Contrasting Effects of Lower Body Positive Pressure on Upper Airways Resistance and Partial Pressure of Carbon Dioxide in Men With HF and OSA or CSA
Editor's Note: Based on Kasai T, Motwani SS, Yumino D, Gabriel JM, Montemurro LT, Amirthalingam V, Floras JS, Bradley TD.Contrasting effects of lower body positive pressure on upper airways resistance and partial pressure of carbon dioxide in men with heart failure and obstructive or central sleep apnea.J Am Coll Cardiol 2013;61:1157-66.
Overnight rostral fluid shift may relate to severity of obstructive (OSA) or central sleep apnea (CSA) in men with HF. Rostral fluid displacement may facilitate OSA if it shifts into the neck and increases transpharyngeal resistance (Rph), because pharyngeal obstruction causes OSA. Rostral fluid displacement may also facilitate CSA if it shifts into the lungs and induces reflex augmentation of ventilation and reduces partial pressure of carbon dioxide (PCO2), because a decrease in PCO2 below the apnea threshold causes CSA. This study sought to test the effects of rostral fluid displacement from the legs on Rph, minute volume of ventilation (Vmin), and PCO2 in men with heart failure (HF) and either OSA or CSA.
Men with HF were divided into those with mainly OSA (obstructive-dominant, n =18) and those with mainly CSA (central-dominant, n = 10). While patients were supine, antishock trousers were deflated (control) or inflated for 15 minutes (lower body positive pressure [LBPP]) in random order. Within each group, two-way repeated-measures analysis of variance, followed by a post hoc analysis with Bonferroni correction for multiple comparisons, was used to compare values obtained during the baseline and either LBPP or control periods.
LBPP reduced leg fluid volume and increased neck circumference in both obstructive- and central-dominant groups. However, in contrast to the obstructive-dominant group in whom LBPP induced an increase in Rph, a decrease in Vmin, and an increase in PCO2, in the central-dominant group, LBPP induced a reduction in Rph, an increase in Vmin, and a reduction in PCO2.
These findings suggest mechanisms by which rostral fluid shift contributes to the pathogenesis of OSA and CSA in men with HF. Rostral fluid shift could facilitate OSA if it induces pharyngeal obstruction, but could also facilitate CSA if it augments ventilation and lowers PCO2.
Sleep apnea occurs in approximately 50% of patients with heart failure (HF), where it is associated with increased mortality.1-3 This mechanistic study provides several insights relevant to the pathogenesis of OSA and CSA in men with HF. In the obstructive-dominant group, application of LBPP, which displaced ~ 260 ml of fluid from the legs, increased neck circumference and induced a degree of upper airway obstruction, reflected by an increase in Rph. This was sufficient to reduce minute ventilation and increase transcutaneous partial pressure of carbon dioxide. In the central-dominant group, LBPP displaced a similar amount of fluid from the legs and resulted in an increase in neck circumference similar to that in the obstructive-dominant group. However, in contrast to the obstructive-dominant group, LBPP induced a reduction in Rph accompanied by an increase in minute ventilation. These changes were sufficient to reduce partial pressure of carbon dioxide by 1.4 mm Hg and a decrease of this magnitude can induce central apnea during sleep in HF patients.4,5
Several limitations of the study needs to be pointed out which includes conducting the study during wakefulness instead of during sleep, inclusion of only men, lack of assessment of differing chemosensitivity on the ventilatory and Rph responses to LBPP and inability to determine whether fluid movement into the lungs during LBPP was related to increased Vmin and reduced Rph in the central-dominant group.
Despite these limitations, the study provides evidence to suggest that nocturnal rostral fluid shift may contribute to the pathogenesis of both OSA and CSA in men with HF. The data suggest that in those in whom rostral fluid shift induces an increase in transpharyngeal resistance, susceptibility to OSA will increase, whereas in those in whom it induces an increase in respiratory drive with reductions in transpharyngeal resistance and PCO2, susceptibility to CSA will increase. The findings raise the possibility that prevention of fluid accumulation in the legs during the daytime or rostral fluid shift at night may alleviate OSA or CSA in some men with HF but additional research is needed to examine these possibilities fully. Further understanding of the complex interaction among the diverse, pathogenic mechanisms that lead to OSA or CSA may help with identification of those needing a targeted treatment and subsequent development of novel therapeutic strategies that could be tailored for the individual patient.)6
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- Naughton M., Benard D., Tam A., Rutherford R., Bradley T.D.; Role of hyperventilation in the pathogenesis of central sleep apneas in patients with congestive heart failure. Am Rev Respir Dis 1993;148:330-338.
- Xie A., Skatrud J.B., Puleo D.S., Rahko P.S., Dempsey J.A.; Apnea-hypopnea threshold for CO2 in patients with congestive heart failure. Am J Respir Crit Care Med 2002;165:1245-1250.
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Keywords: Airway Obstruction, Carbon Dioxide, Heart Failure, Sleep Apnea, Central, Sleep Apnea Syndromes
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