Mr. Smith presented to the ED for a complaint of shortness of breath. The history and physical is below. 

CC: Shortness of breath for the last 2 weeks. 

HPI: 
Mr. Smith is a 52y/o Caucasian male who presented to the ED with a complaint of chest pain and shortness of breath for 2 weeks. He has had some degree of shortness of breath for the last 2-3 months and it has progressively gotten worse over the last 2 weeks. Home nebulizer treatments have not relieved his shortness of breath.  He endorses a history of orthopnea, paroxysmal nocturnal dyspnea and lower extremity edema all of which have become worse over the last two weeks. His chest pain has been constantly present for the last two weeks, is substernal, sharp in nature, and does not radiate. He denies any previous history of heart failure, does not follow a special diet. He is on a number of medications and brought the bottles with him. His medications were reviewed and the list is below. He reports medication compliance. 

Review of Systems: 
Constitutional: Positive for fatigue. Negative for fever, chills, weight loss and diaphoresis.
Skin: Negative for rash or itching. 
HENT: Negative for headaches, hearing loss, tinnitus.
Eyes: Negative for blurred vision, double vision, and photophobia. 
Cardiovascular: Positive for chest pain, orthopnea, PND, and leg swelling. Denies palpitations.
Pulmonary: Positive for cough and shortness of breath. Negative for sputum production.
Gastrointestinal: Negative for heart burn, nausea, vomiting, abdominal pain, diarrhea, constipation, and blood in stool.
Genitourinary: Negative for dysuria, urgency, frequency and hematuria.
Musculoskeletal: Negative for myalgias and neck pain. Positive for chronic pain and joint pain. 
Endo/Heme/Allergies: Negative for environmental allergies. Does not bruise/bleed easily. 
Neurological: Negative for dizziness, tingling, tremors, sensory change and speech changes. 
Psychiatric: Negative for depression, suicidal and homicidal ideations. 

Past Medical History: 

1. COPD
2. Asthma
3. HIV Infection
4. Coronary artery disease S/P 4 drug eluting stents 7 months ago
5. Myocardial Infarction
6. Hyperlipidemia
7. Peptic Ulcer Disease
8. Hypertension 

Surgical History: 

1. CABG x2 7 years ago
2. Appendectomy 

Social History: 
Mr. Smith quit smoking 2 weeks ago and has a 10 pack year history of smoking cigarettes. He denies any current or past use of alcohol or recreational drug use. He works full time as a computer programmer. 

Family History:
Father- hypertension, COPD, alive, current age 75
Mother- stroke, myocardial infarction and heart failure, alive, current age 76
Brother- hypertension 

Home Medications:

1. Diltiazem 120mg PO daily
2. Lisinopril 25mg PO daily
3. Amlodipine 5mg PO daily
4. Plavix 75mg PO daily
5. Nexium 40mg PO daily
6. Atorvastatin 40mg PO daily
7. Aspirin 81mg PO daily
8. Metoprolol 50mg PO daily
9. Etodolac 400mg PO BID
10. Atripla 1 PO daily
11. Isosorbide Dinitrate 20mg PO TID 

Allergies:

1. Contrast Dye- rash, itching

Physical Exam: 
Vitals: 36.0-87-18-150/83
Constitutional: Oriented to person, place, and time. Obese.  Non-toxic appearance. Does not appear ill. 
Head: Normocephalic and atraumatic. 
Nose: Nose midline. Right and left maxillary and frontal sinuses are nontender.  
Mouth/Throat: Oropharynx is clear and moist. Normal dentition. No uvula swelling. 
Eyes: Pupils are equal, round, and reactive to light. No nystagmus. No scleral icterus.  
Neck: Full range of motion. Neck supple. No JVD present. No tracheal deviation present. No thyromegaly or thyroid nodules noted. 
Cardiovascular: Normal rate, S1 normal, S2 present, without S3, S4, gallop, friction rub or murmur. 2-3+ pitting edema of lower extremities bilaterally. 
Pulses: Brachial, Radial, dorsalis pedis, and posterior tibial pulses are 2+/4+ bilaterally.  
Pulmonary/Chest: Respirations regular and even. Dyspneic, not using accessory muscles. Lungs are with rales in the posterior bases bilaterally otherwise they are clear. 
Abdominal: Soft. Bowel sounds are active. Nontender, no masses noted. No CVA tenderness. No hepatosplenomegaly. There is no rigidity, rebound, or guarding. 
Musculoskeletal: Full ROM noted in the bilateral shoulders, wrists, elbows, hips and knees. 
Lymphadenopathy: No cervical lymphadenopathy.  
Neurological: Alert and oriented to person, place, and time. Cranial nerves II –XII intact.   Sensation to lower and upper extremities is intact to light and dull touch. 
Skin: Skin is warm, dry and intact. No abrasion, no bruising, no burn, no laceration, no lesion and no rash noted. 
Psychiatric: Mood and affect normal. Calm and cooperative behavior. Judgment intact. 

Diagnostic Results (results are from the day of admission unless stated otherwise)
WBC- 10.6
Hgb- 8.0
HCT- 26.6
MCV- 92.0
Platelets-289,000 
Na- 139
K- 5.6
BUN- 25
Creatinine- 1.8 (baseline creatinine is 0.8)
Glucose- 102
Ca- 8.6
Magnesium- 2.3
Phosphorus- 2.7
Albumin- 3.8
AST-32
ALT- 37
Total Bilirubin – 0.4
Urinalysis- completely normal 
PT 10.1, INR 1.0
CK MB 3
Troponin T < 0.01 x2 values 
CD4 count was 700 and HIV viral load undetectable (results are from 1 month ago) 

CXR- mild pulmonary edema
BNP- 1761
12 Lead ECG- NSR, no ST or T wave changes. Rate 90. QTc 400, PR 0.10 

Echocardiogram (completed 3 months ago)
Mildly depressed LV systolic function. Estimated ejection fraction of 40%. Septal and inferior wall motion abnormalities. Thickened mitral leaflets with trace mitral regurgitation. 

Answer the following questions:

1. What are Mr. Smith’s risk factors for coronary artery disease and experiencing an acute coronary syndrome?
2. What is a BNP and why is Mr. Smith’s BNP value 1761?
3. What diagnosis explains Mr. Smith’s chest pain and shortness of breath? Provide your rationale and support your answer.
4. Why is Mr. Smith on lisinopril and Metoprolol? Using a computer program such as Microsoft word, power point, visio, draw a concept map showing the steps of the pathological process which lisinopril and Metoprolol are given to prevent. Describe below the drawing how the medications alter the process. The concept map must be your own work. A copy of a picture pasted into your case study is not allowed and 10 points will be deducted it this occurs. If the concept map is not completed 10 points will be deducted from the case study. 
5. How does the process described in question 4 affect afterload?
6. What is preload, what factors affect preload and what is the purpose of preload. How is preload affected by systolic failure and diastolic failure? How does the difference affect the way you diurese an individual?
7. What are the pathological steps that lead to the development of Mr. Smith’s pulmonary edema? What likely triggered this acute decompensation?
8. What other medication is Mr. Smith on that could potentially have adverse cardiac effects which he should not be taking?
9. What things may trigger an acute decompensation in the diagnoses you identified in question 3?

Instructions

This week’s case study will introduce concepts related to cardiac contractility, medications which affect the myocardium, and the consequences of alterations in contractility. Read the scenario and thoroughly complete the questions. Some of the answers will be short answers and may not require a lot of details. For example: what is the most common organism to cause a hospital acquired infection? The answer is pseudomonas aeruginosa. Answers to questions that relate to the pathogenesis of a disease must include specific details on the process. For example: How does hypoxia lead to cellular injury? Simply writing that a lack of blood flow, causes a lack of oxygen available to the cell and the cell cannot function without oxygen is not sufficient. This type of response is NOT reflective of an advanced understanding of the concept or graduate level work. This answer should discuss the cascade of events leading to the lack of oxygen and how it specifically impairs cellular function. All answers to these type of questions should address the effects at the cellular level, then the effects on the organ and then the body as a whole. Additionally describing the normal anatomical and/or physiologic processes underlying the pathogenesis will be necessary to thoroughly answer the question.