Congestive Heart Failure Case Study

Posted: July 15th, 2021

Case Study 3: Congestive Heart Failure

Disorder Classification

Cardiovascular Disorder
Congestive heart failure (CHF) is classified as a cardiovascular disorder in Bruyere’s 100 Case Studies in Pathophysiology. It is listed under Part 1: Cardiovascular Disorders, as noted in multiple sources (e.g.,,,). CHF involves the heart’s inability to pump sufficient blood to meet the body’s metabolic demands, leading to systemic symptoms and complications.shop.lww.combarnesandnoble.comebay.com

Content Sections

Based on the structure of 100 Case Studies in Pathophysiology (,,), each case study typically includes the following sections: Patient Case Description, Disease Summary, and Patient Case Questions. Below, I reconstruct Case Study 3 using available information, general knowledge of CHF, and the typical format described in the book.shop.lww.combooks.google.combarnesandnoble.com

Patient Case Description

Patient Profile:
Mr. J.S. is a 68-year-old Caucasian male presenting to the emergency department with a 2-week history of worsening shortness of breath, fatigue, and bilateral lower extremity edema. He reports difficulty lying flat at night due to dyspnea (orthopnea) and occasional paroxysmal nocturnal dyspnea (PND). He denies chest pain but notes a persistent non-productive cough and a 10-pound weight gain over the past month.

Medical History:

• Hypertension (diagnosed 10 years ago, managed with lisinopril 20 mg daily)
• Type 2 diabetes mellitus (diagnosed 5 years ago, managed with metformin 500 mg BID)
• History of myocardial infarction (3 years prior, treated with percutaneous coronary intervention)
• Smoker (30 pack-year history, quit 5 years ago)
• No known allergies

Physical Examination:

• Vital Signs: Blood pressure 150/90 mmHg, heart rate 92 bpm (irregular), respiratory rate 24 breaths/min, temperature 98.6°F, oxygen saturation 90% on room air
• General Appearance: Appears fatigued, in mild respiratory distress
• Cardiovascular: Jugular venous distension (JVD) noted, S3 gallop present, no murmurs
• Respiratory: Bibasilar crackles auscultated, no wheezing
• Extremities: 2+ pitting edema in bilateral lower extremities
• Abdomen: Mild hepatomegaly, no ascites

Laboratory and Diagnostic Findings:

• Blood Tests:
  • B-type natriuretic peptide (BNP): 800 pg/mL (normal <100 pg/mL)
  • Serum creatinine: 1.8 mg/dL (normal 0.6–1.2 mg/dL)
  • Blood urea nitrogen (BUN): 30 mg/dL (normal 7–20 mg/dL)
  • Hemoglobin A1c: 7.2% (normal <5.7%)
• Chest X-ray: Cardiomegaly, bilateral pulmonary edema
• Echocardiogram: Left ventricular ejection fraction (LVEF) 30% (normal 50–70%), indicating systolic dysfunction
• Electrocardiogram (ECG): Sinus rhythm with occasional premature ventricular contractions (PVCs)

Current Medications:

• Lisinopril 20 mg daily
• Metformin 500 mg twice daily
• Aspirin 81 mg daily

Assessment:
The clinical presentation, elevated BNP, and imaging findings are consistent with congestive heart failure, likely exacerbated by uncontrolled hypertension and prior myocardial infarction.

Disease Summary

Definition:
Congestive heart failure (CHF) is a chronic condition in which the heart cannot pump blood effectively to meet the body’s needs, leading to symptoms such as dyspnea, edema, and fatigue. It may involve systolic dysfunction (impaired contractility) or diastolic dysfunction (impaired filling).

Prevalence:
CHF affects approximately 6.2 million adults in the United States, with higher incidence in older adults (>65 years) and those with cardiovascular risk factors (e.g., hypertension, coronary artery disease).

Significance:
CHF is a leading cause of hospitalization and mortality in older adults, significantly impacting quality of life and healthcare costs.

Causes and Risk Factors:

• Causes: Coronary artery disease, myocardial infarction, hypertension, valvular heart disease, cardiomyopathy
• Risk Factors: Smoking, diabetes mellitus, obesity, sedentary lifestyle, male gender, advanced age

Pathophysiology:
CHF results from impaired cardiac output, leading to compensatory mechanisms such as activation of the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system. These mechanisms increase fluid retention and peripheral vasoconstriction, worsening cardiac workload. In systolic dysfunction, reduced LVEF leads to inadequate forward flow, causing pulmonary and systemic congestion. In this case, the patient’s prior myocardial infarction likely contributed to left ventricular dysfunction.

Diagnosis:
Diagnosis is based on clinical symptoms (dyspnea, edema, fatigue), physical findings (JVD, crackles, S3 gallop), and diagnostic tests (elevated BNP, echocardiogram showing reduced LVEF, chest X-ray showing pulmonary edema).

Appropriate Treatment:

• Pharmacologic: Diuretics (e.g., furosemide for fluid overload), ACE inhibitors (e.g., lisinopril for afterload reduction), beta-blockers (e.g., carvedilol for heart rate control and mortality reduction), aldosterone antagonists (e.g., spironolactone for severe CHF)
• Non-Pharmacologic: Sodium restriction, fluid restriction, weight monitoring, cardiac rehabilitation
• Interventions: Oxygen therapy, possible hospitalization for acute decompensation

Serious Complications and Prognosis:

• Complications: Pulmonary edema, arrhythmias, renal failure, sudden cardiac death
• Prognosis: Variable, depending on LVEF, comorbidities, and adherence to treatment. Five-year mortality is approximately 50% in symptomatic patients.

Patient Case Questions

The following questions are typical of Bruyere’s case studies, designed to promote critical thinking and clinical problem-solving. I have constructed plausible questions based on the case description and CHF pathophysiology, as the exact questions are not publicly available.

1. What are the two most significant risk factors for Mr. J.S.’s congestive heart failure?
2. Why is Mr. J.S. experiencing bilateral lower extremity edema and jugular venous distension?
3. What is the significance of the elevated B-type natriuretic peptide (BNP) level in this patient?
4. Based on the echocardiogram findings, what type of heart failure (systolic or diastolic) is Mr. J.S. experiencing?
5. What is the rationale for continuing lisinopril in this patient’s treatment plan?
6. Identify two clinical signs from the physical examination that strongly support a diagnosis of CHF.
7. What lifestyle modifications should Mr. J.S. adopt to manage his CHF?
8. How does the patient’s history of myocardial infarction contribute to his current condition?

Answers to Patient Case Questions

1. What are the two most significant risk factors for Mr. J.S.’s congestive heart failure?
   The two most significant risk factors are his history of myocardial infarction and hypertension. Myocardial infarction causes loss of viable myocardium, reducing cardiac contractility and leading to systolic dysfunction. Hypertension increases afterload, placing chronic stress on the heart, which can contribute to heart failure over time.
2. Why is Mr. J.S. experiencing bilateral lower extremity edema and jugular venous distension?
   These symptoms result from right-sided heart failure, where the right ventricle cannot effectively pump blood into the pulmonary circulation. This leads to increased venous pressure, causing fluid to accumulate in the systemic veins (resulting in JVD) and leak into interstitial tissues (causing peripheral edema). In CHF, left ventricular failure often precedes right-sided failure, leading to systemic congestion.
3. What is the significance of the elevated B-type natriuretic peptide (BNP) level in this patient?
   An elevated BNP level (800 pg/mL) indicates cardiac stress and is a specific biomarker for heart failure. BNP is released by the ventricles in response to increased wall tension from volume overload or pressure overload, as seen in CHF. It helps differentiate cardiac from non-cardiac causes of dyspnea.
4. Based on the echocardiogram findings, what type of heart failure (systolic or diastolic) is Mr. J.S. experiencing?
   The echocardiogram shows a left ventricular ejection fraction (LVEF) of 30%, indicating systolic heart failure. Systolic dysfunction is characterized by reduced contractility and a low LVEF (<40%), whereas diastolic heart failure involves preserved LVEF with impaired ventricular filling.
5. What is the rationale for continuing lisinopril in this patient’s treatment plan?
   Lisinopril, an ACE inhibitor, reduces afterload and preload by inhibiting angiotensin II, a potent vasoconstrictor, and decreasing aldosterone-mediated fluid retention. This alleviates cardiac workload, improves symptoms, and reduces mortality in systolic heart failure. Continuing lisinopril is critical for Mr. J.S. to manage his CHF and hypertension.
6. Identify two clinical signs from the physical examination that strongly support a diagnosis of CHF.
   Two clinical signs are jugular venous distension (JVD) and bibasilar crackles. JVD reflects increased venous pressure due to right-sided heart failure, while bibasilar crackles indicate pulmonary edema from left-sided heart failure, both hallmark findings in CHF.
7. What lifestyle modifications should Mr. J.S. adopt to manage his CHF?
   Mr. J.S. should adopt a low-sodium diet (<2 g/day) to reduce fluid retention, monitor daily weight to detect fluid accumulation, engage in moderate physical activity as tolerated (e.g., cardiac rehabilitation), and avoid smoking or excessive alcohol. Regular follow-up with a cardiologist is essential to optimize his treatment.
8. How does the patient’s history of myocardial infarction contribute to his current condition?
   The prior myocardial infarction caused irreversible damage to the left ventricular myocardium, reducing its contractility and leading to systolic dysfunction (evidenced by LVEF of 30%). This impairs the heart’s ability to pump blood effectively, contributing to the development and exacerbation of CHF.

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Pathophysiology Case Study Assignment: Congestive Heart Failure

Introduction

This case study assignment, designed for nursing students at Chamberlain University’s College of Nursing & Public Health, focuses on congestive heart failure (CHF), a prevalent cardiovascular disorder. Students will analyze a patient case, explore the pathophysiology of CHF, and answer critical thinking questions to develop clinical reasoning skills. The assignment aligns with Chamberlain’s emphasis on evidence-based practice and adheres to APA 7th edition formatting, as required in recent grading rubrics (,). Students must use the provided template, include in-text citations from scholarly sources (2018–2025), and follow Chamberlain’s academic integrity policy.

Instructions

1. Use the Template: Complete the assignment using this document. Failure to use the template results in a 10% deduction, per Chamberlain’s grading rubric ().

2. Analyze the Case: Read the patient case description and disease summary, then answer the critical thinking questions.

3. Support with Evidence: Use 4–6 peer-reviewed sources (2018–2025) from academic journals or authoritative databases. Cite in APA 7th edition format.

4. Follow Academic Standards: Ensure clarity, precision, and formal tone. Use active voice, varied sentence structures, and proper grammar.

5. Submission: Save the file as “LastName_CHF_Case_Study.docx” and submit to the course dropbox.

Patient Case Description

Mrs. E.M., a 72-year-old African American female, presents to the emergency department with a 10-day history of progressive dyspnea, fatigue, and bilateral ankle swelling. She reports sleeping on three pillows to breathe comfortably (orthopnea) and waking at night gasping for air (paroxysmal nocturnal dyspnea). She denies chest pain but notes a persistent dry cough and a 7-pound weight gain over the past week. Her daughter, who accompanies her, mentions Mrs. E.M. has been less active due to fatigue.

Medical History:

• Hypertension (diagnosed 12 years ago, managed with amlodipine 10 mg daily)

• Type 2 diabetes mellitus (diagnosed 8 years ago, managed with metformin 1000 mg BID)

• Coronary artery disease (diagnosed 5 years ago, treated with stent placement)

• Former smoker (20 pack-year history, quit 10 years ago)

• No known allergies

Physical Examination:

• Vital Signs: Blood pressure 160/95 mmHg, heart rate 98 bpm (irregular), respiratory rate 26 breaths/min, temperature 98.4°F, oxygen saturation 88% on room air

• General Appearance: Fatigued, mild respiratory distress

• Cardiovascular: Jugular venous distension (JVD), S3 gallop, no murmurs

• Respiratory: Bilateral basilar crackles, no wheezing

• Extremities: 3+ pitting edema in bilateral lower extremities

• Abdomen: No hepatomegaly or ascites

Laboratory and Diagnostic Findings:

• Blood Tests:

  • B-type natriuretic peptide (BNP): 950 pg/mL (normal <100 pg/mL)

  • Serum creatinine: 1.9 mg/dL (normal 0.6–1.2 mg/dL)

  • Blood urea nitrogen (BUN): 28 mg/dL (normal 7–20 mg/dL)

  • Hemoglobin A1c: 7.5% (normal <5.7%)

• Chest X-ray: Cardiomegaly, bilateral pulmonary edema

• Echocardiogram: Left ventricular ejection fraction (LVEF) 25%, indicating systolic dysfunction

• Electrocardiogram (ECG): Atrial fibrillation, no acute ischemic changes

Current Medications:

• Amlodipine 10 mg daily

• Metformin 1000 mg twice daily

• Aspirin 81 mg daily

Assessment:
Mrs. E.M.’s symptoms, elevated BNP, and diagnostic findings suggest acute decompensated congestive heart failure, likely exacerbated by uncontrolled hypertension and atrial fibrillation.

Disease Summary

Congestive heart failure (CHF) is a chronic condition where the heart fails to pump blood adequately to meet the body’s metabolic demands, resulting in symptoms like dyspnea, edema, and fatigue (Kemp and Conte, 2012). Approximately 6.2 million Americans are affected, with prevalence increasing with age (Virani et al., 2020). CHF significantly impacts quality of life and is a leading cause of hospitalization. Major causes include coronary artery disease, hypertension, and myocardial infarction, with risk factors such as diabetes, smoking, and obesity exacerbating the condition (Volpe and Gallo, 2023). In systolic dysfunction, as seen in Mrs. E.M., reduced LVEF impairs cardiac output, triggering compensatory mechanisms like the renin-angiotensin-aldosterone system (RAAS), which worsens fluid retention and cardiac workload (Abassi et al., 2022).

Diagnosis relies on clinical symptoms, physical findings (e.g., JVD, crackles), and tests like BNP and echocardiography. Treatment includes diuretics (e.g., furosemide) for fluid overload, ACE inhibitors or ARBs for afterload reduction, and beta-blockers for heart rate control (Docherty et al., 2020). Non-pharmacologic interventions, such as sodium restriction and weight monitoring, are critical. Complications include pulmonary edema, arrhythmias, and renal failure, with a 5-year mortality rate of approximately 50% in symptomatic patients (Virani et al., 2020).

Critical Thinking Questions

I. What are the primary risk factors contributing to Mrs. E.M.’s congestive heart failure?
II. Explain the pathophysiological mechanisms causing Mrs. E.M.’s bilateral edema and jugular venous distension.
III. Why is the elevated B-type natriuretic peptide (BNP) level significant in this case?
IV. Based on the echocardiogram, what type of heart failure is Mrs. E.M. experiencing, and how does it differ from the alternative type?
V. What is the rationale for initiating a loop diuretic like furosemide in Mrs. E.M.’s treatment plan?
VI. Identify two physical examination findings that support a CHF diagnosis in this patient.
VII. What lifestyle interventions should Mrs. E.M. adopt to manage her CHF?
VIII. How does Mrs. E.M.’s history of coronary artery disease contribute to her current condition?

Analysis and Answers to Critical Thinking Questions

I. Primary Risk Factors for Mrs. E.M.’s CHF
Mrs. E.M.’s CHF is primarily driven by her history of coronary artery disease and hypertension. Coronary artery disease, treated with stent placement, likely caused myocardial ischemia, reducing cardiac contractility and contributing to systolic dysfunction. Hypertension increases afterload, forcing the heart to work harder, which over time leads to ventricular remodeling and failure (Volpe and Gallo, 2023). Additionally, her type 2 diabetes and former smoking history are significant risk factors, as they promote atherosclerosis and endothelial dysfunction, further impairing cardiac function (Virani et al., 2020). These factors collectively exacerbate her condition.

II. Pathophysiology of Bilateral Edema and Jugular Venous Distension
Bilateral edema and JVD result from right-sided heart failure secondary to left ventricular dysfunction. In CHF, the left ventricle’s reduced pumping capacity (LVEF 25%) leads to pulmonary congestion, increasing pressure on the right ventricle. The right ventricle, unable to pump effectively against this pressure, causes blood to back up into the systemic veins, elevating venous pressure. This results in JVD and fluid leakage into interstitial tissues, causing peripheral edema (Abassi et al., 2022). The RAAS activation further promotes sodium and water retention, worsening these symptoms.

III. Significance of Elevated BNP Level
The BNP level of 950 pg/mL is a critical diagnostic marker for CHF. BNP is secreted by ventricular myocytes in response to increased wall stress from volume or pressure overload. In Mrs. E.M., the elevated BNP reflects cardiac strain due to systolic dysfunction and fluid overload. This biomarker helps confirm CHF as the cause of her dyspnea, distinguishing it from non-cardiac causes like chronic obstructive pulmonary disease (Docherty et al., 2020). It also guides treatment decisions and monitors disease severity.

IV. Type of Heart Failure and Comparison
Mrs. E.M.’s echocardiogram shows an LVEF of 25%, indicating systolic heart failure, characterized by impaired ventricular contractility and reduced cardiac output. In contrast, diastolic heart failure involves preserved LVEF (>50%) but impaired ventricular filling due to stiff myocardium. Systolic failure, as in Mrs. E.M.’s case, often results from myocardial damage (e.g., coronary artery disease), while diastolic failure is associated with hypertension or hypertrophic cardiomyopathy. The distinction is critical for tailoring therapy, as systolic failure responds well to afterload-reducing agents like ACE inhibitors, whereas diastolic failure requires different management (Kemp and Conte, 2012).

V. Rationale for Furosemide
Furosemide, a loop diuretic, is initiated to alleviate fluid overload in Mrs. E.M. It acts on the loop of Henle to inhibit sodium reabsorption, promoting water excretion and reducing blood volume. This decreases preload, relieving pulmonary edema and peripheral edema, as evidenced by her crackles and ankle swelling. Furosemide improves symptoms like dyspnea and enhances ventricular function by reducing cardiac workload (Docherty et al., 2020). Monitoring renal function is essential due to potential electrolyte imbalances.

VI. Physical Examination Findings Supporting CHF Diagnosis
Two key findings are jugular venous distension and bilateral basilar crackles. JVD indicates elevated venous pressure from right-sided heart failure, a common consequence of left ventricular dysfunction. Basilar crackles reflect pulmonary edema due to increased left ventricular filling pressures, causing fluid leakage into alveoli. These findings, combined with her symptoms, strongly support a CHF diagnosis (Abassi et al., 2022). They align with clinical guidelines for diagnosing heart failure.

VII. Lifestyle Interventions for Mrs. E.M.
Mrs. E.M. should adopt a low-sodium diet (<2 g/day) to minimize fluid retention, as sodium exacerbates edema. Daily weight monitoring helps detect fluid accumulation, prompting early intervention. Engaging in supervised physical activity, such as cardiac rehabilitation, improves exercise tolerance and cardiovascular health. She should avoid smoking and limit alcohol intake to prevent further cardiac stress. Regular follow-up with a healthcare provider ensures medication adherence and disease monitoring (Virani et al., 2020).

VIII. Contribution of Coronary Artery Disease
Mrs. E.M.’s coronary artery disease, treated with stent placement, likely caused myocardial ischemia or infarction, leading to loss of functional myocardium. This damage reduces the left ventricle’s contractility, as evidenced by her LVEF of 25%, resulting in systolic heart failure. The compromised cardiac output triggers compensatory mechanisms like RAAS activation, worsening fluid retention and cardiac strain. Her history of coronary artery disease is a primary driver of her current CHF exacerbation (Kemp and Conte, 2012).

Conclusion

This case study on congestive heart failure provides nursing students with an opportunity to apply pathophysiological principles to clinical practice. By analyzing Mrs. E.M.’s case, students develop skills in identifying risk factors, understanding disease mechanisms, and formulating evidence-based interventions. The assignment emphasizes the importance of integrating diagnostic findings, such as BNP and echocardiography, with clinical symptoms to guide treatment. Furthermore, it highlights the role of lifestyle modifications in managing CHF. Completing this assignment prepares students for real-world nursing challenges in cardiovascular care.

References

Abassi, Z., Khoury, E. E., Karram, T. and Aronson, D., 2022. Edema formation in congestive heart failure and the underlying mechanisms. Frontiers in Cardiovascular Medicine, 9, p.933215.

Docherty, K. F., Vaduganathan, M., Solomon, S. D. and McMurray, J. J. V., 2020. Neprilysin inhibition in heart failure: A review. Journal of the American Heart Association, 9(11), p.e015071.

Kemp, C. D. and Conte, J. V., 2012. The pathophysiology of heart failure. Cardiovascular Pathology, 21(5), pp.365-371.

Virani, S. S., Alonso, A., Benjamin, E. J., Bittencourt, M. S., Callaway, C. W., Carson, A. P., Chamberlain, A. M., Chang, A. R., Cheng, S., Delling, F. N. and Djousse, L., 2020. Heart disease and stroke statistics—2020 update: A report from the American Heart Association. Circulation, 141(9), pp.e139-e596.

Volpe, M. and Gallo, G., 2023. Obesity and cardiovascular disease: An executive document on pathophysiological and clinical links. Frontiers in Cardiovascular Medicine, 10, p.1136340.

Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Colvin, M. M., Drazner, M. H., Filippatos, G. S., Fonarow, G. C. and Givertz, M. M., 2017. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure. Journal of the American College of Cardiology, 70(6), pp.776-803.

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