symmetric.Temporal arteries non-tender to palpation. Frontal and maxillary sinuses non-tender. Eyes: Normal conjunctivae on inspection. Visual acuity with Snellen pocket card: OD 20/20, OS 20/20. Throat/Neck: Mucous membranes moist. Oropharynx without erythema, edema, or exudate. No stridor, no foreign body. No visible scars, deformities, or other lesions on neck inspection. Trachea is midline and freely mobile. JVP WNL Cardiovascular PMI nondisplaced. JVP WNL. No significant change while standing, squatting, during Valsalva maneuver or with sustainedhandgrip. Chest / Respiratory Thorax atraumatic; no postsurgical scars. Respirations shallow, normal rate, nonlabored. No visible bounding of the chest. No tenderness to chest wall or vertebral body palpation. No palpable thrill. Normal tactile fremitus. Thorax normal/symmetrical to percussion. Normal lungs sounds bilaterally. Abdomen Abdomenatraumatic, obese, nondistended. Normoactive bowel sounds. No hepatosplenomegaly or palpable masses. Soft, nontender throughout exam. Genitourinary / Rectal Normal pelvic exam. No masses or tenderness. Normal external genitalia. Musculoskeletal / Osteopathic Structural Examination Normal muscle bulk. No evidence of swelling. No calf tenderness or inflammatory signs. No peripheral edema. No asymmetry or deformity of the back. No tenderness or spasm of the paraspinal muscles. No localized tenderness of the spinous processesor pelvic structures. Neurologic PERRLA.CN II-XII intact. Psychiatric AOx Lymphatic No pathologically enlarged lymph nodes in the cervical, supraclavicular, axillary or inguinal chains. *History of present illness Patient known to be ischemic heart. Recently he developed retrosternal burning and compressing chest pain, with acute onset intermittent course for 5 hours. Not radiating , not relieved by sublingual nitrates , not associated with dyspnea. there is no history of syncope, palpitation, bluish discoloration of peripheries or lower limb oedema.
The pain is not aggravated by chest movement and not relieved by changing posture. There is no cough, haemoptysis, or audible breathing sounds. There is no history of dysphagia, odynophagia, hematemesis or heartburn. There is no history of chest trauma. There were no symptoms suggesting other systems affection. *Past History Patient has history of PCI since 2 years. The patient condition started 3 years ago when he had similar attacks of chest pain that occurred repeatedly despite receiving sublingual Nitro glycerine tablets. There are no other chronic diseases, no drug allergy, no history of operations and no blood transfusion *Family History There are no chronic disease running in family or similar attacks. Emergency Department Examination 1ry Survey: Airway: The patient has patent airways Breathing: By Inspection, the Respiratory Rate is 14 breathes / minute, there is symmetrical chest movements and there is no chest deformity. By Palpation, There is no chest tenderness, there is symmetrical chest expansion & there is no shifting of trachea. By Percussion, No Hyper-resonance By Auscultation, No Abnormal Breathing sounds. Circulation: Central Pulsation is felt, central to peripheral pulsation is comparable & peripheral- toperipheral pulsation is also comparable. Radial pulsation is 63 beats per min, regular, of average volume, symmetrical in both sides and has no special characters. Blood Pressure: 115 / 85 mmHg (Normal) Capillary Filling time: less than 2 seconds. Disability:
PHYSICAL EXAMINATION
DIAGNOSIS AND DIFFERENTIAL Electrocardiography Of all the diagnostic tools clinically used in assessing chest pain, the electrocardiogram (ECG) is the most reliable when used and interpreted correctly. Patients with acute infarctions may have ECG findings that range from acute ST-segment elevations to completely normal. This range means that the ECG is useful only when it has a positive, or diagnostic, finding. New ST-segment elevations, Q waves, bundle branch block,
SPECIFIC CAUSES OF CHEST PAIN Angina Pectoris The pain of chronic stable angina is episodic and lasts 5 to 15 minutes. It is precipitated by exertion and relieved with rest or sublingual nitroglycerin within 3 minutes. The pain is typically visceral in nature (aching, pressure, and squeezing), with radiation to the neck, jaw, arm, or hand. In individual patients the character of each attack varies little with recurrent episodes. Most patients can differentiate their usual angina from other causes of pain. Physicians evaluating patients with stable angina should screen carefully for changes in the pattern that would suggest a shift from stable to unstable angina or even suggest a different diagnosis. Unstable Angina : Patients who complain of recent onset of angina, changes in the character of the angina, or angina at rest are thought to have an unstable pattern of their angina. They are at risk for an AMI or sudden cardiac death (see Chapter 21 for management). Variant (Prinzmetal) Angina This form of angina is thought to be due to spasm of the epicardial vessels in patients with normal coronary arteries (one third of cases) or in patients with underlying atherosclerotic disease (two thirds of cases). Pain typically occurs at rest and may be precipitated by the use of tobacco or cocaine. The ECG typically shows ST- segment elevations during an acute attack. Acute Myocardial Infarction Ischemic pain that lasts longer than 15 minutes, is not relieved by nitroglycerin, or is accompanied by diaphoresis, dyspnea, nausea, or vomiting suggests the diagnosis of AMI. The clinician must understand the limitations of the screening tools used in the ED and should have a high level of suspicion for AMI in patients with risk factors and prolonged or persistent symptoms for whom there is no other clear diagnosis. Aortic Dissection This diagnosis should be suspected in the patient who complains of sudden onset of severe, tearing pain in the retrosternal or midscapular area. High-risk patients are also those at risk for AMI, specifically the middle-age hypertensive male. The patient may be hypertensive or
Gastrointestinal Causes Esophageal reflux, dyspepsia syndromes, and esophageal motility disorders can produce chest pain that is difficult to distinguish from ischemic pain. Patients may complain of burning, gnawing pain associated with an acid taste radiating into the throat. Pain may be exacerbated by meals, worsen when supine, and may be associated with belching. Clinicians should determine whether the symptoms are due to a GI disorder based on the clinical presentation and the absence of findings and/or risk factors suggesting an ischemic cause. Diagnostic decisions should not be made on the basis of a response to a therapeutic trial of antacids, GI cocktails, or nitroglycerin. EMERGENCY DEPARTMENT CARE AND DISPOSITION Assume that every patient complaining of chest pain might be having an AMI. Patients with suspicious histories should have large-bore IV line established, a cardiac monitor, supplemental O 2 , and ECG obtained as soon as possible. Vital signs and pulse oximetry should be monitored continuously. Ask patients about cardiac risk factors, preexisting coronary artery disease, quality of chest pain, time of onset and duration of symptoms, and whether the pattern has been stable, unstable, continuous, or intermittent. Ask specifically for clues to noncardiac causes of chest pain: ability to elicit pain by movement or cough; the relation of pain to meals; or pain that is of sudden onset, referred to the back, or pleuritic in nature. Examine patients while noting evidence of heart failure or valvular insufficiency, pericardial rubs, or tenderness of the chest wall. Specifically, physicians should ask whether pain elicited on palpation of the chest wall exactly reproduces the patient's pain. An ECG should be obtained on all patients for whom there is a reasonable suspicion of myocardial ischemia. A normal ECG, although minimizing the likelihood of an AMI, does not definitively rule out the possibility of MI. If the etiology of chest pain remains unclear in some patients, clinicians should consider more diagnostic tests as guided by clinical suspicion and findings. Clinicians should not use patients' clinical response to GI cocktails, nitroglycerin, or NSAIDs to exclude the possibility of myocardial ischemia. In patients with nondiagnostic ECGs for whom there is a clinical suspicion for ischemia, clinicians should consider provocative testing, echocardiography, or admission and observation.
Physicians should not rely on serum enzyme testing to rule out the possibility of clinically significant disease.