Nurse Practitioner Nashville, Tennessee, United States
Disclosure(s):
Ashley Bernard, DNP, AGACNP-BC: No financial relationships to disclose
Background: Atrial fibrillation (AF) and pulmonary edema have rarely been reported as manifestations of multiple sclerosis (MS). Lesions affecting the insular cortex or brainstem can disrupt autonomic regulation and precipitate arrhythmias or acute heart failure leading to cardiogenic shock.
Methods: A 35-year-old healthy woman with recent onset transient left-sided numbness presented with acute dyspnea, palpitations, and weakness. EKG revealed AF with rapid ventricular response. Physical exam showed normal motor function. Lab work was notable for elevated lactate, leukocytosis and mild troponin elevation. Chest imaging confirmed pulmonary edema. Transthoracic echocardiogram showed EF was mildly depressed (40-45%). After emergent cardioversion, the patient rapidly decompensated into cardiogenic shock requiring intubation, vasopressors, and inotropic support. She had gradual EF recovery and resolution of her shock with medical management. Following extubation, she had an episode of flash pulmonary edema that was treated with sodium nitroprusside and loop diuretics. Throughout her hospitalization, she described waves of transient left-sided numbness, similar to the episodes she experienced prior to presentation.
Outcome: AF was managed with cardioversion, rate and rhythm control using carvedilol, flecainide, and anticoagulation. Brain MRI revealed demyelinating lesions in the periventricular region and brainstem, highly suspicious for MS. LP was performed and CSF analysis showed pleocytosis. The patient was diagnosed with new-onset MS. Given her normal filling pressures at the time of flash pulmonary edema episode, her pulmonary edema was considered neurogenic in etiology. The overlap of neurological disease and cardiac instability required multidisciplinary management.
Conclusion: This case highlights AF and pulmonary edema as a possible presentation of MS. Demyelinating lesions involving the autonomic and respiratory centers can provoke arrhythmias and pulmonary edema, mimicking primary cardiac disease. Clinicians should consider neurogenic causes in unexplained cardiopulmonary decompensation, particularly when neurological symptoms are present.
