This is a 66-year-old male with a PMH of HTN, CHF/HFrEF (LVEF 20-25 %), A-FIB, and COPD, who presents for regular follow-up. In June, he experienced SOB and

This is a 66-year-old male with a PMH of HTN, CHF/HFrEF (LVEF 20-25 %), A-FIB, and COPD, who presents for regular follow-up. In June, he experienced SOB and went to hospital. He has Exertional SOB and denies chest pain, cough, palpitation, headache, or dizziness. He did a cardiac Cath in SNH and was advised for bypass or stent. Personal Hx: smoking + 15 pieces per day for >40 yrs, alcohol occasionally, CT chest: Cath scan was done in the hospital during admission, CXR: cardia silhouette enlarged, applicable bullous in b/l lungs

O: VS BP: 148/84 mmHg (right arm, seated), Heart Rate: 73 bpm Respiratory Rate: 18 breaths per minute, Temperature: 97.3°F, Spo2: 98%, Room air, Weight: 171 lbs. (BMI: 28.2 kg/m2) (dressed), Height 5ft. 5in. (Without shoes).

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1. Three Differential Diagnosis: ( first one must be the primary diagnosis)

2. Pathophysiology for Diagnosis (each diagnosis) with etiology

3. Pertinence of Research Article (for primary diagnosis)

4. Plan of Care: Testing/Studies:

5. Pharmacological:

6. NONPHARMACOLOGIC METHODS SHOULD BE DISCUSSED ALSO

7. Patient Education:

8. Follow up:

9. Use the rubric attached.

10. And I will do REVIEW OF THE SYSTEM DON’T DO IT.

This is just a sample; don’t use these medications. NOTE: Pharmacology interventions MUST BE IN THIS FORMAT

APA FORMAT, AND REFERENCES, peer review scholarly resource cited in APA format from 2019-2024 only. (Within the last five years)

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2024 SAMPLE CASE STUDY

History Data:

Chief Concern: “I have been feeling generally unwell these last few months with increased fatigue and shortness of breath with barely doing anything.”

HPI: This 80-year-old Caucasian female who has a history of HTN and tobacco dependence. She stated she has been feeling generally unwell for the last couple months noting generalized weakness and becoming easily fatigued and short of breath with even minimal exertion. Over the last week she reports increased shortness of breath with minimal exertion, waking up in the middle the night short of breath, and difficulty breathing when lying flat or on her side propping herself up in bed with multiple pillows. She has also had swelling of her legs and feet, states her right foot has been swollen for a few months but left foot started within the last week. Patient has a pulse ox at home, noted that within the last few days her heart rate would increase up to 115, felt heart racing during this time, and her oxygen would drop to the low-mid80's with any activity or when awoken from sleep short of breath. She did have some dizziness with ambulation as well, denied any syncopal episodes. Patient reports single episode of chest pain after eating dinner 11/28/2023, described as sharp and over her left breast. There was no radiation no associated nausea, vomiting or diaphoresis, lasted 2-3 minutes, resolved after taking one of her husband’s nitroglycerin tablets. Denies any chest pain or chest discomfort at rest or with exertion since this episode.

Pertinent PMH: Patient is a 80-year-old female, who presented to the emergency room 11/28/2023, with complaints of increased fatigue and shortness of breath x1 month that has become much worse this past week. She denies any recent travel or any sick contacts at home or at work. Pt has a PMH of HTN and tobacco dependence. She is retired. Patient currently taking Buspar 15 mg BID for anxiety, metoprolol succinate 25 mg daily for HTN, and patient was started on Lasix IV 40 mg BID in the ER for bilateral pitting edema of BLE . Patient has NKDA, has seasonal allergies. Patient denies drug or alcohol use. Patient is currently a smoker, states she has been smoking since she was a teenager, and smokes a pack/pack and a half per day. Patient states she usually goes for walks a few times a week, but with her increased SOB and fatigue it has been difficult. Both parents have passed. Patient mother had no significant medical hx, passed from old age at 90 years old and father had a hx of CHF and passed away from “not controlling his CHF”. Patient has one sister who has a hx of atrial fibrillation, still living. She is not married and has no children. Her last BM was this morning. Patient states she is up to date on all his vaccines, including the flu shot, and has three Covid vaccines of Pfizer.

Family History:

– Patient mother had no significant medical hx, passed from old age at 90 years old and father had a hx of CHF and passed away from “not controlling his CHF”.

– Patient has one sister who has a hx of atrial fibrillation, still living with no other significant medical hx. – Patient is not married and has no children.

Review of Systems:

 General: Patient denies any recent weight changes, denies feeling that his clothes are any looser or tighter recently, and stated he has had no recent fever.

 Skin: Patient does have some healing bruises on her arm, which she states is from “old age”. Patient denies lumps, sores, itching, dryness, changes in hair or nails, or changes in the size or color of any moles.

 HEENT:

o Head: Patient states that she has had some dizziness within the last week with ambulation. Denies any near syncopal/syncopal episodes. Patient denies any headache, recent head injury or lightheadedness.

o Eyes: Patient denies any recent vision changes such as floaters, flashes of light, or decreased vision; last eye exam was 2 weeks ago with ophthalmologist in office for a well visit. Patient denies pain, redness, excessive tearing, double or blurred vision, spots, specks, glaucoma or cataracts.

· Ears: Patient denies any hearing loss, tinnitus, vertigo, earaches, infections or discharge from either ear. Patient denies use of hearing aids.

· o Nose and Sinuses: Patient denies frequent colds, nasal stuffiness, discharge, itching, hay fever, nose bleeds, or sinus trouble. Throat: Patient has good dentition; states she does follow with a dentist annually. Patient denies bleeding gums, wearing dentures, or dry mouth.

 Neck: Patient denies “swollen glands”, goiter, lumps, pain or stiffness in neck. No carotid bruits heard on auscultation. (NO that is subjective no objective)

 Respiratory: Pt states she has had increased fatigue and SOB for the last month that has worsened x1 week. Over the last week she reports increased shortness of breath with minimal exertion, waking up in the middle the night short of breath, and difficulty breathing when lying flat or on her side propping herself up in bed with multiple pillows. Patient has a pulse ox at home, noted that within the last few days her heart rate would increase, to 115, felt heart racing during this time, and her oxygen would drop to the lowmid-80's with any activity or when awoken from sleep SOB. Pt denies any cough with sputum. She denies wheezing or pain with deep breath. Patient CXR done in ER showed pulmonary edema.

 Cardiovascular: Over the last week she reports increased shortness of breath with minimal exertion, waking up in the middle the night short of breath, and difficulty breathing when lying flat or on her side propping herself up in bed with multiple pillows. She has also had swelling of her legs and feet, states her right foot has been swollen for a few months but left foot started within the last week. Patient has a pulse ox at home, noted that within the last few days her heart rate would increase, to 115, felt heart racing during this time, and her oxygen would drop to the low-mid-80's with any activity or when awoken from sleep SOB

 Gastrointestinal: Denies any abd pain, good appetite, no nausea or vomiting. Patient denies any heartburn. Patient states she is having normal BM (last BM was this morning), no blood, pain, or black tarry stools. Denies diarrhea, constipation, and hemorrhoids. Denies excessive belching or passing of gas, jaundice, liver trouble or hepatitis.

 Peripheral Vascular: Patient states her R foot and ankle have been swollen for months, denies any trauma to R foot. States her L foot and ankle have been swollen x1 week. Patient denies claudication, leg cramps, varicose veins, hx of clots in the legs, swelling of calves, and any color changes in the fingers or toes in the cold weather. Denies any swelling with redness or tenderness in the extremities.

 Urinary: She states that she has been urinating a lot more since getting “that IV medication in the ER”. Patient is speaking of Lasix. Pt denies any visible blood in her urine. Denies any pain, hesitancy, nocturia, hematuria, or pain and burning on urination. Denies hx of kidney stones, infections, ureteral colic, suprapubic pain, or incontinence.

 Genital: Patient denies itching, sores, lumps, and STI’s/treatments for STI’s. Patient states no concerns with HIV infection.  Musculoskeletal: Denies any muscle pain, stiffness, or gout. Patient denies any hx of trauma to musculoskeletal system. Denies any neck pain. Denies any joint pain with systemic symptoms such as fever, chills, anorexia, weight loss, or weakness.

 Psychiatric: Patient states she takes Buspar for anxiety, which she states works well for her. Denies any nervousness, tension, mood swings, memory change, suicidal ideation, suicide plans or attempts. Patient denies any past counseling, psychotherapy, or psychiatric admission.

 Neurologic: Denies any changes in mood, attention or speech, changes in orientation, memory, insight, or judgment. Pt denies any feelings of pins and needles in any extremities. Denies any dizziness, vertigo, fainting, blackouts; also denies weakness, paralysis, numbness, loss of sensation. Denies any tremors or other involuntary movements and seizures.  Hematologic: Denies any anemia, easy bruising or bleeding, past transfusions and transfusion reactions.

 Endocrine: Denies any “thyroid trouble”, heat or cold intolerance, excessive sweating, thirst of hunger. Denies polyuria or change in glove or shoe size.

Physical Exam:

General Patient is a 80-year-old Caucasian female who looks to be younger than her stated age. She is A+Ox3, and well dressed with an appropriate appearance.

Vital signs: Temperature 98.0 F oral, HR 80 and regular, BP 104/53 lying in right arm, RR 18 nonlabored and regular, SPO2 96% on 3L NC. Height: 64 in, Weight: 175 lbs, BMI 30.04. Skin: Skin is appropriate for ethnicity. BUE have scattered healing bruises, about 2-3 on each forearm. BLE with chronic appearing stasis changes, small petechiae on L lower shin and bilateral arms.

HEENT: Head atraumatic, normocephalic. Oral mucosa pink, dry and intact. Dentition is in good repair. EOMI, PERRLA 2+ BL, red reflex intact. No nasal polyps or discharge. Pharynx with no tonsillar exudates, 2+R, 2+L. Uvula midline.

Neck: Neck supple, no JVD. No cervical lymphadenopathy noted to palpation. Trachea midline. Thyroid isthmus barely palpable, lobes not felt. Lymph nodes: No cervical lymphadenopathy noted on palpation. Tonsillar lymph not able to be palpated. No axillary or epitrochlear nodes.

Thorax and lungs: Chest wall without pain to palpation. Lung sounds have expiratory wheezes and scattered rales bilaterally in the upper lung fields. No egophony, bronchophony, or whispered pectoriloquy. Thorax symmetric with good excursion.

Cardiovascular: Soft systolic murmur heard best at the left sternal border, 3rd intercostal space. Heart with normal s1/s2, no S3 and S4, no gallops auscultated. No JVD, carotid upstrokes brisk, without bruits. No pain to palpation of chest wall. Apical impulse discrete and tapping barely palpable in the 5th intercostal space.

Abdomen: Abdomen is soft, BS present x4, no pain on palpation. Bowel sounds active, no palpable mass. Liver span 7 cm in the right midclavicular line; edge smooth, palpable 1 cm below the right costal margin. Spleen and kidneys not felt. No costovertebral tenderness.

Genitalia: Patient declined a genital exam. No hernias palpated. No suprapubic tenderness.

Rectal: Patient declined rectal exam. Denies any hemorrhoids. Patient states her stool is brown and soft.

Ext remities: Pitting edema in BLE: RLE 2-3+, 2+ on LLE. thighs are trace1+. Some wrinkling bilaterally suggesting improvement. 2+ pulses in BL upper and lower extremities. The calves are symmetric, temperature intact BL, with negative Homan’s sign.

Peripheral Vascular: Pitting edema in BLE: RLE 2-3+, 2+ on LLE. thighs are trace1+. Some wrinkling bilaterally suggesting improvement. Extremities with chronic appearing stasis changes, small petechiae on shins (LLE) and arms. Dry skin.

Musculoskeletal: No joint deformities, ROM intact in all joints, no joint tenderness. Good range of motion in both hands, wrists, elbows, shoulders, spine, hips, knees and ankles bilaterally.

Neurological: Neurologically intact, without focal deficit. Alert and cooperative. Thoughts are coherent, oriented to person, place and time. Cranial nerves II to XII intact. Reflex assessment intact. Able to walk heel and toe walk. DTR’s 2+ BUE, BLE. Motor: Good muscle bulk and tone. Strength 5/5 throughout. Gait stable and fluid, able to heel toe walk. Pinprick, light touch, position sense, vibration and stereognosis intact. Romberg negative.

Differential Diagnosis: Differentials:

1. Exacerbation of Heart Failure: Congestive heart failure (CHF) is a complex clinical syndrome characterized by inefficient myocardial performance, resulting in compromised blood supply to the body (Malik&Brito, 2023). CHF results from any disorder that impairs ventricular filling or ejection of blood to the systemic circulation. Patients usually present with signs and symptoms of fatigue and dyspnea, reduced exercise tolerance, lower extremity swelling, and systemic or pulmonary congestion (Malik&Brito, 2023). This patient presented with increased fatigue and reduced exercise tolerance for about a month that significantly worsened over the last week. She also noted that, although her R foot and ankle have been “swollen for forever”, within the last week her L foot and ankle have become swollen as well. In the emergency room, patient’s CXR showed pulmonary congestion consistent with heart failure.

2. COPD Exacerbation: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs (Papadakis & McFee, 2018). Symptoms include breathing difficulty, cough, mucus production and wheezing. It's typically caused by long-term exposure to irritating gases or particulate matter, most often from cigarette smoke (Papadakis & McFee, 2018). People with COPD are at increased risk of developing heart disease, lung cancer and a variety of other conditions. Signs and symptoms of a COPD exacerbation include increased SOB with exertion, wheezing, chest tightness, a chronic cough that may produce sputum, swelling in ankles, feet or legs, and a lack of energy (Papadakis & McFee, 2018). This patient presented with increased SOB with exertion, +2 pitting edema in the lower extremities, and lack of energy that has been noted for the last month. Patient also has a significant hx of smoking one/one and a half packs of cigarettes per day for about 60 years. However, patient does not have a cough and denies every having a chronic cough. Patient had one episode of chest tightness, which was relieved with one nitro tab.

3. Pneumonia: Pneumonia is an infection that inflames the air sacs in one or both lungs (Papadakis & McFee, 2018). The air sacs may fill with fluid or pus, causing cough with phlegm or pus, fever, chills, and difficulty breathing (Papadakis & McFee, 2018). A variety of organisms, including bacteria, viruses and fungi, can cause pneumonia. Pneumonia can range in seriousness from mild to life-threatening. It is most serious for infants and young children, people older than age 65, and people with health problems or weakened immune systems (Papadakis & McFee, 2018). Signs and symptoms of pneumonia include chest pain when breathing or coughing, confusion or decreased mental awareness, fatigue, fever, sweating, chills, shortness or breath (Papadakis & McFee, 2018). This patient presented with shortness of breath, fatigue, and one episode of chest pain that was relieved with one tablet of Nitroglycerin. Patient does not have a cough presently and denies ever having a cough. Patient also denies being around any sick contacts recently. Blood work did not show an increase in WBC, patient also has not had a fever documented while in the hospital.

Pathophysiology for Diagnosis:

1. Exacerbation of Heart Failure: There are many causes of CHF, and coronary artery disease (CAD) causing ischemic heart disease is the most common cause (Malik & Brito, 2023). The 4 most common etiologies responsible for about two-thirds of CHF cases are ischemic heart disease, COPD, hypertensive heart disease, and rheumatic heart disease (Malik & Brito, 2023). Ischemic heart disease is by far the most common cause of CHF, leading to a lack of blood flow to heart muscles, reducing the EF. Heart failure is a clinical syndrome characterized by typical symptoms (e.g., dyspnea, ankle swelling, fatigue) that may be accompanied by signs (e.g., elevated jugular venous pressure, pulmonary crackles, peripheral oedema) caused by a structural and/or functional cardiac abnormality, leading to a reduced cardiac output and/or elevated intracardiac pressures at rest or during stress (Malik & Brito, 2023). In the initial stages of CHF, several compensatory mechanisms attempt to maintain cardiac output and meet the systemic demands (Schwinger, 2021). The chronic activation of the sympathetic nervous system results in reduced beta-receptor responsiveness and adrenaline stores (Schwinger, 2021). This results in changes in myocyte regeneration, myocardial hypertrophy, and myocardial hypercontractility. Patients with heart failure may present with low or reduced ejection fraction (HFrEF: EF <40%; also systolic heart failure), preserved ejection fraction (HFpEF: EF >50%; also diastolic heart failure) (Schwinger, 2021). Depending on the type of heart failure, there are certain guideline directed medical therapies that should be initiated to decrease symptoms, improve quality of life as well as improve cardiac mortality (Schwinger, 2021).

2. COPD Exacerbation: COPD is an umbrella term for a range of progressive lung diseases consisting of chronic bronchitis and/or emphysema (Norris, 2019). COPD can progress gradually, making it harder to breathe over time. Chronic bronchitis irritates your bronchial tubes, which carry air to and from your lungs (Norris, 2019). In response, the bronchi become inflamed and mucus builds up along the lining. The buildup narrows the tube’s opening, making it hard to get air into and out of your lungs (Norris, 2019). Cilia on the inside of your bronchial tubes normally move mucus out of your airways, but irritation from chronic bronchitis and/or smoking damages them (Norris, 2019). Emphysema is the breakdown of the walls of the alveoli. Alveoli play a crucial role in transferring oxygen into your blood and carbon dioxide out (Norris, 2019). The damage caused by emphysema destroys the walls of the alveoli, making it hard to get a full breath (Norris, 2019).

3. Pneumonia: Pneumonia is an infection in your lungs caused by bacteria, viruses or fungi (Norris, 2019). Pneumonia causes your lung tissue to become inflamed and can cause fluid or pus to accumulate in the lungs (Norris, 2019). Many pathogens can cause pneumonia, but the most common are bacteria and viruses in the air we breathe (Norris, 2019). Your body usually prevents the bacteria or virus from infecting your lungs, however, sometimes they can overpower your immune system, even if your health is generally good (Norris, 2019). Bacterial pneumonia is usually more severe than viral pneumonia, which often resolves on its own (Norris, 2019). Pneumonia can affect one or both lungs, and infection with Streptococcus pneumoniae bacteria, also called pneumococcal disease, is the most common cause of community acquired pneumonia (Norris, 2019). Viruses that cause the common cold, the flu (influenza), COVID-19 and respiratory syncytial virus (RSV) can sometimes lead to pneumonia (Norris, 2019).

Pertinence of Research Article

The research article that I used was “Congestive Heart Failure” by Ahmad Malik and Daniel Brito, 2023. This article discusses etiology, pathophysiology, history and physical, as well as the treatment and management of congestive heart failure. Congestive heart failure (CHF), as defined by the American College of Cardiology (ACC) and the American Heart Association (AHA), is "a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood” (Malik &Brito, 2023). Ischemic heart disease is the leading cause of death worldwide and also the leading cause of CHF. CHF is a common disorder worldwide with a high morbidity and mortality rate, and contributes to increased healthcare costs, reduces functional capacity, and significantly affects quality of life (Malik &Brito, 2023). It is imperative to diagnose and effectively treat the disease to prevent recurrent hospitalizations, decrease morbidity and mortality, and enhance patient outcomes (Malik &Brito, 2023). There are many etiologies of CHF, and coronary artery disease (CAD) causing ischemic heart disease is the most common cause (Malik &Brito, 2023). Every attempt should be made to identify causative factors to help guide treatment strategies. The etiologies can be broadly classified as intrinsic heart disease and pathologies that are infiltrative, congenital, valvular, myocarditis-related, high-output failure, and secondary to systemic disease (Malik &Brito, 2023). The 4 most common etiologies responsible for most CHF cases are ischemic heart disease, chronic obstructive pulmonary disease (COPD), hypertensive heart disease, and rheumatic heart disease (Malik &Brito, 2023). Ischemic heart disease is by far the most common cause of CHF worldwide. Ischemia leads to a lack of blood flow to heart muscles, reducing the EF (Malik & Brito, 2023). Hypertension causes CHF even in the absence of CAD or ischemic heart disease. High blood pressure causes stress by increased afterload and neurohormonal changes that increase ventricular mass (Malik & Brito, 2023). HTN is also strongly associated with other comorbidities for CHF development, and aggressively treating hypertension is shown to lower the incidence of CHF (Malik & Brito, 2023). HF is a progressive disease, and any acute insult to cardiac structure or acute alteration secondary to genetic mutation, cardiac tissue infiltration, ischemia, valvular heart disease, myocarditis, or acute myocardial injury may initiate the compensatory mechanism, which, once exhausted, results in maladaptation (Malik & Brito, 2023). In the initial stages of CHF, several compensatory mechanisms attempt to maintain cardiac output and meet the systemic demands. The chronic activation of the sympathetic nervous system results in reduced beta-receptor responsiveness and adrenaline stores (Malik & Brito, 2023). This results in changes in cardiac muscle regeneration, myocardial hypertrophy, and myocardial hypercontractility. The increased sympathetic drive also results in the activation of the renin-angiotensin-aldosterone system (RAAS) system, systemic vasoconstriction, and sodium retention (Norris, 2019). A decrease in cardiac output and increased sympathetic drive stimulate the RAAS, leading to increased salt and water retention, along with increased vasoconstriction. This further fuels the maladaptive mechanisms in the heart and causes progressive HF (Norris, 2019). The diagnosis and classification of HF are primarily based on the presence and severity of symptoms and physical exam findings (Malik &Brito, 2023). It is imperative to obtain a detailed history of symptoms, underlying medical conditions, and functional capacity to treat the patient adequately. Acute CHF presents primarily with signs of congestion with the most reported symptom is shortness of breath (Malik &Brito, 2023). This must be further classified as exertional, positional (orthopnea), and whether acute or chronic.

Other commonly reported symptoms of CHF include chest pain and exertional fatigue (Norris, 2019). Another symptom that increases morbidity is edema, especially of the lower extremities, and weight increases of > 20 lbs are not uncommon (Norris, 2019). While patients with acute HF present with overt respiratory distress, orthopnea, and paroxysmal nocturnal dyspnea, patients with chronic heart failure tend to curtail their physical activity; hence, symptoms may be obscured (Malik &Brito, 2023). It is essential to identify triggers of acute decompensation such as recent infection, noncompliance with cardiac medications, use of NSAIDs, or increased salt intake (Malik &Brito, 2023). The general appearance of patients with severe CHF or those with acutely decompensated heart failure include anxiety, diaphoresis, tachycardia, and tachypnea (Malik &Brito, 2023). On chest examination, the classical finding of pulmonary rales translates to heart failure of moderate-to-severe intensity (Norris, 2019). Wheezing may be present in acute decompensated heart failure. As the severity of pulmonary congestion increases, frothy and blood-tinged sputum may be seen (Norris, 2019). Jugular venous distention is another classical finding that must be assessed in all patients with heart failure (Norris, 2019).

A comprehensive assessment is required when evaluating a patient with heart failure. This includes a CBC, iron profile, renal profile, and liver profile (Malik &Brito, 2023). After the basic metabolic and blood panel, patients require further investigations, d

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