ICU · Physiology / cellular
Cellular Physiology & Membrane Potentials
Also known as Membrane potential · Resting membrane potential · Action potential · Na/K ATPase · Nernst equation · Goldman equation · Ion channels · Excitation-contraction coupling · Oxidative phosphorylation · Cytopathic hypoxia · HIF-1 alpha · Apoptosis versus necrosis
Cellular physiology and membrane potentials: the resting membrane potential (minus 70 mV; the Na/K ATPase — 3 Na out, 2 K in; the K leak the dominant). The Nernst equation (the equilibrium potential). The Goldman equation (the permeability-weighted). The action potential (the depolarisation Na influx, the repolarisation K efflux, the refractory). The cell membrane (the phospholipid bilayer, the channels, the receptors). Excitation-contraction coupling (the skeletal, the cardiac, the smooth). Cellular metabolism (glycolysis, Krebs cycle, oxidative phosphorylation, the ATP). Oxygen sensing (the HIF-1 alpha, the mitochondrial oxygen utilisation). Cellular hypoxia (the hypoxic, the stagnant, the anemic, the histotoxic; the cytopathic in sepsis). The cell death (the apoptosis, the necrosis, the necroptosis). The reactive oxygen species and the antioxidant defenses. The clinical correlations (the hyperkalaemia, the hypocalcaemia, the local anaesthetics, the channelopathies).
Checked against its sources on 3 Sept 2026
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A 62-year-old man in septic shock from an obstructed, infected urinary tract is on noradrenaline 0.35 mcg/kg/min, MAP 68, ScvO2 78 per cent, ventilated for ARDS. He has had his 30 mL/kg of crystalloid. Over six hours the lactate has climbed from 3.2 to 5.8 mmol/L — yet the mixed venous SvO2 is 82 per cent and the haemoglobin is 102 g/L. The registrar wants to push the MAP to 85 and add dobutamine.[6][7]
Two beds away, a 24-year-old arrives at 2 am with flaccid, areflexic quadriparesis that began three hours after a large carbohydrate meal. Potassium is 2.4 mmol/L, the ECG shows flattened T waves and prominent U waves, and his father has had identical attacks for thirty years. He is paralysed — and the potassium is not even that low.[24]
Two patients, one question hiding in both: when is a high lactate not hypoxia, and why does dropping potassium paralyse muscle? Both answers live in the cell membrane and the mitochondrion — the two structures this whole topic is built on.[1]
References27ShowHide
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- [24]Gao Z, Xing H, Zhang H, et al. Hypokalemic periodic paralysis: novel perspectives from genetic mutations to clinical management Gene, 2026.PMID 42013926
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