Precision and consistency of the passive leg raising maneuver for determining fluid responsiveness with bioreactance non-invasive cardiac output monitoring in critically ill patients and healthy volunteers.

OBJECTIVE: The passive leg raising (PLR) maneuver has become standard practice in fluid resuscitation. We aim to investigate the precision and consistency of the PLR for determining fluid responsiveness in critically ill patients and healthy volunteers using bioreactance non-invasive cardiac output monitoring (NiCOM™, Cheetah Medical, Inc., Newton Center, Massachusetts, USA). METHODS: This study is prospective, single-center, observational cohort with repeated measures in critically ill patients admitted to the medical intensive care unit and healthy volunteers at a tertiary academic medical center. Three cycles of PLR were performed, each at 20-30 minutes apart. Fluid responsiveness was defined as a change in stroke volume index (ΔSVI) > 10% with each PLR as determined by NiCOM™. Precision was the variability in ΔSVI after the 3 PLR's, and determined by range, average deviation and standard deviation. Consistency was the same fluid responsiveness determination of "Yes" (ΔSVI > 10%) or "No" (ΔSVI ≤ 10%) for all 3 PLR's. RESULTS: Seventy-five patients and 25 volunteers were enrolled. In patients, the precision was range of 17.2±13.3%, average deviation 6.5±4.0% and standard deviation 9.0±5.2%; and for volunteers, 17.4±10.3%, 6.6±3.8% and 9.0±6.7%, respectively. There was no statistical difference in the precision measurements between patients and volunteers. Forty-nine (65.3%) patients vs. twenty-four (96.0%) volunteers had consistent results, p < 0.01. Among those with consistent results, twenty-four (49.0%) patients and 24 (100%) volunteers were fluid responsive. CONCLUSIONS: The precision and consistency of determining ΔSVI with NiCOM™ after PLR may have clinical implication if ΔSVI > 10% is the absolute cutoff to determine fluid responsiveness.

Altered fast and slow inactivation of the N440K Nav1.4 mutant in a periodic paralysis syndrome.

OBJECTIVE: To electrophysiologically characterize the Na(v)1.4 mutant N440K found in a Korean family with a syndrome combining symptoms of paramyotonia congenita, hyperkalemic periodic paralysis, and potassium-aggravated myotonia. METHODS: We characterized transiently expressed wild-type and mutant Na(v)1.4 using whole-cell voltage-clamp analysis. RESULTS: N440K produced a significant depolarizing shift in the voltage dependence of fast inactivation and increased persistent current and acceleration in fast inactivation recovery, which gave rise to a 2-fold elevation in the dynamic availability of the mutant channels. In addition, the mutant channels required substantially longer and stronger depolarization to enter the slow-inactivated state. CONCLUSIONS: N440K causes a gain of function consistent with skeletal muscle hyperexcitability as observed in individuals with the mutation. How the same mutation results in distinct phenotypes in the 2 kindreds remains to be determined.