NR 545 Week 6 Conflicting Findings Analysis Example

Integrated Case Analysis: Lightheadedness on Standing Six Weeks Into Heart Failure Therapy, Where the Mechanism Calls for More Drug and the Examination Warns Against It, and the Finding That Settles Which Drug to Cut

Student Name

College of Nursing, Chamberlain University

NR 545: Pharmacology, Physical Assessment, and Pathophysiology

Instructor Name

Month Day, Year

Integrated Case Analysis: Lightheadedness on Standing Six Weeks Into Heart Failure Therapy, Where the Mechanism Calls for More Drug and the Examination Warns Against It, and the Finding That Settles Which Drug to Cut

The Presentation

Six weeks into treatment for a ventricle ejecting 30%, the 64-year-old patient returns for a planned visit to continue building therapy. Current medications are lisinopril 20 mg once a day; carvedilol 6.25 mg morning and night (begun three weeks ago at 3.125 mg, raised 10 days ago); dapagliflozin 10 mg each morning; furosemide 40 mg on waking; and metformin, 1,000 mg at breakfast and at the evening meal. Coronary angiography two weeks ago showed no significant coronary disease, so the cardiomyopathy is considered nonischemic, most likely hypertensive.

The patient reports feeling much less breathless, now sleeping flat, but describes lightheadedness on standing over the past week, twice needing to sit down after getting out of bed. No fainting, no chest pain, no palpitations. The patient has been eating less in hot weather and reports a dry mouth. Home weights have fallen steadily and this morning's was 85.0 kg.

Examination: blood pressure 98/62 mmHg seated and 84/56 mmHg after three minutes standing, with lightheadedness on standing. Heart rate 70 seated, 78 standing. Jugular venous pressure not visible above the clavicle at 45 degrees and visible at 3 cm above the sternal angle only when lying flat. Lungs clear. No edema. Warm peripheries with refill in under two seconds. Mucous membranes dry. Third heart sound no longer heard.

Laboratory results: creatinine 1.62 mg/dL (1.35 four weeks ago), eGFR 46 mL/min/1.73 m², blood urea nitrogen 38 mg/dL (22 four weeks ago), potassium 4.5 mmol/L, sodium 138 mmol/L.

Two Readings

The plan for today was to continue increasing guideline-directed therapy: raise carvedilol toward its target, switch lisinopril to sacubitril/valsartan and add spironolactone. Each of these lowers blood pressure. The patient now has symptomatic orthostatic hypotension. Two explanations are reasonable, and each leads to a different plan.

Reading A: the weak ventricle cannot tolerate the beta-blocker increase. The physiology supports this. A ventricle with an ejection fraction of 30% depends partly on sympathetic support to maintain output. Carvedilol blocks beta-adrenergic receptors, reducing heart rate and contractility, and also blocks alpha-1 receptors, causing vasodilation. The dose was increased 10 days ago, and the symptoms began about a week ago. If output has fallen, blood pressure would fall, kidney perfusion would fall and creatinine would rise. Under this reading, the carvedilol should be reduced, and further increases in therapy delayed.

Reading B: the patient is volume depleted from overlapping diuresis. This also has support. Furosemide was set at a dose chosen when the patient was congested. Dapagliflozin was added with its own natriuretic effect. The patient has since reached and passed the estimated dry weight of 86 kg, and has been eating and drinking less in hot weather. Volume depletion reduces preload, which in a patient with a dilated ventricle can reduce stroke volume and cause orthostatic hypotension, and reduces kidney perfusion, raising creatinine and urea. Under this reading, the furosemide should be reduced or stopped and the carvedilol kept.

The Pivot

Several findings favor Reading B, but one settles it: the patient is warm and dry, not cold.

If the problem were low cardiac output, the examination should show signs of poor perfusion: cool extremities, slow capillary refill and a narrow pulse pressure. In chronic heart failure, a proportional pulse pressure below 25% has been associated with a low cardiac index (Stevenson & Perloff, 1989). This patient's proportional pulse pressure is 98 minus 62, divided by 98, or 0.37, well above that threshold. The extremities are warm with brisk refill. In the hemodynamic profiles used to classify heart failure, the patient is now warm and dry (Nohria et al., 2003), which is where therapy aimed to take the patient, except that the patient has overshot.

The other findings point the same way. Weight is 85.0 kg, 1 kg below the estimated dry weight and 6.4 kg below the weight at diagnosis. The jugular venous pressure is low. Mucous membranes are dry. The urea has risen proportionally more than the creatinine, from 22 to 38 mg/dL while creatinine rose from 1.35 to 1.62 mg/dL, a ratio of about 23 that is consistent with reduced kidney perfusion from low volume. The heart rate rises on standing, from 70 to 78, which is a limited response because of the beta-blocker, but the direction is consistent with volume depletion.

The timing that seemed to favor Reading A, the carvedilol increase 10 days ago, fits Reading B equally well, since the patient passed dry weight at about the same time. Timing alone cannot separate them; the perfusion examination can.

A Plan That Depends on the Answer

Under Reading B, the plan is as follows. Furosemide is stopped as a daily medication and changed to 40 mg as needed, taken only when the morning weight has gone up by over a kilogram since the day before, or two kilograms since the week before, or if ankle swelling returns. Carvedilol is continued at 6.25 mg twice daily, not reduced. Dapagliflozin is continued. The patient is advised to drink normally, about 1.5 to 2 liters a day in hot weather, rather than restricting fluid. The planned switch to sacubitril/valsartan and addition of spironolactone are postponed by one to two weeks, until blood pressure recovers and creatinine returns toward baseline. Guidelines support adjusting diuretic doses to the lowest dose that maintains euvolemia once congestion has resolved (Heidenreich et al., 2022).

Under Reading A, the plan would have been different: reduce carvedilol back to 3.125 mg twice daily, continue the furosemide and consider referral for evaluation of low output. That difference is the proof that the conflict mattered. Reducing the beta-blocker in a patient who was actually volume depleted would have removed a drug that lowers mortality in reduced ejection fraction, while leaving the cause of the symptoms in place.

What Remains Uncertain

The resolution is probable, not certain. The carvedilol increase may be contributing modestly, and the two causes can coexist. The plan is built to reveal that. If lightheadedness and orthostatic hypotension resolve within a week after stopping daily furosemide, with weight stable near 86 kg and creatinine falling, Reading B is confirmed. If symptoms persist once the patient is back to dry weight, or if extremities become cool or the pulse pressure narrows, the question reopens, and carvedilol would be reduced and output assessed. The patient will have blood pressure, weight and a basic metabolic panel checked in one week, and will call sooner if fainting, chest pain or worsening lightheadedness occurs.

References

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: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 145(18), e895-e1032. https://doi.org/10.1161/CIR.0000000000001063

Nohria, A., Tsang, S. W., Fang, J. C., Lewis, E. F., Jarcho, J. A., Mudge, G. H., & Stevenson, L. W. (2003). Clinical assessment identifies hemodynamic profiles that predict outcomes in patients admitted with heart failure. Journal of the American College of Cardiology, 41(10), 1797-1804. https://doi.org/10.1016/S0735-1097(03)00309-7

Stevenson, L. W., & Perloff, J. K. (1989). The limited reliability of physical signs for estimating hemodynamics in chronic heart failure. JAMA, 261(6), 884-888. https://doi.org/10.1001/jama.1989.03420060100040