In severe Guillain-Barré syndrome, extreme blood pressure fluctuations may result from parallel changes in vascular resistance and heart rate due to dysautonomia and baroreflex dysfunction.
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May explain BP lability via dysautonomia in severe GBS; leaves open validation in prospective cohorts.
A 76-year-old man with severe Guillain-Barré syndrome had extremes of hypotension alternating with hypertension. His blood pressure paralleled both systemic vascular resistance and cardiac output. Heart rate, rather than stroke volume, was the major determinant of cardiac output over a wide range of blood pressures. It was at times invariant for several hours and was unresponsive to carotid massage or respiratory cycles, but slowed slightly with each episode of hypotension. Trend monitoring indicated that hypotension preceded reductions in pulmonary artery diastolic pressure. These findings suggest that hypotension resulted from a vasodepressor response with a vagotomized heart and that hypertension was the result of increased sympathetic activity. Both extremes were caused by parallel changes in vascular resistance and heart rate. Dysfunction of baroreflex buffering may have accounted for the rapid swings in pressure.
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Ropper et al. (1990) studied this question.
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