CAR-3. An unnerving case of heart failure.

To discuss the spectrum of dysautonomia associated with Guillain-Barre syndrome (GBS), including characteristics, proposed pathophysiology and treatment options. We report a 59-year-old Hispanic male diagnosed with GBS as evidenced by clinical picture, characteristic cerebral spinal fluid analysis, EMG data and initial response to plasmapheresis. As patient was recovering, he complained of chest pain and a cardiac nuclear stress test was performed to assess possible ischemic etiology. This showed no evidence of ischemia and an estimated left ventricular ejection fraction (LVEF) of 69%. The patient was discharged with minimal disability. Three weeks later he presented with rapid ascending paralysis and neuromuscular respiratory failure leading to intubation. Nasal swab revealed influenza A infection. Our patient then developed hypotension and an inappropriate bradycardia with heart rates in the 40s. Laboratory evaluation revealed alarming elevations in cardiac specific markers declaring myocardial injury. Echocardiogram showed global hypokinesis with a LVEF of <20%. The patient then developed congestive heart failure with pulmonary congestion and a basic natriuretic protein (BNP) of 1650. Gradually the patient's paralysis resolved with intravenous immunoglobulin therapy. Simultaneously, there was resolution of the patient's hypotension, bradycardia and congestive heart failure physiology. Two weeks later, echocardiogram demonstrated normal appearing ventricles with a LVEF of 60-65%. This case illustrates a severe GBS dysautonomia resulting in a reversible congestive cardiomyopathy. Dysautonomias are relatively common in GBS, possibly occurring in up to 60-70% of GBS sufferers. Intensive care unit monitoring and preparation for demand pacemaker placement is crucial for these patients, although the mainstay of treatment is supportive and aimed at the underlying GBS. There have been several reported cases of GBS dysautonomias presenting with EKG evidence of ischemia and elevated cardiac enzymes. Pathophysiology is theorized to involve alterations in transmural myocardial blood flow secondary to autonomic dysfunction.

Kevin Luce, MD, James Byrd, MD, and Mukta Panda, MD. University of Tennessee-Chattanooga Unit, Chattanooga, TN.