Medical hypotheses
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Rocuronium is an aminosteroid non-depolarizing neuromuscular relaxant, which is metabolized in the liver and excreted through bile. The duration of neuromuscular blockade of rocuronium at equipotent bolus dose may be prolonged and variable in patients with liver and kidney failure. However, very few studies have been reported its pharmacodynamics in patients with obstructive jaundice. We propose that the effect of rocuronium is prolonged in patients with obstructive jaundice, and a caution should be taken in monitoring postoperative residual neuromuscular blockade.
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Obesity has reached global pandemic that threatens the health of millions of people and is associated with numerous morbidities such as hypertension, type II diabetes mellitus, dyslipidemia, cor pulmonale, gallbladder disease, obstructive sleep apnea (OSA), certain cancers, osteoarthritis, increased surgical risk and postoperative complications, lower extremity venous and/or lymphatic problems, pulmonary embolism, stroke/cerebrovascular diseases and coronary arterial disease. Despite all these adverse associations, numerous studies and meta-analyses have documented an "obesity paradox" in which overweight and obese population with established cardiovascular disease have a better prognosis than do their lean counterparts. ⋯ Chronic intermittent hypoxia, one of the physiological markers of OSA, is characterized by transient periods of oxygen desaturation followed by reoxygenation, and is a major cause of its systemic harmful (oxidative stress, inflammation, sympathetic activity, vasculature remodelling and endothelial dysfunction) and/or protective (preconditioning-like cardioprotective) effects. Since many OSA subjects are obese, and obesity is an independent risk factor for many comorbidities associated with OSA; and also most OSA has never been diagnosed in obese patients, we hypothesed that the chronic intermittent hypoxia caused by OSA in obese patients may be one of the underlying mechanisms in morbi-mortality paradox of obesity.
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Cardiac arrhythmias cause significant morbidity and mortality in patients with coronary heart disease, hypertension, and congestive cardiac failure and in the elderly. Inflammation, oxidative injury, altered myocyte metabolism, extracellular matrix remodeling and fibrosis initiate and perpetuate cardiac arrhythmias, especially atrial fibrillation. Enhanced myeloperoxidase (MPO) activity by infiltrating activated leukocytes could bind to myocardial cells and cause fibrosis resulting in the initiation and progression of arrhythmias. ⋯ EPA and DHA form precursors to anti-inflammatory lipid molecules: lipoxins, resolvins, protectins and maresins that are known to suppress inflammation, have anti-fibrotic actions and inhibit MPO activity. Hence, it is likely that leukocyte and/or myocardial deficiency of EPA and DHA and consequent reduced formation of lipoxins, resolvins, protectins and maresins enhance inflammation and MPO activity that leads to myocardial damage and fibrosis and initiation and progression of cardiac arrhythmias. Based on these evidences, I propose that lipoxins, resolvins and protectins function as endogenous anti-arrhythmic molecules and their stable synthetic analogs could be useful in the management of cardiac arrhythmias.
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Acute coagulopathy of trauma predicts a poor clinical outcome. Tissue trauma activates the sympathoadrenal system resulting in high circulating levels of catecholamines that influence hemostasis dose-dependently through immediate effects on the two major compartments of hemostasis, i.e., the circulating blood and the vascular endothelium. There appears to be a dose-dependency with regards to injury severity and the hemostatic response to trauma evaluated in whole blood by viscoelastic assays like thrombelastography (TEG), changing from normal to hypercoagulable, to hypocoagulable and finally hyperfibrinolytic in severely injured patients. ⋯ Given this, the rise in circulating catecholamines in trauma patients may favor a switch from hyper- to hypocoagulability in the blood to keep the progressively more procoagulant microvasculature open. The hypothesis delineated in the present paper thus infers that the state of the fluid phase, including its cellular elements, is a consequence of the degree of the tissue injury and importantly, critically related to the degree of endothelial damage, with a progressively more procoagulant endothelium inducing a gradient of increasing anticoagulation towards the fluid phase. The implications of this hypothesis may include targeted treatment strategies according to the degree of sympathoadrenal response as evaluated by whole blood viscoelastical hemostatic assays in trauma patients.
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Awareness under anaesthesia is an uncommon but serious phenomenon, which continues to occur despite the use of commercially available depth-of-anaesthesia (DOA) monitors. Many of these monitors use processed electroencephalographic (EEG) data to give an indication of anaesthetic depth. ⋯ I hypothesise that an audio signal derived from the raw EEG waveform could form the basis of a DOA monitor, enabling humans to directly determine whether a patient is awake or anaesthetised from sound alone. I propose to call the sounds derived from amplification of the EEG trace the 'audio EEG'.