Abstract

Excessive augmentation of peripheral chemoreceptors`(PChR) activity is a well described and common phenomenon in congestive heart failure syndrome. It is related to exercise intolerance, arrhythmic events, periodic breathing and increased mortality. Recent studies also suggest its role in pathophysiology of resistant hypertension. Elevated sympathetic tone resulting from the excitation of brainstem nuclei by hyperactive PChR is believed to be responsible for the above ominous clinical consequences. Therefore, strategies targeting PChR (e.g. carotid bodies) seem particularly interesting especially in such high-risk populations. However, several issues require particular attention regarding potential interventions on PChR in heart failure and/or hypertensive patients. These caveats include: excessive lowering of sympathetic tone, problems with surgical / endovascular approach and decreased ventilatory drive. Moreover, the clinical predictors of favourable response to the therapeutic modulation of PChR are currently unknown. Additionally, it must be acknowledged that different types of PChR (i.e. carotid vs. aortic bodies) exert various hemodynamic and ventilatory responses. For example blood pressure response seems to be controlled mostly by carotid bodies, while heart rate response is believed to be mediated through aortic bodies. Another important clinical aspect of PChR physiology is the effect of dopamine – inotropic and vasoactive drug commonly used in critically ill patients. By blocking the release of neurotransmitters from PChR dopamine may lead to dangerous hypoxia and complicate the process of weaning from the ventilatory support. All the above issues will be discussed in detail in the context of most recent publications and speaker`s personal experience.

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