Delirium as an Atypical Presentation of Severe Aortic Stenosis in a Cognitively Intact Nonagenarian With Atrial Fibrillation

A 90-year-old woman with well-established severe calcific aortic stenosis (aortic valve area 0.6 cm², gradient 60 mmHg on echocardiography six months earlier) and chronic atrial fibrillation was brought to the emergency department with a three-day history of acute confusion, inattention, and agitation. She had no fever, urinary symptoms, recent medication changes, or falls. Critically, her baseline cognition was documented as fully intact — she had scored 10/10 on the Abbreviated Mental Test Score (AMTS) just two weeks prior. On this admission, her AMTS had fallen to 4/10, marking significant deterioration.

She lived semi-independently with a Clinical Frailty Score of 5 (mild frailty) and ambulated with a walker. Her current medications included bisoprolol 2.5 mg, apixaban 5 mg twice daily, lansoprazole, macrogol, and Adcal D3 — no recent additions or dose changes. A Do Not Attempt Resuscitation (DNAR) order was in place consistent with her expressed preferences. Vital signs on arrival showed blood pressure 130/60 mmHg, heart rate 68 bpm in an irregularly irregular rhythm, respiratory rate 18 breaths/min, and oxygen saturation 96% on 2L supplemental oxygen. Cardiovascular examination revealed a prominent grade 4/6 systolic ejection murmur at the right upper sternal border, elevated jugular venous pressure, and bibasal crepitations. No focal neurological deficits were detected.

A structured delirium workup was performed to exclude common precipitants. The white blood cell count and C-reactive protein (6 mg/L) were near-normal, urine dipstick was clear, and there was no consolidation on chest X-ray to suggest infection. Electrolytes, glucose, liver function, calcium, and thyroid-stimulating hormone were all within acceptable limits. No recent medication changes or high-risk drugs were identified. A venous blood gas showed normal pH (7.44), and adequate lactate clearance, with no evidence of hypoxia or hypercapnia.

The chest X-ray on admission demonstrated bilateral pulmonary congestion — a stark contrast to a baseline film taken three months earlier that showed no pulmonary vascular redistribution.

Figure 1

Chest X-ray — Admission

Bilateral pulmonary congestion with vascular redistribution and perihilar haziness, consistent with acute decompensated heart failure. This finding was absent on a chest film taken three months prior, confirming acute decompensation rather than chronic baseline changes.

The ECG demonstrated the patient's known atrial fibrillation with no new ischemic changes — specifically no ST-segment shifts or T-wave inversions to suggest acute coronary syndrome.

Figure 2

Electrocardiogram — Atrial Fibrillation, No Ischemic Changes

12-lead ECG showing an irregularly irregular rhythm consistent with atrial fibrillation. No ST-segment depression, elevation, or acute T-wave changes to suggest myocardial ischemia. The mildly elevated troponin was attributed to type 2 myocardial injury from hemodynamic stress rather than plaque rupture.

Figure 3

Chest X-ray — Baseline (3 Months Prior)

Comparison film demonstrating clear lung fields without pulmonary venous congestion. The marked difference between this baseline radiograph and the admission film confirms acute-on-chronic decompensation rather than chronically elevated pulmonary pressures misread as new pathology.

Transthoracic echocardiography confirmed the previously documented severe calcific aortic stenosis, with an indexed aortic valve area of 0.6 cm² and a peak aortic jet velocity of 3.84 m/s with a mean gradient exceeding 40 mmHg. No new wall motion abnormalities or pericardial effusion were identified. The markedly elevated NT-proBNP of 9,807 pg/mL (normal <400 pg/mL) and mildly elevated troponin with a stable trend (220 falling to 216 ng/L) confirmed acute decompensated heart failure with type 2 myocardial injury rather than a primary ACS event.

Figure 4

Transthoracic Echocardiography — Aortic Valve Area

Doppler echocardiogram demonstrating an indexed aortic valve area of 0.6 cm², consistent with very severe aortic stenosis. This measurement, confirmed on repeat study, places the patient well below the severe AS threshold of 1.0 cm² (indexed <0.6 cm²/m²). The fixed outflow obstruction severely limits the ability to increase cardiac output in response to physiologic demand.

Figure 5

Transthoracic Echocardiography — Peak Velocity and Mean Gradient

Continuous-wave Doppler across the aortic valve showing a peak velocity of 3.84 m/s with a mean gradient exceeding 40 mmHg, confirming hemodynamically severe aortic stenosis. The elevated gradient in the context of atrial fibrillation — where preload is reduced by loss of atrial kick — likely underestimates the true degree of obstruction under normal sinus conditions.

The clinical diagnosis was delirium secondary to cerebral hypoperfusion from acute decompensated heart failure, precipitated by severe aortic stenosis and chronic atrial fibrillation. The patient was managed conservatively with intravenous furosemide 40 mg once daily for two days, followed by oral bumetanide 1 mg daily once stable. Within 72 hours, her delirium completely resolved without use of antipsychotics or sedatives. Pulmonary congestion improved clinically and on repeat radiograph, and renal function remained stable throughout. She was discharged home at her baseline cognitive status. Cardiothoracic surgery consultation was deferred at her request, consistent with her care preferences for conservative management.

Discussion

This case illustrates a critical and under-recognized mechanism of delirium in elderly patients: low cardiac output from severe aortic stenosis compounded by atrial fibrillation. Severe AS creates a fixed obstruction at the left ventricular outflow tract, limiting the heart's ability to augment stroke volume during periods of increased physiologic demand or hemodynamic stress. In the setting of chronic atrial fibrillation, loss of the atrial kick — which normally contributes 20–30% of ventricular filling, especially important in a hypertrophied, stiff left ventricle — further reduces preload and stroke volume. The result is a "perfect storm": systemic hypoperfusion that disproportionately affects the aging brain, which is exquisitely sensitive even to mild reductions in cerebral blood flow. The structured delirium workup excluding infection, metabolic disturbance, CNS pathology, and medication effects is essential because cardiogenic delirium requires an entirely different treatment trajectory (diuresis and hemodynamic optimization) than the usual precipitants.

The rapid resolution of delirium within 72 hours of IV diuretic therapy serves as its own diagnostic confirmation. This temporal relationship between decongestion and cognitive recovery reinforces the cardiac etiology and underscores why NT-proBNP should be measured early in elderly patients with unexplained cognitive deterioration and no obvious infectious or metabolic cause. The mildly elevated troponin with a stable trend — typical of type 2 myocardial injury rather than plaque rupture — should not redirect the clinical team toward an ACS pathway. In very elderly, frail patients with severe AS who decline or are not candidates for valve replacement, IV diuretics remain the most effective intervention available, capable of dramatically improving symptoms and quality of life even without definitive valve therapy.