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Brief Review: Mechanisms of Hyperbaric Bradycardia

高壓力性心律遲緩之機制

摘要


人類在高壓力狀況下不論是處於靜息或運動時均會表現心律遲緩之現象,根據已知的資料顯示引致高壓力性心律遲緩之機制有二:其一與高氧壓有關;另一則否。高氧壓可以引致心律遲緩已是不爭之事實,而與高氧壓無關,但可導致高壓力性心律遲緩的其他機制則不甚瞭解。在正常氧壓下,本文攷慮到二種可能引致高壓力性心律遲緩的原因:呼吸型態的改變與循環性條件反射之解除,我們認爲高氧壓是引發與維持高壓性心律遲緩最主要的因子,而呼吸型形態的改變是正常氧壓下造成心律遲緩之因子。

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並列摘要


Lin, Y. C. and K. K. Shida: Brief review: Mechanisms of hyperbaric bradycardia. Chinese J. Physiol. 31(1): 01-22, 1988. Relative bradycardias have been reported to occur in humans both at rest and during exercise under a variety of hyperbaric conditions. Review of existing data reveals that there are two major mechanisms operating: one depends on hyperoxia and the other does not. While it is clear that hyperoxia produces bradycardia b a variety of well understood mechanisms, the non-oxygen-dependent causes of hyperbaric bradycardia have not been defined. Experimental results from animals studies have eliminated the involvement of increased ambient pressure and gas density in the development of hyperbaric bradycardia, in all normoxic conditions. This review considers two other possibilities, the altered respiratory pattern which may modify the HR secondarily, and circulatory deconditioning under hyperbaric environments, which masks the hyperbaric bradycardia. We propose that the return of a normal sea level HR following the initial bradycardia represents, in effect, bradycardia which would be seen if cardiovascular deconditioning were not present. It is concluded that hyperoxia is the major factor responsible for initiating and maintaining hyperbaric bradycardia, whereas non-oxygen dependent hyperbaric factors may alter respiratory patterns and secondarily cause a reduction in HR.

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