Case study

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Case Study 2.1 – Coronary Artery Thrombosis and Heart Failure

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Ruth Olson, a 73-year-old female presented to the emergency department with a recent (4-hour) history of severe chest pain radiating to her left arm. She was suspected of having had a “heart attack.” Coronary angiography revealed complete occlusion of the left anterior descending branch about 2 cm from its origin. She was given a therapeutic dose of recombinant human tissue plasminogen activator (tPA). This treatment restored coronary artery blood flow, and her chest pain improved. Simultaneously, she was started on one tablet of aspirin per day.

Seven days later, she noted swelling of both legs and feet and was found to have pitting edema of the legs; her liver was enlarged, and her neck veins (jugular) appeared full. She was given diuretics and asked to consume a salt-restricted diet. Because of considerable weakness, she remained in bed most of the time.

A few days later, she developed sudden pain in the lower right part of her chest, aggravated by taking a deep breath. Physical examination revealed that her left leg had more swelling than the right. X-ray of her chest showed a faint shadow in the peripheral part of the lower lobe of the right lung. Intravenous heparin was started.

The following images may help guide your discussion:

ALL STUDENTS WILL ANSWER QUESTIONS #1 & QUESTION #8. Then, for your INITIAL POST, students with the LAST name beginning with the letter:

  • A – C | Will answer Questions 2
  • D – F | Will answer Questions 3
  • G – J | Will answer Questions 4
  • K – O | Will answer Questions 5
  • P – T | Will answer Questions 6
  • U – Z | Will answer Questions 7

Initial posts and responses must be based on various current resources such as textbooks, articles, and journals. Medscape, Up-to-Date, and ePocrates as supplemental resources are acceptable. It must be evidence-based and published within the last five years. The posts must be professionally written and in the correct APA 7th Edition Manual format for in-text and references applied. 

  1. What is the epidemiology of coronary artery disease in the United States? (CDC; WHO; American Heart Association, and other sources)
  2. What is the basis of thrombosis in the coronary artery? What are the factors that predispose to arterial versus venous thrombosis?
  3. Why was t-PA given? What is the mechanism of action of t-PA? What are the other naturally occurring anticoagulants?
  4. Why is aspirin given in such cases? What stage of hemostasis is affected by aspirin?
  5. Why did the patient develop edema initially? What are the factors that predispose to generalized edema? Why did he later develop more edema in one leg? Why are patients with edema given a salt-free diet?
  6. What are the clinical settings in which venous thrombosis of leg veins occurs? What is the most feared consequence?
  7. What are other causes of arterial thrombosis?
  8. What is the Primary Diagnosis? What are two possible differential diagnoses? What is the likely outcome of this case?

NB

LAST NAME BEGINS WITH “R”

 

Case Study 2.3 – Atrial Fibrillation and Left Ventricular Hypertrophy

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You received a call from the local emergency department.  The patient in question (Irving Olson) is a 75-year-old man recently evaluated in your office after an episode of syncope shortly after a funeral for a 71-year-old cousin who had also died suddenly.  Irving’s medical record indicated that he has an active diagnosis of emphysema.  Your patient’s episode of syncope was associated with transient mild dyspnea on exertion and palpitations.  There was no associated chest pain.  The patient denied prior medical illness.  He had never been told he had a heart murmur, and there was nothing in his history to suggest before acute rheumatic fever.  Physical examination revealed a forceful systolic heave and an apical precordial impulse displaced far to the left on the chest wall.  The chest radiograph showed cardiomegaly with slight atrial enlargement.  An ECG confirmed the presence of left ventricular hypertrophy.  His liver enzymes were slightly elevated, but serum markers of cardiac injury (enzymes, troponin) were negative for myocardial infarction.  The patient had been referred to a cardiologist for an echocardiogram to rule out hypertrophic cardiomyopathy, valvular heart disease, or coarctation of the aorta.

The medical examiner relates that the patient collapsed suddenly at work while unloading a truck.

The following images may help guide your discussion:

ALL students will answer Question #1 & Question #10. Then for your INITIAL POST, students with the LAST name ending in:

  • A – C: Will answer Questions 2
  • D – F: Will answer Questions 3
  • G – J: Will answer Questions  4
  • K – O: Will answer Questions  5 & 7
  • P – T: Will answer Questions  6 & 8
  • U – Z: Will answer Questions  9

Initial posts and responses must be based on various resources such as textbooks, articles, and journals.  Medscape, Up-to-Date, ePocrates, Primary Care Pocket Guide, and/or others as supplemental resources are acceptable.

  1. What is the epidemiology of Atrial Fibrillation and Left Ventricular Hypertrophy?  (CDC; WHO; other sources)
  2. Describe the physiology of hypertrophic cardiomyopathy.  What would have been found if an echocardiogram had been done? 
  3. Are there other types of cardiomyopathy?  What must the clinician do before the term cardiomyopathy is applied? 
  4. What does the heart look like in dilated cardiomyopathy?  What is the physiology of dilated cardiomyopathy? 
  5. Define myocarditis, and list some common etiologic agents. 
  6. What is the primary physiologic problem in restrictive cardiomyopathy? 
  7. Compare and contrast hypertrophic versus dilated cardiomyopathy concerning ventricular morphology, hemodynamics, genetics, and pathophysiology.
  8. Define myocarditis.  Describe the histologic criteria for myocarditis.  List some crucial etiologies for myocarditis.
  9. List three known myocardial toxins.
  10. What is the Primary Diagnosis?  What are two possible differential diagnoses?  What is the likely outcome of this case?

 

Case Study 2.4 – STEMI vs. NSTEMI

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Victoria is a 44-year-old Vietnamese woman who was evaluated in the emergency department for chest pain. She had a history of hypertension. Her medications included antihypertensives and cholesterol-lowering agents. She had a prior admission two years ago for a small, uncomplicated, myocardial infarct. There were no clinical changes until 2 weeks before her emergency department admission when she began having daily anginal attacks that lasted > 30 minutes. In the hour before her admission, she had awakened with severe chest pain, nausea, and dyspnea. There had been severe unrelenting pain for 45 minutes, and it had not been relieved by nitroglycerin. Vital signs were HR 105 beats/min, BP 100/50 mm Hg (usual BP was about 155/95 mm Hg), and temperature 100° F. She was obese and diaphoretic (sweating profusely) with pale skin and labored respirations. Rales were heard over both lung fields. An ECG and serial cardiac markers were ordered.

Laboratory ValuesTime Total CKIUCK-MBng/mLCK index Troponinng/mL

Admission

150

3

20

<0.4

8 hr

320

8

25

0.8

16 hr

500

30

60

10.4

24 hr

750

60

80

22

48 hr

300

18

60

14

72 hr

80

2

25

9.3

Normal

8-120

0-3

0-3

<0.4

The following images may help guide your discussion:

ALL Students will answer Question #1 and Question #8.  Then for your INITIAL POST, students with the LAST name ending in:

  • A – C: Will answer Questions 2
  • D – F: Will answer Questions 3
  • G – J: Will answer Questions 4
  • K – O: Will answer Questions 5
  • P – T: Will answer Questions 6
  • U – Z: Will answer Questions 7

Initial posts and responses must be based on various resources such as textbooks, articles, and journals. Medscape, Up-to-Date, ePocrates, Primary Care Pocket Guide, and/or others as supplemental resources are acceptable.

  1. What is the epidemiology of STEMI vs. NSTEMI? (CDC; WHO; other sources)
  2. Could you still have made the diagnosis of acute myocardial infarction based on laboratory data if the patient had waited for 24- 48 hours before coming to medical attention?
  3. When would a negative CK profile not be helpful in ruling out acute MI?
  4. What additional test would be valuable in the assessment of a patient with a suspected acute MI and a negative CK profile?
  5. Which test is more sensitive for myocardial injury, CK or CK-MB?
  6. Which test is more specific for myocardial injury, CK or CK-MB?
  7. Which test is most specific for myocardial injury?
  8. What is the Primary Diagnosis?  What are 2 possible differential diagnoses?  What is the likely outcome of this case?