Format

Send to:

Choose Destination
See comment in PubMed Commons below
Arq Bras Cardiol. 2011 Feb;96(2):161-7. Epub 2011 Jan 7.

Behavior of central and peripheral chemoreflexes in heart failure.

[Article in English, Portuguese, Spanish]

Author information

  • 1Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, Rua Dr. Baeta Neves 98, Pinheiros São Paulo, SP, Brazil. gvguima@usp.br.

Abstract

The heart failure (HF) syndrome can be defined as the final pathway of any type of heart disease. The sympatho-inhibitory cardiovascular reflexes, such as the arterial baroreceptor reflex, are significantly decreased in HF. Patients with HF present higher ventilation for a certain workload when compared with normal individuals. This fact generates low ventilatory efficiency and is related to higher ventilation associated with the carbon dioxide production, which is a predictor of bad prognosis, in addition to being a limiting factor for the practice of exercises. There is evidence that the autonomic imbalance contributes to the pathogenesis and the progression of heart failure. The chemoreflexes are the main mechanisms of control and regulation of the ventilatory responses to the changes in concentrations of arterial oxygen and carbon dioxide. The chemoreflex activation causes an increase in the sympathetic activity, heart rate, arterial pressure and minute volume. However, the increase in the minute volume and the arterial pressure, due to negative feedback, cause inhibition of the sympathetic response at the chemoreflex activation. In spite of the functional alterations of the reflexes, their behavior in normal and pathological conditions, especially their contribution to the sympathoexcitatory state observed in HF has not been broadly studied. Therefore, this review aims at integrating the knowledge on central and peripheral chemoreflexes in HF syndrome, as well as clarifying the influence of the heart failure drug therapy on the chemoreflexes.

PMID:
21448511
[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Scientific Electronic Library Online
    Loading ...
    Write to the Help Desk