OBJECTIVE: To test the hypothesis that muscle fibers are depolarized in patients with critical illness myopathy by measuring velocity recovery cycles (VRCs) of muscle action potentials. METHODS: VRCs were recorded from brachioradialis muscle by direct muscle stimulation in 10 patients in intensive care with evidence of critical illness myopathy (CIM). Two sets of recordings were made, mean 3.9 d apart, and compared with those from 10 age-matched controls. RESULTS: Muscle supernormality was reduced in the patients by 50% compared with controls (P<0.002) and relative refractory period was increased by 59% (P<0.01). Supernormality was correlated with plasma potassium levels (R=-0.753, P<0.001), and the slope of this relationship was much steeper than previously reported for non-critically ill patients with renal failure (P<0.01). CONCLUSIONS: The abnormal excitability properties indicate that the muscle fibers in CIM were depolarized, and/or that sodium channel inactivation was increased. The heightened sensitivity to potassium is consistent with the hypothesis that an endotoxin reduces sodium channel availability in depolarized muscle fibers. SIGNIFICANCE: VRCs provide a practicable means to monitor muscle membrane changes in intensive care and to investigate the pathogenesis of CIM.
OBJECTIVE: To test the hypothesis that muscle fibers are depolarized in patients with critical illness myopathy by measuring velocity recovery cycles (VRCs) of muscle action potentials. METHODS: VRCs were recorded from brachioradialis muscle by direct muscle stimulation in 10 patients in intensive care with evidence of critical illness myopathy (CIM). Two sets of recordings were made, mean 3.9 d apart, and compared with those from 10 age-matched controls. RESULTS: Muscle supernormality was reduced in the patients by 50% compared with controls (P<0.002) and relative refractory period was increased by 59% (P<0.01). Supernormality was correlated with plasma potassium levels (R=-0.753, P<0.001), and the slope of this relationship was much steeper than previously reported for non-critically ill patients with renal failure (P<0.01). CONCLUSIONS: The abnormal excitability properties indicate that the muscle fibers in CIM were depolarized, and/or that sodium channel inactivation was increased. The heightened sensitivity to potassium is consistent with the hypothesis that an endotoxin reduces sodium channel availability in depolarized muscle fibers. SIGNIFICANCE: VRCs provide a practicable means to monitor muscle membrane changes in intensive care and to investigate the pathogenesis of CIM.
Authors: Daniel Tuchscherer; Werner J Z'graggen; Christina Passath; Jukka Takala; Christer Sinderby; Lukas Brander Journal: Intensive Care Med Date: 2011-11-03 Impact factor: 17.440
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