From Reduced Ejection Fraction to Alveolar Flooding: A Case Analysis of Acute Decompensated Heart Failure in a 68-Year-Old Man
[Author Name]
Nursing Program, Southern New Hampshire University
NUR 315: Pathophysiology for Nurses
Module 4 Assignment
[Instructor Name]
August 11, 2026
Composite case written as a model document. No real patient, employer or clinician is described.
Case Presentation
Mr. A is a composite 68-year-old retired maintenance supervisor who arrived at a community hospital emergency department at 9:15 p.m. after six days of worsening breathlessness. Six days earlier he could walk the length of his driveway to collect the mail without stopping; on the day he came in he stopped twice and rested against the fence to finish the trip. He now sleeps propped on three pillows rather than the single pillow he has used for years, and on two of the past three nights he woke at about 2 a.m. gasping and sat on the edge of the bed for twenty minutes before the breathlessness eased. His home log shows a weight rise from 82.1 kg to 85.5 kg across those six days, a gain of 3.4 kg.
His history includes an anterior myocardial infarction four years ago treated with a stent, after which an echocardiogram measured a left ventricular ejection fraction of 30 percent. He also carries a fifteen-year history of hypertension and stage 3a chronic kidney disease. His routine medicines include a loop diuretic taken each morning, a beta blocker and an angiotensin converting enzyme inhibitor. He reports skipping the diuretic on three of the past seven days because he was away from home and did not want to be caught without a bathroom, and he ate restaurant food on four of those days. At triage his blood pressure was 158/94 mm Hg, heart rate 104 and regular, respiratory rate 26, temperature 36.8 C, and oxygen saturation 89 percent on room air, rising to 95 percent on 3 L per minute by nasal cannula.
On examination the jugular venous column was visible to 10 cm above the sternal angle with the head of the bed at 45 degrees. Crackles were audible in both lung bases to the level of the mid-scapula, an S3 gallop was present at the apex, and pitting edema of 2+ extended to mid-shin on both legs. His hands were cool and capillary refill took three seconds. Urine output over the first two hours was 20 mL per hour. Laboratory results showed a B-type natriuretic peptide of 1,860 pg per mL against a reference value below 100, serum sodium 132 mmol per L, potassium 4.1 mmol per L, and creatinine 1.6 mg per dL against a baseline of 1.2 mg per dL three months earlier. The chest radiograph showed cardiomegaly, redistribution of blood flow to the upper lobes, and small bilateral pleural effusions.
The Mechanism: How a Weakened Left Ventricle Produces Congestion
The chain begins in the muscle. The infarction four years ago replaced a section of left ventricular wall with fibrous scar, which stretches under pressure but does not contract. Stroke volume fell, and an ejection fraction of 30 percent means that under a third of the blood held in the ventricle at the end of filling is moved forward with each beat. For a time the body held cardiac output near normal by raising heart rate and by keeping more volume in the circulation, so his symptoms at rest stayed mild. Arterial baroreceptors read the lower pressure and smaller pulse volume as underfilling and increased sympathetic outflow, which raised heart rate and contractility and constricted arterioles. Each of those responses defends blood pressure in the short run and costs the ventricle oxygen and workload in the long run.
The kidney reads the same signal and adds a second layer. Reduced renal perfusion pressure prompts the juxtaglomerular cells to release renin, which starts the sequence that produces angiotensin II. Angiotensin II constricts systemic arterioles, raising the resistance the failing ventricle must eject against, and it stimulates aldosterone release, which drives sodium and water reabsorption in the distal nephron. Angiotensin II also triggers thirst and the release of antidiuretic hormone, so water is retained out of proportion to sodium. That last step, and not a loss of body sodium, is the reason his serum sodium reads 132 mmol per L while his total body sodium and total body water are both high. Plasma volume expands, and the expansion is delivered straight back to the ventricle that could not manage the volume it already had.
Expanded volume raises left ventricular end-diastolic pressure. A healthy ventricle answers extra stretch with a stronger contraction, but a dilated ventricle sits on the flat part of that relationship and gains almost nothing, so pressure banks up instead of moving forward. It is transmitted to the left atrium and then to the pulmonary veins and capillaries. Once capillary hydrostatic pressure passes plasma oncotic pressure and outruns the lymphatic drainage of the lung, fluid crosses into the interstitium and then into the alveoli. The raised pressure in the pulmonary circulation also increases the load on the right ventricle, so systemic venous pressure rises in turn, and constant wall stress stretches myocytes that release B-type natriuretic peptide in proportion to that stretch. The compensations that protected his blood pressure in the months after the infarction are the same processes now moving fluid into his alveoli.
Reading Each Finding Back Through the Chain
Every respiratory finding in the case sits at a named step. The crackles are the sound of small airways and alveoli popping open against interstitial and alveolar fluid, and they are heard at the bases first because hydrostatic pressure is highest in the dependent lung. Orthopnea has the same explanation from the other direction: lying flat returns volume from the legs and the splanchnic bed to a central circulation that is already overfilled, so pressure rises and breathing worsens within minutes, which is why he now needs three pillows. Waking at 2 a.m. gasping follows the same shift after several hours spent lying down. The saturation of 89 percent reflects a thicker path for oxygen to cross and lung that is perfused but poorly ventilated, and the radiographic redistribution to the upper lobes is that same congestion seen in outline.
The systemic findings follow the pressure backward. A jugular venous column at 10 cm and pitting edema to mid-shin both report a raised central venous pressure rather than a local leg problem. The weight matters more than the edema: a gain of 3.4 kg is about 3.4 L of retained fluid, which is why the scale detects congestion days before pitting edema appears, because the interstitial space absorbs several liters before it holds a thumbprint. Sodium of 132 mmol per L marks water retention driven by antidiuretic hormone rather than a sodium deficit. The B-type natriuretic peptide of 1,860 pg per mL reports myocyte stretch. Creatinine rising from 1.2 to 1.6 mg per dL reflects a kidney that is underperfused from the front and congested from the back, and cool hands with a three second refill show the arteriolar constriction the sympathetic response produced.
The chain also predicts what nursing care watches and what teaching has to change. Because the problem is volume and pressure rather than infection or airway disease, the measures that matter are a daily weight taken at the same hour on the same scale after voiding and before breakfast, intake and output, respiratory rate, oxygen saturation, and how many pillows he needs to sleep. Improvement should show as urine output above 0.5 mL per kg per hour, a falling weight, and an ability to lie flatter, and the team follows potassium and creatinine because moving that volume moves both. The teaching point comes from the cause and not the symptom: three missed diuretic doses and four restaurant meals restarted the retention step, so he leaves with a scale, a written call rule of a 2 kg gain across three days, and a sodium plan he helped write.
References
Centers for Disease Control and Prevention. (2024). About heart failure. U.S. Department of Health and Human Services. https://www.cdc.gov/heart-disease/about/heart-failure.html
Hall, J. E., & Hall, M. E. (2021). Guyton and Hall textbook of medical physiology (14th ed.). Elsevier.
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.
National Heart, Lung, and Blood Institute. (2022). Heart failure. National Institutes of Health. https://www.nhlbi.nih.gov/health/heart-failure
Norris, T. L. (2019). Porth's essentials of pathophysiology (5th ed.). Wolters Kluwer.
How this NUR 315 Module 4 example is structured
In many sections the module 4 assignment in a pathophysiology course asks for a written case analysis that follows one disease process from mechanism to presentation; your classroom's instructions and rubric decide the exact form, so read them before you use this NUR 315 Module 4 example as a shape. The paper moves in three steps. The case comes first, so every later claim has a finding to point at. The mechanism comes second and is written as a single chain rather than a list of facts, because causal order is what a pathophysiology grader is reading for. The mapping section comes last and does the work most papers leave out: it returns to each finding in the case, names the step that produced it, and then says what the chain predicts for monitoring and patient teaching.
NUR 315 Module 4 questions, answered
What does a NUR 315 Module 4 paper usually ask for?
In many sections the module 4 assignment in a pathophysiology course is a written case analysis: one patient, one disease process, and a mechanism traced to the findings at the bedside. Your classroom's instructions and rubric decide the exact form, including how many sources are expected and whether a diagram is welcome. Read those first, then use this example as a shape.
How much pharmacology belongs in a BSN pathophysiology case paper?
Enough to explain the mechanism, not enough to prescribe. Naming a drug class and what it does to the chain, such as a diuretic lowering preload, keeps the paper at practice level. Dosing tables, titration schedules and prescriber decision rules belong to a later course, and adding them usually costs the space the mechanism needed.
Why do students search for labels like 4-2 or 4-3?
SNHU numbers graded items by module and sequence, so a paper landing in the fourth module gets typed as 4-2 or 4-3 in search boxes and message boards. The convention is real, but the number attached to any given paper varies by section and term, so match the label your classroom shows rather than one found online.
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 Southern New Hampshire 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.