From Crackles to Quadruple Therapy: An Integrated Case Analysis of Heart Failure With Reduced Ejection Fraction in a 61 Year Old Primary Care Patient
[Student Name]
Edson College of Nursing and Health Innovation, Arizona State University
NUR 503: Advanced Health Assessment, Pathophysiology and Pharmacotherapeutics for Health Promotion II
Dr. [Course Faculty]
October 6, 2025
Model document. All patient details are composite and illustrative.
Presentation and Focused Assessment Findings
Heart failure affects roughly 6.7 million adults in the United States, and about half of those diagnosed die within five years (Centers for Disease Control and Prevention, 2024). The patient in this case is a composite built for teaching and describes no real person. He is a 61 year old man who came to a primary care clinic with two months of progressive exertional dyspnea, orthopnea that had grown from one pillow to three, and a 4.5 kg weight gain over the preceding 21 days. His history included hypertension treated with amlodipine 10 mg daily, type 2 diabetes with a most recent hemoglobin A1C of 7.4 percent, and 30 pack years of cigarette exposure that ended nine years ago. He reported stopping twice on a flight of stairs he had climbed without difficulty in the spring, and he denied chest pain, syncope and fever.
On examination the blood pressure was 148/92 mm Hg, the heart rate 96 beats per minute and regular, the respiratory rate 22, oxygen saturation 94 percent on room air, and the weight 96.2 kg, up from 91.7 kg at a visit four months earlier. The jugular venous pulsation was visible at 9 cm above the sternal angle with the head of the bed raised to 45 degrees. Auscultation found a soft S1, a preserved S2, and a low pitched S3 at the apex that was audible only with the bell in the left lateral decubitus position. The point of maximal impulse was displaced laterally to the anterior axillary line. Bibasilar inspiratory crackles reached the mid scapula and did not clear with coughing, and pitting edema was 3+ to the mid tibia bilaterally.
Diagnostics ordered at the visit returned an N terminal pro B type natriuretic peptide of 1,840 pg/mL, serum creatinine 1.2 mg/dL with an estimated glomerular filtration rate of 62 mL/min/1.73 m2, potassium 4.1 mEq/L, sodium 136 mEq/L, and a chest radiograph showing cardiomegaly with cephalization of the pulmonary vasculature. Transthoracic echocardiography reported a left ventricular ejection fraction of 32 percent with global hypokinesis and a left ventricular end diastolic diameter of 6.4 cm. Read as a cluster rather than as a list, the displaced impulse, the S3, the elevated venous pressure and the natriuretic peptide converge on a single process: a dilated ventricle that cannot empty adequately and a circulation that has answered by holding volume.
The Mechanism That Produces These Findings
Every finding above is downstream of one event. When the left ventricle dilates and its contractile efficiency falls, stroke volume drops, and the arterial baroreceptors read the smaller pulse pressure as hypovolemia. Sympathetic outflow rises, which explains a resting heart rate of 96 in a man taking no stimulant. Reduced renal perfusion and beta 1 stimulation at the juxtaglomerular apparatus release renin, and the renin angiotensin aldosterone cascade follows: angiotensin II raises afterload through vasoconstriction, and aldosterone drives sodium and water reabsorption at the distal nephron. The circulation therefore expands the very volume that a failing ventricle cannot move, which is why his weight climbed 4.5 kg while his effort tolerance fell (Heidenreich et al., 2022).
The same signals remodel the muscle. Sustained angiotensin II and aldosterone exposure promotes myocyte hypertrophy, interstitial collagen deposition and chamber dilation, so the ventricle grows rounder and its end diastolic diameter of 6.4 cm reflects months of adaptation rather than days of illness. Wall stretch also triggers a counter regulatory arm. Atrial and ventricular myocytes release natriuretic peptides that promote natriuresis, vasodilation and inhibition of aldosterone, and the elevated N terminal pro B type value of 1,840 pg/mL is the measurable trace of that response. The defense is losing, in part because neprilysin degrades the active peptides almost as fast as the stretched ventricle can make them (McDonagh et al., 2021).
From there each physical sign has an address. Elevated left atrial pressure transmits backward into the pulmonary capillary bed, and once hydrostatic pressure exceeds plasma oncotic pressure, fluid enters the interstitium and then the alveoli, producing crackles that do not clear with coughing and the radiographic cephalization already noted. The S3 is the sound of rapid early diastolic filling striking a ventricle that is already stretched and noncompliant. On the right side, elevated filling pressure raises systemic venous pressure, which the jugular column displays at 9 cm. Dependent edema is the joint product of that venous pressure and aldosterone driven sodium retention, which is why it is bilateral and gravity dependent rather than focal.
Pharmacotherapy Aimed at the Same Mechanism
Because the mechanism is neurohormonal, the therapy is neurohormonal, and each agent is chosen for the arm of the cascade it interrupts rather than for the symptom it relieves. Sacubitril valsartan blocks the angiotensin II type 1 receptor while inhibiting neprilysin, so the natriuretic peptides the stretched ventricle is already producing survive long enough to act. In the PARADIGM HF trial that combination lowered the rate of cardiovascular death or heart failure hospitalization against enalapril, reached by 21.8 percent of the sacubitril valsartan group and 26.5 percent of the enalapril group (McMurray et al., 2014). With a systolic pressure of 148 mm Hg and no prior angiotensin converting enzyme inhibitor, a starting dose of 49/51 mg twice daily is defensible, and no washout interval applies because there is no inhibitor to wash out.
Three additions complete guideline directed therapy. A blocker with proven benefit in reduced ejection fraction, such as carvedilol 3.125 mg twice daily, blunts the sympathetic arm and is begun at low dose once congestion is improving rather than during active volume overload. Spironolactone 12.5 mg daily antagonizes aldosterone at the mineralocorticoid receptor, which answers both the sodium retention and the interstitial fibrosis described above, and a potassium of 4.1 mEq/L with an estimated glomerular filtration rate of 62 mL/min/1.73 m2 places this patient inside the accepted range for starting it. Dapagliflozin 10 mg daily is added for its heart failure benefit rather than for glycemic control; in DAPA HF the primary composite occurred in 16.3 percent of the dapagliflozin group and 21.2 percent of the placebo group (McMurray et al., 2019).
Two remaining decisions are subtractions as much as additions. Furosemide 40 mg daily is prescribed for congestion alone, on the understanding that a loop diuretic relieves symptoms without altering the remodeling that drives outcomes, so the dose is expected to fall as the four disease modifying agents take effect. Amlodipine is stopped, because a dihydropyridine calcium channel blocker is neutral in reduced ejection fraction and the renin angiotensin blockade now carries the blood pressure. Monitoring follows the pharmacology rather than the calendar: a basic metabolic panel and blood pressure seven days after each start or titration, daily home weights with a two kilogram gain as the reported threshold, and repeat echocardiography at three months (Heidenreich et al., 2022).
References
Centers for Disease Control and Prevention. (2024). Heart failure. U.S. Department of Health and Human Services. https://www.cdc.gov/heart-disease/about/heart-failure.html
Heidenreich, P. A., Bozkurt, B., Aguilar, D., Allen, L. A., Byun, J. J., Colvin, M. M., Deswal, A., Drazner, M. H., Dunlay, S. M., Evers, L. R., Fang, J. C., Fedson, S. E., Fonarow, G. C., Hayek, S. S., Hernandez, A. F., Khazanie, P., Kittleson, M. M., Lee, C. S., Link, M. S., ... Yancy, C. W. (2022). 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation, 145(18), e895-e1032. https://doi.org/10.1161/CIR.0000000000001063
McDonagh, T. A., Metra, M., Adamo, M., Gardner, R. S., Baumbach, A., Bohm, M., Burri, H., Butler, J., Celutkiene, J., Chioncel, O., Cleland, J. G. F., Coats, A. J. S., Crespo-Leiro, M. G., Farmakis, D., Gilard, M., Heymans, S., Hoes, A. W., Jaarsma, T., Jankowska, E. A., ... Skibelund, A. K. (2021). 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. European Heart Journal, 42(36), 3599-3726. https://doi.org/10.1093/eurheartj/ehab368
McMurray, J. J. V., Packer, M., Desai, A. S., Gong, J., Lefkowitz, M. P., Rizkala, A. R., Rouleau, J. L., Shi, V. C., Solomon, S. D., Swedberg, K., & Zile, M. R. (2014). Angiotensin-neprilysin inhibition versus enalapril in heart failure. New England Journal of Medicine, 371(11), 993-1004. https://doi.org/10.1056/NEJMoa1409077
McMurray, J. J. V., Solomon, S. D., Inzucchi, S. E., Kober, L., Kosiborod, M. N., Martinez, F. A., Ponikowski, P., Sabatine, M. S., Anand, I. S., Belohlavek, J., Bohm, M., Chiang, C.-E., Chopra, V. K., de Boer, R. A., Desai, A. S., Diez, M., Drozdz, J., Dukat, A., Ge, J., ... Langkilde, A. M. (2019). Dapagliflozin in patients with heart failure and reduced ejection fraction. New England Journal of Medicine, 381(21), 1995-2008. https://doi.org/10.1056/NEJMoa1911303
How this NUR 503 Module 4 example is structured
Arizona State University publishes no module by module deliverable names for Advanced Health Assessment, Pathophysiology and Pharmacotherapeutics for Health Promotion II, so this NUR 503 Module 4 example is written as the genre the module almost certainly wants: in many sections this module asks for an integrated case analysis, and your course instructions and rubric decide the exact form. The first sheet reports the presentation, the focused examination and the diagnostics as findings, with measures and reference points attached and no interpretation yet. The second sheet explains the mechanism once, in order, then gives every physical sign an address inside it. The third sheet selects therapy by naming the arm of the cascade each agent interrupts, adds trial evidence with both comparison groups, and closes with monitoring and one deprescribing decision. That order is the argument: findings, then cause, then the drug that answers the cause.
NUR 503 Module 4 questions, answered
What does NUR 503 Module 4 usually ask for?
ASU does not publish module by module deliverable names for this course, so treat the genre as the safe target. In many sections this module asks for an integrated case paper in which assessment findings, the mechanism behind them and the drug therapy connect. Your course instructions and rubric decide the exact form, the sections and the citation expectations.
How long is a paper like this in a short ASU session?
This model document runs about 1,100 words of body prose across three sections plus a title page and references, which is a common size for a graduate case paper in a short session. No official length is claimed here. Check the assignment instructions and rubric in your course for the length your section expects.
Can I write about a real patient from my clinical site?
No. Build a composite instead, as this example does. Composite patients let you keep the clinical reasoning realistic while removing every identifier, so there is nothing to de-identify because no real case is used. State plainly in the paper that the patient is a composite, and keep employer names, dates of service and site details out of the document.
Write yours, or have the desk draft it
This paper is an original model document written by our desk, not a submitted student paper and not an official Arizona State University document. Read it for the moves, then write your own to the instructions in your classroom. If you want one built to your exact prompt and rubric, the first custom sample is free and arrives in 24 to 48 hours.